In my last post on Health Optimization, one commenter inadverntently brought up a topic which I find interesting, although it is highly contraversial—which is HIV/AIDS skepticism and rationality in science.
The particular part of that which I am interested in is proper levels of uncertainty and rationality errors in medical science.
I have some skepticism for the HIV/AIDS theory, perhaps on the level of say 20-30%. More concretely, I would roughly say I am only about 70% confident that HIV is the sole cause of AIDS, or 70% confident that the mainstream theory of HIV/AIDS is solid.
Most of that doubt comes from one particular flaw I in the current mainstream theory which I find particularly damning.
It is claimed that HIV is a sexually transmitted disease. However, the typical estimates of transmission rate are extremely low:
0.05% / 0.1% per insertive/receptive P/V sex act
0.065% / 0.5% per insertive/receptive P/A sex act
This data is from wikipedia—it lists a single paper as a source, but from what I recall this matches the official statistics from the CDC and what not.
For comparison, from the wikipedia entry on Gonorrhea, a conventional STD:
Men have a 20% risk of getting the infection from a single act of vaginal intercourse with a woman infected with gonorrhea. Women have a 60–80% risk of getting the infection from a single act of vaginal intercourse with a man infected with gonorrhea.[7]
So it would appear that HIV is roughly 100-500 times less sexually transmittable than a conventional STD like gonorrhea.
So in my mind this makes it technically impossible for HIV to be an STD. These transmission rates are so astronomically low that for it to spread from one infected person to an uninfected partner would take years and years of unprotected sex.
If you plug that it to a simulation, it just never can spread—even if everyone was having unprotected sex with a random stranger every single day, it would still require an unrealistic initial foothold in the population by other means before it could ever spread sexually.
And of course, if you plug in actual realistic data about frequency of unprotected sexual intercourse with strangers, it’s just completely impossible. Bogus. It doesn’t work. It can not be an STD.
As gonorrhea (and I presume other STDs) are hundreds of times more transmissable than HIV, their low rates in the population place bounds on HIV’s sexual transmission.
Finally, these rates of transmission are so low that one should question the uncertainty and issues with false positives—how accurate are these numbers really?
A few years ago, I entered an online discussion with some outspoken HIV-AIDS skeptics who supported the theories of Peter Duesberg, and in the course of that debate, I read quite a bit of literature on the subject. My ultimate conclusion was that the HIV-AIDS link has been established beyond reasonable doubt after all; the entire web of evidence just seems too strong. For a good overview, I recommend the articles on the topic published in the Science magazine in December 1994: http://www.sciencemag.org/feature/data/cohen/cohen.dtl
Regarding your concerns about transmission probabilities, in Western countries, AIDS as an STD has indeed never been more than a marginal phenomenon among the heterosexual population. (Just think of the striking fact that, to my knowledge, in the West there has never been a catastrophic AIDS epidemic among female prostitutes, and philandering rock stars who had sex with thousands of groupies in the eighties also managed to avoid it.) As much as it’s fashionable to speak of AIDS as an “equal opportunity” disease, it’s clear that the principal mechanism of its sexual transmission in the First World has been sex between men, because of both the level of promiscuity and the nature of the sexual acts involved. (And it may well be that HIV among heterosexuals would be even rarer if it weren’t constantly reintroduced into the heterosexual population via women having sex with bisexual men, let alone if the sexual transmissions from intravenous drug users were also absent.)
On the other hand, when it comes to African AIDS, it’s hard to say anything reliably. The public discussions of First World AIDS are full of nonsense, but at least there are enough reliable raw data to make some sense out of the situation; in the case of Africa, however, we don’t know anything beyond what we’re told from people with highly suspect interests in the matter, either careerist or ideological, and even if there are some truthful and reasonable voices in the whole mess, it’s impossible to filter them out in the sea of misinformation.
Quite interesting. I didn’t really know much about Medical Hypotheses until I posted a link in another thread (as a minor side point) to an article my dad wrote which happened to be in that very journal, and someone pointed out what it was. Strange connection.
A long while ago I found Duesberg’s papers and entered into some online debates taking his position. The end result of all that reading moved me into a position closer to yours, but more uncertain. I just went and re-read Duesberg’s most recent 2003 paper and noticed it still has a noticeable pull on me after reading it, but after going back and forth several times between the two camps I usually end up somewhere lost in the middle.
Duesberg, even though probably ill-fated in his main quest, has I believe shown that the orthodox establishment has gone wrong at least in part. The history of the whole affair seems like it should be a lesson that we should learn from, a lesson that somehow results in learning and moving towards a more rational scientific establishment, more cleanly divorced from politics. That may be an interesting discussion to have here, if it hasn’t already been discussed much. Deusberg suggests a jury process to replace the current peer-review system, which he is highly critical of. That could be an interesting rationalist angle on this.
So in my mind this makes it technically impossible for HIV to be an STD.
To say that this makes it not an STD is to misunderstand what an STD is.
An STD is not a disease whose transmission method is specialised to the act of copulation. It is merely a disease which is so difficult to transmit at all that only the most intimate of contact has any substantial chance of doing so. What is important about the sexual contact is not the sex, but the blood contact.
In HIV we have something that is so difficult to transmit that even conventional heterosexual intercourse has difficulty. Closer blood contact is required for a high chance of transmission, such as in anal intercourse (the intestinal lining is fragile and not adapted to contact with foreign bodies) or injection from infected needles. This has been known practically since the start from the epidemiology, before any pathogen was identified.
I’m not in quite agreement with both of your points. Yes of course HIV is transmissable only through blood, but I don’t agree with that being a good criteria for use of the term “sexually transmitted”, especially when other STD’s such as gonorrhea are actually effective—they are measurably hundreds of times more sexually transmissable than HIV. This is probably due to both evolved mechanisms that those STDs have (such as ulceration formation) and overall low virality and transmissability of HIV.
So it is ingenous I think to change the categorization. HIV is clearly at an extremum, and perhaps would be better classified as a weakly transmissable blood borne disease, not an STD.
The evolutionary relevance is important here. How did this evolve?
However, the typical estimates of transmission rate are extremely low: 0.05% / 0.1% per insertive/receptive P/V sex act 0.065% / 0.5% per insertive/receptive P/A sex act
These transmission rates are so astronomically low that for it to spread from one infected person to an uninfected partner would take years and years of unprotected sex.
At an (unrealistically?) independent 0.5% chance per act, a 50% chance of transmission would require 139 sex acts — hardly “years and years”.
(ETA: yes, unrealistically, according to this abstractfound by Perplexed: “However, in comparison with nonparametric estimates, the model assuming constant infectivity appears to seriously underestimate the risk after very few contacts and to seriously overestimate the risk associated with a large number of contacts. Our results suggest that the association between the number of unprotected sexual contacts and the probability of infection is weak and highly inconsistent with constant per-contact infectivity.”)
So in my mind this makes it technically impossible for HIV to be an STD.
At best, this can show that pandemic AIDS can’t primarily result from sexual transmission of HIV, which is evidence that AIDS has causes other than HIV, but also that pandemic AIDS spreads through other means (as suggested here, e.g.).
As gonorrhea (and I presume other STDs) are hundreds of times more transmissable than HIV, their low rates in the population place bounds on HIV’s sexual transmission.
If you’re thinking of rates in the modern developed world, STDs are unsurprisingly more common when and where treatment is less available:
...in New York City, serologic testing in 1901 indicated that 5%-19% of all men had syphilitic infections. (source)
Studies of pregnant women in Africa have found rates for gonorrhea ranging from 0.02% in Gabon to 3.1% in Central African Republic and 7.8% in South Africa.… [syphilis] rates of 17.4% in Cameroon, 8.4% in South Africa, 6.7% in Central African Republic and 2.5% in Burkina Faso.… (source)
However, the typical estimates of transmission rate are extremely low: 0.05% / 0.1% per insertive/receptive P/V sex act 0.065% / 0.5% per insertive/receptive P/A sex act
At an (unrealistically?) independent 0.5% chance per act, a 50% chance of transmission would require 139 sex acts — hardly “years and years”.
That is for the highest transmission activity—receptive A, so be careful not to cherry pick. Yes − 139 unprotected sex acts. It would take 1390 unprotected insertive A sex acts to reach a 50% chance of transmission.
So with some assumptions, mainly—gay bathouses and no condom use—yes the virus could spread horizontally, in theory. Although that population would necessarily first acquire every other STD known to man, more or less.
But in the general heterosexual population, not a chance. If you compare to the odds of pregnancy from unprotected sex, the insane requisite amounts of unprotected sex with strangers would result in a massive baby epidemic and far more vertical transmissions long before it could ever spread horizontally in the hetero population.
I don’t know why you mention “modern developed-world rates” and then have a link to 1901 NY and Africa . . .
So in my mind this makes it technically impossible for HIV to be an STD.
At best, this can show that pandemic AIDS can’t primarily result from sexual transmission of HIV, which is evidence that AIDS has causes other than HIV, but also that pandemic AIDS spreads through other means (as suggested here.
You don’t need the “at best” qualifier, but yes I agree that is what this shows. Showing that however opens a crack in the entire facade. Perhaps not a critical failure, but a significant doubt nonetheless.
If the orthodox position had updated on the evidence, and instead changed their claim to “HIV is a borderline infectious disease that spreads primarily through the prenatal and blood-borne routes”, then I would give them more creedence. Of course, for political reasons alone they could never admit that.
Funny to think of pregnancy as curable, but yes of course that’s true. However, it doesn’t really change the numbers much.
Also, from what I have read about the early 80′s bathouse scene, it is possible that many of those guys did acquire every STD known to man, so at least in that case the sexual transmission route could work even with such terribly low efficiency.
Regardless, it seems strange to label it as a STD from an evolutionary perspective, it doesn’t fit that profile, and it seems incredibly unlikely it could have evolved as such.
Essentially the government committed to a public awareness campaign that HIV was ‘rapidly growing’ in the heterosexual community, and this became part of the dogma. It is politically motivated—it’s anti-sex message appeases religious conservatives while also shifting attention away from the gay bathouse scene, so it sort of benefits everyone politically, regardless of whether it’s actually true.
At an (unrealistically?) independent 0.5% chance per act, a 50% chance of transmission would require 139 sex acts — hardly “years and years”.
I don’t see why epidemiology should care about the 50% threshold. The relevant number is the expected number of transmissions per year. Thus independence is irrelevant.[1] At 200 anal tops per year per infected person, incidence should double yearly. And every top requires a bottom, so that’s 400 anal sex acts per year for just doubling. It seemed to spread more quickly than that, but maybe 800 and 4x per year works. It seems just barely plausible with this transmission rate. I’m not sure of the details of bathhouses, but I thought that there was a lot of non-anal sex, too.
[1] independence is relevant if 70s gays were systematically different from the people in the study; and they probably were, eg, they probably had higher rates of STDs
And every top requires a bottom, so that’s 400 anal sex acts per year for just doubling. It seemed to spread more quickly than that, but maybe 800 and 4x per year works.
It took 8 years (until August 1989) for the first 100,000 cases to be reported; the second 100,000 were reported in just 2 years (by November 1991). The half million total was passed in October of 1995.
This seems to indicate a doubling time of about 2 years.
ETA: Also according to that page, the patient with the first confirmed HIV infection died of AIDS in 1968, so the growth rate of AIDS before 1989 was at most 1.73x per year.
OK, maybe doubling works. But it’s important to distinguish different populations. You should expect it to spread faster through the bathhouse scene than through the rest of the gay community than through the straight community. So it should slow down once it exhausted the bathhouse regulars (something like weekly visits) or when AIDS shut down that scene. If that happened around 1985 and there’s a 10 year incubation period, then the 1995 numbers still include bathhouse effects. Diagnoses were increasing at 3x or 4x in the early 80s: 100 in fall ’81 to 250 in mid ‘82 to 1000 in early ‘83 to 3000 by the end of the year. From ‘83 to ’89 it was merely doubling and it slowed after that. Of course, there are problems with diagnosis numbers early in an epidemic, but death followed quickly, in weird ways, so these numbers are probably good enough. Yes, there were people with AIDS in 60s, but that 1.73x includes time to get to the bathhouse scene.
One problem with this simplified model is assuming every sexual act is with a new partner, which would only be true in the very early stages.
I think your analysis is on the right track though, and it seems barely plausible with this transmission rate, assuming negligible condom use and an intense bathhouse scene. However, in standard theory HIV progresses to AIDS in about 10 years, so this sets a timer which starts removing vectors from the population.
Thus the exact exponent matters considerably. If incidence can only double every year, then after 10 years you get 2^10 ~ 1000 cases.
If incidence doubles every 6 months (quadruples every year), then you get a million cases after ten years.
If you consider that all other STD’s would infect this population before HIV, then one has to wonder how that would effect condom use, and how that changes the model.
So do you find the transmission rate and make the model before you decide that HIV was an STD which spread this way, or after?
One problem with this simplified model is assuming every sexual act is with a new partner, which would only be true in the very early stages.
It assumes that every sexual act is with an uninfected partner. Perhaps that’s what you meant, but then I wouldn’t have used “very.”
If you consider that all other STD’s would infect this population before HIV, then one has to wonder how that would effect condom use, and how that changes the model.
I think this is pretty well documented. STDs were routine and not a big deal (treatable!) in the 70s gay scene. Thus they did not cause condom use.
I’d point out that nobody is claiming that HIV is exclusively sexually transmitted; there are other methods of transmitting it, such as infected needles. Also, Wikipedia cites a paper suggesting that those rates you mentioned are “4 to 10 times higher in low-income countries” and as high as 1.7% for anal intercourse.
I don’t know whether or not these facts are sufficient to address your fundamental complaint, but they would make a pretty big difference.
I have some skepticism for the HIV/AIDS theory, perhaps on the level of say 20-30%.
It takes courage to voice a low but not negligible degree of doubt in a emotionally salient mainstream position. I would expect it to result in almost as much social punishment as in the case of outright denial. (Emotional backlash isn’t good at math.)
More concretely, I would roughly say I am only about 70% confident that HIV is the sole cause of AIDS, or 70% confident that the mainstream theory of HIV/AIDS is solid.
I am surprised that those two confidences happen to be the same. Is it not a distinct possibility that HIV is, in fact, the sole cause of AIDS even when the mainstream theory is itself rubbish? (For example, if the theory got important details such as mechanism completely wrong.)
I tend to think of “HIV being the sole cause of AIDS” as the central tenet of the mainstream theory, but sure that could be true even if much of the details are wrong. Actually, I think many within the mainstream would admit most of the details are wrong—last I checked all the important details, such as how the retrovirus could come active after many years and damage T-cells and what not are all still hot research items.
And most of the specific results have been failures—no vaccine yet, just some drugs with a bunch of side effects which may or may not even improve mortality, etc etc.
I find hypotheses in the middle more likely overall—examples: that HIV is a mostly harmless retrovirus but in some people with (X, Y, Z cofactors) it can cause immune damage.
And I yes, I am at least mildly concerned about taking an HIV skeptic position in a public internet forum—and just thinking about the reasons for that causes me to slightly update to be more skeptical.
Note that in general low-transmission rates aren’t that good an argument against it. First of all, a lot of transmission in the US occurred through other forms, especially early in the epidemic (intravenous needle sharing and transfusion of infected blood being two major ones). As others have noted the transmission issue is also generally higher for homosexual rather than heterosexual intercourse.
Frankly, the thing that I most don’t understand about people who are skeptical about the HIV-AIDS link is how one explains the fact that anti-virals tailored to deal with HIV work. Even the first-gen treatments such as AZT were used due to the biochemistry of HIV (often targeting reverse transcriptase). And they worked in delaying the onset of AIDS and worked for giving people with AIDS higher life-expectancy. I don’t see how one can easily reconcile that with HIV not being the cause of AIDS and I’ve never heard anything remotely resembling a coherent explanation about this.
The extremely low official transmission rates indicate that HIV is probably not a sexually transmitted disease, as typically understood. According to the published transmission data, it’s only effective natural means of transmission is vertical—from mother to child. From what we know about symbiosis and parasites, this should lead one to suspect it is not that lethal.
However that doesn’t destroy the hypothesis that HIV could be a unique disease of civilization—a mutation of a formerly limited retrovirus into a more damaging form that spreads horizontally only through extremely unnatural novelties of the modern world—needle sharing and epic promiscuity in some subgroups. It does of course make the overall hypothesis more complex and overall less likely, but it doesn’t destroy it outright.
Frankly, the thing that I most don’t understand about people who are skeptical about the HIV-AIDS link is how one explains the fact that anti-virals tailored to deal with HIV work.
This is very difficult to prove ethically, and certainly hasn’t been shown to satisfaction. Consider how immensely difficult it has been to understand the real health effects of fat in the diet, for example. In the 80′s and 90′s, we thought it was oh so simple. Today we (the wise) realize how profoundly ignorant we were then, and still are today. I think part of the rational reappraisal for the strength of the HIV hypothesis should come from a similar update.
In other words one can only cling to a high degree of certainty about the HIV hypothesis when one is profoundly ignorant concerning the depth of one’s ignorance about the complexity of human health.
Even the first-gen treatments such as AZT were used due to the biochemistry of HIV (often targeting reverse transcriptase).
That’s the theory.
And they worked in delaying the onset of AIDS and worked for giving people with AIDS higher life-expectancy.
Ahh the world would be so simple if that was true. The AZT clinic trial was ended prematurely and double-blindness could not be maintained due to side effects. The skeptics claim that later studies show that AZT increases long term mortality, not the other way around.
I don’t see how one can easily reconcile that with HIV not being the cause of AIDS and I’ve never heard anything remotely resembling a coherent explanation about this.
You need to realize how impossible it would be to concretely show what you presume to high certainty. You would basically need a double blind study with two control groups, one receiving plazebo, and compare total mortality. One immediate problem is any noticeable side effects would immediately end the blindness—and the retrovirals certainly have side effects.
And even showing that AZT or drug X reduces mortality in HIV+ patients does not lead to the conclusion that HIV is the cause, or that AZT or drug X has any effect on HIV. Supplementing patients with vitamin D, or changing their diet, or feeding them aspirin, or any number of other changes could also decrease mortality, but have nothing to do with the viral theory.
This is very difficult to prove ethically, and certainly hasn’t been shown to satisfaction.
Ahh the world would be so simple if that was true. The AZT clinic trial was ended prematurely and was generally bogus. The skeptics claim that studies show that AZT increases mortality, not the other way around.
So I don’t know what evidence you have for these claims. The original AZT study can be found here. It handled placebos just fine.
And AZT is just one example of many anti-retrovirals. 3TC and ABC have also been used. Moreover, there are studies which show that the the standard drug cocktails work better than AZT or 3TC alone. That makes sense for the standard model of HIV as the cause of AIDS.
And even showing that AZT or drug X reduces mortality in HIV+ patients does not lead to the conclusion that HIV is the cause, or the AZT or drug X has any effect on HIV. Supplementing patients with vitamin D, or changing their diet, or feeding them aspirin, or any number of other changes could also decrease mortality, but have nothing to do with the viral theory.
There seems to be an issue here involving what level of evidence is necessary. From a Bayesian stand point you can’t ever “show” anything in the sense that you want. But the overall pattern of evidence can still give you a probability close to 1 that HIV is the primary cause of AIDS.
Notice that it has serious toxicity side effects, including bone marrow supression, and thus it can massively damage the innate immune system.
This is evident in the abstract itself:
We conducted a double-blind, placebo-controlled trial of oral azidothymidine (AZT) in 282 patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex. Although significant clinical benefit was documented (N Engl J Med 1987; 317:185-91), serious adverse reactions, particularly bone marrow suppression, were observed. Nausea, myalgia, insomnia, and severe headaches were reported more frequently by recipients of AZT; macrocytosis developed within weeks in most of the AZT group. Anemia with hemoglobin levels below 7.5 g per deciliter developed in 24 percent of AZT recipients and 4 percent of placebo recipients (P less than 0.001). Twenty-one percent of AZT recipients and 4 percent of placebo recipients required multiple red-cell transfusions (P less than 0.001). Neutropenia (less than 500 cells per cubic millimeter) occurred in 16 percent of AZT recipients, as compared with 2 percent of placebo recipients (P less than 0.001).
The original AZT study could not possibly be placebo controlled, due to the high toxicity—this is basically chemotherapy. Now chemotherapy can be effective, but it can not be double blind.
Furthermore, due to high toxicity, only a fraction of patients actually completed the intended trial:
The subjects were stratified according to numbers of T cells with CD4 surface markers and were randomly assigned to receive either 250 mg of AZT or placebo by mouth every four hours for a total of 24 weeks. One hundred forty-five subjects received AZT, and 137 received placebo. When the study was terminated, 27 subjects had completed 24 weeks of the study, 152 had completed 16 weeks, and the remainder had completed at least 8 weeks
Only 27 out of 245 AZT subjects completed the full 24 weeks! One in the AZT group of 245 died in this period, but how many more in the AZT group would have died if they had been able to complete the full 24 week chemotherapy trial?
These were crazy times. These patients were very ill and very worried. It was a full scale terror panic. It was obvious who was on placebo and who wasn’t, and from what I have read, placebo patients were swapping and trading pills with AZT patients who couldn’t finish. It was many things, but not double-blind.
There seems to be an issue here involving what level of evidence is necessary.
Here is what would be required to prove with > 99% certainty that HIV is the sole cause of AIDS:
Take a random sample of perfectly healthy test subjects. Now inject half of them with HIV and half with a placebo, and follow their health over the long term. That is about the only test that could get you 99% accuracy, and it is obviously not ethical.
So, instead we have to make due with what we have.
And again, showing that AZT improves long-term mortality—which the AZT trial clearly did not show, only shows that AZT improves mortality in sick AIDS patients. It doesn’t tell you much else about HIV as a theory.
It’s important that we agree on that subpoint—for it has nothing to do with the level of evidence.
There are many, many things that could improve mortality in sick AIDS patients. Stoss therapy, better diet, more sex, aspirin, etc etc. Do you think that proving a mortality decrease correlation in any of these categories would ‘prove’ they are the true cause of AIDS?
Moreover, there are studies which show that the the standard drug cocktails work better than AZT or 3TC alone. That makes sense for the standard model of HIV as the cause of AIDS.
It also makes sense for the common sense model that reducing AZT doses down from outright lethal to mildly poisonous but tolerable ‘works better’.
Take a random sample of perfectly healthy test subjects. Now inject half of them with HIV and half with a placebo, and follow their health over the long term. That is about the only test that could get you 99% accuracy, and it is obviously not ethical.
There have been documented cases of accidental HIV infection of lab workers and dental patients that are not too terribly far from such a controlled experiment. See: S.J. O’Brien and J.J. Goedert, “HIV causes AIDS: Koch’s postulates fulfilled,” Current Opinion in Immunology, Vol. 8, Issue 5, October 1996, pp. 613-618.
The article (listed as a “guest editorial”, I note for completeness) has the following citations in the relevant section:
52. Weiss SH, Goedert JJ, Gartner S, Popovic M, Waters D, Markham P, Veronese FD, Gall MH, Barkley WE, Gibbons J et al.: Risk of human immunodeflciency virus (HIV-1) infection among laboratory workers.Science 1988, 239:68-71.
53. Reitz MS Jr, Hall L, Robert-Guroff M, Lautenberger J, Hahn BH, Shaw GM, Kong LI, Weiss SH, Waters D, Gallo RC, Blattner W: Viral variability and serum antibody response in a laboratory worker infected with HIV-1 (HTLV-IIIB).AIDS Res Hum Retroviruses 1994, 10:1143-1155.
54. Guo HG, Waters D, Hall L, Louie A, Popovic M, Blattner W, Streicher H, Gallo RC, Chermann JC, Reitz MS: Nucleotide sequence analysis of the original isolate of HIV-1.Nature 1991, 349:745-746.
55. Wain-Hobson S, Vartanian JP, Henry M, Chenciner N, Cheynier R, Delassus S, Martins LP, Sala M, Nugeyre MT, Guetard D et al.: LAV revisited: origins of the early HIV-t isolates from Institut Pasteur.Science 1991, 252:961-965.
56. Wolinsky SM, Wike CM, Korber BTM, Hutto C, Parks WP, Rosenblum LL, Kunstman KJ, Furtado MR, Munoz JL: Selective transmission of human immunodeficiency virus type-1 variants from mothers to infants.Science 1992, 255:1134-1137.
57. Morbidity Mortality Weekly Report of the Center for Disease Control: Revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults (1993). 1992:1-19.
I’m not a skeptic, but I am a bit surprised that three infected lab workers is considered evidence worth mentioning. I’m accustomed to seeing clinical studies with fewer than 100 patients treated as merely suggestive, and several hundred or even thousands of patients necessary to convince regulatory authorities that there is a real phenomenon. So when I read that “three laboratory workers...became infected”, it strikes me as anecdotal. Of course you take what you can get, but still, it seems a small group.
My experience is with pharmaceuticals, which could explain the difference. But still, there’s a difference to be explained.
On the upside, if three is worth mentioning, then maybe one is worth mentioning, which would mean that Seth Roberts’s self-experimentation may be worthwhile.
Ok, so I have finished reading O’Brien and JJ Goedert. I think the accidental lab worker cases probably have low utility in distinguishing between pathologic HIV and passenger HIV theories, but the animal SIV studies potentially fulfill the ideal experiment design. If animals injected with pure close SIV analogs to HIV develop AIDS-like illness, that is about as good as evidence as one could hope for.
For the lab worker infections, they say that the genomes are close to the clonal strain used in the lab, but they don’t have a good probalistic model for this:
The sequence divergence
between LW virus envelope genes and clonal HTLV-IIIB
is <3%, which is the same genetic distance from LAV-LAI
to HTLV-IIIB, viral strains now agreed by all to have
been derived from a single patient [54,55]. This low
level of sequence divergence is equivalent to the variation
observed between HIV-infected infants and their mothers,
and threefold less than the extent of variation of HIV
between unconnected patients [56].
threefold more or less variation doesn’t sound like much to me, and regardless even assuming they did all get infected via the lab, it doesn’t mention treatment, so we don’t know if they were treated with AZT or what.
I think the animal models are more interesting—as all the drug cofounding variables are eliminated and everything is controlled.
The authors discuss 3 animal models—baboons, some wierd knockout mice with human t-cell graphs, and finally SIV injected into rhesus monkeys. They spend the most time discussing the latter paper so I looked into it.
“Induction of AIDS in Rhesus Monkeys by Molecularly Cloned Simian Immunodeficiency”.
In short, all 5 of the monkeys injected later become seropositive, and 50% of them progress to AIDs-like illnesses and die. Presumably some are naturally resistant.
There is a potential issue to this otherwise smoking gun, which is that it appears they had to inject whole culture of T-cells, as the virus can not be isolated directly into plasmid vectors:
We, and others, have experienced considerable considerable difficulty in subcloning the full-length proviral DNA into plasmid vectors.
SIV mac239-cloned DNA was transfected into primary macaque PBLs and into Hut 78 cells (a human CD4+ T cell line) by a DEAE-dexxtran procedure, and stock virus was frozen for subsequent animal inoculations
But if all they had then was provirus integrated into PBL ( peripheral blood lymphocytes ), then one must wonder about the risk of graft versus host disease, and transfusion reaction in general. Basically, the foreign T-cell line can actively invade and cause all kinds of havoc. Perhaps they have controlled for that and I’m completely off, but I don’t see where they mention it.
OBrien and Goodart conclude:
Control macaques inoculated with
saline, with inactivated SIVMAcA239 or with SIVMACA239
carrying mutations/deletions in the nef gene failed to
induce AIDS in the same macaque species [80,83,84].
Because SIV strains cause AIDS in monkeys and because
they are the closest phylogenetic relatives of HIV, they
provide an animal model fulfillment of Koch’s transmission
I haven’t seen mention of ‘inactivated’ sivmaca239 yet in 80, but maybe it is in 83 or 84. However, if they are forced to infect live T-cells because they can’t produce viable clonal plasmid, this seems to have a major confounding factor in graft vs host disease. I’d like to find a knowledge skeptic take on this—perhaps Duesberg confronts it, not sure yet.
If he doesn’t confront it, then that doesn’t look so good for his position.
It appears to me that you are noting different weaknesses, different alternative explanations of the results, in each experimental protocol. I imagine that could appear to happen if there were a strong publication bias for results in favor of the hypothesis (e.g. with medicinal prayer studies), but that has not been demonstrated.
From what I understand, there is strong reason to suspect such bias in the animal models, as many other animal tests were conducted previously attempting to show SIV causing AIDS, and they uniformly failed. From what I have read, the SIV injections failed to do anything in chimps. We don’t know how many other rhesus monkeys were injected, but I find it highly unlikely that the five in this study (3 out of 5 of which developed immune defeciency) were the first.
That bias is interesting and it would be useful to have a metastudy covering all the animals that have been injected, but of course most naturally occuring strains of species specific virus should be expected to be harmless. So the ‘bias’ doesn’t really tell you much and is expected either way.
I’ll look to see if there is any skeptic review of the SIV injections which did succeed, because in my mind that is fairly strong evidence. If HIV analogs cause AIDS-like illness in primates when they hop species or traditional barriers, this is a good experiemental model for HIV crossing over into humans and causing illness, and is far stronger in my mind than the murky epidimelogical data with all of it’s drug cofactor issues.
The lab monkeys are in a controlled environment—we know they weren’t using drugs, weren’t fed AZT, etc etc.
Yes, but were they treated with chemotherapy agents such as AZT which cause bone marrow and immune supression? (I am asking before I read the article)
For the controlled experiment example, it would have to be double blind the entire time. Nobody would ever know who got placebo and who didnt’, and no difference in treatment regimens either way—all on the same diet, same lifestyle, etc etc. I highly doubt the accidental cases fit that profile.
Yes, but were they treated with chemotherapy agents such as AZT which cause bone marrow and immune supression?
From what I see, O’Brien and Goedert don’t report about this. However, Cohen’s Science article to which I linked above provides more details about the cases of infected lab workers, claiming that two of them didn’t receive any antivirals until the progress of AIDS was well underway: http://www.sciencemag.org/feature/data/cohen/266-5191-1647a.pdf
I have seen that, but I don’t take it as strong evidence of anything either way.
Clearly HIV antibodies are correlated with ill-health, poor immune function and low CD4 counts—that was established in the very beginning by Gallo et all and is the entire basis of their original claim.
But the competing hypothesis is not the null hypothesis, the competing hypothesis is that the HIV presence is a marker of some severe immune function failure, and that HIV itself is a largely harmless vertically transmitted retrovirus—like all the others. If it does become active, it is because something is already seriously wrong.
So of course if you have a lab, and you are testing lab-workers deathly afraid of contracting HIV, in either theory some may come up HIV+, and in either theory those that test positive will be ill.
This is very different than the intentional infection test you need to establish strong causation along a koch’s postulate principle. I think one of the stronger flaws in current HIV theory is the chimpanzee models—they have many HIV similar retroviruses (SIV’s), they are common in wild chimps, are all vertically transmitted, and don’t appear to be problematic for chimps. If HIV killed chimps outright, the mainstream theory would have some more ammo.
Instead the theory is that HIV came from a chimp SIV and somehow became lethal and horizontally transmissable at the same time in humans. But from the studies of sexual transmission—it is only weakly blood transmissable. So overall, it’s alot to swallow. I think it is plausible that this happened and HIV causes novel problems in humans, but it certainly has not been well demonstrated, mainly because HIV doesn’t cause specific symptoms and it is extremely difficult to properly dissociate other causitive factors. As Duesberg notes, the cocaine/meth craze boomed in the 80′s right as the AIDS epidemic started—they overlap perfectly.
Deusberg’s theory is that drugs specifically are a major cause of the immunosupression, which I think has some absolute validity, but we should also notice that there are other causes, and some people just have poor immune health, and this has been the case for long before HIV came on the scene.
I think one of the stronger flaws in current HIV theory is the chimpanzee models—they have many HIV similar retroviruses (SIV’s), they are common in wild chimps, are all vertically transmitted, and don’t appear to be problematic for chimps. If HIV killed chimps outright, the mainstream theory would have some more ammo.
I think that, in general, viruses that jump species barriers are more lethal in their new hosts than their old ones. Selection pressure tends to make viruses that are transmitted from individual to individual less dangerous over time, not more, because a dead host can’t spread the virus. So the fact that chimps tolerate SIV better than humans tolerate HIV isn’t a strike against the “HIV is mutated SIV” theory.
Also, there exists a more direct counterexample: FIV, feline immunodeficiency virus, is an HIV-like virus that is commonly found in lions. It doesn’t harm lions very much, but it’s lethal to domestic cats, which haven’t co-evolved with the virus the way lions have. (Specifically, lions compensate for the loss of T-cells to the virus by producing them in much larger numbers than other animals do.)
Perhaps not all viruses that jump species barriers are more lethal, but we care most about the lethal ones for sure, and lethality or host damage is a side effect of high replication, so yes I agree with your analysis.
I also said:
I think it is plausible that this happened and HIV causes novel problems in humans, but it certainly has not been well demonstrated, mainly because HIV doesn’t cause specific symptoms and it is extremely difficult to properly dissociate other causitive factors.
I’m reading the OBrien Goddert response now that cites some animal studis showing how some animal HIV analogs do fulfill koch’s postulate now. I am reading into the sources, but I wasn’t aware overall that they had found animal HIV analogs that caused AIDS like symptoms. I’ll have to update towards the ‘HIV is more pathogenic’ stance if this all checks out.
But the competing hypothesis is not the null hypothesis, the competing hypothesis is that the HIV presence is a marker of some severe immune function failure, and that HIV itself is a largely harmless vertically transmitted retrovirus—like all the others. If it does become active, it is because something is already seriously wrong. So of course if you have a lab, and you are testing lab-workers deathly afraid of contracting HIV, in either theory some may come up HIV+, and in either theory those that test positive will be ill.
According to O’Brien and Goedert, however, the strains of HIV found in these accidentally infected individuals were effectively identical to those from the source of their accidental infection, showing much less difference than is usual for strains taken from two random patients. This looks like powerful evidence against the competing hypothesis. On the other hand, it seems like there have been disputes about the validity of these identification procedures, and Duesberg and other skeptics raised some specific objections to them back then. However, this gets into technical issues that I’m definitely not competent to judge on.
(I should add that I haven’t delved into the references provided by O’Brien and Goedert, which Robin has conveniently listed in his above comment, to see if their summary of the facts is accurate and complete.)
Also, while we are looking at evidence for one side or the other, I should present some of the recent evidence that supports the Deusberg hypothesis, namely that cocaine use can cause HIV progression and AIDS-defining illness. Heavy cocaine use and HIV+ status are extremely correlated, the question is one then of causation.
Just search for “cocaine cd4 counts”|
From a rat study linked here
We noted a 200- to 300-fold increase in HIV RNA copy numbers in the peripheral blood obtained from cocaine-treated, HIV-infected animals when compared with HIV-infected controlsExposure to cocaine alone did not affect the implantation of PBL, suggesting a specific interaction between cocaine and HIV. This report describes a model for evaluating HIV cofactors and supports cocaine’s role in the development and progression of AIDS.
Even more interesting—an abstract from a more recent study showing that crack cocaine can cause AIDS independently (in women at least)
CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women.
I was under the impression that there was only 2 HIV strains, and only HIV-1 is of concern in the west, but I’m no expert on this.
Do you have the O’Brien/Goedert paper link or any of this discussion? Your earlier link was just an editorial summary. Sounds interesting, I’d like to read more into it. (i am going to search now, but if you have the link . . .)
If O’Brien and Goedert are right, it would depend on how many strains there are and what their prevalence is ahead of time—I think Bayes’ Theorem would apply, no? Also, I guess we just have to presume that no other sick people from the sample were not reported. And finally, the sample size of 1 or 2 raises some theoretical issues, but still it would be interesting.
I was under the impression that there was only 2 HIV strains, and only HIV-1 is of concern in the west, but I’m no expert on this.
No. There are two major HIV strains, HIV-1 and HIV-2, with the vast majority of infections in the US being HIV-1. However, there are many substrains of both. In general, since HIV has a high mutation rate, there are individual genetic markers for different people. No one who has HIV for more than a few weeks has a single form of HIV in them but already will have a population of slightly distinct forms. This is part of what makes HIV so pesky for the immune system, for developing vaccines, and for developing drugs to combat it. Note that this isn’t that rare. For example, influenza does something similar although my impression is that this is not nearly as extreme an example.
Frankly, this is a very basic aspect of HIV biology, which you could find on any primer on the subject. If one doesn’t know about this, this suggests major gaps in one’s knowledge base about HIV and I’m not at all sure that one who doesn’t know about this has enough background to discuss issues related to whether HIV causes AIDS.
and I’m not at all sure that one who doesn’t know about this has enough background to discuss issues related to whether HIV causes AIDS.
Because he said “2 HIV strains” rather than “2 major HIV strains with many substrains”? He should be disqualified from participating in debate on a topic because he failed to use sufficiently precise language on a point not relevant to the current discussion?
I’m a non-partisan on this issue, having not researched it enough to have a firm opinion… but the consistent use of these kinds of dark side debate tactics by one side makes me seriously tempted to update in the opposite direction.
the strains of HIV found in these accidentally infected individuals were effectively identical to those from the source of their accidental infection, showing much less difference than is usual for strains taken from two random patients.
It seemed pretty clear from context that Vlad was talking about substrains. If there’s anything that went wrong here, judging from Jacob’s followup remark, it was an illusion of transparency failure on my part in that Vlad’s meaning seemed clear to me, and I then made the (erroneous) conclusion that someone with a basic background would also get what Vlad was talking about.
Note incidentally, that using heuristics about whether or not someone has enough background to understand or discuss something is not intrinsically a dark side issue to start with. Indeed, sometimes it is very necessary. See for example some of the discussion on cousin it’s recent post where it seemed that some individuals (well, primarily one individual) were making repeated subtle but highly relevant errors about certain ideas related to Godel’s theorems and Turing machines. After repeated attempts to explain, the mathematicians in the thread (including myself) started trying to explain that the errors in question were basic enough that further attempts to explain would likely be fruitless. That’s not a dark side tactic, sometimes that’s just true.
Note incidentally, that using heuristics about whether or not someone has enough background to understand or discuss something is not intrinsically a dark side issue to start with
Yes, I absolutely agree. But that’s not the tactic I was referring to. The tactic in question consists of finding some nitpicky objection to something your opponent said, something not directly relevant to the issue at hand, and something which isn’t even wrong, just insufficiently precise, and discounting the substance of their argument on that basis.
The tactic in question consists of finding some nitpicky objection to something your opponent said, something not directly relevant to the issue at hand, and something which isn’t even wrong, just insufficiently precise, and discounting the substance of their argument on that basis.
Hrrm? Imprecision if anything occurred on Vlad’s part, not Jacob’s. Again, see issue of illusion of transparency matter. See also Vlad’s remark below.
It seemed pretty clear from context that Vlad was talking about substrains.
Yes, of course. I’m not familiar with the finer points of terminology in this area, but the O’Brien-Goedert paper uses the term “strain” both for the two major strains and their sub-strains, and I’ve noticed the same in many other papers too. So I don’t think this was imprecise in any way.
Vlad originally used the word ‘strains’, not substrains, and I have only ever heard ‘strains’ used in reference to HIV1 and HIV2 as you say. But yes I am at least somewhat aware of sub-strains through protein coding variation in viruses in general, and how mutations lead to new epidemics.
I’m not sure what the proper ‘background’ is just to discuss an issue, but I probably don’t have it, regardless.
(I initially posted an excerpt from the paper in this comment, but in the meantime, I found an ungated version. The stuff about the accidental transmissions is on page 615.)
Do you have the O’Brien/Goedert paper link or any of this discussion? Your earlier link was just an editorial summary. Sounds interesting, I’d like to read more into it. (i am going to search now, but if you have the link . . .)
The article cited here? I downloaded a copy if anyone wants to PM me an email address.
For the controlled experiment example, it would have to be double blind the entire time. Nobody would ever know who got placebo and who didnt’, and no difference in treatment regimens either way—all on the same diet, same lifestyle, etc etc. I highly doubt the accidental cases fit that profile.
If you want absolute certainty, you need to fulfill koch’s postulates, which is the medical disease variant of experimental physics, and is well grounded.
So yes, in questions of science, we do demand specific evidence for near-certain proof, but naturally when that is not possible for whatever reason, we can still update based on other evidence and reach well grounded conclusions.
First of all, you never have absolute certainty. Proof is for math and alcohol. You may also want to read the Sequences relevant to Bayesian reasoning especially about how 0 and 1 are not probabilities.
Note also that even outside a Bayesian context, Koch’s postulates are a rough framework. For example, sometimes there is great difficulty growing an organism in a culture (Koch’s second postulate requires this), and sometimes only a fraction of a population may be symptomatic. Even Koch was willing to treat the first postulate as a guideline rather than a hard and fast rule; he worked with multiple examples of microorganisms that showed up in some healthy people but didn’t cause disease In fact we know now that this very common. Many causes of minor infections, such as staph, are present on everyone. It then takes some problem, such a wound, or disruption of the immune system to cause the person to become unhealthy. For viral examples, look at asymptomatic herpes or HPV.
Frankly, referring to Koch’s postulates like this are one of the things that makes many people with medical knowledge not take the HIV-AIDS skeptics very seriously. As a general heuristic, cranks like to take old ideas and try to use them to argue against some modern result even when that idea isn’t used in the current form or isn’t as absolute as they make it out to be. This seems for example to occur frequently with creationists who use an oversimplified form of Mendelian genetics that seems to date prior to the work of Hardy, Weinberg, and Fisher. As a way of preventing this signal, referring to such things as Koch’s work can be done, but you need to be clear that you understand the limitations it has. Otherwise, it just sets off alarm bells.
As a general heuristic, cranks like to take old ideas and try to use them to argue against some modern result even when that idea isn’t used in the current form or isn’t as absolute as they make it out to be.
Note also that even outside a Bayesian context, Koch’s postulates are a rough framework. For example, sometimes there is great difficulty growing an organism in a culture (Koch’s second postulate requires this), and sometimes only a fraction of a population may be symptomatic.
It is also difficult to empirically test elements of String Theory or evolutionary history. This difficulty isn’t taken to be evidence for against those theories. Lack of easy clear cut empirical tests is just that—lack of a simple theorem discriminator. I am not claiming that it is some magic pass required for any theory to be credible.
On the other hand, nor can one use lack of said simple theorem discriminator to get a free pass and somehow claim to have extra certainty—that most come from evidence regardless.
However, in this case I do think that the general idea of Koch’s postulate is highly relevant, it is not ‘cranky’ to invoke it, and in fact it is probably the single strongest piece of evidence for the mainstream position—as Vlad M pointed out to me.
I am currently reading:
”
HIV causes AIDS: Koch’s postulates fulfilled”
Guest editorial
Stephen .I O’Brien* and .lames ,i Goederff
It reviews SIV models where SIV can be prepared and injected into monkeys and in some cases does cause AIDS like disease progression (usually more quickly than HIV).
So I don’t think your associations between “referring to Koch’s postulates” and cranks, and your general heuristic are valid at all, not when the mainstream is listing this as a centerpiece of evidence.
I haven’t read the editorial yet, but I’m not sure where the notion that this was a centerpiece of evidence comes from. I was vaguely aware of this result but never have paid it much attention. I suspect that if one talked to active AIDS and HIV researchers they’d say that there was a very strong case even without this. But yes, conservation of expected evidence does come into play here, so you have a valid point. In any event, the upshot that Koch’s postulates are not seen as any sort of absolute is very much relevant.
S.J. O’Brien and J.J. Goedert (1996) (the paper cited by Vladimir_M) specifically references Koch’s postulates. The accidental infection of laboratory workers is only one of five items cited in reference to (I believe) #3, “The cultured microorganism should cause disease when introduced into a healthy organism.”
Ever since I’ve read in Guinea Pig Zero about test subjects who feel that they’ll never be able to afford medical care and cheat on the requirements of an experiment (for example, not following dietary changes they’ve signed on for), I’ve been that little bit more dubious about drug studies.
Have you seen these two recentmeta-analysis of HIV transmission rates? Comparing them to your numbers, it seems that Wikipedia/CDC have greatly understated the risk for P/A sex acts (due to using older studies?).
Also, according to this page, the transmission rates for genital herpes are similar to HIV for P/V sex acts, so AIDS is not the only STD to have such low transmission rates.
it would still require an unrealistic initial foothold in the population by other means before it could ever spread sexually
I think the conventional theory is that HIV established an initial foothold by means such as needle sharing, blood transfusions, and P/A sex acts. That seems quite realistic to me. Why do you think it’s unrealistic?
No I haven’t seen them until now. I haven’t really been looking into or thinking about this until just recently.
I originally quoted the wikipedia data, which several us tracked down and analyzed in another thread (it comes from the CDC and originally from a single medium-ish European study which I think did a fairly good job to control for factors such as condom use and what not given the complexities):
It is claimed that HIV is a sexually transmitted disease. However, the typical estimates of transmission rate are extremely low: 0.05% / 0.1% per insertive/receptive P/V sex act 0.065% / 0.5% per insertive/receptive P/A sex act
Let’s compare to the 1st meta-analysis:
it finds 0.04/0.08% for insertive/receptive P/V sex in the 1st world, very similar but slightly lower to the older CDC study (from europe). They find the rates are around 5 times higher in the 3rd world.
For P/A receptive, they find a pooled per-act rate of 1.7%, about 3.5 times higher than the 1st world CDC study. I suspect this is simply because they pooled 1st and 3rd world data together.
This does not show that Wikipedia/CDC have “greatly understated” the risk for P/A sex acts—this data is in agreement. The variance is between 1st and 3rd world studies. The 1st world data is of paramount concern for the historical origin theory of the disease. The 3rd world data is a side point—not historically important and suspect in general, as in fact mentioned in the abstract.
The abstract:
We did a systematic review and meta-analysis of observational studies of the risk of HIV-1 transmission per heterosexual contact. 43 publications comprising 25 different study populations were identified. Pooled female-to-male (0·04% per act [95% CI 0·01—0·14]) and male-to-female (0·08% per act [95% CI 0·06—0·11]) transmission estimates in high-income countries indicated a low risk of infection in the absence of antiretrovirals. Low-income country female-to-male (0·38% per act [95% CI 0·13—1·10]) and male-to-female (0·30% per act [95% CI 0·14—0·63]) estimates in the absence of commercial sex exposure (CSE) were higher. In meta-regression analysis, the infectivity across estimates in the absence of CSE was significantly associated with sex, setting, the interaction between setting and sex, and antenatal HIV prevalence. The pooled receptive anal intercourse estimate was much higher (1·7% per act [95% CI 0·3—8·9]). Estimates for the early and late phases of HIV infection were 9·2 (95% CI 4·5—18·8) and 7·3 (95% CI 4·5—11·9) times larger, respectively, than for the asymptomatic phase. After adjusting for CSE, presence or history of genital ulcers in either couple member increased per-act infectivity 5·3 (95% CI 1·4—19·5) times versus no sexually transmitted infection. Study estimates among non-circumcised men were at least twice those among circumcised men. Low-income country estimates were more heterogeneous than high-income country estimates, which indicates poorer study quality, greater heterogeneity of risk factors, or under-reporting of high-risk behaviour. Efforts are needed to better understand these differences and to quantify infectivity in low-income countries.
So this supports the original CDC data for the 1st world.
The second meta-study finds a receptive A per act rate of 1.4%, a little lower than the 1st study, and about 2.8 times the 1st world CDC data. They make no mention of what countries, and I assume it mixes 3rd and 1st world data—it is a large meta-analysis of many studies.
There is also some serious wierdness in the 2nd study:
Per-partner combined URAI–UIAI summary estimates, which adjusted for additional exposures other than AI with a ‘main’ partner [7.9% (95% CI 1.2–14.5)], were lower than crude (unadjusted) estimates [48.1% (95% CI 35.3–60.8)].
Our modelling demonstrated that it would require unreasonably low numbers of AI HIV exposures per partnership to reconcile the summary per-act and per-partner estimates, suggesting considerable variability in AI infectiousness between and within partnerships over time.
So something doesn’t fit—the per act and per partner numbers don’t square up at all. Somewhere else someone posted an abstract with a similar result, how basically your chance of infection levels off quickly in couples and is much lower than you think—you are either going to get it or not irregardless of number of sex acts. This suggests that there are some major unknown immunity factors at work or the entire model is wrong.
I think the conventional theory is that HIV established an initial foothold by means such as needle sharing, blood transfusions, and P/A sex acts. That seems quite realistic to me. Why do you think it’s unrealistic?
I think the needle sharing and blood transfusions is far more credible, but the 0.5% ish per act of receptive A in the 1st world could possibly support a sexual vector in the gay bathouse scene, but it is debatable.
The conventional theory requires that HIV came over as a mutated form of harmless simian SIV and spread here, through a single source vector from what I recall. Blood donation might make more sense, but one would have to look at the epidemiological models for that.
Perhaps vulnerability to transmission is partially dependent on prior immune health. That would predict faster spread where health-in-general is worst, ie Africa, as observed, and also explain the discrepancy between prevalence and observed traqnsmission rates. I also recall reading an article about a widely afflicted demographic in the US (a particular subset of gays in a particular city—I don’t recall which one), which suggested that they had already weakened their immune systems with drugs and sleep deprivation.
The other possibilities are that the transmission rate you quoted is wrong for some reason, or that the sexual transmission aspect has been overstated, and most transmission is through reused needles and other blood-borne vectors.
Note that spreading the idea that the transmission rate of AIDS is low has negative utility, regardless of whether it’s true or not, since it would encourage dangerous behavior.
Note that spreading the idea that the transmission rate of AIDS is low has negative utility, regardless of whether it’s true or not, since it would encourage dangerous behavior.
This is untrue. Consider a similar claim: “spreading the idea that very few passengers on planes are killed by terrorists has negative utility, regardless of whether it is true or not, since it would encourage dangerous behavior.”
Informing people of the true risks of any activity will not in general have negative utility. If you believe a particular case is an exception you need to explain in detail why you believe this to be so.
In the case of infectious diseases, there are large unpriced negative externalities involved. Everyone doing what is individually rational, given true beliefs about transmission rates, is likely not socially optimal, because the expected individual cost of a risky action is less than the expected social cost. Giving people false beliefs about transmission rates can improve social welfare by shifting the expected individual cost closer to the expected social cost.
Are you talking about free rider problems with health care costs under a partly or fully socialized health care system or something else? STDs seem to be less of a problem than more easily transmitted diseases like flu for most negative externalities I can think of.
Are you talking about free rider problems with health care costs under a partly or fully socialized health care system or something else?
And also, if you take some risky action that increases your chances of get infected, that also increases the chances of everyone else getting infected (causally, via yourself getting infected and then infecting others).
STDs seem to be less of a problem than more easily transmitted diseases like flu for most negative externalities I can think of.
I’m not sure I get your point here. Whether it’s more or less of a problem doesn’t seem relevant to the original claim that spawned this subthread.
I’m not sure I get your point here. Whether it’s more or less of a problem doesn’t seem relevant to the original claim that spawned this subthread.
It’s relevant to using your negative externality argument to support the original claim. To be consistent you would have to argue that we should make even more effort to avoid spreading the idea that airborne diseases like flu have low transmission rates (if true) than the idea that STDs have low transmission rates. Are you advocating a general policy of deliberately misleading people about the risks of various activities in an effort to correct for negative externalities? I’m pretty sure more efficient and robust approaches could be found.
It would be consistent with Wei Dai’s claim just to argue that we should make an effort to not reveal how low the transmission rate of influenza is among people who don’t wash their hands; we know that hand-washing is a large factor in transmission, but actual transmission rate numbers are still low enough to fail to convince people to wash their hands.
From a brief study of those particular numbers (I worked on a team modeling the spread of H1N1), I feel like we already mislead the public about the numbers themselves by being truthful as to the societal benefits and somewhat optimistic about the individual benefits of hand washing. If you believe more robust methods are more efficient, by all means, advocate for them, but I’m reasonably happy with the current situation.
From another perspective, blood-borne pathogens are particularly worth focusing on because they are easier to control. If we could encourage the entire population of the world to behave safely (not reuse needles, use condoms for sex, etc.), it would be a fairly minor change for individuals, but could eradicate or nearly eliminate HIV over time. With the flu, safe behavior will limit the damage of seasonal infections, but it’s not realistic to actually eliminate the virus. Thus, over the long term, I think the negative externalities of HIV might outweigh those of influenza.
I’m pretty sure more efficient and robust approaches could be found.
I think government policy makers and public health authorities already use a variety of approaches to reduce negative externalities related to infectious diseases, including subtle misinformation, such as making efforts to correct people’s beliefs about transmission rates when they are too low, but not when they are too high (anything really obvious wouldn’t work in a free society like ours). But it seems clear that large negative externalities still exist. What other approaches do you have in mind, and why haven’t they thought of it already?
I think we’re starting from quite different assumptions about how society works. I don’t believe that government policy makers or public health authorities are very rational. Even to the extent that they are rational, I don’t believe that their incentives are such as to reliably lead them to decisions that maximize utility by the kind of utilitarian calculus you seem to be assuming. So to the extent that we agree negative externalities exist (and I suspect we differ a fair bit on what they are and to what extent they exist) I have very little expectation that government policy makers or public health authorities will tend to take actions that minimize them.
What did you mean when you said “I’m pretty sure more efficient and robust approaches could be found”? You’re not offering any concrete ideas yourself, and apparently you weren’t thinking of government health authorities when you wrote that, so who is supposed to find and apply these approaches?
Think ‘market based’. Internalize negative externalities. To a first approximation this usually means reducing government involvement rather than increasing it. This is straying into politics though so maybe we should avoid further discussion of this topic.
Compared to the rest of this open thread, I don’t think you have anything to worry about!
Seriously though, I think we’d both like to hear you elaborate upon your market-based idea. I don’t think I got any useful information out of your blurb.
Let me first clarify the points I was making in this thread (which were not intended to lead to a debate about healthcare or politics in general). If you still feel we have substantive disagreements that we might be able to resolve through more explicitly political discussion I’m willing to continue the conversation unless there are strong objections from others.
First my points were not intended to imply any particular opinion on AIDS transmission rates specifically. My initial post was simply intended to point out that the utility of spreading the idea that AIDS transmission rates are low is dependent on the truth of the claim.
This was intended to be a more general point that exaggerating the risks of any particular activity is not a good general policy. In the AIDS case there are genuine costs to taking precautions against transmission, even if they are in fact greatly outweighed by the benefits. In a hypothetical world where transmission rates are negligible, maintaining that they are high would have negative utility.
Wei Dai responded by claiming that because of negative externalities associated with infectious diseases, exaggerating the transmission rate can improve social welfare. Now this is not incompatible with my original point, it is rather a claim of a mechanism by which exaggerating the risks of an activity can have positive utility. It is probably worth noting at this point that I am not a utilitarian so I am likely to disagree with utilitarians on what outcomes have positive utility but we can probably agree that in general internalizing negative externalities is a good thing.
I concede that it is possible in theory to imagine a situation where deliberately exaggerating risks has positive utility. The fun thing about negative externalities though is that it is very easy for an intelligent person to think of some and to propose plausible mechanisms by which any given action can be justified. I could easily argue for example that the credibility of science and scientists is undermined when they are caught making false claims and that the negative utility resulting from this outweighs any positive utility from individual acts of well intentioned deception.
Ultimately though I have what you might call a deontological normative belief about science that it should always pursue the truth and leave the task of judging when to strategically lie to others. I also suspect that this is a winning strategy for agents with imperfect powers of prediction but that is mere supposition.
Regardless, if negative externalities associated with infectious diseases are the real concern I’m pretty confident that you’d start with much higher expected value actions than lying about the facts in an effort to influence individual choices. If individuals are not bearing the full costs of their actions then there are more direct ways of changing their incentives such that the costs are better reflected than trying to influence their beliefs away from the truth by spreading false facts. This is the point at which I’d start to get into the politics of healthcare however and I don’t particularly want to do that here.
My initial post was simply intended to point out that the utility of spreading the idea that AIDS transmission rates are low is dependent on the truth of the claim.
Agreed. I think Wei Dai and I also agree (without speaking for Wei Dai), but think that the idea transmission rate to spread is conceivably a function of the true transmission rate, rather than locked to the true transmission rate itself. It sounds like you agree with that too, but are a little more stringent with what makes that “conceivably” true.
I concede that it is possible in theory to imagine a situation where deliberately exaggerating risks has positive utility.
To my mind, one such situation is one where a super-majority of the population don’t understand probability, and 1% effectively means “never” to those people. In this case, specifically lying about the number is less helpful than phrasing it alternate true ways, but because they don’t understand probability, if you asked them to estimate a probability based on the true facts you just gave, they might say 10%; I might consider them deceived, even if you weren’t doing anything that would deceive a rational agent.
Ultimately though I have what you might call a deontological normative belief about science that it should always pursue the truth and leave the task of judging when to strategically lie to others. I also suspect that this is a winning strategy for agents with imperfect powers of prediction but that is mere supposition.
This is a good point, much like Ends Don’t Justify Means (Among Humans). One small caveat I’d like to make is that I don’t think we are talking about science (or more accurately) scientists lying to the populace. I think what we are discussing are administrators, media outlets and policy makers that are informed of the numbers (it would probably be too generous to say informed of the science) choosing not to widely disseminate them in favor of reporting non-numerical information that might lead the populace to adopt an inaccurate belief about those numbers.
If individuals are not bearing the full costs of their actions then there are more direct ways of changing their incentives such that the costs are better reflected than trying to influence their beliefs away from the truth …
Yes. Please elaborate, this seems to be the most interesting part of the conversation, and the way you’re conversing now, I don’t see why you’re worried about a backlash. It would probably be wise to be as general as possible and not make any specific reference to a given countries system of healthcare (if that’s where you’re going), but if you have a real point I’d really like to hear it.
… by spreading false facts.
Again, I wasn’t purely speaking about false facts, more about choosing which true facts to announce, and in what way to achieve the desired impact. One doesn’t have to lie to manipulate, and it’s generally not the best strategy. I’m also not claiming that manipulation should be a primary goal, but selective revelation of data (which will always happen because of time and attention constants) is bound to be manipulative, even if accidentally, and it would be better to produce desired action than undesired action, so we should be aware of the manipulative potential of what we plan to say.
Ok, we’ve had two examples of negative externalities associated with infectious diseases. I brought up the free-rider / moral hazard problem of the costs of treating the disease not being fully born by an individual who engages in high risk activities. Wei Dai brought up the problem of an individual who gets infected as a result of high risk activities increasing the risks of others getting infected by increasing the incidence of the disease.
Now if negative externalities are your true concern then you should address them as directly as possible. There are a variety of a variety of possible solutions to addressing negative externalities. Note that lying about the actual damage caused is not a standard solution.
The moral hazard / free-rider problem is a general problem that affects healthcare as it is organized in most developed nations. A significant number of people consider this a feature rather than a bug however. If you actually wanted to internalize these negative externalities the most direct way would be to allow insurers (or the government, though that would be less efficient) to set their healthcare premiums on the basis of any relevant health or lifestyle information.
While this happens to some extent (smokers or the obese may pay extra under various systems for example) it would be controversial in others (charging homosexuals higher premiums if they were at greater risk of contracting STDs for example). It would likely be even more controversial for conditions that are not generally perceived as due to bad personal choices (as smoking related illnesses or obesity are by many and homosexuality is by some on the Christian right). The suggestion that insurance companies might charge higher premiums based on genetic testing is widely regarded as unreasonable for example and I’m sure the same would apply if premiums for a government run system were so determined. Why such discrimination is considered outrageous for healthcare but is routine in some other areas of life is left as an exercise for the reader.
As to the problem of an infected individual increasing the risk of others getting infected, criminalization, civil tort law and pigovian taxes are all possible approaches to internalizing the externalities. My point that STDs present less of a problem in this regard than airborne infectious diseases like flu was that the parties put at risk are generally more able to control the risks themselves (easier to limit your exposure to STDs than to the flu) and that the source of the infection is generally easier to identify (most people have a much shorter list of candidates for infecting them with an STD than with the flu). There are fairly significant practical difficulties to prosecuting individuals who get infected with the flu and then spread it, to suing someone who has so infected you or to targeting taxes at those who put themselves at high risk of flu infection. All of these are practical to some degree with STDs.
Fundamentally my point is that if negative externalities related to infectious diseases are the real problem you are concerned about, there are standard ways of internalizing negative externalities that could be applied. Trying to justify misleading the general public about the actual risks of certain activities and the actual benefits of certain precautions on the basis of negative externalities raises the question of why you are not focusing your efforts on these other more direct and efficient means of internalizing those negative externalities.
Thank you very much for your reply. I really did want you to specify more clearly what you were talking about. It seems obvious to me (now) that anyone following your line of thought would have understood what you were talking about from your earlier comments, but I didn’t, and I hope you can forgive me for not understanding without further clarification.
As an aside, smoking has an obvious externality in second-hand smoke, which is often directly regulated by outlawing smoking in certain areas. What are the negative externalities of obesity? If we are to believe some recent studies, fat people may make the people around them fatter, which is a non-obvious externality, but does obesity have any commonly-recognized effects on people other than the obese when not considering subsidized healthcare, or is it only considered to have that externality when healthy-weight individuals are contributing to the costs of obese individuals?
to suing someone who has so infected you
This is at least possible with in some places regarding HIV, as well as pursuing criminal charges (examples).
Even more off topic, but on topic with the much more inflamed discussion in the adjacent thread, while looking for that reference I found this. I was thinking at first that a man infecting 13 women would be in contradiction with the extremely low transmission numbers for HIV. Here are what my numbers look like: with (2006 estimates—I couldn’t find number for late 1990′s) 8e5 HIV+ men in the US, a 50-50 chance that one of them would infect 13 women requires that they each engage in an average of 2845 acts with a 0.08% tx rate (unprotected P/V), 762 0.3% tx rate acts (low-income P/V) or a mere 139 acts with 1.7% tx rate (unprotected P/A). The probabilities get much more complicated when dividing demographics, but while those are unrealistically high numbers, they aren’t off by an order of magnitude; at least, the low-income P/V figure probably isn’t. Actually pulling any information off that data point, given that it is singular and unreliable is stupid, but if it were too be believed we should expect that HIV has a true aggregate transmission rate closer to 0.45%, given reasonable assumptions about average frequency of intercourse. Of course that aggregate can easily be composed by a few high-risk activities and lots and lots of low risk activities.
EDIT: I got so distracted I forgot what the main point was
Trying to justify misleading the general public about the actual risks of certain activities and the actual benefits of certain precautions on the basis of negative externalities raises the question of why you are not focusing your efforts on these other more direct and efficient means of internalizing those negative externalities.
I point out only your use of the word “efficient”. Misleading people is so easy it’s almost impossible not to do it, so the cost / benefit ratio doesn’t have to be very high to make it an efficient activity. As far as effectiveness, I agree that other, more direct measures can be much better.
As I mentioned earlier, negative externalities are easy to dream up. Many people consider it legitimate to complain about negative externalities caused by ugly buildings (such as power plants, wind farms or architecture that doesn’t fit with its surroundings) but complaining about the aesthetic negative externalities associated with unattractive people in public places is not generally considered legitimate.
In practice in democratic society these issues are generally resolved by who can shout the loudest or wield most political influence and not by any direct rational accounting of costs. It is not clear for example that the relatively small risks associated with second hand smoke justify trampling on the rights of smokers to indulge outside of their own homes, especially given that smoking is already subject to large Pigovian taxes in most countries with such bans.
Misleading people is so easy it’s almost impossible not to do it, so the cost / benefit ratio doesn’t have to be very high to make it an efficient activity.
It should at least be positive. It is not clear that it is in practice. It seems plausible to me that the general public distrust of government advice on risk that underlies phenomena like anti-vaccination movements is a direct result of an ongoing pattern of deliberately misleading people about risks. Overall I don’t see a strong reason to suppose the net effect is beneficial.
It seems plausible to me that the general public distrust of government advice on risk that underlies phenomena like anti-vaccination movements is a direct result of an ongoing pattern of deliberately misleading people about risks.
Best point brought up yet. While to some extent I think that mistrust of authority is indefatigable, increasing the risk of that is probably much more costly.
How do you feel about the specific example I mentioned, where the true risk of transmission of something is 1%, but the media outlet or whatever decides to omit the number and instead say something like “over the course of a week, an individual can spread disease X to over a hundred people”, and while true, that convinces individuals that the specific risk is much higher than 1%?
I personally find it a little irritating when the media omits information that would be necessary to work out actual risk numbers for myself. I don’t object if they communicate the numbers in a way designed to have maximum impact on the typical human mind (it’s been suggested that using frequencies rather than probabilities may help for example) but I do object if they leave out crucial information required to figure out true risk estimates. Of course I don’t generally assume this is some grand conspiracy but rather reflective of the innumeracy of the media in general.
I don’t believe in grand conspiracies because they just require too many contingencies. All this discussion, from my perspective, is about the potential for a tacit agreement between most (not all) of those disseminating information in various ways that the best method of talking about public risks is not necessarily to directly discuss low numbers associated with them.
As I indicated earlier, I think that this agreement effectively already exists regarding influenza, and probably also HIV and other infections as well.
To be consistent you would have to argue that we should make even more effort to avoid spreading the idea that airborne diseases like flu have low transmission rates (if true) than the idea that STDs have low transmission rates. Are you advocating a general policy of deliberately misleading people about the risks of various activities in an effort to correct for negative externalities?
Strictly speaking, Wei never claimed anything about what we should do. (Even if everything he said is correct — and it seems obviously so to me — it’s plausible that we’re best off with a policy of authorities never lying about risks, due to unintended consequences, public trust, slippery slopes, &c.)
I think you’re on to something, but wouldn’t that cause officials to overstate transmission rates rather than understate them?
What is especially strange to me is that the government pushed a fear campaign for HIV and promoted as a dangerous STD for the mainstream hetero community, but neglected to double-check their official statistics, which rather clearly destroy the STD theory. Perhaps it’s just an honest mistake, but I don’t think so. From what I have read, they have spent time trying to get honest statistics. So they overpromoted the STD message, regardless of the actual statistics.
Regardless of what HIV actually does or is, public campaigns to reduce needle sharing and reduce unprotected sex are probably net public goods.
However, on the other hand, if AIDS is really caused by drug toxicity, then at least some people are actively being harmed by spending energy in the wrong protections.
But I agree with your central point, and it applies to vaccines especially—they don’t really have much of an individual benefit, but if enough people can be convinced to vaccinate, the entire epidemic can be curtailed or completely avoided.
That needs some clarification. Most people cannot distguish between a risk being somewhat low, and it being extremely low, so we need to be careful about the transition from numbers to qualitative divisions. The risks of being killed in a plane crash are so low that unless you’re a pilot, you should ignore them; and overestimating the risks of flying would cause too much driving, which is more dangerous. In the case of AIDS, the probability of transmission may be “low”, but none of the numbers given are so low that they would justify skipping any of the common safety precautions, so we shouldn’t describe the probabilities involved as low in the presence of people who can’t do the utility computations themselves.
So as an addendum to this, I found this blog which I am now reading as it has an updated view from the HIV skeptic position. Here is a post analyzing a recent study showing that cocaine can cause AIDS
CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women
The 1st commenter had an inside view which I thought was especially interesting:
This certainly supports my eyewitness accounts of back in 1987 when several friends and acquaintances consciously or subconsciously decided that an HIV positive diagnosis surely meant death in 2 to 5 years, which led them onto severe crack and cocaine binges up until they were finally put on AZT monotherapy. Sad to say what the results were. Now they’re all part of the statistics. Can I say self-fulfilling prophecy?
Cocaine is a drug that a) can damage the immune system and b) reduce appetite. It isn’t at all unreasonable that HIV positive individuals who were heavy cocaine users would therefore progress to full AIDS faster than others. Note also that a 2-5 timespan isn’t that far off from the timespan one would expect from HIV infection to emergence of AIDS given no treatment. Note that the study authors don’t seem to think that this is at all unusual and nowhere do they claim that the use of crack cocaine was somehow causing AIDS.
Sure, but it makes it more difficult to dissociate what the cocaine and virus are doing independent of each other, ie it makes it difficult to tease out the cause and effect from the correlation.
Well not quite, because cocaine was causing AIDs-like symptoms before HIV was presumed to be around, even if the great rise of cocaine use in the 80′s in the west happens to correspond exactly with the rise of AIDS.
the great rise of cocaine use in the 80′s in the west happens to correspond exactly with the rise of AIDS
What’s your source for this? Looking at the cocaine statistics and AIDS statistics myself, I’m not seeing this correspondence. What I do see is that cocaine use dropped to a fraction of its peak level by 1990, while AIDS kept rising.
Just go down to the graph in your first link and look at the emergency room drug mentions and see the cocaine serge—it does indeed correspond to the AIDS epidemic. Deusberg’s 2003 paper has more on this, but it’s in the data you linked. From the emergency room data it looks like cocaine use was still growing up to 2001, but my point was with the rise. AIDS peaked in the mid 90′s from your data link.
I have some skepticism for the HIV/AIDS theory, perhaps on the level of say 20-30%. More concretely, I would roughly say I am only about 70% confident that HIV is the sole cause of AIDS,
This much at least is something that should be relatively easy to confirm to a reasonable level of satisfaction. It would seem to require only a microscope, as syringe and a sufficient sample of people with AIDS. Has anybody ever founds someone with AIDS who did not have HIV? If not is that because nobody has bothered to take a close look? If so then I would certainly support your questioning of the standard of research supporting the mainstream position.
Has anybody ever founds someone with AIDS who did not have HIV?
According to skeptics, yes, in all but name. The standard skeptical argument is that AIDS, as it is currently defined, includes HIV+ as a necessary diagnostic criterion, and that this is a circular definition: if someone presents with all the symptoms of AIDS, but tests HIV-, then they are defined to not have AIDS. This means that 100% of diagnosed AIDS patients will be HIV+, just by definition, not due to a meaningful correlation.
It would seem to require only a microscope, as syringe and a sufficient sample of people with AIDS
The skeptical position here is that you can’t actually see a virus with an optical microscope (which I believe is true), and “HIV tests” are actually just testing for HIV antibodies (or substances alleged to be HIV antibodies), not HIV itself.
I’m not endorsing these positions, just passing them along, btw.
I have some skepticism for the HIV/AIDS theory, perhaps on the level of say 20-30%. More concretely, I would roughly say I am only about 70% confident that HIV is the sole cause of AIDS,
This is something that should be relatively easy to confirm to a reasonable level of satisfaction. It would seem to require only a microscope, as syringe and a sufficient sample of people with AIDS. Has anybody ever founds someone with AIDS who did not have HIV?
Yes, unless one defines AIDS as a collection of symptoms plus HIV. I forget the name, but any definition of AIDS which does not include HIV has some HIV-.
Now on the other hand, AIDS is a syndrome of immune supression, not a disease, so there of course could be other things that cause a similar syndrome.
If not is that because nobody has bothered to take a close look? If so then I would certainly support your questioning of the standard of research supporting the mainstream position.
If you are interested in venturing down that rabbit hole, read a little Duesberg:
(warning: reading his papers may result in general increased skepticism about the medical establishment)
Now on the other hand, AIDS is a syndrome of immune supression, not a disease, so there of course could be other things that cause a similar syndrome.
Now that is a familiar mistake—and a negligence that does real damage. I’m more familiar with the mental side of the medical establishment so have seen, for example, ADD symptoms lumped together and medicated presuming there is only one distinct etiology. Looking at a brain scan could tell them the difference easily enough.
(warning: reading his papers may result in general increased skepticism about the medical establishment)
That would be surprising—purely because my existing skepticism is already significant. All the more so after I spent some time involved in medical research myself. Scary stuff. “Hang on, wait. you want me to do what with the data?”
it’s just completely impossible. Bogus. It doesn’t work. It can not be an STD.
I find denialism in all forms simply fascinating. I wonder if you could indulge my curiosity.
You find your arguments completely convincing. Yet they are based on publicly available statistics and rather obvious and common-sense kinds of reasonings. So, I have to wonder, what do you think is wrong with the cognitive apparatus of all those medical and research professionals who believe that HIV == AIDS and is an STD?
Why don’t they reach the same conclusions as you? Are they stupid? Just haven’t thought of the train of thinking you use? What are your guess as to where they are all going wrong? Why none of them has realized the simple truth and shared it with colleagues?
Incidentally, I have a hypothesis as to what is wrong with your reasoning, which I will share on request, but I really want to understand how you reconcile your own certainty with the opposing certainty of people who (on paper) seem far better qualified on this subject.
I find denialism in all forms simply fascinating. I wonder if you could indulge my curiosity.
I will indulge your curiosity in a moment, but I’m curious why you use the politically loaded term “denialism”.
As far as I can tell, it’s sole purpose is to derail rational dicussion by associating one’s opponent with a morally perverse stance—specially invoking the association of Holocaust Denialism. Politics is the mind-killer. In regards to that, I have just been spectating your thread with Vladimir M, and I concur wholeheartedly with his well-written related post.
There is no rational use of that appelation, so please desist from that entire mode of thought.
So, I have to wonder, what do you think is wrong with the cognitive apparatus of all those medical and research professionals who believe that HIV == AIDS and is an STD?
Firstly, I don’t think nearly as many quality researchers believe HIV == AIDS as you claim, at least not internally. The theory has gone well past the level of political mindkill and into the territory of an instituitionalied religion, where skeptics and detractors are publically shamed as evil people. I hope we can avoid that here. Actually, I think most intelligent researchers, if they could afford to be honest, would admit that HIV is the major indirect causitive factor, but this is not the same as saying HIV == AIDS. Likewise, I think most would admit that HIV is not quite an STD, not really at all.
Finally, even though I just said what I think is “wrong [with] the cognitive apparatus of all those medical and research professionals”, namely that it is more an issue of politically charged public positions; I should also point out that even by the standard of your implied criteria—which seems to consist of counting up scientists for or against, it is even less clear that HIV == AIDS can be supported on that criteria. (which I do not favor as a rational criteria regardless). There are a large number of skeptics on public record for that hypothesis even considering the huge social stigma associated with adopting such a position in public. The HIV==AIDS hypothesis has far more skeptics on record than String Theory, for comparison.
But regardless, counting scientists is not a good rational criteria.
If you want to get into a discussion about rationality and reasoning in highly politicized issues such as this, that is an interesting side topic. But otherwise don’t stoop to the moral high ground of politicized orthodoxy—just provide your hypothesis.
I find denialism in all forms simply fascinating. I wonder if you could indulge my curiosity.
I will indulge your curiosity in a moment, but I’m curious why you use the politically loaded term “denialism”.
As far as I can tell, it’s sole purpose is to derail rational dicussion by associating one’s opponent with a morally perverse stance—specially invoking the association of Holocaust Denialism.
The wikipedia article on HIV that you reference has a section entitled “AIDS Denialism”.
But now that you mention it, why do you consider Holocaust denialism morally perverse? I thought that questioning PC conventional wisdom was considered a Good Thing here.
If you want to get into a discussion about rationality and reasoning in highly politicized issues such as this, that is an interesting side topic.
No, I don’t believe I do. I wouldn’t want to further offend you.
But otherwise don’t stoop to the moral high ground of politicized orthodoxy—just provide your hypothesis.
My hypothesis is pretty simple. You are using the wrong numbers.
When I Googled, the firstfew hits I found suggested 0.3% per coital act as a lower bound on heterosexual transmissibility with the risks increasing by 1-2 orders of magnitude in case of genital ulcers and/or high viral loads. I don’t think that it is particularly difficult to understand the epidemic spreading in Africa as an STD when these higher numbers are used.
I did look at this study providing smaller numbers and this paper critiquing it, as well as this abstract mentioned in the wikipedia article. It was pretty clear to me that the kinds of low numbers you were using to argue against HIV being an STD are actually based on monogamous couples who are regularly examined by physicians and have been instructed in the use of condoms to prevent transmission. Those numbers don’t apply to the most common cases of transmission, in which ulcers and other factors make transmission much more likely.
That is the hypothesis I was going to offer. When you suggested that you only had a 20-30% level of doubt of the orthodox position, I simply had no idea that it was such a strong and assured 30%.
Please see my response below concerning the perjorative “Denialist”, and why such perjoratives have no place here.
If you want to get into a discussion about rationality and reasoning in highly politicized issues such as this, that is an interesting side topic.
No, I don’t believe I do. I wouldn’t want to further offend you.
You haven’t offended me.
When I Googled, the first few hits I found suggested 0.3% per coital act as a lower bound on heterosexual transmissibility with the risks increasing by 1-2 orders of magnitude in case of genital ulcers and/or high viral loads
The google hits you mention are just websites, not research papers—not relevant. There is no reason apriori to view the ~0.3% per coital act transmission rate as a lower bound, it could just as easily be an upper bound. You need to show considerably more evidence for that point.
The data on wikipedia comes from the official data from the CDC1, which in turn comes from a compilation of numerous studies. I take that to be the ‘best’ data from the majoritive position, and overrides any other lesser studies for a variety of reasons.
It was pretty clear to me that the kinds of low numbers you were using to argue against HIV being an STD are actually based on monogamous couples who are regularly examined by physicians and have been instructed in the use of condoms to prevent transmission. Those numbers don’t apply to the most common cases of transmission, in which ulcers and other factors make transmission much more likely.
This may be ‘clear to you’, but the Wikipedia data comes from a large CDC sponsored review considering aggregates of other studies to get overall measures of transmission. This is the orthodox data! I highly doubt it has the simple methodological errors you claim. And even if you did prove that it does have those errors, then you are only helping the skeptic case—by showing methodological errors in the orthodox position, and the next set of data should then come from the heterodox camp.
The google hits you mention are just websites, not research papers—not relevant. There is no reason apriori to view the ~0.3% per coital act transmission rate as a lower bound, it could just as easily be an upper bound. You need to show considerably more evidence for that point.
If I can take the liberty of butting in...
The data on wikipedia comes from the official data from the CDC1, which in turn comes from a compilation of numerous studies. I take that to be the ‘best’ data from the majoritive position, and overrides any other lesser studies for a variety of reasons.
Here’s the table of data I believe you’re referring to:
It cites references 76, 77 & 79, all of which turn out to be publiclyavailableonline. That’s good, because now I can check the validity of Perplexed’s claim that the studies backing your CDC data used samples of relatively healthy, well-off people who lack some risk factors.
I took ref. 76 first. It reports data from the “European Study Group on Heterosexual Transmission of HIV”, which recruited 563 HIV+ people, and their opposite-sex partners, from clinics and other health centres in 9 European countries. (Potential sampling bias no. 1: HIV+ people in European countries are more likely to have access to adequate healthcare than many Africans and Americans.) It also says:
Study participants were tested and interviewed individually on entry and the contacts [subjects who repeatedly had sex with their infected partner] who were HIV seronegative were followed up every six months. At each interview the couples were counselled about the risk of HIV infection and safer sex practices. At entry to the study a questionnaire was administered by the interviewer. [...] If partners gave a different description of their sexual behaviour the couple was excluded.
That fits Perplexed’s claim that the study’s couples were “regularly examined by physicians” and “instructed in the use of condoms to prevent transmission”. It’s not clear whether they were “monogamous”, but the study did exclude “[c]ontacts reporting other risks of HIV infection and those with other heterosexual partners with major risks for HIV infection”. I also see another sampling bias: if the man & the woman in a couple disagreed on their questionnaires, that couple was blocked from the study. I would think that such couples have a higher risk of transmitting HIV (as I’d guess they’re more likely to be couples where someone’s lying about their sexual history); if so, the study’s more likely to lowball HIV transmission risks.
What about refs. 77 & 79? Where did their data came from? It’s pretty clear that they used the same European Study Group data. From 77:
Between March 1987 and March 1991, a total of 563 heterosexual couples were enrolled in a European multi-center study involving 13 centers in nine different countries. Each couple consisted of an HIV-infected index case and a regular heterosexual partner, whose only known risk factor for HIV infection was sexual intercourse with the index case.
And 79:
From March 1987 to June 1992, 13 research centers in nine European countries participated in a study of heterosexual transmission of HIV.
To be explicit: the three studies you’re citing (via the CDC) are based on one data set, and Perplexed’s characterization of that data is essentially accurate. That adds credence to his claim that the transmission rates you’re citing don’t represent HIV transmission rates in other situations.
Incidentally, tables 2 & 3 of ref. 76 suggest that HIV transmission risk is not only associated with type of sex act, but also with the HIV+ partner’s infection stage, especially (I did not expect this!) for male partners of HIV+ women. Maybe more evidence that there’s more to HIV transmission risk than who’s putting which organ in which orifice?
By all means. While you were writing this I was reading 76 and writing my own reply.
That’s good, because now I can check the validity of Perplexed’s claim that the studies backing your CDC data used samples of relatively healthy, well-off people who lack some risk factors.
Ah I hope he wasn’t claiming this, because they certainly were anything but healthy, with around 20% being hardcore IV drug users, 23% transfusion recipients, 10% hemophiliacs, and overall high rates of STD’s.
I noticed the discrepancy about sexual history part but I didn’t see how to factor it. They are relying on self-reporting to make any of these links.
To be explicit: the three studies you’re citing (via the CDC) are based on one data set, and Perplexed’s characterization of that data is essentially accurate.
Err, no, because his characterization is based on the idea that these couples were using condoms frequently, but the study specifically shows that is not the case—see my reply to Perplexed.
If you want to characterize this study, fine, but don’t pretend that these are “regular couples regularly using condoms”—that is not what the study claims.
And finally this is the orthodox data. I mean if you want to reject … ok .. and then we move to searching for other data which supports our relative positions . . . to the extent we have positions.
Perhaps it would be best to agree what the ideal study would be and precommit to that ideal in a sense? And then we could look for other studies that may be closer. Of course in the real world they will rarely be clear cut.
That’s good, because now I can check the validity of Perplexed’s claim that the studies backing your CDC data used samples of relatively healthy, well-off people who lack some risk factors.
Ah I hope he wasn’t claiming this, because they certainly were anything but healthy, with around 20% being hardcore IV drug users, 23% transfusion recipients, 10% hemophiliacs, and overall high rates of STD’s.
I quite agree that they weren’t healthy in absolute terms; I just meant that they were relatively healthy for people with HIV. Compared to HIV+ people in much of the rest of the world, especially sub-Saharan Africa, I’d expect this European study’s subjects to have (on average) better nourishment, better healthcare, stronger immune systems, less exposure to infectious disease, much less exposure to parasites, and a far lower rate of promiscuity & prostitution. I should’ve been more explicit that that was the sort of comparison I had in mind.
To be explicit: the three studies you’re citing (via the CDC) are based on one data set, and Perplexed’s characterization of that data is essentially accurate.
Err, no, because his characterization is based on the idea that these couples were using condoms frequently, but the study specifically shows that is not the case—see my reply to Perplexed.
Looking at your reply, I think we disagree about whether or not Perplexed was hinting that the couples were consistently using condoms. I didn’t think Perplexed was implying anything more than that most cases of HIV transmission involve people who weren’t regularly reminded to use condoms. So I took his statement at face value, in which case it’s surely true (unless European doctors have come up with a way of counselling couples “about the risk of HIV infection and safer sex practices” that doesn’t involve advising condom use!).
If you want to characterize this study, fine, but don’t pretend that these are “regular couples regularly using condoms”—that is not what the study claims.
I don’t believe Perplexed or I are pretending that these are normal couples who continually use condoms. I think it goes without saying that these weren’t “regular couples” — after all, “regular couples” don’t visit hospitals and clinics to get HIV infections checked out. Whom are you quoting?
And finally this is the orthodox data. I mean if you want to reject … ok .. and then we move to searching for other data which supports our relative positions . . . to the extent we have positions.
I reject your interpretation of the data, rather than the data. The study probably gives a fair idea of transmission risks among faithful Western couples living in the 1980s/90s who regularly see doctors...but for that reason (among others) it’s likely to underestimate transmission risks in other demographics.
Perhaps it would be best to agree what the ideal study would be and precommit to that ideal in a sense? And then we could look for other studies that may be closer. Of course in the real world they will rarely be clear cut.
I think you’re probably right on that point. I suspect that looking at per-sex act transmission risks isn’t going to be very enlightening about whether or not HIV causes AIDS. It would be better to have data from
previously healthy people
who were accidentally infected with HIV
and don’t engage in risky behaviour
and are followed up regularly
for at least 20 years
(each bullet point getting more restrictive). I don’t know if there are such data, but it would get us closer to the original question than big-picture arguments about transmission risks.
Compared to HIV+ people in much of the rest of the world, especially sub-Saharan Africa, I’d expect this European study’s subjects to have (on average) better nourishment, better healthcare, stronger immune systems, less exposure to infectious disease, much less exposure to parasites, and a far lower rate of promiscuity & prostitution.
I generally agree with most of this except perhaps the last part—I doubt that promiscuity and prostitution varies that much from 3rd and 1st world.
I didn’t think Perplexed was implying anything more than that most cases of HIV transmission involve people who weren’t regularly reminded to use condoms. So I took his statement at face value, in which case it’s surely true (unless European doctors have come up with a way of counselling couples “about the risk of HIV infection and safer sex practices” that doesn’t involve advising condom use!).
I think he was implying that the reminders led to condom use, but this was in fact not the case according to the study itself (possibly because they excluded many of the condom users, some aspects of the study’s design are not all that clear to me).
I think it goes without saying that these weren’t “regular couples” — after all, “regular couples” don’t visit hospitals and clinics to get HIV infections checked out. Whom are you quoting?
Not quoting, just paraphrasing. He was implying that the heterosexual couples receiving counseling were not indicative of a typical HIV hetero population, but the study designers of course realized that and were at least attempting to gather representative data.
Ok, whether HIV causes AIDS is a larger topic. My original point was just about the orthodox claim that HIV is sexually transmitted, which I believe is rather obviously bogus according to the orthodox’s own data. I hope you can see how the orthodox could go wrong there and some of the political factors at work.
As to the larger HIV == AIDS issue, I largely agree with your ideal data criteria, but one potential issue is whether we are comparing HIV to the null hypothesis or to some other hypothesis. I don’t think any reasonable skeptic claims that HIV is not at least correlated with AIDS—Richard Gallo may be many things, but he is probably not stupid nor a charlatan.
So it would be better to compare the orthodox HIV hypothesis vs the Drug/Lifestyle Hypothesis (which predated HIV). Some immediate concerns are that one must take care to then define AIDS reasonably without circular reference to HIV (which precludes some data)
The next concern would be that either way, previously healthy people don’t get HIV or AIDS, in reality or according to either theory. The risk groups are all unhealthy in various ways.
All that being said, Duesberg does indeed provide data very close to what you are proposing. There are some groups of HIV+ who, for whatever reason, have refused mainstream treatment. There aren’t many such people, but he cites a study about a group in Germany—they are called long term non-progressors (which is kind of funny when you think about it—AIDS is progress?).
Anyway, this study is small, only 30-40 people IIRMC, but it is long lasting and only a handful have died. He calculates their death rate as measurably lower than the death rate of HIV+ treated patients, and uses this as a major piece of evidence.
here .. that part is on page 402 (it’s a large journal excerpt or something—not really that long)
An interesting read overall, would like to read a good rebuttal.
I generally agree with most of this except perhaps the last part—I doubt that promiscuity and prostitution varies that much from 3rd and 1st world.
Quite possibly, but note that I was comparing the subjects in the European study with the rest of the world, rather than all of the 1st world. The study’s screening procedures probably cut out quite a few people who have a lot of sex.
Ok, whether HIV causes AIDS is a larger topic. My original point was just about the orthodox claim that HIV is sexually transmitted, which I believe is rather obviously bogus according to the orthodox’s own data. I hope you can see how the orthodox could go wrong there and some of the political factors at work.
I think I do. (I hope I do!) Still, I do see the orthodox belief that HIV can be transmitted sexually as being compatible with the CDC numbers. The CDC transmission rates are surely below the average real-world HIV transmission rate (due to the nature of the European study sample), and there are features of the data that are easier to explain if we acknowledge that HIV’s sexually transmitted: the condom-using couples had lower HIV transmission rates than the non-condom users, men who (claimed to have) had period sex with HIV+ women were at higher risk of transmission than men who (claimed to have) avoided period sex, and so forth. So I continue to disagree that the HIV-is-an-STI view is “obviously bogus according to the orthodox’s own data”.
So it would be better to compare the orthodox HIV hypothesis vs the Drug/Lifestyle Hypothesis (which predated HIV). Some immediate concerns are that one must take care to then define AIDS reasonably without circular reference to HIV (which precludes some data)
It might even preclude the Duesberg/Koehnlein data you link. Page 402 says the study’s of “AIDS patients”, and it’s not clear from the immediate context what definition of “AIDS” was used for the study. All 36 of the patients (you were right about the study’s size!) are listed as being HIV+, which suggests to me that the AIDS diagnoses were made (at least partly) based on HIV+ status, as is standard practice.
The next concern would be that either way, previously healthy people don’t get HIV or AIDS, in reality or according to either theory. The risk groups are all unhealthy in various ways.
I would have thought that healthy people are capable of getting HIV? Getting pricked with an HIV-infected needle works, as does sexual transmission. A lot of people in high-risk groups are unhealthy, of course, but there are surely unlucky people who get HIV without prior major illness.
All that being said, Duesberg does indeed provide data very close to what you are proposing. There are some groups of HIV+ who, for whatever reason, have refused mainstream treatment. There aren’t many such people, but he cites a study about a group in Germany—they are called long term non-progressors (which is kind of funny when you think about it—AIDS is progress?).
I looked up long-term nonprogressors on Wikipedia (not the most reliable source, but anyway), and it looks like many long-term non-progressors have genetic traits that make them better able to resist HIV, or have a weaker form of HIV.
I also saw that the group in Germany Duesberg’s talking about all come from Kiel, a relatively small city (population about 240,000). I’m wondering whether the people living there could be more likely to have HIV-resistant genes. Or maybe the form of HIV circulating there is less virulent? (Or both?)
Anyway, this study is small, only 30-40 people IIRMC, but it is long lasting and only a handful have died. He calculates their death rate as measurably lower than the death rate of HIV+ treated patients, and uses this as a major piece of evidence.
here .. that part is on page 402 (it’s a large journal excerpt or something—not really that long)
An interesting read overall, would like to read a good rebuttal.
I should say upfront that there’s no way I’m rebutting all 30 pages of the article (I really doubt the game’s worth the candle), but I can comment a bit more on the little German study.
The first thing that jumps out at me is the lack of detail. I’m curious about how Koehnlein discovered the subjects for the study (personal contact?) and whether they included all of the eligible patients they found. I also wonder how Koehnlein followed up patients, and how regularly. How rigorously do they track the patients to make sure they’re staying off HIV drugs & illicit drugs? How often do they check on them to see whether they’re still alive? When was the last follow-up? The article’s dated mid-2003, but it looks like Koehnlein’s added no new subjects to the study since 2000, and the latest update is from 2001 (when the 3 dead patients died). It would be very interesting to know how many of the remaining 33 patients are still alive 7-9 years on. I looked for later publications by Koehnlein on his study and didn’t find any (which is a bit of a red flag in itself).
I’m also not sure that some of these “AIDS patients” had AIDS in the first place. This looks like the CDC’s definition of AIDS: typically, you have to HIV, and either a CD4 count below 200 (“or a CD4+ T-cell percentage of total lymphocytes of less than 15%”) or one of a list of AIDS-defining illnesses. (You might dispute using HIV+ status as part of the definition of AIDS, but it makes no difference with Koehnlein’s subjects because they all had HIV.) The table doesn’t offer enough information about CD4 T-cell percentages to check whether they’re less than 15%, but it does give CD4 counts and list what appear to be the patients’ “initial AIDS-indicator symptoms”.
So I look at case 1. His CD4 count is 256. His initial symptom was “Herpes zoster”. The Wikipedia/CDC list of AIDS-defining diseases does not include herpes zoster, only chronic ulcers due to herpes simplex. It’s not clear that the patient actually had AIDS when Koehnlein included him in the study. Moving on to case 2, she’s marked as asymptomatic and no CD4 count is given. What was the basis for her AIDS diagnosis?
I sorted the 36 cases into 3 groups: a “questionable diagnosis” group (patient was asymptomatic/had symptoms clearly not on the AIDS-defining illness list, and their CD4 count was explicitly given as >200), a “definite AIDS” group (patient had an illness clearly on the AIDS-defining list, and/or a CD4 count explicitly <200), and an “unsure” group (cases that didn’t fit the other two groups). I put cases 1, 8, 9, 17, 19, 20, 23, 24, 25, 27 & 35 in the “questionable” group; cases 3, 4, 6, 12, 13, 21, 30, 31, 32 & 36 in the “definite AIDS” group; and cases 2, 5, 7, 10, 11, 14 (they had pneumonia, but only recurrent pneumonia and/or PJP is AIDS-defining), 15, 16 (they had toxoplasmosis, but it’s not said whether it was in the brain), 18, 22, 26, 28, 29, 33 & 34 in the “unsure” group.
So the Koehnlein’s study’s effective sample size & death rate seems to be sensitive to how rigorously one defines AIDS. As I see it, only 10 of the 36 cases unambiguously have AIDS, and counting deaths in that subgroup leads to a death rate of 20% as opposed to “only 8%”. I think Koehnlein’s data are interesting, but there are a multitude of reasons not to take Duesberg’s 8% vs. 63% comparison at face value.
The CDC transmission rates are surely below the average real-world HIV transmission rate (due to the nature of the European study sample),
I would have given more creedence to this view at the beginning of this whole inquiry, but in another branch several other posters found some large meta-analysis studies, and low and behold they confirm and agree with the old CDC European study. I discuss that here
Of note is that the infection rate in 1st world countires agrees with the original CDC European Study, and the infection rate in Africa/3rd world appears to be 3-6 times higher. Metastudies which mix 1st and 3rd world results get rates somewhere in between.
Some of these metastudies were of thousands of individual studies, and say what we will about them, I think they nail down the real world transmission rates, and the 1st world rates are just as low as I originally quoted (or lower)
and there are features of the data that are easier to explain if we acknowledge that HIV’s sexually transmitted: the condom-using couples had lower HIV transmission rates than the non-condom users, men who (claimed to have) had period sex with HIV+ women were at higher risk of transmission than men who (claimed to have) avoided period sex, and so forth. So I continue to disagree that the HIV-is-an-STI view is “obviously bogus according to the orthodox’s own data”.
Effects like this surely can increase transmission rates in specific instances, but for epidemilogical modelling we are interested in the average rates—and note as I analyzed elsewhere, the original CDC European study does attempt to control for condom use—it intends to show infection rates for unprotected sex. I don’t think you can so easily dismiss all these studies and the work that has gone into computing these transmission rates.
I looked up long-term nonprogressors on Wikipedia (not the most reliable source, but anyway), and it looks like many long-term non-progressors have genetic traits that make them better able to resist HIV, or have a weaker form of HIV.
This is certainly a possibility and fits what we know with viruses—variable genetic resistance is to be expected.
However, what is important is how one samples and when. If you take a sampling of survivors years later, then sure you can expect to be finding survivors due to genetic resistance.
But if you sample a subset based only on the criteria that they refuse medication after testing seropositive, then that is a very different sampling, and you should expect it to be largely uncorrelated from genetic resistance (unless you want to argue that people with genetic resistance are strongly expected to resist medication!, but I hope you won’t take that route)
You do bring up a potentially valid criticism:
I also saw that the group in Germany Duesberg’s talking about all come from Kiel, a relatively small city (population about 240,000). I’m wondering whether the people living there could be more likely to have HIV-resistant genes. Or maybe the form of HIV circulating there is less virulent? (Or both?)
Possibly, but I don’t find a reason why we should expect this without specific evidence—from what I understand the HIV-1 virus variants spread diffusely in specific at-risk subgroups. It would help the case if the study had more widely distributed patients, and maybe there are other such studies, but it isn’t strong evidence against. We can’t expect many patients to have resisted medicating, and those that did would tend to be clustered geographically in regions where some cluster of doctors were allowed to hold that view and resist medication for a long period of time and study the patients. From what I understand, this was not allowed to happen in the states.
You raise some further methodological questions:
The first thing that jumps out at me is the lack of detail. I’m curious about how Koehnlein discovered the subjects for the study (personal contact?) and whether they included all of the eligible patients they found. I also wonder how Koehnlein followed up patients, and how regularly. How rigorously do they track the patients to make sure they’re staying off HIV drugs & illicit drugs? How often do they check on them to see whether they’re still alive? When was the last follow-up?
I don’t know, and yes these are interesting questions, and it would be useful if there was a meta-study of all long-term survivors/non-progressors.
The article’s dated mid-2003, but it looks like Koehnlein’s added no new subjects to the study since 2000, and the latest update is from 2001 (when the 3 dead patients died). It would be very interesting to know how many of the remaining 33 patients are still alive 7-9 years on
Yes, this would be interesting, but note that we shouldn’t expect these people to have full life expectancy, in either theory—as seropositive status is clearly a marker for ill-health. The bigger question is does refusing medication increase lifespan? That is the central point.
Even if they all died after 12 years on average, that still may be better than typical, for example.
I looked for later publications by Koehnlein on his study and didn’t find any (which is a bit of a red flag in itself).
A follow up would be interesting, but lack thereof isn’t necessarily a red-flag. They are going to die at some point, and probably much earlier than seronegatives. The question is one of statistics.
As to your questioning of whether these are “AIDS patients”, I find that is rather irrelevant—we are only concerned with the fact that they tested positive for HIV. If HIV doesn’t strongly cause AIDS, but medication does, then of course we shouldn’t expect these medication refusers to progress into AIDS and become AIDS-patients, which is exactly what the study is showing. So I dont’ understand why you are trying to show that they are not AIDS patients—that’s the whole point! You may be unknowling arguing for the opposition (or perhaps I am confused on your position or you have none).
I would have given more creedence to this view at the beginning of this whole inquiry, but in another branch several other posters found some large meta-analysis studies, and low and behold they confirm and agree with the old CDC European study. I discuss that here
Of note is that the infection rate in 1st world countires agrees with the original CDC European Study, and the infection rate in Africa/3rd world appears to be 3-6 times higher. Metastudies which mix 1st and 3rd world results get rates somewhere in between.
Some of these metastudies were of thousands of individual studies, and say what we will about them, I think they nail down the real world transmission rates, and the 1st world rates are just as low as I originally quoted (or lower)
All of this is consistent with the CDC statistics underestimating the general transmission rate. You write that the rate estimated from the European study “agrees with” meta-analyses of 1st world data, and that the 3rd world rate estimated by meta-analysis is higher still. So pooling the two meta-analytic results gives a global average rate greater than the 1st world average rates, i.e. averages greater than the CDC rates.
and there are features of the data that are easier to explain if we acknowledge that HIV’s sexually transmitted [snip]
Effects like this surely can increase transmission rates in specific instances, but for epidemilogical modelling we are interested in the average rates—and note as I analyzed elsewhere, the original CDC European study does attempt to control for condom use—it intends to show infection rates for unprotected sex. I don’t think you can so easily dismiss all these studies and the work that has gone into computing these transmission rates.
I don’t think I am dismissing these studies and the work. The bit of my comment you’re quoting refers, after all, to secondary analyses in one of those studies. The point I’m trying to make by drawing attention to those analyses isn’t something like “look, the transmission rates are higher if you don’t use condoms, clearly they’re high enough for HIV to spread through the population”, but instead “associations between condom use and transmission rates, and between sex during menses and transmission rates, have a far higher likelihood in a model where HIV is an STI than in a model where it’s not”. It’s much easier for me to explain why having sex with a woman at particular times in her menstrual cycle would correlate with HIV transmission if I presume HIV’s sexually transmitted, which I interpret as evidence for [edited: I had a brain fart and originally wrote “against”] the view that HIV’s an STI.
However, what is important is how one samples and when. If you take a sampling of survivors years later, then sure you can expect to be finding survivors due to genetic resistance.
But if you sample a subset based only on the criteria that they refuse medication after testing seropositive, then that is a very different sampling, and you should expect it to be largely uncorrelated from genetic resistance (unless you want to argue that people with genetic resistance are strongly expected to resist medication!, but I hope you won’t take that route)
Don’t worry, I’m not. I’m suggesting that because the sampled people all come from the same small geographic region, it’s possible that genetic resistance and/or weaker HIV variants are more common among them.
Possibly, but I don’t find a reason why we should expect this without specific evidence—from what I understand the HIV-1 virus variants spread diffusely in specific at-risk subgroups. It would help the case if the study had more widely distributed patients, and maybe there are other such studies, but it isn’t strong evidence against.
The specific evidence I have in mind is the geographic restriction of the sample. A group of people from one place will tend to be more genetically similar than a worldwide sample, and will be more likely to share strains of a disease. I expect HIV-1 variants do spread diffusely in subgroups, but I don’t think that rules out my point. Particular alleles of genes spread throughout humanity, but spatial proximity still correlates with genetic similarity among people. Sure, geographic restriction is hardly strong evidence of these things — a sample of people who live on the same street could quite easily contain just as much variety in genes that affect HIV resistance (or variety in HIV substrains) as a wider sample. But with geographic restrictions, the variance is likely to be less. (Notice also that the sample seems to be relatively racially homogeneous — only one of the 36 cases is described as black. That’s more evidence of less genetic variance, though very weak evidence, as racial groupings don’t represent much genetic variance.)
Yes, this would be interesting, but note that we shouldn’t expect these people to have full life expectancy, in either theory—as seropositive status is clearly a marker for ill-health.
Yes, but you originally presented the study as “data very close to what [I am] proposing”, and part of my proposal was that the study’s subjects “are followed up regularly” for 20+ years. Koehnlein’s study started in 1985, most of the subjects entered it in the 1990s or later, the latest update is from 2001, and the published report is from 2003. So most subjects don’t seem to have had anything like a 20-year (or more) follow-up.
The bigger question is does refusing medication increase lifespan? That is the central point.
The bigger question we’re looking at is whether HIV causes the complex of conditions we recognize as AIDS (and, before that, HIV transmission rates).
Even if they all died after 12 years on average, that still may be better than typical, for example.
True, but the question is how much better than average their lifespan was, and the causes of death also matter. If the patients lived for many post-HIV years more than average, but most of them died of Kaposi’s sarcoma, I would strongly suspect AIDS.
A follow up would be interesting, but lack thereof isn’t necessarily a red-flag.
It doesn’t mean the study is somehow wrong, but I see it as a warning sign. It’s very unusual for someone to spend 16+ years on a unique, systematic study of untreated HIV patients, and then not publish it anywhere except as a one-page summary in the middle of a review article that I suspect was mostly written by someone else. I have a hunch that Koehnlein’s unable to get the study published in full.
As to your questioning of whether these are “AIDS patients”, I find that is rather irrelevant—we are only concerned with the fact that they tested positive for HIV.
I can think of two reasons why it’s very relevant. First off, if most of the subjects didn’t have AIDS, that might well explain why their death rate’s less than that of AIDS patients (and Duesberg & Koehnlein quite explicitly compare the sample’s death rate to that of “German AIDS patients”) — one dies of AIDS instead of HIV per se, and it normally takes years to go from being HIV+ to having AIDS. Secondly, Duesberg & Koehnlein say the study is of “AIDS patients”; if it turns out that there are people in the study who didn’t have AIDS, D&K have made a specious comparison, and a false claim about the nature of the study. That would raise questions about how much I should trust their report of it.
If HIV doesn’t strongly cause AIDS, but medication does, then of course we shouldn’t expect these medication refusers to progress into AIDS and become AIDS-patients,
Agreed, with the proviso that one would have to wait a long time to be sure that HIV didn’t eventually progress to AIDS.
which is exactly what the study is showing.
Disagreed. If you’re agreeing with my suspicion that some of the people in Koehnlein’s study didn’t have AIDS, you’re implicitly accepting my guess that the clinic symptoms and CD4 counts in the table are those observed for each subject when they entered the study, because that forms the basis for my suspicion. And if you believe that, it follows that you can only infer whether a subject had AIDS when they entered the study, and not whether they later developed AIDS.
So I dont’ understand why you are trying to show that they are not AIDS patients—that’s the whole point! You may be unknowling arguing for the opposition (or perhaps I am confused on your position or you have none).
So pooling the two meta-analytic results gives a global average rate greater than the 1st world average rates, i.e. averages greater than the CDC rates.
For a variety of reasons, I find it useful to separate the two, and the 1st world rates are the most important—the virus outbreak started in San Francisco essentially (following the end tail of the massive hippie/drug liberation social experiment). Also, the 3rd world rates are suspect in general, as one of the meta-studies notes, for a variety of reasons. And regardless, even the 3rd world rates are 30 times lower than typical STD’s, even if they were accurate (which is dubious).
The specific evidence I have in mind is the geographic restriction of the sample.
Yes, but as you admit,
Sure, geographic restriction is hardly strong evidence
So at this point I think it is more time profitable to switch gears and spend a little effort investigating other LTP reports other than this single study. And just a little google searching shows that there appears to be now a number of other LTPs from across the world that are similar to the Koehnlein group—and avoiding traditional treatment appears to be a common link. You can google it as well, but here are some links:
from an article in Health Care Industry (older − 2000):
An adjunct to immune-based research has been the close study, since the early 1990s, of HIV-infected individuals who have not progressed to AIDS in 10 or more years and who have not taken antiretroviral therapy
It has been 16 years since Brothers learned he was HIV-positive.
Since then, he has never taken AIDS drugs or had any illnesses associated with the disease. Despite his good fortune, Brothers says he feels isolated.
And finally here is a compilation of another dozen studies or cases of untreated LTNPs (older hasn’t been updated recently)
So it doesn’t look like the Koenhnlein study is an isolated incident. I am still looking for more recent studies or follow ups.
From everything I know so far, the vast majority of patients were treated, so if treatment has a beneficial effect at all, then it follows that the ratio of treated LTNPs to untreated LTNPs must be equal or greater to the original treatment ratio. I understand that in the west that treatment ratio was very high, probably > 95%
And as far as I can tell, we aren’t seeing anything like that ratio in LTNPs, so this could be very strong support indeed for at least part of the Deusberg hypothesis: that the treatment can itself cause the disease.
Edit: I completely guessed on that 95%, and later found this telling quote in the NYT article (I am reading these as I go):
Levy believes that about 5 percent of people with HIV are medicine-free and still healthy after 10 years.
But what it would really need is a big long term study with the sampling precommitted early based only on choice of treatment strategy. Actually, this should be how our entire medical system works in general. If the drug companies produce a treatment like AZT, doctors and patients get to choose treatment strategies, and overall mortality data is collected slowly over time. Survival of the fittest strategy.
which is exactly what the study is showing.
I should have said here “what the study intends to show”
Disagreed. If you’re agreeing with my suspicion that some of the people in Koehnlein’s study didn’t have AIDS, you’re implicitly accepting my guess that the clinic symptoms and CD4 counts in the table are those observed for each subject when they entered the study, because that forms the basis for my suspicion. And if you believe that, it follows that you can only infer whether a subject had AIDS when they entered the study, and not whether they later developed AIDS.
I was under the impression they tested them when they entered the study and then periodically thereafter just as you’d expect. The overall concern is the long term result—the death rate. I thought the entire point Deusberg was making was that overall mortality was lower in this untreated group than in the general treated population, and the medications themselves were actually causing AIDS progression.
For a variety of reasons, I find it useful to separate the two, and the 1st world rates are the most important—the virus outbreak started in San Francisco essentially (following the end tail of the massive hippie/drug liberation social experiment).
As I understand things, HIV jumped into the human population in Africa decades before hippies and the 1960s counterculture, and that only after being established in West/Central Africa did it reach the US. As such, the 3rd world transmission rates have just as big a role to play as 1st world transmission rates. With an external pool of infected people established, it became possible for HIV to be reintroduced to the US over & over again until it landed in US subpopulations that spread it with needle sharing & frequent anal sex.
Also, the 3rd world rates are suspect in general, as one of the meta-studies notes, for a variety of reasons. And regardless, even the 3rd world rates are 30 times lower than typical STD’s, even if they were accurate (which is dubious).
Without being more specific about what’s wrong with the rates, I’m not sure why this means the 3rd world rates are necessarily about equal to (or less than) the 1st world rates. At any rate, HIV is not a “typical STD”, and a lower transmission rate than other STDs doesn’t mean much as long as HIV’s rates are sufficient to enable its spread. Also, Wei_Dai suggested that the P/V sexual transmission rate for HIV is comparable to that of genital herpes, a point you didn’t seem to dispute in your reply. Do you believe that genital herpes has too low a transmission rate to be an STD?
So at this point I think it is more time profitable to switch gears and spend a little effort investigating other LTP reports other than this single study. And just a little google searching shows that there appears to be now a number of other LTPs from across the world that are similar to the Koehnlein group—and avoiding traditional treatment appears to be a common link.
But here’s the thing: the lone fact that a case report or study has some LTNPs doesn’t necessarily mean much in terms of questioning the HIV-AIDS link. For example, the studies in the 2000 Research Initiative/Treatment Action! article (I think “Health Care Industry” is just the name of the section on findarticles.com where the article’s mirrored) seem to focus on gathering together people already known to be treatment-refusing LTNPs, and finding out what makes them LNTPs. Simply observing that treatment-refusing LTNPs exist doesn’t convince me. Even if 99% of HIV+ people progress to AIDS within some time frame, with so many HIV+ people there are going to be a lucky few who turn out to be treatment-refusing non-progressors.
By contrast, Koehnlein’s methodology seemed to be different, which was why I initially thought that work might be compelling. I’d assumed that Koehnlein systematically recruited people into the study when they originally tested HIV+, not later, which would prevent Koehnlein gaming the study by excluding non-LTNPs. (Of course, with all the questions I now have about the study, I’m questioning even that. D&K don’t say when the subjects were recruited into the study, only when they were diagnosed HIV+. Possibly Koehnlein recruited subjects years after their HIV+ diagnoses.)
And finally here is a compilation of another dozen studies or cases of untreated LTNPs (older hasn’t been updated recently)
The catch with those 14 reports (the last of which is just a second-hand anecdote) is the same as for the other ones you linked: the page listing them doesn’t say what their sampling strategies were, and I think it’s likely that a lot of the reports’ authors deliberately sought out treatment-refusing LTNPs instead of representative samples. (The list is probably also a selective one, considering the website hosting it.) For example, the first report in the list is “based on 10 HIV+ people” who didn’t use antiviral drugs. I find it unlikely that doctors would bother publishing a study of only 10 LTNPs if those people had taken antiviral medication; it wouldn’t be very informative. It’d effectively be a tiny drug trial, and there are already far bigger trials of anti-HIV drugs. So I’d guess the doctors’ aim was to deliberately search for as many treatment-refusing LTNPs as they could find, because other doctors have something to learn from how their bodies work. If so, it wouldn’t be surprising that they found a handful.
From everything I know so far, the vast majority of patients were treated, so if treatment has a beneficial effect at all, then it follows that the ratio of treated LTNPs to untreated LTNPs must be equal or greater to the original treatment ratio.
That only follows if there aren’t any confounding factors associated with treatment status. If (making up an example here) HIV+ people being treated use treatment as an excuse to resume risky behaviour, and the treatment is only marginally effective, we might well end up with relatively few treated LTNPs. (I haven’t looked into this. Maybe it turns out that there aren’t any major confounding factors, but I wouldn’t want to assume them away without evidence.)
And as far as I can tell, we aren’t seeing anything like that ratio in LTNPs, so this could be very strong support indeed for at least part of the Deusberg hypothesis: that the treatment can itself cause the disease.
If you’re basing this on counting reports of LTNPs, you might be getting a skewed picture, since treatment-refusing LTNPs are much more newsworthy than LTNPs who accept treatment, and the latter probably don’t get so many of their own journal articles and magazine profiles. To count them, you’d probably have to locate reports of HIV drug trials that happen to have data on how the testees progress.
Edit: I completely guessed on that 95%, and later found this telling quote in the NYT article (I am reading these as I go):
Levy believes that about 5 percent of people with HIV are medicine-free and still healthy after 10 years.
It usually takes several years for HIV to progress with AIDS, with or without treatment. So it wouldn’t be that surprising if there’s a large minority of people who don’t develop AIDS within a decade of HIV infection, and a fair few of them are probably, yes, medicine-free. (Plus, of course, we’re looking at a newspaper’s paraphrase of something a scientist said, so I’m inclined to exercise caution.)
I should have said here “what the study intends to show”
I was under the impression they tested them when they entered the study and then periodically thereafter just as you’d expect. The overall concern is the long term result—the death rate. I thought the entire point Deusberg was making was that overall mortality was lower in this untreated group than in the general treated population, and the medications themselves were actually causing AIDS progression.
To be honest, I think D&K are confused themselves about what the study’s meant to show. D&K call it “a study of AIDS patients”, but then they write “our relatively small sample supports the hypothesis that without anti-HIV drugs and/or recreational drugs HIV fails to cause AIDS.” But if the subjects were all AIDS patients, how could the study show that they failed to progress to AIDS? They would already have had AIDS!
If you’re correct that Duesberg’s intent was to make the point “that overall mortality was lower in this untreated group than in the general treated population, and the medications themselves were actually causing AIDS progression”, then he’s trying to have it both ways. He can’t infer the first thing (lower mortality) unless the study subjects are AIDS patients, because other AIDS patients are his comparison group, and he can’t infer the second thing (medications causing AIDS) unless some of the subjects aren’t AIDS patients.
Also, I doubt Koehnlein did systematically test the subjects periodically for AIDS. CD4 counts are missing for some of the asymptomatic patients, and to test them for AIDS, they would have needed CD4 counts. So either Koehnlein didn’t have their CD4 counts (which implies that Koehnlein wasn’t periodically testing them for AIDS), or Koehnlein’s selectively withholding CD4 counts (and something funny’s going on).
Whew. The more I go over this study, the more worrying it gets.
Ah, unfortunately this got too long, so I had to split it.
To be honest, I think D&K are confused themselves about what the study’s meant to show. D&K call it “a study of AIDS patients”, but then they write “our relatively small sample supports the hypothesis that without anti-HIV drugs and/or recreational drugs HIV fails to cause AIDS.” But if the subjects were all AIDS patients, how could the study show that they failed to progress to AIDS? They would already have had AIDS!
I think this was a confusion of terminology, and “AIDS patient” in the general sense was used to just refer to all HIV+ patients he was treating. It did not refer to only a subset that had later stage ‘AIDS’ symptoms. At least, that’s how it read to me.
From what I understand, Koehnlein somehow found a way to treat patients without antivirals legally, so patients seeking non-antiviral treatment came to him. His ‘study’ is just a record of all such patients, when they first came under his care, their backgrounds, and eventual prognosis (a couple of deaths out of thirty or so patients so far).,
Also, I doubt Koehnlein did systematically test the subjects periodically for AIDS. CD4 counts are missing for some of the asymptomatic patients, and to test them for AIDS, they would have needed CD4 counts. So either Koehnlein didn’t have their CD4 counts (which implies that Koehnlein wasn’t periodically testing them for AIDS), or Koehnlein’s selectively withholding CD4 counts (and something funny’s going on).
Koehnlein may subscribe to the Duesberg hypothesis, and as such wouldn’t place any special value on persistent tracking of CD4 counts.
Ah, unfortunately this got too long, so I had to split it.
It might be for the best! This splits the Koehnlein study discussion and the general HIV discussion into their own separate subthreads.
I think this was a confusion of terminology, and “AIDS patient” in the general sense was used to just refer to all HIV+ patients he was treating. It did not refer to only a subset that had later stage ‘AIDS’ symptoms. At least, that’s how it read to me.
Yes, we initially read the phrase differently. I originally interpreted it at face value, figuring that in a review article about HIV & AIDS, D&K would take care to avoid confusing having AIDS with being HIV+. I now think I might’ve given them too much credit.
Nonetheless, at one point, D&K must be using “AIDS patients” with its narrow meaning (patients with AIDS proper) and not its informal one (patients with HIV who may or may not also have AIDS), because the statistics they quote for German AIDS patients match the Robert Koch Institut’s AIDS statistics, but not the organization’s HIV+ headcount.
Whatever D&K’s intentions or confusions, my earlier point that the study can’t provide strong, simultaneous support of all the conclusions drawn from it still stands.
Koehnlein may subscribe to the Duesberg hypothesis, and as such wouldn’t place any special value on persistent tracking of CD4 counts.
If so, Koehnlein’s testing his (her?) own definition of AIDS, not an orthodox one, and all bets are off.
As I understand things, HIV jumped into the human population in Africa decades before hippies and the 1960s counterculture, and that only after being established in West/Central Africa did it reach the US. As such, the 3rd world transmission rates have just as big a role to play as 1st world transmission rates. With an external pool of infected people established, it became possible for HIV to be reintroduced to the US over & over again until it landed in US subpopulations that spread it with needle sharing & frequent anal sex.
That’s a theory, but it has some critical flaws. Namely one must wonder why did it not spread via prostitutes, needle sharers and blood transfusions earlier? Condom use dropped with the adoption of the pill in the 1960′s and the sexual liberation opened up a hetero transmission channel which has about the same net transmission rate (always limited by the insertive step).
AIDS became an epidemic in San Francisco in the early 80′s, and it grew quickly from a handful of cases to effect a large portion of the gay population, and was closely correlated with a diverse number of fundamental lifestyle differences. It is this phenomena, this quick sudden outbreak in a very specific subgroup, which I find extremely difficult to reconcile with the transmission data. Tops and bottoms tend to specialize so the rate-limiting factor for expansion in the gay community would be closer to the insertive A rate, at around 0.06% vs receptive at 0.5%. Needle sharing is about 10 times more effective, and blood transfusion is around 1,000 times more effective.
But all the early cases are in this one specific group, which is not even the highest risk group. I mean, the transmission rates for insertive V and A are about the same, and there are far more heteros than homos, so it just doesn’t make any sense. And don’t tell me the homos are having all the sex—they may be having more individually, but not when considering prostitutes and sexually liberated women in the 60′s and 70′s, the fact that heteros have anal as well, and the 100 to 1 hetero to homo ratio. The overall hetero transmission channel is much much larger, especially after considering needle sharing and transfusions, and yet the disease only appears in the homo subgroup, time and time again. Why?
Ignore for a second all high level conceptions about HIV. Don’t privilege the orthodox HIV hypothesis, instead compartmentalize and consider just this evidence concerning transmission rates, and how that evidence should cause one to update from an initial 50⁄50 split between two alternate hypotheses:
HIV spreads primarily horizontally and is novel in homo sapiens
HIV spreads primarily vertically and has been in homo sapiens for a long time
The transmission rates clearly favor 2 - the virus can barely spread sexually, but can spread fairly easily antenatally.
Also, if you actually read into the depths of these studies, it becomes clear that there is a strong framing bias to favor the default sexual transmission theory. The actual sexual transmission rates are not known with certainty, and all of these studies depend on the orthodox HIV model. The actual horizontal transmission rate may be . .. zero.
One of the more interesting hetero sero-discordant studies is the Padian 10 year study. Trying to isolate for hetero sexual transmission, they actually strictly eliminated all drug users by using actual drug tests—something that others have not done to my knowledge. They then did the typical questionnaire analysis trying to determine how each seropositive index member in the couple actually caught HIV—which is more or less just a random guessing game, and then they applied regression techniques to look for risk factors.
The risk factors they found are more or less random, and do not point to a sexually transmitted disease. For instance:
We found only marginal significance
for enrollment in the study prior to 1990 (OR = 1.9),
not using condoms (OR = 1.7), and >300 unprotected
penile-vaginal or penile-anal contacts (the median
number of contacts) (OR = 1.6), all of which had been
found to be significant in previous analyses (2, 6, 14).
So large amounts of unprotected sex did not appear to be a very significant risk factor. The highest risk factor was just anal sex as a practice, not the number of contacts.
But what was really interesting in this group of some 600ish hetero non-drug users was that during the length of the study, there was not a single seroconversion, even though condom use in these couples was imperfect:
We observed no seroconversions after entry into the study. [ ] Nevertheless,
only 75 percent reported consistent condom
use in the 6 months prior to their final follow-up visit.
Forty-seven couples who remained in follow-up for 3
months to 6 years used condoms intermittently, and no
seroconversions occurred among exposed partners.
There is zero evidence that non-drug using heterosexuals acquire the disease sexually, and studies such as this are evidence favoring a vertically transmitted virus.
At any rate, HIV is not a “typical STD”, and a lower transmission rate than other STDs doesn’t mean much as long as HIV’s rates are sufficient to enable its spread.
Why does it only spread laterally into gay men and drug users, even though this is extraordinarily unlikely if it truly is horizontally transmitted?
Also, Wei_Dai suggested that the P/V sexual transmission rate for HIV is comparable to that of genital herpes, a point you didn’t seem to dispute in your reply. Do you believe that genital herpes has too low a transmission rate to be an STD?
I haven’t analyzed genital herpes and know very little about it, and regardless it is irrelevant. If the data says that HIV can not be sexually transmitted, and another disease has the same epidemologial data and is also called an STD, that somehow doesn’t magically change the data. It just makes both classifications wrong.
Simply observing that treatment-refusing LTNPs exist doesn’t convince me. Even if 99% of HIV+ people progress to AIDS within some time frame, with so many HIV+ people there are going to be a lucky few who turn out to be treatment-refusing non-progressors.
There is no ‘luck’ and it all depends on the ratios. If only 1% of HIV+ people refuse treatment, but even just 10% of all “long-term non progressors” refuse treatment, then clearly treatment itself is part of the problem.
From everything I know so far, the vast majority of patients were treated, so if treatment has a beneficial effect at all, then it follows that the ratio of treated LTNPs to untreated LTNPs must be equal or greater to the original treatment ratio.
That only follows if there aren’t any confounding factors associated with treatment status. If (making up an example here) HIV+ people being treated use treatment as an excuse to resume risky behaviour, and the treatment is only marginally effective, we might well end up with relatively few treated LTNPs. (I haven’t looked into this. Maybe it turns out that there aren’t any major confounding factors, but I wouldn’t want to assume them away without evidence.)
It is strange and interesting that you think the cofactors only could work in favor of your privileged hypothesis. There is also the placebo effect to consider, and in a drug trial that is not double blind (as the AZT trials could not be) those who found out they were getting placebo believed they were going to die, and that encouraged wreckless behavior, not the other way around. Also, all the reports on LTNPs I have read are unanimous on lifestyle change being a distinguishing factor- reduction in drug use and bathouse type partying, general increase in healthier behavior. However, they still die at accelerated rates, and some eventually get AIDS.
Overall though it is pretty clear that even with some placebo benefit in it’s favor, AZT had no net benefit. If one could factor in the placebo bias, I expect it actually increases mortality a little on the whole. However, the data on the original AZT trial and later the more extensive concorde trial show that AZT has little effect or a small net negative effect. I think it is difficult to pin all of the modern deaths on AZT, and clearly AZT was not the main killer during the trials, but the fact of the matter is we simply do not have a control group to compare to in the long term.
This is the first cohort to basically be on sustained chemotherapy for life. It’s hard to imagine that this could not have negative long term effects.
That’s a theory, but it has some critical flaws. Namely one must wonder why did it not spread via prostitutes, needle sharers and blood transfusions earlier?
I’m not sure which specific time period you’re referring to with “earlier”. If you’re talking about the 1970s, I’d guess it’s because HIV simply hadn’t been introduced to those subpopulations often/early enough to stick. If you’re talking about the early 1980s, well, it looks like HIV did spread, at least among needle sharers and people who had blood transfusions. (I haven’t seen data on prostitutes.) According to this 1985 Science article, 12,932 AIDS sufferers were reported to the CDC by August 30, 1985. 1.5% of them had received blood transfusions within 5 years of diagnosis, and 17% were heterosexuals who’d used IV drugs. (Also, 12% of the homosexual & bisexual men diagnosed were IV drug users.)
It is this phenomena, this quick sudden outbreak in a very specific subgroup, which I find extremely difficult to reconcile with the transmission data. Tops and bottoms tend to specialize so the rate-limiting factor for expansion in the gay community would be closer to the insertive A rate, at around 0.06% vs receptive at 0.5%.
Although I’m sure tops & bottoms “tend to specialize”, I doubt men with dozens of sexual partners are completely picky about which role they play. If men are inconsistent about being the top/bottom, the insertive anal transmission rate is going to be an underestimate. In fact, it’s likely to be an underestimate twice over, because preexisting STIs make transmission more likely, and promiscuous men will have more STIs on average. You’ve also got the handful of IV drug users among these men. If I’d had to bet on where HIV would rear its head first, the bathhouse subculture would’ve been a great choice to put my money on.
Needle sharing is about 10 times more effective, and blood transfusion is around 1,000 times more effective.
But neither of those can have an impact until HIV’s introduced to the subpopulations of needle sharers/blood donors, and even after that, their effect will depend on when HIV reached those subgroups, and how many people in those subgroups start off with HIV.
But all the early cases are in this one specific group, which is not even the highest risk group.
Only if you define “early” as really early: the first reports of IV drug users with AIDS came out in the same year as the first reports of AIDS in gay men. And again, risk isn’t everything. Even if group X has much higher transmission risks than group Y, if the virus reaches group Y first, the earliest infections are likely to emerge in group Y.
I mean, the transmission rates for insertive V and A are about the same,
While the receptive A rate is higher than the receptive V rate.
and there are far more heteros than homos, so it just doesn’t make any sense.
Ease of person-to-person transmission within a subgroup matters more to how quickly a disease spreads through that subgroup than the subgroup’s absolute size.
And don’t tell me the homos are having all the sex—they may be having more individually,
Which increases the ease of transmission.
but not when considering prostitutes and sexually liberated women in the 60′s and 70′s,
Which doesn’t much matter if there’s hardly any HIV among those women to start off with. I’d also guess that the proportion of “sexually liberated women” having as much sex and injecting as much drugs as gay men in the 1970s/1980s bathhouse culture is relatively small.
the fact that heteros have anal as well
As often as promiscuous gay men?
and the 100 to 1 hetero to homo ratio.
See above about subpopulation size.
The overall hetero transmission channel is much much larger, especially after considering needle sharing and transfusions, and yet the disease only appears in the homo subgroup, time and time again. Why?
To extend your own metaphor, the “hetero” channel was wider than the “homo” channel, but the “homo” channel had faster flow. Plus, again, there were gay men who engaged in IV drug use, and if gay men were among the first US citizens exposed to HIV, as is very possible, that would’ve given them a head start.
Ignore for a second all high level conceptions about HIV.
Not sure what that means specifically.
Don’t privilege the orthodox HIV hypothesis,
It’s the hypothesis favoured by the medical establishment and the scientific mainstream on the basis of evidence that is at least circumstantial, and at best definitive, which suggests it’s a good starting point. I’m not plucking an arbitrary hypothesis to defend out of thin air.
instead compartmentalize and consider just this evidence concerning transmission rates, and how that evidence should cause one to update from an initial 50⁄50 split between two alternate hypotheses:
HIV spreads primarily horizontally and is novel in homo sapiens
HIV spreads primarily vertically and has been in homo sapiens for a long time
The transmission rates clearly favor 2 - the virus can barely spread sexually, but can spread fairly easily antenatally.
I really disagree with how you’re framing things here. It’s screwy to split horizontal transmission & vertical transmission into separate hypotheses, since both processes are happening right now throughout the human race, and both processes happen at different rates across time & place. I don’t understand why the mode of transmission corresponds to how long HIV’s been circulating in humanity, either.
Mother-child HIV transmission rates per child (without anti-HIV prophylaxis) are generally higher than sexual transmission rates per sex act, sure. But there’re a lot more sexual acts happening than childbirths. So there’s more to the situation than raw transmission rates.
That’s a theory, but it has some critical flaws. Namely one must wonder why did it not spread via prostitutes, needle sharers and blood transfusions earlier?
I’m not sure which specific time period you’re referring to with “earlier”. If you’re talking about the 1970s, I’d guess it’s because HIV simply hadn’t been introduced to those subpopulations often/early enough to stick.
There are several documented cases of early AIDS where we have stored tissue that later tested positive for HIV, such as the gay teenager who died in St Louis in 1969. This poses a serious problem for the standard theories that HIV is transmitted horizontally (unlike any other retroviruses) and presumably came out of Africa. So how did it get into this teenager? You would need some world travelling gay subculture at the time to link the disease to Africa, but not a big enough subculture to create an epidemic. Since only a small portion of men are gay, we should expect that if it came out of Africa the first vectors would have been heterosexual, not homosexual. And as there are several of these strange early cases, it would have had to come over from Africa multiple times, but always only in gay men. This theory is just not salvageable.
Also, consider that the different genetic subtypes are closely associated with particular risk groups—subtype M appears in MSM and IV drug users but not others, which doesn’t make any sense for a horizontally transmitted viral vector. Most of the subtypes are linked to particular geographical regions in Africa, which points to a long history in humans (with M representing a novelty linked to novel behaviour).
Also consider that all other primates have naturally occurring lentivirus family retroviruses very similar to HIV. Consider that the entire family of retroviruses are more symbionts than parasites—humans are ‘infected’ with thousands of different retroviruses, many of which are integrated into our genome, and they have functional roles in gene expression and even the formation of the placenta.
So if all other primates have naturally occurring lentiviruses, why don’t humans? There is a clear evolutionary niche for a lentivirus in mammals, and it seems odd that homo sapiens somehow lost their naturally occurring lentivirus at some point in our evolutionary divergence, only to re-acquire it very recently in the last one hundred years. It just doesn’t make any sense at all.
Retroviruses generally are not horizontally transmittable, and there is no evidence that HIV is an exception. The Padian study in the other thread branch directly shows that HIV is probably not sexually transmittable.
There are several documented cases of early AIDS where we have stored tissue that later tested positive for HIV, such as the gay teenager who died in St Louis in 1969. This poses a serious problem for the standard theories that HIV is transmitted horizontally (unlike any other retroviruses) and presumably came out of Africa.
But most of the earliest confirmed AIDS cases were retracted (David Carr) or have a direct connection to Africa (anonymous Congolese adults & Arvid Noe). It’s only Robert R. (the “gay teenager” you refer to) who didn’t have a direct African connection, but that doesn’t mean there wasn’t one, and such a connection wouldn’t even be necessary with Haiti available as a closer source of HIV.
So how did it get into this teenager? You would need some world travelling gay subculture at the time to link the disease to Africa, but not a big enough subculture to create an epidemic.
This is one teenager. He only had to be unlucky once when having sex with just one infected man.
Since only a small portion of men are gay, we should expect that if it came out of Africa the first vectors would have been heterosexual, not homosexual.
I’m confused. This PNAS paper presents good phylogenetic evidence that the HIV strains causing the North American epidemic came from Haiti, and that Haiti’s HIV came from Africa in the 1960s, which “suggests its arrival in Haiti may have occurred with the return of one of the many Haitian professionals who worked in the newly independent Congo in the 1960s”. So it’s Haitian economic migrants who would’ve been the “first vectors” to carry HIV out of Africa in any real number, and I have no reason to think they were disproportionately homosexual.
And as there are several of these strange early cases,
If by “strange” you mean that all those cases are inexplicable, I disagree.
it would have had to come over from Africa multiple times, but always only in gay men.
Not at all.
Also, consider that the different genetic subtypes are closely associated with particular risk groups—subtype M appears in MSM and IV drug users but not others, which doesn’t make any sense for a horizontally transmitted viral vector.
I’m not an epidemiologist (or a geneticist), but couldn’t that just be a founder effect perpetuated by MSM and IV drug users transmitting HIV much better amongst themselves than they transmit it to everyone else?
Most of the subtypes are linked to particular geographical regions in Africa, which points to a long history in humans (with M representing a novelty linked to novel behaviour).
I’m not seeing why this would be evidence for/against orthodox theories of HIV & AIDS. (And if I were being pedantic, again I’d suggest the relative insularity of MSM and injecting drug users as why subtype M’s linked with them, rather than the novelty of their behaviour as such.)
I’ll pass on commenting on your last three paragraphs, since what I know about retroviruses would fit on the back of a postage stamp. I will try checking Padian et al. again, though.
One of the more interesting hetero sero-discordant studies is the Padian 10 year study. Trying to isolate for hetero sexual transmission, they actually strictly eliminated all drug users by using actual drug tests—something that others have not done to my knowledge.
Yes, I don’t know any other studies that used direct drug tests. There is this Madrid study of heterosexual transmission that used indirect testing of “markers related to drug addiction (e.g., hepatitis C serology)” to check for drug use in addition to questionnaires, and its recorded transmission rate is quite high: 26%, out of 38 couples. However, it looks like a retrospective study.
We found only marginal significance for enrollment in the study prior to 1990 (OR = 1.9), not using condoms (OR = 1.7), and >300 unprotected penile-vaginal or penile-anal contacts (the median number of contacts) (OR = 1.6) [snip]
So large amounts of unprotected sex did not appear to be a very significant risk factor. The highest risk factor was just anal sex as a practice, not the number of contacts.
Although quantity of sex doesn’t seem to have made much difference, the unadjusted odds ratio associated with not using condoms bordered on statistical significance with a confidence interval of 0.95 to 3.01. After adjusting for the number of sexual contacts, that odds ratio went up to 2.1, becoming significant and equal to the adjusted odds ratio associated with anal sex. I notice too that after adjustment, STI history — a risk factor elsewhere associated with HIV transmission — was the risk factor with the highest odds ratio.
But what was really interesting in this group of some 600ish hetero non-drug users was that during the length of the study, there was not a single seroconversion, even though condom use in these couples was imperfect:
It would be more interesting if the relevant sample did contain 600 heterosexual non-drug users followed for the length of the study. However, the “no seroconversions” result comes from the study’s prospective part, which involved only “175 HIV-discordant couples over time, for a total of approximately 282 couple-years of follow-up [...] attrition was severe”. That’s a mean follow-up time of only 19 months per couple. Most couples probably got less follow-up time than that, because severe attrition would tend to negatively skew the follow-up time distribution, depressing the median.
That’s not all. The investigators didn’t just counsel the couples on safe sex, but also set up a 24-hour telephone support line, a newsletter and regular meet-ups. These measures were very effective in changing the couples’ behaviour: by the final follow-up, 15% of the 175 couples abstained from sex and 74% used condoms. So, at final follow-up, only 11% of the couples — nineteen in absolute terms — were at substantial risk of HIV transmission. The study’s statistical power to detect the small (in absolute terms) risk of heterosexual HIV transmission wouldn’t have been that great, especially given “the lack of incident STDs during the course of the study” (page 355).
There is zero evidence that non-drug using heterosexuals acquire the disease sexually, and studies such as this are evidence favoring a vertically transmitted virus.
You’re exaggerating. Even ignoring all other work on HIV’s epidemiology, there’s evidence of heterosexual HIV transmission in this very study! Its prospective aspect is just half of the research; there’s also the cross-sectional sample, which includes 230 couples recruited after the researchers began screening subjects for drug use in 1990. HIV transmission occurred in this subgroup, and after adjusting for estimated number of sex acts across the entire cross-sectional sample, there was no association between being enrolled before 1990 and HIV transmission (adjusted odds ratio = 1.0, 95% confidence interval = 0.98-1.0), so the transmissions in the cross-sectional group can’t just be attributed to the pre-1990 (i.e. unscreened) subgroup. (And again, recall the higher odds ratio for failing to use condoms and having a history of STIs. That sounds like more evidence of sexual transmission to me!)
Why does it only spread laterally into gay men and drug users, even though this is extraordinarily unlikely if it truly is horizontally transmitted?
But...it doesn’t only spread laterally into gay men and drug users?
I haven’t analyzed genital herpes and know very little about it, and regardless it is irrelevant. If the data says that HIV can not be sexually transmitted, and another disease has the same epidemologial data and is also called an STD, that somehow doesn’t magically change the data.
That’s true!
It just makes both classifications wrong.
Or your definition of an STI too restrictive.
There is no ‘luck’ and it all depends on the ratios. If only 1% of HIV+ people refuse treatment, but even just 10% of all “long-term non progressors” refuse treatment, then clearly treatment itself is part of the problem.
I think you have some implicit assumptions there to unpack.
It is strange and interesting that you think the cofactors only could work in favor of your privileged hypothesis. There is also the placebo effect to consider, and in a drug trial that is not double blind (as the AZT trials could not be) those who found out they were getting placebo believed they were going to die, and that encouraged wreckless behavior, not the other way around.
Do you have references for this?
Also, all the reports on LTNPs I have read are unanimous on lifestyle change being a distinguishing factor- reduction in drug use and bathouse type partying, general increase in healthier behavior.
Well, I expect that helps. (Which is not to say that switching to a healthy lifestyle halts the progression into AIDS.) I can’t imagine doing poppers and having casual sex is a good thing for anyone with HIV. (Come to think of it, isn’t it possible for someone who already has HIV to reinfect themselves with other substrains and make their infection worse?)
However, they still die at accelerated rates, and some eventually get AIDS.
Makes sense.
I think I’ll hold off on commenting on the last couple of paragraphs about AZT since (1) I really don’t know much about AZT, and (2) this discussion is becoming quite extensive and too much of a time sink for my liking.
Ok, so concerning the Padian study, I believe you have misread it, and I am to blame because I originally mislabeled it when I said:
One of the more interesting hetero sero-discordant studies is the Padian 10 year study.
I was wrong—it was not in fact a study of sero-discordant couples, and I apologize for that mistake, for it seems to have mislead you. This is evident in the abstract and is explicitly clarified elsewhere:
To examine rates of and risk factors for heterosexual transmission of human immunodeficiency virus (HIV), the authors conducted a prospective study of infected individuals and their heterosexual partners who have been recruited since 1985.
[...]
Briefly, couples were recruited without regard to the gender of the
index case or to the serostatus of the partner. [,,] Among couples where both were infected, the direction transmission was determined from detailed risk histories. [..] At the recruitment visit, the serostatus of the partner
was ascertained along with a risk history.
So they recruited non-drug using heteros of either sex who had steady partners, and some fraction of those partners were already infected—specifically 19% of the female partners and 2% of the male partners. They explicitly state there were no new infections in the abstract:
Over time, the authors observed increased condom use (p <0.001) and no new infections.
And again later:
However, given the retrospective nature of the cross-sectional aspect of our design (e.g., transmission occurred prior to entry in the study), past
We observed no seroconversions after entry into the study.
The last part happens to be in the ‘prospective results’ portion (where they switched focus to only serodiscordant couples), but should not be interpreted to somehow only apply to the post 1990 time period—as it says “after entry into the study”, and agrees with the “no new infections” in the abstract.
So I believe you have misinterpreted when you say:
However, the “no seroconversions” result comes from the study’s prospective part,
There was not a single new infection (seroconversion) during the entire ten years across all couples.
You are correct that they were counseled on condom use, but this does not seem to have influence actual reported condom use, even though the percentage of couples using condoms upon entry increased from around 50% to 75%, a significant fraction reported inconsistent usage:
Nevertheless, only 75 percent reported consistent condom use in the 6 months prior to their final follow-up visit. Forty-seven couples who remained in follow-up for 3 months to 6 years used condoms intermittently
So the key of this study and really all of the heterosexual transmission studies is that it is all just guess work. The 19% female and 2% male seropositive partners were just assumed to have acquired HIV sexually, but as this occurred prior to the study, the drug controls were not in place (and testing didn’t start until 1990). They are just assuming sexual transmission in these cases based on the strong unfounded assumption that HIV is sexually transmittable, they really have no idea.
What they did show, was that over about 4000 couple years, there was not a single new transmission in this drug-screened hetero sample. Using the 75% consistent condom use number, lets say then 1000 couple years of inconsistent usage, and perhaps then taking that to conservatively imply 80% condom usage on average for ‘intermittent’ users, you still have 200 couple years of unprotected sex, and not a single transmission. Remember that most of the partners (80%) are female, some practise anal, and that condom usage was reported as highest only for female index patients (male partners—paradoxically). Also, condoms are not at all 100% effective, even when used properly.
If there had been just a single seroconversion, that would correspond to a rate of transmission of 1 per 200 to 1000 years of sex, or perhaps a rate of 1 in 20,000 to 1 in 100,000 sex acts − 0.01 to 0.05%. But that single seroconversion did not happen. The actual transmission rate was exactly zero. As this study actually controlled for drug use cofactors it is the most accurate data I’ve seen for actual sexual transmission, and it shows that most studies grossly overestimate sexual transmission—the reality is there is no M->F transmission or it involves iv drug use.
The problem is simple—as untreated HIV presumably leads to death in 5-10 years, it needs to infect more than one person on average in that timespan just to maintain HIV population rate. To achieve a doubling in 10 years, it would need to infect 3 new people on average in that time.
To explain the growth rate in the early 80′s requires an absurdly faster doubling rate. This is not an STD. It is something else.
this discussion is becoming quite extensive and too much of a time sink for my liking.
Alright, I’ve had another look at Padian et al.’s paper. I did follow your lead in thinking the study was solely of sero-discordant couples, and I agree with you now that it actually wasn’t. However, the relevant part of the study is the prospective sample, which was solely of HIV-discordant couples, so my overall interpretation of the study’s nominally zero transmission rate remains unchanged.
They explicitly state there were no new infections in the abstract:
Over time, the authors observed increased condom use (p <0.001) and no new infections.
And again later:
[snip] We observed no seroconversions after entry into the study.
The last part happens to be in the ‘prospective results’ portion (where they switched focus to only serodiscordant couples), but should not be interpreted to somehow only apply to the post 1990 time period—as it says “after entry into the study”, and agrees with the “no new infections” in the abstract.
Right, but Padian et al. refer to the retrospective part of the study as the “cross-sectional” part (see page 351: “the retrospective nature of the cross-sectional aspect of our design”), implying there was no follow-up in that part. Without follow-up, they couldn’t have detected seroconversion after entry into the study, so the retrospective method wouldn’t pick up on post-entry transmissions however often they actually happened. So it’s a mistake to argue that no transmission happened in the retrospective group on the grounds that no transmission was observed, because the retrospective method can’t detect new transmissions.
So, although it’s technically true that the “no seroconversions” result applies to the whole period of the study, it would’ve been disingenuous for me to say so, because the researchers could only spot new seroconversions from 1990 onwards.
So I believe you have misinterpreted when you say:
However, the “no seroconversions” result comes from the study’s prospective part,
The study’s non-prospective part was incapable of detecting post-recruitment seroconversions, so the basis for the “no seroconversions” result is indeed the prospective part.
There was not a single new infection (seroconversion) during the entire ten years across all couples.
Well, there might’ve been new infections between 1985 & 1996 among the retrospective sample, but the study wouldn’t have detected those. The retrospective method would only detect those that happened in a couple before they entered the study.
You are correct that they were counseled on condom use, but this does not seem to have influence actual reported condom use, even though the percentage of couples using condoms upon entry increased from around 50% to 75%, a significant fraction reported inconsistent usage
The fact that a minority of the couples still didn’t use condoms consistently at their final follow-up doesn’t mean the counselling had no influence!
So the key of this study and really all of the heterosexual transmission studies is that it is all just guess work. The 19% female and 2% male seropositive partners were just assumed to have acquired HIV sexually, but as this occurred prior to the study, the drug controls were not in place
Only for the retrospective sample.
The calculations you do in the next couple of paragraphs seem to be based on both the retrospective & prospective subsamples, which exaggerates the number of couples in which new HIV transmissions could have been observed. New transmissions would only be observable among the couples in the prospective group.
So let’s run the numbers again for just that group. That group had 282 couple-years of follow-up, just 7% of your starting point of 4000 couple-years. Multiplying your final unprotected sex estimates by 0.07 gives me just 14 to 70 couple-years of unprotected sex.
Following on from that, how likely was a seroconversion for some hypothetical transmission rate? Let’s take 0.05%; 0.1% is unusually high for heterosexual couples, if I remember rightly, and 0.01% feels too low. Supposing the couples had 100 sex acts a year, we have (with a lot of simplifying assumptions) 1400 to 7000 sex acts. With 7000 acts at 0.05% a time, I get a 3% chance of no seroconversions. With 1400 acts, I get a 50% chance. This suggests that the likelihood of no seroconversions was not insignificant, so inferring a transmission rate of zero is likely to be a type II error. I also haven’t accounted for the 15% of prospective subgroup couples who became abstinent during the study.
As this study actually controlled for drug use cofactors it is the most accurate data I’ve seen for actual sexual transmission, and it shows that most studies grossly overestimate sexual transmission
Not with this lack of statistical power it doesn’t.
the reality is there is no M->F transmission or it involves iv drug use.
Whaaa?! Wouldn’t that imply that every female partner who became seropositive in the other studies got infected from secret lesbian sex or injecting drugs?
The problem is simple—as untreated HIV presumably leads to death in 5-10 years, it needs to infect more than one person on average in that timespan just to maintain HIV population rate. To achieve a doubling in 10 years, it would need to infect 3 new people on average in that time.
I don’t see that as a prohibitively high barrier. Especially because there’s not really just one transmission rate for each kind of sex act: transmission rate is moderated by other factors like stage of HIV infection, being infected with other STIs, and so forth.
To explain the growth rate in the early 80′s requires an absurdly faster doubling rate. This is not an STD. It is something else.
The early 80s growth rate wasn’t just driven by heterosexual sex.
Right, but Padian et al. refer to the retrospective part of the study as the “cross-sectional” part (see page 351: “the retrospective nature of the cross-sectional aspect of our design”), implying there was no follow-up in that part.
There was follow up starting in 1990. Basically they started the study by recruiting in 1985 and were originally focused on the retrospective aspect. Couples come in, fill out a questionairre and they attempt to screen out drug users and look for patterns in infected partners (couples where both are seropositive). Then in 1990, they began bringing couples in for examinations and follow up tests—“Physical examinations for both partners were initiated in 1990.” This is the beginning of the prospective part, but it doesn’t mean it is only valid for couples starting after that date, which comes from the very first sentence of the abstract:
To examine rates of and risk factors for heterosexual transmission of human immunodeficiency virus (HIV), the authors conducted a prospective study of infected individuals and their heterosexual partners who have been recruited since 1985.
The prospective part was not limited to only couples enrolling after 1990. That is only the beginning of the biannual checkups.
So, although it’s technically true that the “no seroconversions” result applies to the whole period of the study, it would’ve been disingenuous for me to say so, because the researchers could only spot new seroconversions from 1990 onwards.
Technically yes, but immediately in 1990 on the first follow-up they would have spotted any new seroconversions in any serodiscordant couples currently in the study. And they would have clearly mentioned any such detected seroconversions, and indeed they clearly mentioned that they detectected exactly zero.
But regardless, yes I did botch the total couple-years. The text implies that the 175 couple group with follow up was the total set of persistent couples:
Risk behavior at baseline and most recent (final) follow-up visit among 175 human immunodeficiency virus (HIV)-discordant couples recruited in Northern California from 1985 to 1996 (n = 175 couples with a total of 3,384 couple-months of follow-up)
Abstenence was between 0 and 14.5%, consistent condom use betwen 32% and 74%, and anal between 37 and 8%. We should probably also factor in that condoms are not 100% effective. Lets ignore that for a second and assume midpoints of the above numbers, with around 100 sex acts per year, or 10 per month. If ‘inconsistent’ means ~50%, I get ~2 unsafe acts per month, or ~6,000 unsafe acts. The majority of these couples (80%) are male seropositive, so the higher M->F numbers apply 0.1% to 0.5%.
The infection rate for P->V is supposedly 10 in 10,000, or 0.1% according to the CDC from the European study. The infection rate for P->A is supposedly 50 in 10,000, or 0.5%.
Sure it would have been better with 10,000 couples over many years, but how much specific negative evidence for sexual transmission does one require? Is there any specific positive evidence?
There is a larger set of data Deusberg points to for lack of sexual transmission, which is the hemophiliac population, around 75% of which tested positive for HIV in the 80′s. There were about 5,000 wives of HIV+ hemophiliacs, and the CDC reports 131 were diagnosed with miscellaneous AIDS diseases between 1985 and 1992. However, the particular diseases were age-related opportunistic infections, including 81% pneumonia—no KS, demantia, lymphoma, or wasting syndrome generally characteristic of typical AIDS. The 131 / 5000 appears to just be regular background rates for those illnesses. If AIDS was sexually transmitted, we should have seen evidence in this population of wives. Many of these couples were having sex for years before the blood was tested. This strongly contradicts any theories of a sexually transmitted etiological agent.
And if it is not sexually transmittable, then it is either only vertically transmittable or the entire theory is hopelessly flawed at a deeper level. I suspect the latter because the measured vertical transmission rates are not high enough to sustain plausible viral population.
the reality is there is no M->F transmission or it involves iv drug use.
Whaaa?! Wouldn’t that imply that every female partner who became seropositive in the other studies got infected from secret lesbian sex or injecting drugs?
Not at all—the data just shows that seropositivity is not sexually transmittable. A great deal of other evidence, combined with this clear lack of sexual transmission shows that seropositivity is clearly linked to risk groups with immunosuppression in general.
What you’re saying about Padian et al. just clicked for me. I’d got it into my head that they were allocating each recruited couple to either a retrospective track or a prospective track, with couples switching from the retrospective track to the prospective track after 1990, but without their data being carried over. But you’re saying the couples already enrolled in the study pre-1990 were automatically entered into the prospective part with their earlier questionnaires & lab work retained, right? That’d make more sense than how I first interpreted the paper. (Serves me right for skipping the abstract and diving straight into the methods section. Twice.)
Alright, let’s crunch some numbers.
Abstenence was between 0 and 14.5%, consistent condom use betwen 32% and 74%, and anal between 37 and 8%. We should probably also factor in that condoms are not 100% effective. Lets ignore that for a second and assume midpoints of the above numbers, with around 100 sex acts per year, or 10 per month.
Using the midpoints of the ranges is a good first guess in the absence of other information. However, I think there’s a good reason to use estimates much closer to the follow-up percentages (14.5%, 74% & 8%) than the baseline percentages (0%, 32% & 37%). The prospective results section says that “approximately 97 percent of behavior change was reported between baseline and the first follow-up visit”. That is, when couples started/stopped using condoms consistently (or abstaining, or having anal sex), they almost always did so before their first follow-up visit, suggesting the couples changed their behaviour shortly after counselling, not gradually. If so, then the baseline percentages only represent the couples’ behaviour distribution for a few weeks; after that, the distribution would be much better represented by the rates at final follow-up.
This could have a big impact on the surprisingness of the zero seroconversions result. Switching from the midpoint rates to the final follow-up rates boosts the abstinence rate to 14.5% and the consistent condom use rate to 74%, while cutting the “[a]ny anal intercourse” rate from 22.5% to 8%. So the neither-abstinent-nor-consistently-condom-using rate sinks from 39.7% to 11.5%. Carrying that forward, I get an unsafe act count ≈1600 instead of ≈5600 (assuming 50% condom use in that 11.5% of couples).
That of course makes a big difference: with a 0.1% risk per act (and I’d peg the risk as being far closer to 0.1% than 0.5%, given the low rate of couples admitting to any anal sex, let alone repeated anal sex), 1600 sex acts have a 20% chance of not causing any transmissions, but 5000 sex acts have only a 0.03% chance. Evidently the unlikeliness of getting no seroconversions under a hypothesis of low-but-nonzero transmission rates hinges on the numerical assumptions made about sexual behaviours. (And there are yet more tweaks one could make to the numbers: whether to adjust for the couples that were female HIV+ instead of male HIV+, how much to adjust for condom unreliability, how much to adjust for the time lag between HIV infection and showing up as HIV+ on a blood test, and so on.) A claim that HIV isn’t an STI is a hefty claim to hang on this single result.
Sure it would have been better with 10,000 couples over many years, but how much specific negative evidence for sexual transmission does one require?
If I’m remembering correctly, the only pieces of specific negative evidence I’ve seen cited here were the transmission rates’ small sizes (which I don’t see as evidence that HIV isn’t an STI, because the fact that a number is small doesn’t mean I can safely assume it’s nil), and the zero seroconversions result from Padian et al., the strength of which is arguable.
Is there any specific positive evidence?
I think the other studies of heterosexual transmission are at least suggestive. Explaining away the hundreds of female HIV seroconversions detected in those studies by assuming that each case of male-to-female transmission “involves iv drug use” does not seem credible to me. IV drug use is more common that it once was, but surely it’s not that common!
My scepticism is stronger still because a few of the studies have methodological features that would make transmission via needle sharing even less likely. I mentioned this Madrid study before. There’s also this ingenious study, which used sequence analysis on the subjects’ HIV samples to confirm that transmission was within pairs, making it less likely that non-index partners who seroconverted caught HIV from sharing needles with strangers.
Not at all—the data just shows that seropositivity is not sexually transmittable. A great deal of other evidence, combined with this clear lack of sexual transmission shows that seropositivity is clearly linked to risk groups with immunosuppression in general.
Immunosuppressed or not, a person won’t get infected by a virus unless that virus makes it into their body. Even with immunosuppression as a cofactor for HIV transmission, it can’t substitute for HIV transmission.
I almost forgot to ask for a reference for this:
There is a larger set of data Deusberg points to for lack of sexual transmission, which is the hemophiliac population, around 75% of which tested positive for HIV in the 80′s.
I’m unwilling to take Duesberg’s synopsis of these data on trust, and would want to see where he got his numbers from, and which methodological issues he might’ve glossed over. I can think of a few issues already, without even looking. The fact that the couples were having sex for years before getting tested in the 1980s wouldn’t mean much if HIV hadn’t been circulating in the blood supply for long. Different AIDS risk groups often have different constellations of AIDS-defining illness: Haitians often present with diarrhoea & TB, whereas US gay men often present with KS, for example, so I would guess haemophiliacs & their wives might have their own distinct AIDS-associated illnesses. Counting AIDS cases would underestimate HIV transmissions, because only some HIV+ wives would have progressed to AIDS. And so forth.
Also note this ‘ingenious’ study has an important point of evidence that does agree with the Padian study and points to a non-sexually transmitted etiology:
There was no significant difference in the rate of HIV transmission per coital act with inconsistent condom use, compared with no reported use, at any stage of infection.
The circumcision studies from Africa don’t tell us much either, as circumcision is associated with ethnic/cultural groups and thus drug use and other factors.
Immunosuppressed or not, a person won’t get infected by a virus unless that virus makes it into their body. Even with immunosuppression as a cofactor for HIV transmission, it can’t substitute for HIV transmission.
There are other more parsimonious explanations that don’t rely on a ‘virus’ at all, and HIV—as far as it exists as a rather arbitrary collection of DNA/RNA sequences, may not be a virus at all. It could just as easily be trash RNA being secreted in exosomes tagged for immune system garbage collection. It could be regulatory RNA exosome messages intended for other cells. It could be a mutant form of an endogenous regulatory RNA exosome. It could be an endogenous ‘virus’ that forms as a cancer-like mutation of normal endogenous regulatory RNA exosome communication. And yes, it could actually be a true exogenous RNA virus that just happens to be remarkably similar to sequences embedded in the human genome (such as the so called “HERV” sequences) - and just happens to look like typical RNA exosomes in the microscope.
But even if it is a true exogenous virus that can jump between cells and that is a huge if, there is astonishingly little evidence it causes much harm.
There is a mountain of evidence that drug use causes harm, and specifically that particular drugs linked especially to the gay community cause specific types of chronic accumulated immune damage.
Methanphetamine (speed) and its derivatives for example is tightly correlated with HIV/AIDS, it is endemic in the “party and play” gay community, and we have a large amount of evidence that Meth does significant long term harm.
Firstly, Meth is a hyper-stimulant of the “flight or fight” stress response. This stress response essentially temporarily shuts down the immune system and digestion to focus the body on a temporary threat. A lion may kill you in a matter of minutes, while your body’s normal symbiotes/parasites such as fungal candida are not going to do much in this time frame—so stress is bad for the immune system, but this is ok because stress normally is temporary.
What happens when go on a multi-day meth binge and hyper-stimulate your stress response? Well, we don’t entirely know, but it appears to be pretty bad for your immune system. And finally, the drug itself has potential DNA damaging effects through oxidative free radicals. This is a particular problem for any drugs that are often heated up and burnt in either the consumption or production phases, resulting in oxidative byproducts. The typical crack-cocaine ‘cooking’ procedure is especially bad in this respect.
The ‘immune system’ - which really should be called the ‘regulatory system’, is second only to the brain in complexity. It is responsible for not only protecting the body from foreign invaders, but also for general regulation of symbiotes/parasites in the gut, identification and control of rebellions (cancer), as well as normal tissue generation and regeneration (healing).
The CD4 cell pathway in particular is especially complex, and these cells are responsible for identification and long-term memory of particular antigens. They go through an extensive selection process to eliminate possible identification errors (auto-immune disorders). This system is especially sensitive to DNA damage, which is happening all the time—and these cells are expected to stick around for many years to hold antigen memory. They also use a random DNA shuffling process early on to generate their antigen recognition system, and these cells are bouncing around constantly in the blood in such a way that makes essential complex DNA repairs—double strand break repairs—much more difficult.
Consider the insults that AIDS patients are inflecting on this system: known potent stress inducing immuno-suppressants such as Meth and Cocaine type drugs, and oxidized byproducts of cooked drugs directly injected or smoked. Also consider that the rectum is second only to injection as a route into the bloodstream, and associated with anal sex are lubricants which can be absorbed. Has anybody seriously evaluated the long-term health effects of anal lubricants? I haven’t seen such a study. Consider that earlier in the AIDS era more toxic oil based lubricants, possibly containing benzoprene deriatives, were more common. Fortunately presumably safer water based lubricants are more common today, as the oil-lubricants can destroy condoms. All of this stuff goes—right up into the bloodstream.
And finally we should look at gay related intestinal disorders—as most of the CD4 cells are actually in the gut, and gut problems are endemic in gay men. Whether it’s semen absorption, lubricants, or anal douching is unclear, but it appears to cause some chronic gut problem—and possibly leaky gut syndrome, allowing more foreign antigens to pass directly into the blood. Exposure to all these strange antigens may simply confuse the immune system. Now combine that with chronic meth use and you have a clear recipe for AIDS which doesn’t require a virus. Overall, the gut/immune system is designed for forward entry.
The hetero groups that get AIDS in the west tend to be hardcore drug users. The other known group is hemophiliacs. The “AIDS” each of these groups gets are quite different and really only have the low CD4 count and blood reaction test in common—which really are just general markers of a dysfunctional immune system. Hemophilliacs have a genetic disorder of the blood and never lived long until the AIDS era anyway, and injecting foreign protein for the clotting agent is immuno-suppressive in itself.
AIDS, like cancer, is something that anybody can get—but most will not progress to AIDS or cancer until they are already quite old, and will usually die of something else well before that. AIDS is really just a common immune disorder—the elderly often have it to some degree—lower CD4 counts and opportunistic infections. You can accelerate the aging of your immune system and progress to AIDS faster by chronic use of immune supressing hyper-stressors such as Meth/coke drugs and or direct toxic DNA damage through injecting or absorbing (anally) foreign matter into the blood.
None of this causes much immediate damage, but like smoking it ages particular vulnerable systems, probably through accumulated DNA damage, and this is why many people who quit eventually will progress to AIDS anyway a decade later or so—the damage has already been done, just as many smokers who quit will still progress to lung cancer at an accelerated rate.
But the insults that these risk groups are doing to their blood and lymph are considerably worse than smoking. Although notice there is a huge amount of overlap—someone who chronically smokes crack cocaine is much more likely to die of some lung infection than say karposi’s sarcoma.
Also note this ‘ingenious’ study has an important point of evidence that does agree with the Padian study and points to a non-sexually transmitted etiology:
There was no significant difference in the rate of HIV transmission per coital act with inconsistent condom use, compared with no reported use, at any stage of infection.
Flicking to page 354 of Padian et al. I see this: “the practice of anal sex and lack of condom use have remained strong predictors of transmission since the beginning of the study”. And table 2 of the paper suggests that not using condoms is a statistically significant transmission risk factor, after adjusting for number of contacts (as I previously mentioned). I would not interpret that as agreement with a finding of “no significant difference”.
The circumcision studies from Africa don’t tell us much either, as circumcision is associated with ethnic/cultural groups and thus drug use and other factors.
This argument might go through for observational studies, although even there I’d want a quantitative argument for why I should expect those confounders to have as strong (or stronger) an effect as circumcision’s apparent effect. But I also referred to three large randomized trials, and randomization reduces the association between confounders and treatment effects to statistical noise — that’s why people conduct randomized trials. So I still regard the trials as strong evidence for circumcision having an effect on HIV transmission; confounders don’t have a substantial effect on the results of randomized trials unless the randomization process was faulty.
(Incidentally, my original links to the 2nd & 3rd trials are now broken. Hereare alternative links, although they may be paywalled.)
I’m skipping over the paragraphs on whether or not HIV is a virus since what HIV is specifically doesn’t bear on the point I was trying to make, which is that cofactors can’t subtitute for exposure to HIV (whatever one thinks HIV is).
There is a mountain of evidence that drug use causes harm,
Agreed.
and specifically that particular drugs linked especially to the gay community cause specific types of chronic accumulated immune damage.
Even if I grant you that, it doesn’t mean much to me unless one of those “specific types” of immune damage is the massive reduction in CD4 cell counts characteristic of AIDS. There are different kinds of immunosuppression, and it won’t do to presume that because something causes one kind of immunosuppression, it causes the kind of immunosuppression associated with AIDS.
At any rate, I suspect properly accounting for HIV+ status eliminates the link between whichever drugs you have in mind and AIDS. (Note that I am not denying any association between drug use and some form of immunosuppression — just non-spurious associations between drug use and substantial depletion of CD4 counts.) This 1993 Nature report describes results from the Multicenter AIDS Cohort Study. Check out the graph: there is a clear difference in CD4 count between seronegatives & seropositives, and only the seropositives suffer a downward slide in CD4 counts over the years, whereas differing levels of drug use show only meagre effects on CD4 count trajectories.
Methanphetamine (speed) and its derivatives for example is tightly correlated with HIV/AIDS, it is endemic in the “party and play” gay community, and we have a large amount of evidence that Meth does significant long term harm.
But how much does it affect CD4 counts?
What happens when go on a multi-day meth binge and hyper-stimulate your stress response? Well, we don’t entirely know, but it appears to be pretty bad for your immune system. And finally, the drug itself has potential DNA damaging effects through oxidative free radicals. This is a particular problem for any drugs that are often heated up and burnt in either the consumption or production phases, resulting in oxidative byproducts.
But how much do they affect CD4 counts?
Skipping the background commentary on the immune system and the speculation about lubricants & intestinal disorders.
The hetero groups that get AIDS in the west tend to be hardcore drug users. The other known group is hemophiliacs. The “AIDS” each of these groups gets are quite different and really only have the low CD4 count and blood reaction test in common -
CD4 counts below 200-400 are AIDS’ key feature. The Nature paper I linked refers to “CD4+ T-lymphocyte depletion” as “the primary pathognomonic feature of AIDS”. Opportunistic infections of course vary in prevalence across subpopulations, but that doesn’t somehow negate the common symptom that allows them to get a foothold: low CD4 counts.
which really are just general markers of a dysfunctional immune system.
Do you have references for this?
Hemophilliacs have a genetic disorder of the blood and never lived long until the AIDS era anyway, and injecting foreign protein for the clotting agent is immuno-suppressive in itself.
But how much does it affect CD4 counts?
AIDS, like cancer, is something that anybody can get -
If they have HIV. Or idiopathic CD4+ T-lymphoctyopenia, come to think of it. Other than that...?
but most will not progress to AIDS or cancer until they are already quite old, and will usually die of something else well before that. AIDS is really just a common immune disorder—the elderly often have it to some degree—lower CD4 counts and opportunistic infections.
Hedging with the phrase “to some degree” makes that statement too vague for me to get a handle on, and it’d help to put a number on it. At any rate, CD4 counts don’t appear to be much lower among the elderly than among younger adults. A quick poke around for CD4 reference counts brings up this Mayo Medical Laboratories page, which gives a range of 424-1509 for people aged 18-55, and a range of 430-1513 for people aged 55+.
You can probably anticipate what I’d say/ask for the rest of the parent post, so I’ll save you the repetition.
This thread is now at 4.5*10^4 words (counted by copying into a text editor, and find/replacing to delete words that’re actually headers or vote/navigation links). I believe it should have been taken off-line at approximately the 5*10^3 word mark, if not sooner.
I admit I’m obsessively addicted. The more I look into it, the more I have found that HIV science has gone horribly, horribly wrong, and ‘HIV’ - whatever it is—if it even exists—is neither necessary nor sufficient to cause AIDS.
Considering that we have spent hundreds of billions of dollars on this hypothesis, this has larger implications for rationality and the scientific establishment in general.
Even if I grant you that, it doesn’t mean much to me unless one of those “specific types” of immune damage is the massive reduction in CD4 cell counts characteristic of AIDS. There are different kinds of immunosuppression, and it won’t do to presume that because something causes one kind of immunosuppression, it causes the kind of immunosuppression associated with AIDS.
This is absolutely true, and is a very good point. However, keep in mind that seropositivity is not a direct measure of HIV, and isn’t even especially correlated with HIV (see my reply in the other thread). Seropositivity is a rather good measure of CD4 cell decline—simply glance at that graph in the Nature paper and you can see that. Although I should point out I’m not sure if it’s actual cell loss that is measured or simply more CD8 expressing T-cells vs CD4.
Also note that there was no body of non-users of nitrates in the homo risk group in this study—they were split simply into ‘light’ and ‘heavy’, and the heavy users were twice as likely to get KS—I’d say that is a rather significant correlation.
This study has some flaws for looking at toxological causes though, as it was only looking at rather recent drug use (24 months), which is not quite the same as use history overall.
But how much does it affect CD4 counts?
I’m not sure about Meth’s effects on CD4 counts in particular, but heavy cocaine use has a strong depleting effect on CD4 counts. First google result
But there are other factors in the homosexual risk group, the most important of which is simply semen. Semen is loaded with immunosuppressants that are designed to temporarily and locally deactivate the female immune system in the vaginal tract. One of those components are the prostglandins. It appears that evolution has struck a balance between semen’s need to disable immunity and the female’s need to regulate opportunistic microbes in the vagina (namely candida) - this balance sometimes fails and yeast infections result.
AIDS is in general associated with candidiasis—yeast infections—which overgrows in the rectal tract and eventually in the blood, and some of the seminal components absorb into the blood. Large-scale overuse of antibiotics to combat STD’s in the gay community is another significant cofactor, but semen itself may be a major part of the problem.
Many papers about semen’s immune suppression effects are a simple google search away—here is one typical example.
They found that just seven daily rectal semen insertions had a marked immune suppression effect, but only in male rats, female rats didn’t seem to be particularly effected.
You seem to think that the CD4 count decline is somehow completely explained by HIV theory. It is not. The CD4 count decline is the defining feature of AIDS, but HIV’s role, if any, is theoretical and not well understood. So it makes sense to look at all the factors involved—for there are many independent immune suppressing factors in the primary AIDs risk groups—homosexuals and injection drug users.
In the original AIDS defining population of homosexuals, AIDS is associated with a tightly bundled set of cofactors:
passive anal sex
drug use
a history of a large number of past sexual partners and STD’s
a history of heavy antibiotic treatment
More on all the known immune suppressing factors in the gay cohort here. All of this needs to be taken into consideration before one starts chasing some new ‘virus’.
The drugs have changed over time (meth and MDMA being more popular now), but the correlation has remained.
The second significant risk group of AIDS patients appears to be injection drug users—really crack cocaine injectors in particular, and cocaine is known to deplete CD4 cells and cause AIDS all by itself.
Hemophilliacs have a genetic disorder of the blood and never lived long until the AIDS era anyway, and injecting foreign protein for the clotting agent is immuno-suppressive in itself.
But how much does it affect CD4 counts?
I don’t know. Do you know? Do you want to investigate this? How? Keep in mind that before the AIDS era, hemophiliacs didn’t live all that long. We simply didn’t have much data on their longer term health problems. Then in 1985 the HIV panic mania spread, and the hemophiliac population was tested with Gallo’s “HIV’ test—which really is just a CD4 decline surrogate test. And we found that a big % of this population had declining CD4 counts and somewhat AIDS-like blood. What does this really mean?
And their wives don’t get it, btw. Neither do non-drug using prostitutes. Porn actresses in general do not appear to be at an elevated risk of developing AIDS either. None of this makes any sense for a sexually transmittable viral theory, but it makes perfect sense if AIDS is caused by primarily toxological chronic immune suppression.
At any rate, CD4 counts don’t appear to be much lower among the elderly than among younger adults.
I’m not so sure about that. I’m not sure that low CD4 counts in particular is common in the elderly, but compromised immune function is a typical problem of the elderly:
“Opportunistic infections occur with greater frequency or severity in patients with impaired host defenses. Growing numbers of HIV-infected persons, transplant recipients, and elderly persons are at increased risk.”
“Elderly persons have defects in T-cell immunity that result in increased incidence and death from TB”
You can probably anticipate what I’d say/ask for the rest of the parent post, so I’ll save you the repetition.
I won’t reply to this comment in full, but there’s a little loose end of my own making here, and I should tie it up:
You can probably anticipate what I’d say/ask for the rest of the parent post, so I’ll save you the repetition.
?
“But how much does it affect CD4 counts?” (In response to the references to meth, cocaine, direct DNA damage due to injection and rectal absorption of foreign matter, and smoking.)
Evidently the unlikeliness of getting no seroconversions under a hypothesis of low-but-nonzero transmission rates hinges on the numerical assumptions made about sexual behaviors.
A claim that HIV isn’t an STI is a hefty claim to hang on this single result.
Strong claims shouldn’t hinge on a single study, but this study can be used to update probabilities for certain theories. You can think of it as eliminating possibilities.
Namely it eliminates or vastly reduces any hypotheses involving a typical STD transmission route. It allows for a very small possible horizontal transmission rate, but the most likely cluster is centered around zero. That doesn’t prove it is zero, it is just that this evidence strongly favors zero transmission rate theories over all others.
Is there any specific positive evidence?
I think the other studies of heterosexual transmission are at least suggestive. Explaining away the hundreds of female HIV seroconversions detected in those studies
The what? I don’t think there is a single “female HIV seroconversion” to be “explained away” in any of those studies. From what I understand, and what Padian et al claim, the Padian study is the only properly controlled prospective study of heterosexual transmission. The other studies are just observational guesswork that are all circularly dependent on the notion that seropositivity is transmissible—they see a couple where both test positive and they just assume it was sexually transmissible—hardly anything resembling evidence for the theory—just circular logic.
by assuming that each case of male-to-female transmission “involves iv drug use” does not seem credible to me. IV drug use is more common that it once was, but surely it’s not that common!
First of all, in the other theories, there is no transmission to explain—and it certainly doesn’t have to involve iv drug use.
You have to understand what exactly seropositivity actually means. It is a blood test that was specifically designed to classify “aids-like” blood. Gallo developed it by comparing and testing a large amount of antibody combinations (biological IDs essentially), until he found a combination which successfully partitioned the AIDS-like and pre-AIDS-like blood from the normal blood. There are a host of other conditions that can cause full or partial seropositivity—think of it as a semi-general measure of CD4 immune malfunction. And actually, ‘malfunction’ is not even the right term, as one can test positive under some normal circumstances as well—such as pregnancy or during the course of some illnesses.
Testing positive multiple times, for no other apparent reasons, is a clear sign of some persistent CD4 immune malfunction which is highly correlated with full-blown AIDS in the future.
I glanced at the Madrid study and find it largely worthless compared to the Padin study. It is small, not properly controlled, and not prospective. They found higher “viral load” in couples that were both positive vs couples where only one partner was positive? That makes sense simply because as viral load loosely correlates with degree of sickness, we expect that to be correlated in couples. More sick people are more likely to not have partners at all or have sick partners.
You would see the exact same effect in smokers, and keep that analogy in mind when looking at any of this data.
Your “ingenious study” is not well controlled for drug use, and in fact barely even mentions it. As HIV/AIDS is highly correlated with drug use in all the epidemological data I have seen in the west, I don’t think this study allows us to differentiate much of anything.
For example, if you want to determine if lung cancer is predominantly caused by a sexually transmittable virus or toxicological effects of smoking, you need to design studies that carefully differentiate between the two. If you don’t screen for drug use (or smoking) you won’t learn much. Smoking (and drug use) are both highly correlated in long-term couples. If you just simply assume from the get go that the sexually transmitted viral theory is correct, you would naturally see an apparent low rate of transmission proportional to the length of time the couple is together (because this correlates with the smoking behavior ‘catching’.)
So to show that lung cancer is caused by a sexually transmitted vector, you would need to focus on non-smokers. That is why the Padian study is useful, and this African study you point to is not useful.
The part that you seem to think is ingenious—the so called “sequence analysis”, I do not find necessarily ingenious or able to “confirm that transmission was within pairs” in the slightest.
If you want to get into the side discussion on “viral load” and viral DNA comparison based on PCR techniques, it’s critical that you understand Kary Mullis’s objection. Kary Mullis won the nobel for inventing PCR, and he is a strong critic of the whole HIV theory, and the entire interpretation of genetic data based on the technique he invented.
Basically, PCR-like techniques allow you to detect DNA sequences that match a partial fragment, and they allow you to massively amplify those matches—allowing one to find a needle in a haystack by duplicating the needle into a new haystack, so to speak. It’s more useful for qualitative vs quantitative results. The problem with the whole idea of using PCR to test for “HIV DNA” is multi-fold. First, HIV-DNA is allowed to be any of a vast set of sequences—presumably because of it’s massive “mutation” potential. The human body is floating in a sea of RNA and DNA sequences, most of which we know little about—large amounts of various types of RNA that is used to control gene expression, regulatory computation, and regulatory signaling between cells.
So out of that sea of DNA/RNA you get in a tube, a huge set of 10bp-ish sequences are rather arbitrarily determined to be “HIV”, and then one tests many partial sequences and usually finds some similar-ish matches. If you use this PCR test on anybody you will always get some positive results—everybody has some amount of “HIV-ish” genetic material circulating in their blood normally. Comparing sequences in this way is fraught with methodological problems—if you pick some random sequence you will probably find something similar in someone else’s blood, so there is a huge amount of potential sample bias—somewhat like looking for pictures of crystals in ice patterns or looking for coded messages in the bible. There is so many random sequences that it is easy to find some that match, focus on those, and then ignore all the non-matches. A real true similarity comparison would involve a tremendous amount of sequencing on a scale that is—as far as I can tell—never done or not even feasible today. It is not as if PCR gives us some complete snapshot pictureof all the DNA/RNA floating around.
And finally, keep in mind that any way you slice it—we should expect to see sequence similarities in these couples, as they are genetically related—from the same area in africa and much more related on average than two random samples of homo sapiens.
Strong claims shouldn’t hinge on a single study, but this study can be used to update probabilities for certain theories. You can think of it as eliminating possibilities.
That’s my issue — I don’t think Padian et al.’s zero seroconversions result is sufficiently strong to outright eliminate a possibility, unless one’s already assigned a low prior to that possibility. Personally, I walked into this discussion with a very high prior (something like 99%) for HIV being sexually transmissible to some nontrivial (more than, say, once in every million unsafe sex acts) extent, and the Padian et al. result is not a strong one, so my prior is essentially unchanged.
Namely it eliminates or vastly reduces any hypotheses involving a typical STD transmission route. It allows for a very small possible horizontal transmission rate, but the most likely cluster is centered around zero.
Since the prior estimates for sexual transmission I’ve seen are already very small (on the order of 0.01% to 0.1%), the Padian et al. result doesn’t really clash with them that much. I also doubt “the most likely cluster” is centred on zero if one accounts for all of the evidence in the study, rather than focusing exclusively on the zero seroconversions result.
That doesn’t prove it is zero, it is just that this evidence strongly favors zero transmission rate theories over all others.
It favours a zero transmission rate strongly only if one makes particular strong assumptions about the sexual behaviour of the study’s subjects, and disregards the evidence of risk factors.
The what? I don’t think there is a single “female HIV seroconversion” to be “explained away” in any of those studies.
Let’s return to one of the papers that kicked off this discussion, as it has a few examples. From page 810: “seroconversions occurred in three male and seven female contacts after enrolment in the study” (that’s not even counting whatever seroconversions had to have occurred in those subjects already HIV+ at the start of the study). There must be some explanation for those seven seroconversions.
From what I understand, and what Padian et al claim, the Padian study is the only properly controlled prospective study of heterosexual transmission. The other studies are just observational guesswork that are all circularly dependent on the notion that seropositivity is transmissible—they see a couple where both test positive and they just assume it was sexually transmissible—hardly anything resembling evidence for the theory—just circular logic.
Whether or not one believes HIV is sexually transmitted, seroconversions occurred. What were their causes, if not HIV infection due to sexual transmission?
First of all, in the other theories, there is no transmission to explain—and it certainly doesn’t have to involve iv drug use.
Where does the HIV come from if not an external source?
I glanced at the Madrid study and find it largely worthless compared to the Padin study. It is small, not properly controlled, and not prospective.
I do not see the Madrid study as “largely worthless”, though I’d give it less weight than the Padian et al. study for the reasons you give. (I should emphasize that I’m talking about the Padian et al. study as a whole there; I maintain my reservations about the zero seroconversions result.) Still, the Madrid study sample’s not particularly small compared to the number of Padian et al. couples who consistently had unprotected sex and were followed up prospectively.
Your “ingenious study” is not well controlled for drug use, and in fact barely even mentions it.
Yes. The point I was making was that with the sequence analysis confirming the source of the transmission, the probability of any given seroconverter having been infected by IV drug use with strangers is less than if the researchers hadn’t done the sequence analysis (although of course still more than zero). So, to have me agree that the HIV infections are due to IV drug use, I would have to be convinced that the seroconverters had been sharing needles with their partners. And...
As HIV/AIDS is highly correlated with drug use in all the epidemological data I have seen in the west,
...as the study took place in Uganda, I find it very unlikely that even half of the seroconverters were infected by sharing needles (especially since none of the subjects reported injection drug use). Unless you are now arguing that seroconversion doesn’t actually indicate HIV infection (and I can’t tell whether you are or not), I expect you can see why I’d want alternative explanations for each of these seroconversions.
So to show that lung cancer is caused by a sexually transmitted vector, you would need to focus on non-smokers. That is why the Padian study is useful, and this African study you point to is not useful.
The African study, I’d say, is weaker evidence than the Padian study. At the same time, I think it’s absurd to write it off as “not useful”. At the risk of repeating myself, my reasoning goes like this: some number of subjects acquired HIV during the Ugandan study; exposure to HIV is necessary for infection; it is not credible to suppose that every HIV exposure that led to seroconversion is attributable to IV drug use. If there were only four or five seroconversions, I’d say it was statistically possible. In fact, the study reports that out of 239 monogamous couples that were initially HIV-discordant, 72 “acquired HIV during follow-up”. The probability that all 72 of these Ugandans acquired HIV by IV drug use is surely astronomically small.
If you want to get into the side discussion on “viral load” and viral DNA comparison based on PCR techniques,
Not especially, to be honest.
it’s critical that you understand Kary Mullis’s objection. Kary Mullis won the nobel for inventing PCR, and he is a strong critic of the whole HIV theory, and the entire interpretation of genetic data based on the technique he invented.
I’m not much impressed by Mullis’s Nobel credentials. There are quiteafewNobelists who got the prize and promptly started dabbling in crankery. (Including, as it happens, Luc Montagnier, so this isn’t just an issue for people who downplay the links between HIV & AIDS.) Jim Watson co-discovered DNA’s structure, but I’m not about to take all his proclamations about genetics at face value.
Anyway, I haven’t seen anything in the Uganda study report to suggest they used PCR in so sloppy a way as you’re suggesting, and I doubt they’d have much to report if they had. As such, it’s hard for me to avoid the feeling that your remarks about PCR are something of a fully general counterargument against HIV sequencing.
And finally, keep in mind that any way you slice it—we should expect to see sequence similarities in these couples, as they are genetically related—from the same area in africa and much more related on average than two random samples of homo sapiens.
Right, but two samples of virus from a couple where one member infected the other will nonetheless be far more genetically similar on average than two samples of virus from randomly selected infected people in Rakai.
Whether or not one believes HIV is sexually transmitted, seroconversions occurred. What were their causes, if not HIV infection due to sexual transmission?
First of all, in the other theories, there is no transmission to explain—and it certainly doesn’t have to involve iv drug use.
Where does the HIV come from if not an external source?
I’m having difficulty squaring some of your comments on seropositivity and HIV testing with the high reported sensitivity & specificity of properly conducted HIV tests.
First off, before we get into anything else, we need to understand and agree on what seropositivity actually means. Seropositivity means a positive result on an antibody test such as western blot, to some combination of antigens identified by Gallo in 1985 in his large scale blood screening tests. He did a large number of tests on transformed (immortalized) cell lines derived from AIDS patients and found a combination of antigens that could screen blood—separating AIDS and pre-AIDS blood from regular blood.
The problem is he (like Motagnier) failed to isolate the ‘virus’, and most or all of the antibodies in the test react or cross-react with antigens to opportunistic microbes (candida namely) and cellular debris. The p24 protein in particular is essentially just a normal cellular wall or microvescile component—so the ‘HIV’ test is really just a general test of opportunistic infection and apoptosis or immune directed killing of CD4 cells (possibly due to widespread viral parasite burden). It is not a measure of ‘HIV’, it is a direct measure of declining CD4 cells and AIDS or pre-AIDS.
The antibody tests are not standardized geographically or temporarily, so it also makes it very difficult to compare across studies—“seropositivity” means different things in different places and times.
As just one random example—most dogs typically have a mix of ‘HIV’ antigens, and are HIV ‘seropositive’ in whole or in part:
reported that 72⁄144 (50%) of dog blood samples “obtained from the Veterinary Medical Teaching Hospital, University of California, Davis” tested in commercial Western blot assays, “reacted with one or more HIV recombinant proteins [gp120--21.5%, gp41--23%, p31--22%, p24-- 43%]”
You post a link to a paper which supposedly shows the ” high reported sensitivity & specificity” of HIV tests. This is not actually what that paper is about, but it references several other papers for this claim—the first I investigated being this. The important quote:
Thirty-fourwomentested HIV-1 positive
with both rapid test and EIA, and all
were confirmed by Western blot
(prevalence=7/1000).
So they are just using Western blot as ‘confirmation’. So they are just using one antibody test to confirm another antibody test—which of course is rather ridiculous.
To actually compute the sensitivity and specificity for a “HIV” test, one needs a gold standard such as viral isolation or perhaps a DNA test. Unfortunately HIV can not be isolated, either because it doesn’t exit or it exists in only minute quantities.
But one can attempt to use the presumed viral DNA as a gold standard, and the result is extremely poor sensitivity and specificity:
Poor sensitivity is perhaps a gross understatement—the study actually shows that around 18-25% of the population at large test positive for ‘HIV DNA’, and this is only weakly correlated with seropositivity.
You completely dismiss Mullis’s argument based solely on an ad hominem “not much impressed by Mullis’s nobel credentials” without seeming to acknowledge or understand the argument itself.
Seroconversion in the west is closely correlated with AIDS or pre-AIDS. This does not appear to be as true in Africa, so we are generally talking about two different worlds. Part of this may be genetic (black americans have amazingly higher seropositvity in general), the other part may relate simply to higher precedence of opportunistic infections and antigens that seropositivity measures. KS for example is vary rare in the west and along with systemic candidaisis was part of the original AIDS definition, but it is one of the most common cancers in Africa.
Unless you are now arguing that seroconversion doesn’t actually indicate HIV infection (and I can’t tell whether you are or not),
I am arguing that.
Seropositivity does not strongly correlate with ‘HIV’ infection (by DNA test), which is why it is better to discuss AIDS itself as being sexually transmittable or not.
The Gallo blood test is tightly correlated with AIDS (at least in the west) - simply because that is what it was designed to do, so you can use that as data for AIDS transmission discussions.
Unless you are now arguing that seroconversion doesn’t actually indicate HIV infection (and I can’t tell whether you are or not),
I am arguing that.
OK. At this point, I’m going to have to disengage and walk away from this debate. I’m realizing that the inferential distance between us is far bigger than I originally thought, and trying to bridge it would need me to considerably ramp up the effort I’m already putting into this. (Even then I can imagine this going on indefinitely, which isn’t a very appealing prospect to me, nor to other Less Wrong posters, by the looks of it.)
I’d still like to respond briefly to one part of your comment, which comments on my own words rather than HIV/AIDS:
You completely dismiss Mullis’s argument based solely on an ad hominem “not much impressed by Mullis’s nobel credentials” without seeming to acknowledge or understand the argument itself.
It’s wholly legitimate for me to respond to someone citing Mullis’s credentials (as if I didn’t know about them already) by explaining why I give them little weight, and my next paragraph was meant to summarize why I gave “your remarks about PCR” (that is, those you paraphrased from Mullis) short shrift. In other words, I acknowledged the argument by rejecting it.
I’m glad you can walk away, I have a harder time initiating that. I’m curious though about the direction of the inferential distance you see—do you have a biology background?
The dissidents point to a rather surprising pile of evidence that the serological HIV tests are based on rather general, cross-reactive antibodies, and this is essentially a fundamental flaw in HIV science which has never been corrected. Now it may be that the orthodoxy has a really good counter to this, but if they do I have yet to find it. The orthodox position on this, from papers linked to wikipedia, points to studies which measure the sensitivity of various HIV antibody tests by comparing them to . . other HIV antibody tests.
The few large double-blind meta-studies that compare the different antibody tests to PCR tests show terrible sensitivity and specificity between the two, and I haven’t seen the orthodox counter to this. So something is wrong with the antibody tests, the PCR tests, or the whole thing. I imagine it’s a little bit of both—the antibody tests are cross-reactive (hence many dogs test positive), and PCR tests are difficult and subject to experimenter bias.
Perhaps the orthodox counter is that there are a whole big host of HIV related viruses, and the antibody tests are cross-reactive across these related species. This seems to then just beg more questions than it answers, and doesn’t circumvent some of the specific non-viral cross-reactions the dissidents point to.
My paraphrase of Mullis’s argument may actually be a mix of other dissident positions. I just rechecked that part of his book and he covers the difficulty of PCR and the confirmation bias but largely in regards to the OJ trial. On HIV he mainly rehashes Deusberg’s argument.
I’m curious though about the direction of the inferential distance you see—do you have a biology background?
None at all. (I expect the inferential distance would be even greater if I did. If I had personal experience of working with retroviruses, for instance, I reckon my prior probabilities for claims like “HIV can not be isolated” or “HIV doesn’t exist” would be far, far less than they are. And they are already very low.)
To actually compute the sensitivity and specificity for a “HIV” test, one needs a gold standard such as viral isolation or perhaps a DNA test. Unfortunately HIV can not be isolated, either because it doesn’t exit or it exists in only minute quantities.
When ‘HIV’ was first ‘discovered’ in the original papers by Gallo and Montagnier, they had difficulty isolating and didn’t publish pictures from what I understand—that didn’t happen until years later. Gallo’s great discovery for HTLVIII was based on running a lager number of antigen/antibody tests with an immortalized cell line to find an antibody test that could screen AIDS and pre-AIDS blood from regular blood. That is the basis of all the current HIV tests.
The first published pictures came more than a decade later, and they showed that “HIV isolate” really consists largely of cellular debris and microvesciles. In these EM photos, they do find some occasional particles of roughly the right size and label them as “HIV”, but they could also just be any of a number of other things, and for all intents and purposes, HIV ‘particles’ look like regular microvesciles.
The titles of the papers say it all:
“Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations”
“Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations”
I have lost the link, but there are better more recent pictures taken with ATM, and they show that for all intents and purposes, it’s impossible to distinguish ‘HIV’ from regular microvesicles that bud from the cell wall naturally. If HIV can be said to exist at all as a unique exogenous virus, it is only because of unique RNA content in the microvesicle, and in this sense is very much unlike all other known viruses.
Of course, the part of HIV’s genome which is supposed to code for the outer envelope is pretty much the same as the endogenous sequences that already exist in the human genome—the HERVs.
I highly doubt it has the simple methodological errors you claim.
Well the best cure for doubt is to actually read the papers referenced. For example, following the links from your reference to the abstract of the actual paper which generated the numbers brought me to this abstract. I think you should read it.
The issue isn’t methodological errors in the studies—the studies clearly describe the methodologies used and their limits. The issue is trying to use the numbers in ways that they are not designed to be used. It is not the orthodox folks that are doing that. It is you that is doing that.
The issue is trying to use the numbers in ways that they are not designed to be used. It is not the orthodox folks that are doing that.
Ah, so do the numbers come with little instruction manuals that say “CAN ONLY BE USED TO SUPPORT ORTHODOX POSITION”? Haha sorry, couldn’t resist.
OK, I’m game, I will now look into the CDC studies, but let’s be clear on the trace ..
it starts with the wikipedia chart which has the ref note 80 linked here, which points to this, which in turn lists refs 76, 77, and 79 for P/V sex, which are (in order):
76:
Comparison of female to male and male to female transmission of HIV in 563 stable couples
77:
Reducing the risk of sexual HIV transmission: quantifying the per-act risk for HIV on the basis of choice of partner, sex act, and condom use
79:
European Study Group on Heterosexual Transmission of HIV. Heterosexual transmission of HIV: variability of infectivity throughout the course of infection
You will find that #77, the Varghese et al paper, can be found online by Googling the title, and that it gets its 0.1% number for heterosexual transmission from the paper whose abstract I recommended.
I’m pretty sure you will find that all of these papers involve monogamous couples. If you give it some thought, you will realize that there is just about no other way to come up with a solid empirically-based number. And I again urge you to read that abstract—particularly the bottom third.
Haha ok this is kinda funny, but the abstract you linked to which is the source of the data in Varghese(77), is just 76! - the couple comparison from the European Study Group which I linked to and have been trying to parse. 79 appears to be another chapter from that same book, but I haven’t looked at it yet.
So before we get into 76 - the source of the stat you don’t like in 77, I need to backup and remember your original claim about the data:
It was pretty clear to me that the kinds of low numbers you were using to argue against HIV being an STD are actually based on monogamous couples who are regularly examined by physicians and have been instructed in the use of condoms to prevent transmission. Those numbers don’t apply to the most common cases of transmission, in which ulcers and other factors make transmission much more likely.
Your implied point appears to be that couples in this study use condoms frequently. Surprisingly, this is not the case—only a surprisingly small number of couples reported consistent condom use (out of 500+),
These people were using other methods of birth control more than condoms.
None of the 24 partners who had used condoms
systematically since the first sexual contact was
infected.
and they further removed consistent condom users from the data:
Assuming that no risk factors for transmission
would be relevant during consistent condom use, eight
male and 16 female contacts who were still negative and
had systematically used condoms since the first sexual
contact with the index case were excluded from the
analysis of risk factors.
Haha ok this is kinda funny, but the abstract you linked to which is the source of the data in Varghese(77), is just 76! - the couple comparison from the European Study Group.
No, it is not. The reference leading to the abstract is the absolute risk described in the first paragraph of page 40 of Varghese. It is reference 28 of Varghese.
You are apparently following the references (21) appearing in Table 1 of Varghese. But these are relative risks (relative to felatio). Not at all what I meant.
My point about condom use came from an earlier reference that I had supplied which discusses a study that took place in Uganda in 2005. And I didn’t say that they used condoms frequently, I said that they were monogamous couples who got regular medical inspections and had been counseled regarding condoms. And in this study, as I recall, there was no exclusion of condom users.
Trial participants were enrolled as individuals; provided written, informed consent; and were guaranteed confidentiality. Condoms and voluntary HIV counseling and testing, for individuals and for couples, were promoted and provided free of charge. … Antiretroviral therapy (ART) was not available in Uganda at the time of the study, but participants were offered free general health care and treatment for opportunistic infections.
The top-level comment of this thread. Comments are nested. Click parent enough times and you’re at a top-level comment. I’m surprised the name is confusing to you.
As for the table, it’s linked in the top-level comment:
The linked table is clearly labeled and indicates that the risk is supposed to be for not using a condom. The table has the same figures as the “Table 1” appearing as an image in a nested comment by satt, which has the same indication. I doubt you missed that.
Given that you appear to be discussing the cites referenced in the table, I’m puzzled as to why you think condom use is implied. Are you saying the table is wrong, or are you talking about some other part of the cite than was used to build it?
the “Table 1” appearing as an image in a nested comment by satt
Well, what do you know. You do know how to provide links to what you are talking about.
I doubt you missed that.
I don’t know why you are doubtful. Have I responded to anything on that branch before now?
Given that you appear to be discussing the cites referenced in the table, I’m puzzled as to why you think condom use is implied. Are you saying the table is wrong, or are you talking about some other part of the cite than was used to build it?
You know something, you are a very effective troll. You have me boiling with fury right now. However, now that I know what is happening, I can become relatively calm, with effort.
If you want to know what I was talking about when I discussed condom use, I would refer you to what I said I was talking about when I discussed condom use.
I’m sorry. I really thought you understood that the papers you were discussing are exactly those that were used to build the table:
it starts with the wikipedia chart which has the ref note 80 linked here, which points to this, which in turn lists refs 76, 77, and 79 for P/V sex, which are (in order):
This entire conversation is definitely mostly a mistake. Nobody can possibly care enough about the answer to my original question, which was: “is the table misrepresenting the studies it’s built out of, or are you mistaken?”, in order to justify reading this crap.
Ah no I haven’t even read Varghese(77) yet. You looked at that one and posted a link to an abstract—this abstract, which comes from the same European Study Group and has the same numbers (563 couples) as 76. So the abstract you wanted me to look at is just 76, it’s all the same source.
I’m not really concerned (at the moment) with what may or may not be happening in Uganda. The CDC data comes from this European Study Group, that is the original data in question - (the data you questioned).
Actually, though you may not believe me, Holocaust denialism hadn’t even occurred to me.
It didn’t occur to me either, and seemed strange. That word does have strong negative connotations in my mind, but only because I associate it with stupid people denying true things and refusing to update on evidence. I thought the comment that referred to was incorrect, but it seemed more like honest confusion of the sort that clarification would dispel than denialism.
Some history then of exactly why the word conjures strong negative correlations is in order.
Look at the wikipedia entry for “denialism”. It originates with holocaust denialism, was then applied to skeptics of HIV==AIDS, and then later to other areas.
Peter Duesberg, the leading HIV==AIDS skeptic, is a German of non-Jewish descent raised in Nazi-era Germany, so it’s use against him and his followers adds extra moral angst. It is just about the deepest insulting connotation one can use. It is a signal of stooping to the ultimate low, that, in running out of any remaining rational argument, one must invoke deep moral revulsion to stigmatize one’s opponent.
In my view, the term is a serious Crime of Irrationality, it is an empty ad-hominem and should be seen as a sign of great failure when one stoops to using it as a name-calling tactic against one’s opponents.
That being said, I don’t think Perplexed has this view, and that wasn’t his intention. I am just giving background on why the word should not be used here.
Those who don’t subscribe to HIV==AIDS, should just be called skeptics.
Do we call proponents of quantum loop gravity String Theory Denialists? It’s ridiculous.
Should we call those who subscribe to HIV==AIDS to be Inquisitors, Mcaurthy-ists, or Witch-hunters?
I don’t think Perplexed has this view, and that wasn’t his intention.
Oh, I certainly was aware that I wasn’t complimenting you in using that term. But I don’t see any reason to waste the perfectly good word “skeptic” on someone who imagines that scientists who disagree with him are mostly doing so out of fear of being attacked by their politically powerful colleagues. I think that “denialist” does the job just fine.
Now, if you told me that several of your scientist friends had confided in you that they are living in fear, well, then that would be the kind of evidence that just might justify the label of skepticism.
So you are actually advocating the use of such perjoratives, even though they have no rational purpose and only serve to incite moral revulsion? Their only purpose is to exploit irrational cognitive bias.
I think that applying the term AIDS denialist to someone who irrationally denies the validity of the scientific consensus on HIV/AIDS is entirely appropriate. It is certainly the standard term for the phenomenon.
As for moral revulsion, I would strongly suggest that you actually read some of the references regarding AIDS denialism that exist in that wikipedia article that you recommended. You will find that moral revulsion for your position is relatively common.
I would say that the purpose of using this terminology would be to signal to the person so labeled that he has stepped over an important line and that many people will disagree that that person deserves to be called a rationalist.
Rationality is a methodology, not a position, and name-calling goes against it’s core principles.
To quote Vlad M:
In many ideologically charged topics that are a matter of culture wars and political battles, a key strategy is to create an association in the public mind between one’s favored position and a vague and general feeling of righteousness and moral rectitude—so that in the future, ideological opponents can be defeated by attacking their moral character, regardless of the quality and accuracy of their arguments and position
I think that applying the term AIDS denialist to someone who irrationally denies the validity of the scientific consensus on HIV/AIDS is entirely appropriate. It is certainly the standard term for the phenomenon.
I don’t think that’s right. “AIDS denialism” is usually used to mean this:
AIDS denialism is the view held by a loosely connected group of people and organizations who deny that the human immunodeficiency virus (HIV) is the cause of acquired immune deficiency syndrome (AIDS).
I’m not sure what your point is. Jacob_cannell has denied that HIV is the cause of AIDS. What is worse, to my mind, he has offered the opinion that many scientists who say that HIV is the direct cause of AIDS are doing so dishonestly—out of fear of retribution. Read the wikipedia article on denialism. He fits the pattern.
Cannell: Actually, I think most intelligent researchers, if they could afford to be honest, would admit that HIV is the major indirect causitive factor, but this is not the same as saying HIV == AIDS.
Nobody thinks that HIV == AIDS. HIV is a virus, and AIDS is a syndrome, that may—or may not—subsequently develop in individuals infected with HIV.
That HIV != AIDS is not even remotely controversial:
HIV progresses to AIDS at a variable rate affected by viral, host, and environmental factors; most will progress to AIDS within 10 years of HIV infection: some will have progressed much sooner, and some will take much longer.
I think you’re reading this in an excessively literalistic manner. “HIV==AIDS” as it’s being used here is just shorthand for “AIDS is caused exclusively and entirely by HIV infection”
The chance of developing AIDS is probably also associated with age of HIV infection, the use of antiretroviral drugs—and other genetic and environmental factors.
Does the non-mutated CCR5 gene do anything important that the mutation disrupts? (In the sort of way the mutation for malaria resistance causes sickle cell anemia if you have two of them.)
That is the way I understand it and the way I assume jacob_cannell is using it. I’m pretty sure all concerned know the difference between viruses and diseases.
The question is whether HIV-1 is the cause of AIDS. Sure, there may be other factors that contribute, but I am claiming “no AIDS without HIV” and “HIV infection if untreated by anti-virals, leads almost inevitably to the diagnosable disease AIDS”. Jacob_cannell is apparently disputing this.
“HIV infection if untreated by anti-virals, leads almost inevitably to the diagnosable disease AIDS”
I’m basically agnostic on the HIV/AIDS question, but my layman’s understanding is that even mainstream thought on AIDS would not support this second statement. I believe it’s well understood that there are nontrivial numbers of people who are HIV+ and do not develop AIDS, decades after infection. This may be the gene mutation(s) referred to by timtyler, or it may be something else (I’m not well-read on the specifics)
First I should point out that even the mainstream, as far as I understand, does not claim that HIV-1 is the sole cause of AIDS, unless one takes AIDS to be a very specific form of immune suppression only caused by HIV, but so far there is little scientific support for that—other causitive factors can mimic AIDS-like immune supression, and I believe this knowledge and view is mainstream.
As to your 2nd point, kodos96 addresses that, and again it’s not even the mainstream position.
So first off, I am not disputing what you are claiming—firstly because it’s not even the mainstream position, but secondly because what I am disputing is something of a meta nature. I am disputing the certainty in the mainstream position.
I hold a range of beliefs about HIV and AIDS, and distribute probabilities amongst them. I naturally tend to simultaneously consider multiple viewpoints. In this case they are:
(orthodox) HIV is the prime cause of a progressive immune deregulation, although riskgroup specific co-factors contribute
(moderate) HIV, like the other exogenous retroviruses, has health negative effects, but is hardly outright lethal. It exists in an evolutionary limbo—it was once more lethal, but is evolving into more of a harmless vertically transmitted symbiote. Other exogenous retroviruses have been implicated in cancers, but not strongly. They are somewhere between epidemic viruses and harmless exogenous retroviruses that long ago were neutered and intergrated into our DNA. Furthemore, there are several genetic variations, and they have differential individual effect—picking up novel retroviruses from someone else’s blood is not good for one’s health.
.. .
I assign highest creedence to 2 atm. Note that it is very difficult to distinguish between these 3 theories. About the only specific differentiator would be koch’s postulate—isolating the virus and then infecting it into new hosts, observing the symptoms, and then reisolating the virus from infected cells. HIV has not been shown to cause AIDS under that criteria—it fails in any animal models.
Yes, that’s the term. Idiopathic just means “crap we have no idea what causes this”, so basically low CD4 counts and weak immune function is usually associated with HIV antibodies, but not always. I’ve seen that term used elsewhere, I think it is mainstream. I don’t think mainstream researchers are claiming HIV is the only thing that can cause low CD4 counts and AIDS-like symptoms—AIDS is not a specific set of symptoms at all, so it’s bound to have many classification errors.
Stop playing dumb—everyone who uses the word “denialist” knows exactly what it’s supposed to connote. Godwining has no place in a rationalist community.
Believing that other people knew (or should have known) how angry they were going to make you is exactly what makes outrage-driven discussions blow up.
Malice and spite exist, but I think they’re very rare compared to incompetence.
“Should have known better” is a very tempting stance to take, but it strikes me as unreasonable.
Believing that other people knew (or should have known) how angry they were going to make you is exactly what makes outrage-driven discussions blow up.
Malice and spite exist, but I think they’re very rare compared to incompetence.
Also note that doing things even when you know that they will make other people angry is not necessarily malicious or spiteful. In most cases it will be because healthy individuals place limits on how much responsibility they assume for other people’s emotions. Doing things because they will cause another person could be spiteful. (Although even then that is not necessarily the case. See, for example, the recent Star Trek movie in which time-travelled Spock tells Kirk to provoke an emotional response in the young Spock, allowing Kirk to save everyone including Spock.)
So I guess what you’re trying to say is that he didn’t intend for the word “denialist” to conjure up images of the Holocaust in the minds of readers. Of course this is possible, but I think it’s pretty unlikely. The modern revival of the word (in the context of climate change) was specifically intended to have that connotation, and this was discussed openly by those who popularized its use in that arena.
Now I suppose it’s possible that he just picked the word up from context and started using it, without realizing that it was designed to provoke an emotional response and shut down rational debate… but based on his tone and overall approach, that’s not what it seems like to me.
So I guess what you’re trying to say is that he didn’t intend for the word “denialist” to conjure up images of the Holocaust in the minds of readers.
That’s it.
Generalizing from the inside of my head, I think “denialist” has a stench from “Holocaust denialist”—it implies refusal to accept a true, important, and morally obligatory mainstream belief.
Perhaps such a word should be tabooed in a rationalist forum.
However, precisely because “denialist” became commonly used for such purposes as “global warming denialist”, the connection to the Holocaust got weakened.
The connotations of words shift, and as Holocaust denial has become less of a public issue (this is called “winning”), ‘denialist’ has acquired other default meanings.
I find denialism in all forms simply fascinating. I wonder if you could indulge my curiosity.
This is a truly impressive bit of sophistry. You have succeeded in phrasing your objection in a manner such that a casual observer, unfamiliar with the topic under discussion, would think that you were being completely sincerely intellectually curious, while at the same time employing a coded epithet unmistakable to those already inclined to agree with you. This is a very common tactic, but I have rarely seen it done so skillfully. Bravo sir!
Now leave and go do it someplace else. This is lesswrong, not realclimate
In my last post on Health Optimization, one commenter inadverntently brought up a topic which I find interesting, although it is highly contraversial—which is HIV/AIDS skepticism and rationality in science.
The particular part of that which I am interested in is proper levels of uncertainty and rationality errors in medical science.
I have some skepticism for the HIV/AIDS theory, perhaps on the level of say 20-30%. More concretely, I would roughly say I am only about 70% confident that HIV is the sole cause of AIDS, or 70% confident that the mainstream theory of HIV/AIDS is solid.
Most of that doubt comes from one particular flaw I in the current mainstream theory which I find particularly damning.
It is claimed that HIV is a sexually transmitted disease. However, the typical estimates of transmission rate are extremely low: 0.05% / 0.1% per insertive/receptive P/V sex act 0.065% / 0.5% per insertive/receptive P/A sex act
This data is from wikipedia—it lists a single paper as a source, but from what I recall this matches the official statistics from the CDC and what not.
For comparison, from the wikipedia entry on Gonorrhea, a conventional STD:
So it would appear that HIV is roughly 100-500 times less sexually transmittable than a conventional STD like gonorrhea.
So in my mind this makes it technically impossible for HIV to be an STD. These transmission rates are so astronomically low that for it to spread from one infected person to an uninfected partner would take years and years of unprotected sex.
If you plug that it to a simulation, it just never can spread—even if everyone was having unprotected sex with a random stranger every single day, it would still require an unrealistic initial foothold in the population by other means before it could ever spread sexually.
And of course, if you plug in actual realistic data about frequency of unprotected sexual intercourse with strangers, it’s just completely impossible. Bogus. It doesn’t work. It can not be an STD.
As gonorrhea (and I presume other STDs) are hundreds of times more transmissable than HIV, their low rates in the population place bounds on HIV’s sexual transmission.
Finally, these rates of transmission are so low that one should question the uncertainty and issues with false positives—how accurate are these numbers really?
A few years ago, I entered an online discussion with some outspoken HIV-AIDS skeptics who supported the theories of Peter Duesberg, and in the course of that debate, I read quite a bit of literature on the subject. My ultimate conclusion was that the HIV-AIDS link has been established beyond reasonable doubt after all; the entire web of evidence just seems too strong. For a good overview, I recommend the articles on the topic published in the Science magazine in December 1994:
http://www.sciencemag.org/feature/data/cohen/cohen.dtl
Regarding your concerns about transmission probabilities, in Western countries, AIDS as an STD has indeed never been more than a marginal phenomenon among the heterosexual population. (Just think of the striking fact that, to my knowledge, in the West there has never been a catastrophic AIDS epidemic among female prostitutes, and philandering rock stars who had sex with thousands of groupies in the eighties also managed to avoid it.) As much as it’s fashionable to speak of AIDS as an “equal opportunity” disease, it’s clear that the principal mechanism of its sexual transmission in the First World has been sex between men, because of both the level of promiscuity and the nature of the sexual acts involved. (And it may well be that HIV among heterosexuals would be even rarer if it weren’t constantly reintroduced into the heterosexual population via women having sex with bisexual men, let alone if the sexual transmissions from intravenous drug users were also absent.)
On the other hand, when it comes to African AIDS, it’s hard to say anything reliably. The public discussions of First World AIDS are full of nonsense, but at least there are enough reliable raw data to make some sense out of the situation; in the case of Africa, however, we don’t know anything beyond what we’re told from people with highly suspect interests in the matter, either careerist or ideological, and even if there are some truthful and reasonable voices in the whole mess, it’s impossible to filter them out in the sea of misinformation.
Also, here’s a pertinent comment I left on OB in a thread about the recent Medical Hypotheses affair: http://www.overcomingbias.com/2010/05/rip-medical-hypotheses.html#comment-447400
Quite interesting. I didn’t really know much about Medical Hypotheses until I posted a link in another thread (as a minor side point) to an article my dad wrote which happened to be in that very journal, and someone pointed out what it was. Strange connection.
A long while ago I found Duesberg’s papers and entered into some online debates taking his position. The end result of all that reading moved me into a position closer to yours, but more uncertain. I just went and re-read Duesberg’s most recent 2003 paper and noticed it still has a noticeable pull on me after reading it, but after going back and forth several times between the two camps I usually end up somewhere lost in the middle.
Duesberg, even though probably ill-fated in his main quest, has I believe shown that the orthodox establishment has gone wrong at least in part. The history of the whole affair seems like it should be a lesson that we should learn from, a lesson that somehow results in learning and moving towards a more rational scientific establishment, more cleanly divorced from politics. That may be an interesting discussion to have here, if it hasn’t already been discussed much. Deusberg suggests a jury process to replace the current peer-review system, which he is highly critical of. That could be an interesting rationalist angle on this.
To say that this makes it not an STD is to misunderstand what an STD is.
An STD is not a disease whose transmission method is specialised to the act of copulation. It is merely a disease which is so difficult to transmit at all that only the most intimate of contact has any substantial chance of doing so. What is important about the sexual contact is not the sex, but the blood contact.
In HIV we have something that is so difficult to transmit that even conventional heterosexual intercourse has difficulty. Closer blood contact is required for a high chance of transmission, such as in anal intercourse (the intestinal lining is fragile and not adapted to contact with foreign bodies) or injection from infected needles. This has been known practically since the start from the epidemiology, before any pathogen was identified.
I’m not in quite agreement with both of your points. Yes of course HIV is transmissable only through blood, but I don’t agree with that being a good criteria for use of the term “sexually transmitted”, especially when other STD’s such as gonorrhea are actually effective—they are measurably hundreds of times more sexually transmissable than HIV. This is probably due to both evolved mechanisms that those STDs have (such as ulceration formation) and overall low virality and transmissability of HIV.
So it is ingenous I think to change the categorization. HIV is clearly at an extremum, and perhaps would be better classified as a weakly transmissable blood borne disease, not an STD.
The evolutionary relevance is important here. How did this evolve?
At an (unrealistically?) independent 0.5% chance per act, a 50% chance of transmission would require 139 sex acts — hardly “years and years”.
(ETA: yes, unrealistically, according to this abstract found by Perplexed: “However, in comparison with nonparametric estimates, the model assuming constant infectivity appears to seriously underestimate the risk after very few contacts and to seriously overestimate the risk associated with a large number of contacts. Our results suggest that the association between the number of unprotected sexual contacts and the probability of infection is weak and highly inconsistent with constant per-contact infectivity.”)
At best, this can show that pandemic AIDS can’t primarily result from sexual transmission of HIV, which is evidence that AIDS has causes other than HIV, but also that pandemic AIDS spreads through other means (as suggested here, e.g.).
If you’re thinking of rates in the modern developed world, STDs are unsurprisingly more common when and where treatment is less available:
That is for the highest transmission activity—receptive A, so be careful not to cherry pick. Yes − 139 unprotected sex acts. It would take 1390 unprotected insertive A sex acts to reach a 50% chance of transmission.
So with some assumptions, mainly—gay bathouses and no condom use—yes the virus could spread horizontally, in theory. Although that population would necessarily first acquire every other STD known to man, more or less.
But in the general heterosexual population, not a chance. If you compare to the odds of pregnancy from unprotected sex, the insane requisite amounts of unprotected sex with strangers would result in a massive baby epidemic and far more vertical transmissions long before it could ever spread horizontally in the hetero population.
I don’t know why you mention “modern developed-world rates” and then have a link to 1901 NY and Africa . . .
You don’t need the “at best” qualifier, but yes I agree that is what this shows. Showing that however opens a crack in the entire facade. Perhaps not a critical failure, but a significant doubt nonetheless.
If the orthodox position had updated on the evidence, and instead changed their claim to “HIV is a borderline infectious disease that spreads primarily through the prenatal and blood-borne routes”, then I would give them more creedence. Of course, for political reasons alone they could never admit that.
Many non-AIDS STIs, and pregnancy, are curable.
Funny to think of pregnancy as curable, but yes of course that’s true. However, it doesn’t really change the numbers much.
Also, from what I have read about the early 80′s bathouse scene, it is possible that many of those guys did acquire every STD known to man, so at least in that case the sexual transmission route could work even with such terribly low efficiency.
Regardless, it seems strange to label it as a STD from an evolutionary perspective, it doesn’t fit that profile, and it seems incredibly unlikely it could have evolved as such.
It’s also funny to call babies an epidemic.
Life is a disease. It is transmitted by sex and ends deadly always.
touche!
What are the political reasons? Staying on-message and retaining funding, or something more specific?
Essentially the government committed to a public awareness campaign that HIV was ‘rapidly growing’ in the heterosexual community, and this became part of the dogma. It is politically motivated—it’s anti-sex message appeases religious conservatives while also shifting attention away from the gay bathouse scene, so it sort of benefits everyone politically, regardless of whether it’s actually true.
I meant “rates are higher outside the modern developed world”. Rephrased for clarity.
I don’t see why epidemiology should care about the 50% threshold. The relevant number is the expected number of transmissions per year. Thus independence is irrelevant.[1] At 200 anal tops per year per infected person, incidence should double yearly. And every top requires a bottom, so that’s 400 anal sex acts per year for just doubling. It seemed to spread more quickly than that, but maybe 800 and 4x per year works. It seems just barely plausible with this transmission rate. I’m not sure of the details of bathhouses, but I thought that there was a lot of non-anal sex, too.
[1] independence is relevant if 70s gays were systematically different from the people in the study; and they probably were, eg, they probably had higher rates of STDs
Why “more quickly than that”? From Epidemiology of HIV/AIDS in the United States:
This seems to indicate a doubling time of about 2 years.
ETA: Also according to that page, the patient with the first confirmed HIV infection died of AIDS in 1968, so the growth rate of AIDS before 1989 was at most 1.73x per year.
OK, maybe doubling works.
But it’s important to distinguish different populations. You should expect it to spread faster through the bathhouse scene than through the rest of the gay community than through the straight community. So it should slow down once it exhausted the bathhouse regulars (something like weekly visits) or when AIDS shut down that scene. If that happened around 1985 and there’s a 10 year incubation period, then the 1995 numbers still include bathhouse effects. Diagnoses were increasing at 3x or 4x in the early 80s: 100 in fall ’81 to 250 in mid ‘82 to 1000 in early ‘83 to 3000 by the end of the year. From ‘83 to ’89 it was merely doubling and it slowed after that. Of course, there are problems with diagnosis numbers early in an epidemic, but death followed quickly, in weird ways, so these numbers are probably good enough. Yes, there were people with AIDS in 60s, but that 1.73x includes time to get to the bathhouse scene.
One problem with this simplified model is assuming every sexual act is with a new partner, which would only be true in the very early stages.
I think your analysis is on the right track though, and it seems barely plausible with this transmission rate, assuming negligible condom use and an intense bathhouse scene. However, in standard theory HIV progresses to AIDS in about 10 years, so this sets a timer which starts removing vectors from the population.
Thus the exact exponent matters considerably. If incidence can only double every year, then after 10 years you get 2^10 ~ 1000 cases.
If incidence doubles every 6 months (quadruples every year), then you get a million cases after ten years.
If you consider that all other STD’s would infect this population before HIV, then one has to wonder how that would effect condom use, and how that changes the model.
So do you find the transmission rate and make the model before you decide that HIV was an STD which spread this way, or after?
It assumes that every sexual act is with an uninfected partner. Perhaps that’s what you meant, but then I wouldn’t have used “very.”
I think this is pretty well documented. STDs were routine and not a big deal (treatable!) in the 70s gay scene. Thus they did not cause condom use.
I’d point out that nobody is claiming that HIV is exclusively sexually transmitted; there are other methods of transmitting it, such as infected needles. Also, Wikipedia cites a paper suggesting that those rates you mentioned are “4 to 10 times higher in low-income countries” and as high as 1.7% for anal intercourse.
I don’t know whether or not these facts are sufficient to address your fundamental complaint, but they would make a pretty big difference.
It takes courage to voice a low but not negligible degree of doubt in a emotionally salient mainstream position. I would expect it to result in almost as much social punishment as in the case of outright denial. (Emotional backlash isn’t good at math.)
More concretely, I would roughly say I am only about 70% confident that HIV is the sole cause of AIDS, or 70% confident that the mainstream theory of HIV/AIDS is solid.
I am surprised that those two confidences happen to be the same. Is it not a distinct possibility that HIV is, in fact, the sole cause of AIDS even when the mainstream theory is itself rubbish? (For example, if the theory got important details such as mechanism completely wrong.)
I like this sentence.
I tend to think of “HIV being the sole cause of AIDS” as the central tenet of the mainstream theory, but sure that could be true even if much of the details are wrong. Actually, I think many within the mainstream would admit most of the details are wrong—last I checked all the important details, such as how the retrovirus could come active after many years and damage T-cells and what not are all still hot research items.
And most of the specific results have been failures—no vaccine yet, just some drugs with a bunch of side effects which may or may not even improve mortality, etc etc.
I find hypotheses in the middle more likely overall—examples: that HIV is a mostly harmless retrovirus but in some people with (X, Y, Z cofactors) it can cause immune damage.
And I yes, I am at least mildly concerned about taking an HIV skeptic position in a public internet forum—and just thinking about the reasons for that causes me to slightly update to be more skeptical.
Note that in general low-transmission rates aren’t that good an argument against it. First of all, a lot of transmission in the US occurred through other forms, especially early in the epidemic (intravenous needle sharing and transfusion of infected blood being two major ones). As others have noted the transmission issue is also generally higher for homosexual rather than heterosexual intercourse.
Frankly, the thing that I most don’t understand about people who are skeptical about the HIV-AIDS link is how one explains the fact that anti-virals tailored to deal with HIV work. Even the first-gen treatments such as AZT were used due to the biochemistry of HIV (often targeting reverse transcriptase). And they worked in delaying the onset of AIDS and worked for giving people with AIDS higher life-expectancy. I don’t see how one can easily reconcile that with HIV not being the cause of AIDS and I’ve never heard anything remotely resembling a coherent explanation about this.
The extremely low official transmission rates indicate that HIV is probably not a sexually transmitted disease, as typically understood. According to the published transmission data, it’s only effective natural means of transmission is vertical—from mother to child. From what we know about symbiosis and parasites, this should lead one to suspect it is not that lethal.
However that doesn’t destroy the hypothesis that HIV could be a unique disease of civilization—a mutation of a formerly limited retrovirus into a more damaging form that spreads horizontally only through extremely unnatural novelties of the modern world—needle sharing and epic promiscuity in some subgroups. It does of course make the overall hypothesis more complex and overall less likely, but it doesn’t destroy it outright.
This is very difficult to prove ethically, and certainly hasn’t been shown to satisfaction. Consider how immensely difficult it has been to understand the real health effects of fat in the diet, for example. In the 80′s and 90′s, we thought it was oh so simple. Today we (the wise) realize how profoundly ignorant we were then, and still are today. I think part of the rational reappraisal for the strength of the HIV hypothesis should come from a similar update.
In other words one can only cling to a high degree of certainty about the HIV hypothesis when one is profoundly ignorant concerning the depth of one’s ignorance about the complexity of human health.
That’s the theory.
Ahh the world would be so simple if that was true. The AZT clinic trial was ended prematurely and double-blindness could not be maintained due to side effects. The skeptics claim that later studies show that AZT increases long term mortality, not the other way around.
You need to realize how impossible it would be to concretely show what you presume to high certainty. You would basically need a double blind study with two control groups, one receiving plazebo, and compare total mortality. One immediate problem is any noticeable side effects would immediately end the blindness—and the retrovirals certainly have side effects.
And even showing that AZT or drug X reduces mortality in HIV+ patients does not lead to the conclusion that HIV is the cause, or that AZT or drug X has any effect on HIV. Supplementing patients with vitamin D, or changing their diet, or feeding them aspirin, or any number of other changes could also decrease mortality, but have nothing to do with the viral theory.
Health is complex.
So I don’t know what evidence you have for these claims. The original AZT study can be found here. It handled placebos just fine.
And AZT is just one example of many anti-retrovirals. 3TC and ABC have also been used. Moreover, there are studies which show that the the standard drug cocktails work better than AZT or 3TC alone. That makes sense for the standard model of HIV as the cause of AIDS.
There seems to be an issue here involving what level of evidence is necessary. From a Bayesian stand point you can’t ever “show” anything in the sense that you want. But the overall pattern of evidence can still give you a probability close to 1 that HIV is the primary cause of AIDS.
http://www.ncbi.nlm.nih.gov/pubmed/3299089
Ah you read this while I was editing it.
Yes I have browsed that abstract, although I can’t see if there is a full copy of the whole thing. Notice the link to the toxicity right next to it:
The toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex. A double-blind, placebo-controlled trial.
Notice that it has serious toxicity side effects, including bone marrow supression, and thus it can massively damage the innate immune system.
This is evident in the abstract itself:
The original AZT study could not possibly be placebo controlled, due to the high toxicity—this is basically chemotherapy. Now chemotherapy can be effective, but it can not be double blind.
Furthermore, due to high toxicity, only a fraction of patients actually completed the intended trial:
Only 27 out of 245 AZT subjects completed the full 24 weeks! One in the AZT group of 245 died in this period, but how many more in the AZT group would have died if they had been able to complete the full 24 week chemotherapy trial?
These were crazy times. These patients were very ill and very worried. It was a full scale terror panic. It was obvious who was on placebo and who wasn’t, and from what I have read, placebo patients were swapping and trading pills with AZT patients who couldn’t finish. It was many things, but not double-blind.
Here is what would be required to prove with > 99% certainty that HIV is the sole cause of AIDS:
Take a random sample of perfectly healthy test subjects. Now inject half of them with HIV and half with a placebo, and follow their health over the long term. That is about the only test that could get you 99% accuracy, and it is obviously not ethical.
So, instead we have to make due with what we have.
And again, showing that AZT improves long-term mortality—which the AZT trial clearly did not show, only shows that AZT improves mortality in sick AIDS patients. It doesn’t tell you much else about HIV as a theory.
It’s important that we agree on that subpoint—for it has nothing to do with the level of evidence.
There are many, many things that could improve mortality in sick AIDS patients. Stoss therapy, better diet, more sex, aspirin, etc etc. Do you think that proving a mortality decrease correlation in any of these categories would ‘prove’ they are the true cause of AIDS?
It also makes sense for the common sense model that reducing AZT doses down from outright lethal to mildly poisonous but tolerable ‘works better’.
jacob_cannell:
There have been documented cases of accidental HIV infection of lab workers and dental patients that are not too terribly far from such a controlled experiment. See: S.J. O’Brien and J.J. Goedert, “HIV causes AIDS: Koch’s postulates fulfilled,” Current Opinion in Immunology, Vol. 8, Issue 5, October 1996, pp. 613-618.
UPDATE: Ungated link to the paper here.
The article (listed as a “guest editorial”, I note for completeness) has the following citations in the relevant section:
52. Weiss SH, Goedert JJ, Gartner S, Popovic M, Waters D, Markham P, Veronese FD, Gall MH, Barkley WE, Gibbons J et al.: Risk of human immunodeflciency virus (HIV-1) infection among laboratory workers. Science 1988, 239:68-71.
53. Reitz MS Jr, Hall L, Robert-Guroff M, Lautenberger J, Hahn BH, Shaw GM, Kong LI, Weiss SH, Waters D, Gallo RC, Blattner W: Viral variability and serum antibody response in a laboratory worker infected with HIV-1 (HTLV-IIIB). AIDS Res Hum Retroviruses 1994, 10:1143-1155.
54. Guo HG, Waters D, Hall L, Louie A, Popovic M, Blattner W, Streicher H, Gallo RC, Chermann JC, Reitz MS: Nucleotide sequence analysis of the original isolate of HIV-1. Nature 1991, 349:745-746.
55. Wain-Hobson S, Vartanian JP, Henry M, Chenciner N, Cheynier R, Delassus S, Martins LP, Sala M, Nugeyre MT, Guetard D et al.: LAV revisited: origins of the early HIV-t isolates from Institut Pasteur. Science 1991, 252:961-965.
56. Wolinsky SM, Wike CM, Korber BTM, Hutto C, Parks WP, Rosenblum LL, Kunstman KJ, Furtado MR, Munoz JL: Selective transmission of human immunodeficiency virus type-1 variants from mothers to infants. Science 1992, 255:1134-1137.
57. Morbidity Mortality Weekly Report of the Center for Disease Control: Revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults (1993). 1992:1-19.
I’m not a skeptic, but I am a bit surprised that three infected lab workers is considered evidence worth mentioning. I’m accustomed to seeing clinical studies with fewer than 100 patients treated as merely suggestive, and several hundred or even thousands of patients necessary to convince regulatory authorities that there is a real phenomenon. So when I read that “three laboratory workers...became infected”, it strikes me as anecdotal. Of course you take what you can get, but still, it seems a small group.
My experience is with pharmaceuticals, which could explain the difference. But still, there’s a difference to be explained.
On the upside, if three is worth mentioning, then maybe one is worth mentioning, which would mean that Seth Roberts’s self-experimentation may be worthwhile.
Ok, so I have finished reading O’Brien and JJ Goedert. I think the accidental lab worker cases probably have low utility in distinguishing between pathologic HIV and passenger HIV theories, but the animal SIV studies potentially fulfill the ideal experiment design. If animals injected with pure close SIV analogs to HIV develop AIDS-like illness, that is about as good as evidence as one could hope for.
For the lab worker infections, they say that the genomes are close to the clonal strain used in the lab, but they don’t have a good probalistic model for this:
threefold more or less variation doesn’t sound like much to me, and regardless even assuming they did all get infected via the lab, it doesn’t mention treatment, so we don’t know if they were treated with AZT or what.
I think the animal models are more interesting—as all the drug cofounding variables are eliminated and everything is controlled.
The authors discuss 3 animal models—baboons, some wierd knockout mice with human t-cell graphs, and finally SIV injected into rhesus monkeys. They spend the most time discussing the latter paper so I looked into it.
“Induction of AIDS in Rhesus Monkeys by Molecularly Cloned Simian Immunodeficiency”.
In short, all 5 of the monkeys injected later become seropositive, and 50% of them progress to AIDs-like illnesses and die. Presumably some are naturally resistant.
There is a potential issue to this otherwise smoking gun, which is that it appears they had to inject whole culture of T-cells, as the virus can not be isolated directly into plasmid vectors:
But if all they had then was provirus integrated into PBL ( peripheral blood lymphocytes ), then one must wonder about the risk of graft versus host disease, and transfusion reaction in general. Basically, the foreign T-cell line can actively invade and cause all kinds of havoc. Perhaps they have controlled for that and I’m completely off, but I don’t see where they mention it.
OBrien and Goodart conclude:
I haven’t seen mention of ‘inactivated’ sivmaca239 yet in 80, but maybe it is in 83 or 84. However, if they are forced to infect live T-cells because they can’t produce viable clonal plasmid, this seems to have a major confounding factor in graft vs host disease. I’d like to find a knowledge skeptic take on this—perhaps Duesberg confronts it, not sure yet.
If he doesn’t confront it, then that doesn’t look so good for his position.
It appears to me that you are noting different weaknesses, different alternative explanations of the results, in each experimental protocol. I imagine that could appear to happen if there were a strong publication bias for results in favor of the hypothesis (e.g. with medicinal prayer studies), but that has not been demonstrated.
From what I understand, there is strong reason to suspect such bias in the animal models, as many other animal tests were conducted previously attempting to show SIV causing AIDS, and they uniformly failed. From what I have read, the SIV injections failed to do anything in chimps. We don’t know how many other rhesus monkeys were injected, but I find it highly unlikely that the five in this study (3 out of 5 of which developed immune defeciency) were the first.
That bias is interesting and it would be useful to have a metastudy covering all the animals that have been injected, but of course most naturally occuring strains of species specific virus should be expected to be harmless. So the ‘bias’ doesn’t really tell you much and is expected either way.
I’ll look to see if there is any skeptic review of the SIV injections which did succeed, because in my mind that is fairly strong evidence. If HIV analogs cause AIDS-like illness in primates when they hop species or traditional barriers, this is a good experiemental model for HIV crossing over into humans and causing illness, and is far stronger in my mind than the murky epidimelogical data with all of it’s drug cofactor issues.
The lab monkeys are in a controlled environment—we know they weren’t using drugs, weren’t fed AZT, etc etc.
Yes, but were they treated with chemotherapy agents such as AZT which cause bone marrow and immune supression? (I am asking before I read the article)
For the controlled experiment example, it would have to be double blind the entire time. Nobody would ever know who got placebo and who didnt’, and no difference in treatment regimens either way—all on the same diet, same lifestyle, etc etc. I highly doubt the accidental cases fit that profile.
jacob_cannell:
From what I see, O’Brien and Goedert don’t report about this. However, Cohen’s Science article to which I linked above provides more details about the cases of infected lab workers, claiming that two of them didn’t receive any antivirals until the progress of AIDS was well underway:
http://www.sciencemag.org/feature/data/cohen/266-5191-1647a.pdf
I have seen that, but I don’t take it as strong evidence of anything either way.
Clearly HIV antibodies are correlated with ill-health, poor immune function and low CD4 counts—that was established in the very beginning by Gallo et all and is the entire basis of their original claim.
But the competing hypothesis is not the null hypothesis, the competing hypothesis is that the HIV presence is a marker of some severe immune function failure, and that HIV itself is a largely harmless vertically transmitted retrovirus—like all the others. If it does become active, it is because something is already seriously wrong.
So of course if you have a lab, and you are testing lab-workers deathly afraid of contracting HIV, in either theory some may come up HIV+, and in either theory those that test positive will be ill.
This is very different than the intentional infection test you need to establish strong causation along a koch’s postulate principle. I think one of the stronger flaws in current HIV theory is the chimpanzee models—they have many HIV similar retroviruses (SIV’s), they are common in wild chimps, are all vertically transmitted, and don’t appear to be problematic for chimps. If HIV killed chimps outright, the mainstream theory would have some more ammo.
Instead the theory is that HIV came from a chimp SIV and somehow became lethal and horizontally transmissable at the same time in humans. But from the studies of sexual transmission—it is only weakly blood transmissable. So overall, it’s alot to swallow. I think it is plausible that this happened and HIV causes novel problems in humans, but it certainly has not been well demonstrated, mainly because HIV doesn’t cause specific symptoms and it is extremely difficult to properly dissociate other causitive factors. As Duesberg notes, the cocaine/meth craze boomed in the 80′s right as the AIDS epidemic started—they overlap perfectly.
Deusberg’s theory is that drugs specifically are a major cause of the immunosupression, which I think has some absolute validity, but we should also notice that there are other causes, and some people just have poor immune health, and this has been the case for long before HIV came on the scene.
I think that, in general, viruses that jump species barriers are more lethal in their new hosts than their old ones. Selection pressure tends to make viruses that are transmitted from individual to individual less dangerous over time, not more, because a dead host can’t spread the virus. So the fact that chimps tolerate SIV better than humans tolerate HIV isn’t a strike against the “HIV is mutated SIV” theory.
Also, there exists a more direct counterexample: FIV, feline immunodeficiency virus, is an HIV-like virus that is commonly found in lions. It doesn’t harm lions very much, but it’s lethal to domestic cats, which haven’t co-evolved with the virus the way lions have. (Specifically, lions compensate for the loss of T-cells to the virus by producing them in much larger numbers than other animals do.)
Perhaps not all viruses that jump species barriers are more lethal, but we care most about the lethal ones for sure, and lethality or host damage is a side effect of high replication, so yes I agree with your analysis.
I also said:
I’m reading the OBrien Goddert response now that cites some animal studis showing how some animal HIV analogs do fulfill koch’s postulate now. I am reading into the sources, but I wasn’t aware overall that they had found animal HIV analogs that caused AIDS like symptoms. I’ll have to update towards the ‘HIV is more pathogenic’ stance if this all checks out.
jacob_cannell:
According to O’Brien and Goedert, however, the strains of HIV found in these accidentally infected individuals were effectively identical to those from the source of their accidental infection, showing much less difference than is usual for strains taken from two random patients. This looks like powerful evidence against the competing hypothesis. On the other hand, it seems like there have been disputes about the validity of these identification procedures, and Duesberg and other skeptics raised some specific objections to them back then. However, this gets into technical issues that I’m definitely not competent to judge on.
(I should add that I haven’t delved into the references provided by O’Brien and Goedert, which Robin has conveniently listed in his above comment, to see if their summary of the facts is accurate and complete.)
Also, while we are looking at evidence for one side or the other, I should present some of the recent evidence that supports the Deusberg hypothesis, namely that cocaine use can cause HIV progression and AIDS-defining illness. Heavy cocaine use and HIV+ status are extremely correlated, the question is one then of causation.
Just search for “cocaine cd4 counts”| From a rat study linked here
Even more interesting—an abstract from a more recent study showing that crack cocaine can cause AIDS independently (in women at least)
CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women.
A blog discussion of this here
Perhaps the tide’s are turning in Deusberg’s favor?
I was under the impression that there was only 2 HIV strains, and only HIV-1 is of concern in the west, but I’m no expert on this.
Do you have the O’Brien/Goedert paper link or any of this discussion? Your earlier link was just an editorial summary. Sounds interesting, I’d like to read more into it. (i am going to search now, but if you have the link . . .)
If O’Brien and Goedert are right, it would depend on how many strains there are and what their prevalence is ahead of time—I think Bayes’ Theorem would apply, no? Also, I guess we just have to presume that no other sick people from the sample were not reported. And finally, the sample size of 1 or 2 raises some theoretical issues, but still it would be interesting.
No. There are two major HIV strains, HIV-1 and HIV-2, with the vast majority of infections in the US being HIV-1. However, there are many substrains of both. In general, since HIV has a high mutation rate, there are individual genetic markers for different people. No one who has HIV for more than a few weeks has a single form of HIV in them but already will have a population of slightly distinct forms. This is part of what makes HIV so pesky for the immune system, for developing vaccines, and for developing drugs to combat it. Note that this isn’t that rare. For example, influenza does something similar although my impression is that this is not nearly as extreme an example.
Frankly, this is a very basic aspect of HIV biology, which you could find on any primer on the subject. If one doesn’t know about this, this suggests major gaps in one’s knowledge base about HIV and I’m not at all sure that one who doesn’t know about this has enough background to discuss issues related to whether HIV causes AIDS.
Because he said “2 HIV strains” rather than “2 major HIV strains with many substrains”? He should be disqualified from participating in debate on a topic because he failed to use sufficiently precise language on a point not relevant to the current discussion?
I’m a non-partisan on this issue, having not researched it enough to have a firm opinion… but the consistent use of these kinds of dark side debate tactics by one side makes me seriously tempted to update in the opposite direction.
This isn’t a “dark side” tactic. Vlad wrote:
It seemed pretty clear from context that Vlad was talking about substrains. If there’s anything that went wrong here, judging from Jacob’s followup remark, it was an illusion of transparency failure on my part in that Vlad’s meaning seemed clear to me, and I then made the (erroneous) conclusion that someone with a basic background would also get what Vlad was talking about.
Note incidentally, that using heuristics about whether or not someone has enough background to understand or discuss something is not intrinsically a dark side issue to start with. Indeed, sometimes it is very necessary. See for example some of the discussion on cousin it’s recent post where it seemed that some individuals (well, primarily one individual) were making repeated subtle but highly relevant errors about certain ideas related to Godel’s theorems and Turing machines. After repeated attempts to explain, the mathematicians in the thread (including myself) started trying to explain that the errors in question were basic enough that further attempts to explain would likely be fruitless. That’s not a dark side tactic, sometimes that’s just true.
Yes, I absolutely agree. But that’s not the tactic I was referring to. The tactic in question consists of finding some nitpicky objection to something your opponent said, something not directly relevant to the issue at hand, and something which isn’t even wrong, just insufficiently precise, and discounting the substance of their argument on that basis.
Hrrm? Imprecision if anything occurred on Vlad’s part, not Jacob’s. Again, see issue of illusion of transparency matter. See also Vlad’s remark below.
JoshuaZ:
Yes, of course. I’m not familiar with the finer points of terminology in this area, but the O’Brien-Goedert paper uses the term “strain” both for the two major strains and their sub-strains, and I’ve noticed the same in many other papers too. So I don’t think this was imprecise in any way.
Vlad originally used the word ‘strains’, not substrains, and I have only ever heard ‘strains’ used in reference to HIV1 and HIV2 as you say. But yes I am at least somewhat aware of sub-strains through protein coding variation in viruses in general, and how mutations lead to new epidemics.
I’m not sure what the proper ‘background’ is just to discuss an issue, but I probably don’t have it, regardless.
Ok. Seems to be an error in communication more than anything else then.
FWIW, you seem to have a much better understanding of a lot of this material than most of the HIV-AIDS skeptics I’ve interacted with in the past.
(I initially posted an excerpt from the paper in this comment, but in the meantime, I found an ungated version. The stuff about the accidental transmissions is on page 615.)
The article cited here? I downloaded a copy if anyone wants to PM me an email address.
I’m not sure you are allowed to demand that specific piece of evidence.
If you want absolute certainty, you need to fulfill koch’s postulates, which is the medical disease variant of experimental physics, and is well grounded.
So yes, in questions of science, we do demand specific evidence for near-certain proof, but naturally when that is not possible for whatever reason, we can still update based on other evidence and reach well grounded conclusions.
First of all, you never have absolute certainty. Proof is for math and alcohol. You may also want to read the Sequences relevant to Bayesian reasoning especially about how 0 and 1 are not probabilities.
Note also that even outside a Bayesian context, Koch’s postulates are a rough framework. For example, sometimes there is great difficulty growing an organism in a culture (Koch’s second postulate requires this), and sometimes only a fraction of a population may be symptomatic. Even Koch was willing to treat the first postulate as a guideline rather than a hard and fast rule; he worked with multiple examples of microorganisms that showed up in some healthy people but didn’t cause disease In fact we know now that this very common. Many causes of minor infections, such as staph, are present on everyone. It then takes some problem, such a wound, or disruption of the immune system to cause the person to become unhealthy. For viral examples, look at asymptomatic herpes or HPV.
Frankly, referring to Koch’s postulates like this are one of the things that makes many people with medical knowledge not take the HIV-AIDS skeptics very seriously. As a general heuristic, cranks like to take old ideas and try to use them to argue against some modern result even when that idea isn’t used in the current form or isn’t as absolute as they make it out to be. This seems for example to occur frequently with creationists who use an oversimplified form of Mendelian genetics that seems to date prior to the work of Hardy, Weinberg, and Fisher. As a way of preventing this signal, referring to such things as Koch’s work can be done, but you need to be clear that you understand the limitations it has. Otherwise, it just sets off alarm bells.
This bears repeating.
It is also difficult to empirically test elements of String Theory or evolutionary history. This difficulty isn’t taken to be evidence for against those theories. Lack of easy clear cut empirical tests is just that—lack of a simple theorem discriminator. I am not claiming that it is some magic pass required for any theory to be credible.
On the other hand, nor can one use lack of said simple theorem discriminator to get a free pass and somehow claim to have extra certainty—that most come from evidence regardless.
However, in this case I do think that the general idea of Koch’s postulate is highly relevant, it is not ‘cranky’ to invoke it, and in fact it is probably the single strongest piece of evidence for the mainstream position—as Vlad M pointed out to me.
I am currently reading: ” HIV causes AIDS: Koch’s postulates fulfilled” Guest editorial Stephen .I O’Brien* and .lames ,i Goederff
It reviews SIV models where SIV can be prepared and injected into monkeys and in some cases does cause AIDS like disease progression (usually more quickly than HIV).
So I don’t think your associations between “referring to Koch’s postulates” and cranks, and your general heuristic are valid at all, not when the mainstream is listing this as a centerpiece of evidence.
I haven’t read the editorial yet, but I’m not sure where the notion that this was a centerpiece of evidence comes from. I was vaguely aware of this result but never have paid it much attention. I suspect that if one talked to active AIDS and HIV researchers they’d say that there was a very strong case even without this. But yes, conservation of expected evidence does come into play here, so you have a valid point. In any event, the upshot that Koch’s postulates are not seen as any sort of absolute is very much relevant.
S.J. O’Brien and J.J. Goedert (1996) (the paper cited by Vladimir_M) specifically references Koch’s postulates. The accidental infection of laboratory workers is only one of five items cited in reference to (I believe) #3, “The cultured microorganism should cause disease when introduced into a healthy organism.”
Ever since I’ve read in Guinea Pig Zero about test subjects who feel that they’ll never be able to afford medical care and cheat on the requirements of an experiment (for example, not following dietary changes they’ve signed on for), I’ve been that little bit more dubious about drug studies.
Have you seen these two recent meta-analysis of HIV transmission rates? Comparing them to your numbers, it seems that Wikipedia/CDC have greatly understated the risk for P/A sex acts (due to using older studies?).
Also, according to this page, the transmission rates for genital herpes are similar to HIV for P/V sex acts, so AIDS is not the only STD to have such low transmission rates.
I think the conventional theory is that HIV established an initial foothold by means such as needle sharing, blood transfusions, and P/A sex acts. That seems quite realistic to me. Why do you think it’s unrealistic?
No I haven’t seen them until now. I haven’t really been looking into or thinking about this until just recently.
I originally quoted the wikipedia data, which several us tracked down and analyzed in another thread (it comes from the CDC and originally from a single medium-ish European study which I think did a fairly good job to control for factors such as condom use and what not given the complexities):
Let’s compare to the 1st meta-analysis:
it finds 0.04/0.08% for insertive/receptive P/V sex in the 1st world, very similar but slightly lower to the older CDC study (from europe). They find the rates are around 5 times higher in the 3rd world.
For P/A receptive, they find a pooled per-act rate of 1.7%, about 3.5 times higher than the 1st world CDC study. I suspect this is simply because they pooled 1st and 3rd world data together.
This does not show that Wikipedia/CDC have “greatly understated” the risk for P/A sex acts—this data is in agreement. The variance is between 1st and 3rd world studies. The 1st world data is of paramount concern for the historical origin theory of the disease. The 3rd world data is a side point—not historically important and suspect in general, as in fact mentioned in the abstract.
The abstract:
So this supports the original CDC data for the 1st world.
The second meta-study finds a receptive A per act rate of 1.4%, a little lower than the 1st study, and about 2.8 times the 1st world CDC data. They make no mention of what countries, and I assume it mixes 3rd and 1st world data—it is a large meta-analysis of many studies.
There is also some serious wierdness in the 2nd study:
So something doesn’t fit—the per act and per partner numbers don’t square up at all. Somewhere else someone posted an abstract with a similar result, how basically your chance of infection levels off quickly in couples and is much lower than you think—you are either going to get it or not irregardless of number of sex acts. This suggests that there are some major unknown immunity factors at work or the entire model is wrong.
I think the needle sharing and blood transfusions is far more credible, but the 0.5% ish per act of receptive A in the 1st world could possibly support a sexual vector in the gay bathouse scene, but it is debatable.
The conventional theory requires that HIV came over as a mutated form of harmless simian SIV and spread here, through a single source vector from what I recall. Blood donation might make more sense, but one would have to look at the epidemiological models for that.
Perhaps vulnerability to transmission is partially dependent on prior immune health. That would predict faster spread where health-in-general is worst, ie Africa, as observed, and also explain the discrepancy between prevalence and observed traqnsmission rates. I also recall reading an article about a widely afflicted demographic in the US (a particular subset of gays in a particular city—I don’t recall which one), which suggested that they had already weakened their immune systems with drugs and sleep deprivation.
The other possibilities are that the transmission rate you quoted is wrong for some reason, or that the sexual transmission aspect has been overstated, and most transmission is through reused needles and other blood-borne vectors.
Note that spreading the idea that the transmission rate of AIDS is low has negative utility, regardless of whether it’s true or not, since it would encourage dangerous behavior.
This is untrue. Consider a similar claim: “spreading the idea that very few passengers on planes are killed by terrorists has negative utility, regardless of whether it is true or not, since it would encourage dangerous behavior.”
Informing people of the true risks of any activity will not in general have negative utility. If you believe a particular case is an exception you need to explain in detail why you believe this to be so.
In the case of infectious diseases, there are large unpriced negative externalities involved. Everyone doing what is individually rational, given true beliefs about transmission rates, is likely not socially optimal, because the expected individual cost of a risky action is less than the expected social cost. Giving people false beliefs about transmission rates can improve social welfare by shifting the expected individual cost closer to the expected social cost.
Are you talking about free rider problems with health care costs under a partly or fully socialized health care system or something else? STDs seem to be less of a problem than more easily transmitted diseases like flu for most negative externalities I can think of.
And also, if you take some risky action that increases your chances of get infected, that also increases the chances of everyone else getting infected (causally, via yourself getting infected and then infecting others).
I’m not sure I get your point here. Whether it’s more or less of a problem doesn’t seem relevant to the original claim that spawned this subthread.
It’s relevant to using your negative externality argument to support the original claim. To be consistent you would have to argue that we should make even more effort to avoid spreading the idea that airborne diseases like flu have low transmission rates (if true) than the idea that STDs have low transmission rates. Are you advocating a general policy of deliberately misleading people about the risks of various activities in an effort to correct for negative externalities? I’m pretty sure more efficient and robust approaches could be found.
It would be consistent with Wei Dai’s claim just to argue that we should make an effort to not reveal how low the transmission rate of influenza is among people who don’t wash their hands; we know that hand-washing is a large factor in transmission, but actual transmission rate numbers are still low enough to fail to convince people to wash their hands.
From a brief study of those particular numbers (I worked on a team modeling the spread of H1N1), I feel like we already mislead the public about the numbers themselves by being truthful as to the societal benefits and somewhat optimistic about the individual benefits of hand washing. If you believe more robust methods are more efficient, by all means, advocate for them, but I’m reasonably happy with the current situation.
From another perspective, blood-borne pathogens are particularly worth focusing on because they are easier to control. If we could encourage the entire population of the world to behave safely (not reuse needles, use condoms for sex, etc.), it would be a fairly minor change for individuals, but could eradicate or nearly eliminate HIV over time. With the flu, safe behavior will limit the damage of seasonal infections, but it’s not realistic to actually eliminate the virus. Thus, over the long term, I think the negative externalities of HIV might outweigh those of influenza.
I think government policy makers and public health authorities already use a variety of approaches to reduce negative externalities related to infectious diseases, including subtle misinformation, such as making efforts to correct people’s beliefs about transmission rates when they are too low, but not when they are too high (anything really obvious wouldn’t work in a free society like ours). But it seems clear that large negative externalities still exist. What other approaches do you have in mind, and why haven’t they thought of it already?
I think we’re starting from quite different assumptions about how society works. I don’t believe that government policy makers or public health authorities are very rational. Even to the extent that they are rational, I don’t believe that their incentives are such as to reliably lead them to decisions that maximize utility by the kind of utilitarian calculus you seem to be assuming. So to the extent that we agree negative externalities exist (and I suspect we differ a fair bit on what they are and to what extent they exist) I have very little expectation that government policy makers or public health authorities will tend to take actions that minimize them.
What did you mean when you said “I’m pretty sure more efficient and robust approaches could be found”? You’re not offering any concrete ideas yourself, and apparently you weren’t thinking of government health authorities when you wrote that, so who is supposed to find and apply these approaches?
Think ‘market based’. Internalize negative externalities. To a first approximation this usually means reducing government involvement rather than increasing it. This is straying into politics though so maybe we should avoid further discussion of this topic.
Compared to the rest of this open thread, I don’t think you have anything to worry about!
Seriously though, I think we’d both like to hear you elaborate upon your market-based idea. I don’t think I got any useful information out of your blurb.
Let me first clarify the points I was making in this thread (which were not intended to lead to a debate about healthcare or politics in general). If you still feel we have substantive disagreements that we might be able to resolve through more explicitly political discussion I’m willing to continue the conversation unless there are strong objections from others.
First my points were not intended to imply any particular opinion on AIDS transmission rates specifically. My initial post was simply intended to point out that the utility of spreading the idea that AIDS transmission rates are low is dependent on the truth of the claim.
This was intended to be a more general point that exaggerating the risks of any particular activity is not a good general policy. In the AIDS case there are genuine costs to taking precautions against transmission, even if they are in fact greatly outweighed by the benefits. In a hypothetical world where transmission rates are negligible, maintaining that they are high would have negative utility.
Wei Dai responded by claiming that because of negative externalities associated with infectious diseases, exaggerating the transmission rate can improve social welfare. Now this is not incompatible with my original point, it is rather a claim of a mechanism by which exaggerating the risks of an activity can have positive utility. It is probably worth noting at this point that I am not a utilitarian so I am likely to disagree with utilitarians on what outcomes have positive utility but we can probably agree that in general internalizing negative externalities is a good thing.
I concede that it is possible in theory to imagine a situation where deliberately exaggerating risks has positive utility. The fun thing about negative externalities though is that it is very easy for an intelligent person to think of some and to propose plausible mechanisms by which any given action can be justified. I could easily argue for example that the credibility of science and scientists is undermined when they are caught making false claims and that the negative utility resulting from this outweighs any positive utility from individual acts of well intentioned deception.
Ultimately though I have what you might call a deontological normative belief about science that it should always pursue the truth and leave the task of judging when to strategically lie to others. I also suspect that this is a winning strategy for agents with imperfect powers of prediction but that is mere supposition.
Regardless, if negative externalities associated with infectious diseases are the real concern I’m pretty confident that you’d start with much higher expected value actions than lying about the facts in an effort to influence individual choices. If individuals are not bearing the full costs of their actions then there are more direct ways of changing their incentives such that the costs are better reflected than trying to influence their beliefs away from the truth by spreading false facts. This is the point at which I’d start to get into the politics of healthcare however and I don’t particularly want to do that here.
Agreed. I think Wei Dai and I also agree (without speaking for Wei Dai), but think that the idea transmission rate to spread is conceivably a function of the true transmission rate, rather than locked to the true transmission rate itself. It sounds like you agree with that too, but are a little more stringent with what makes that “conceivably” true.
To my mind, one such situation is one where a super-majority of the population don’t understand probability, and 1% effectively means “never” to those people. In this case, specifically lying about the number is less helpful than phrasing it alternate true ways, but because they don’t understand probability, if you asked them to estimate a probability based on the true facts you just gave, they might say 10%; I might consider them deceived, even if you weren’t doing anything that would deceive a rational agent.
This is a good point, much like Ends Don’t Justify Means (Among Humans). One small caveat I’d like to make is that I don’t think we are talking about science (or more accurately) scientists lying to the populace. I think what we are discussing are administrators, media outlets and policy makers that are informed of the numbers (it would probably be too generous to say informed of the science) choosing not to widely disseminate them in favor of reporting non-numerical information that might lead the populace to adopt an inaccurate belief about those numbers.
Yes. Please elaborate, this seems to be the most interesting part of the conversation, and the way you’re conversing now, I don’t see why you’re worried about a backlash. It would probably be wise to be as general as possible and not make any specific reference to a given countries system of healthcare (if that’s where you’re going), but if you have a real point I’d really like to hear it.
Again, I wasn’t purely speaking about false facts, more about choosing which true facts to announce, and in what way to achieve the desired impact. One doesn’t have to lie to manipulate, and it’s generally not the best strategy. I’m also not claiming that manipulation should be a primary goal, but selective revelation of data (which will always happen because of time and attention constants) is bound to be manipulative, even if accidentally, and it would be better to produce desired action than undesired action, so we should be aware of the manipulative potential of what we plan to say.
Ok, we’ve had two examples of negative externalities associated with infectious diseases. I brought up the free-rider / moral hazard problem of the costs of treating the disease not being fully born by an individual who engages in high risk activities. Wei Dai brought up the problem of an individual who gets infected as a result of high risk activities increasing the risks of others getting infected by increasing the incidence of the disease.
Now if negative externalities are your true concern then you should address them as directly as possible. There are a variety of a variety of possible solutions to addressing negative externalities. Note that lying about the actual damage caused is not a standard solution.
The moral hazard / free-rider problem is a general problem that affects healthcare as it is organized in most developed nations. A significant number of people consider this a feature rather than a bug however. If you actually wanted to internalize these negative externalities the most direct way would be to allow insurers (or the government, though that would be less efficient) to set their healthcare premiums on the basis of any relevant health or lifestyle information.
While this happens to some extent (smokers or the obese may pay extra under various systems for example) it would be controversial in others (charging homosexuals higher premiums if they were at greater risk of contracting STDs for example). It would likely be even more controversial for conditions that are not generally perceived as due to bad personal choices (as smoking related illnesses or obesity are by many and homosexuality is by some on the Christian right). The suggestion that insurance companies might charge higher premiums based on genetic testing is widely regarded as unreasonable for example and I’m sure the same would apply if premiums for a government run system were so determined. Why such discrimination is considered outrageous for healthcare but is routine in some other areas of life is left as an exercise for the reader.
As to the problem of an infected individual increasing the risk of others getting infected, criminalization, civil tort law and pigovian taxes are all possible approaches to internalizing the externalities. My point that STDs present less of a problem in this regard than airborne infectious diseases like flu was that the parties put at risk are generally more able to control the risks themselves (easier to limit your exposure to STDs than to the flu) and that the source of the infection is generally easier to identify (most people have a much shorter list of candidates for infecting them with an STD than with the flu). There are fairly significant practical difficulties to prosecuting individuals who get infected with the flu and then spread it, to suing someone who has so infected you or to targeting taxes at those who put themselves at high risk of flu infection. All of these are practical to some degree with STDs.
Fundamentally my point is that if negative externalities related to infectious diseases are the real problem you are concerned about, there are standard ways of internalizing negative externalities that could be applied. Trying to justify misleading the general public about the actual risks of certain activities and the actual benefits of certain precautions on the basis of negative externalities raises the question of why you are not focusing your efforts on these other more direct and efficient means of internalizing those negative externalities.
Thank you very much for your reply. I really did want you to specify more clearly what you were talking about. It seems obvious to me (now) that anyone following your line of thought would have understood what you were talking about from your earlier comments, but I didn’t, and I hope you can forgive me for not understanding without further clarification.
As an aside, smoking has an obvious externality in second-hand smoke, which is often directly regulated by outlawing smoking in certain areas. What are the negative externalities of obesity? If we are to believe some recent studies, fat people may make the people around them fatter, which is a non-obvious externality, but does obesity have any commonly-recognized effects on people other than the obese when not considering subsidized healthcare, or is it only considered to have that externality when healthy-weight individuals are contributing to the costs of obese individuals?
This is at least possible with in some places regarding HIV, as well as pursuing criminal charges (examples).
Even more off topic, but on topic with the much more inflamed discussion in the adjacent thread, while looking for that reference I found this. I was thinking at first that a man infecting 13 women would be in contradiction with the extremely low transmission numbers for HIV. Here are what my numbers look like: with (2006 estimates—I couldn’t find number for late 1990′s) 8e5 HIV+ men in the US, a 50-50 chance that one of them would infect 13 women requires that they each engage in an average of 2845 acts with a 0.08% tx rate (unprotected P/V), 762 0.3% tx rate acts (low-income P/V) or a mere 139 acts with 1.7% tx rate (unprotected P/A). The probabilities get much more complicated when dividing demographics, but while those are unrealistically high numbers, they aren’t off by an order of magnitude; at least, the low-income P/V figure probably isn’t. Actually pulling any information off that data point, given that it is singular and unreliable is stupid, but if it were too be believed we should expect that HIV has a true aggregate transmission rate closer to 0.45%, given reasonable assumptions about average frequency of intercourse. Of course that aggregate can easily be composed by a few high-risk activities and lots and lots of low risk activities.
EDIT: I got so distracted I forgot what the main point was
I point out only your use of the word “efficient”. Misleading people is so easy it’s almost impossible not to do it, so the cost / benefit ratio doesn’t have to be very high to make it an efficient activity. As far as effectiveness, I agree that other, more direct measures can be much better.
As I mentioned earlier, negative externalities are easy to dream up. Many people consider it legitimate to complain about negative externalities caused by ugly buildings (such as power plants, wind farms or architecture that doesn’t fit with its surroundings) but complaining about the aesthetic negative externalities associated with unattractive people in public places is not generally considered legitimate.
In practice in democratic society these issues are generally resolved by who can shout the loudest or wield most political influence and not by any direct rational accounting of costs. It is not clear for example that the relatively small risks associated with second hand smoke justify trampling on the rights of smokers to indulge outside of their own homes, especially given that smoking is already subject to large Pigovian taxes in most countries with such bans.
It should at least be positive. It is not clear that it is in practice. It seems plausible to me that the general public distrust of government advice on risk that underlies phenomena like anti-vaccination movements is a direct result of an ongoing pattern of deliberately misleading people about risks. Overall I don’t see a strong reason to suppose the net effect is beneficial.
Best point brought up yet. While to some extent I think that mistrust of authority is indefatigable, increasing the risk of that is probably much more costly.
How do you feel about the specific example I mentioned, where the true risk of transmission of something is 1%, but the media outlet or whatever decides to omit the number and instead say something like “over the course of a week, an individual can spread disease X to over a hundred people”, and while true, that convinces individuals that the specific risk is much higher than 1%?
I personally find it a little irritating when the media omits information that would be necessary to work out actual risk numbers for myself. I don’t object if they communicate the numbers in a way designed to have maximum impact on the typical human mind (it’s been suggested that using frequencies rather than probabilities may help for example) but I do object if they leave out crucial information required to figure out true risk estimates. Of course I don’t generally assume this is some grand conspiracy but rather reflective of the innumeracy of the media in general.
I don’t believe in grand conspiracies because they just require too many contingencies. All this discussion, from my perspective, is about the potential for a tacit agreement between most (not all) of those disseminating information in various ways that the best method of talking about public risks is not necessarily to directly discuss low numbers associated with them.
As I indicated earlier, I think that this agreement effectively already exists regarding influenza, and probably also HIV and other infections as well.
Strictly speaking, Wei never claimed anything about what we should do. (Even if everything he said is correct — and it seems obviously so to me — it’s plausible that we’re best off with a policy of authorities never lying about risks, due to unintended consequences, public trust, slippery slopes, &c.)
I think you’re on to something, but wouldn’t that cause officials to overstate transmission rates rather than understate them?
What is especially strange to me is that the government pushed a fear campaign for HIV and promoted as a dangerous STD for the mainstream hetero community, but neglected to double-check their official statistics, which rather clearly destroy the STD theory. Perhaps it’s just an honest mistake, but I don’t think so. From what I have read, they have spent time trying to get honest statistics. So they overpromoted the STD message, regardless of the actual statistics.
Regardless of what HIV actually does or is, public campaigns to reduce needle sharing and reduce unprotected sex are probably net public goods.
However, on the other hand, if AIDS is really caused by drug toxicity, then at least some people are actively being harmed by spending energy in the wrong protections.
But I agree with your central point, and it applies to vaccines especially—they don’t really have much of an individual benefit, but if enough people can be convinced to vaccinate, the entire epidemic can be curtailed or completely avoided.
That needs some clarification. Most people cannot distguish between a risk being somewhat low, and it being extremely low, so we need to be careful about the transition from numbers to qualitative divisions. The risks of being killed in a plane crash are so low that unless you’re a pilot, you should ignore them; and overestimating the risks of flying would cause too much driving, which is more dangerous. In the case of AIDS, the probability of transmission may be “low”, but none of the numbers given are so low that they would justify skipping any of the common safety precautions, so we shouldn’t describe the probabilities involved as low in the presence of people who can’t do the utility computations themselves.
Topical.
So as an addendum to this, I found this blog which I am now reading as it has an updated view from the HIV skeptic position. Here is a post analyzing a recent study showing that cocaine can cause AIDS
CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women
The 1st commenter had an inside view which I thought was especially interesting:
This certainly supports my eyewitness accounts of back in 1987 when several friends and acquaintances consciously or subconsciously decided that an HIV positive diagnosis surely meant death in 2 to 5 years, which led them onto severe crack and cocaine binges up until they were finally put on AZT monotherapy. Sad to say what the results were. Now they’re all part of the statistics. Can I say self-fulfilling prophecy?
Cocaine is a drug that a) can damage the immune system and b) reduce appetite. It isn’t at all unreasonable that HIV positive individuals who were heavy cocaine users would therefore progress to full AIDS faster than others. Note also that a 2-5 timespan isn’t that far off from the timespan one would expect from HIV infection to emergence of AIDS given no treatment. Note that the study authors don’t seem to think that this is at all unusual and nowhere do they claim that the use of crack cocaine was somehow causing AIDS.
Sure, but it makes it more difficult to dissociate what the cocaine and virus are doing independent of each other, ie it makes it difficult to tease out the cause and effect from the correlation.
Right, but that makes it just weak evidence. So it isn’t very useful for the claim that cocaine somehow causes AIDS.
Well not quite, because cocaine was causing AIDs-like symptoms before HIV was presumed to be around, even if the great rise of cocaine use in the 80′s in the west happens to correspond exactly with the rise of AIDS.
What’s your source for this? Looking at the cocaine statistics and AIDS statistics myself, I’m not seeing this correspondence. What I do see is that cocaine use dropped to a fraction of its peak level by 1990, while AIDS kept rising.
Just go down to the graph in your first link and look at the emergency room drug mentions and see the cocaine serge—it does indeed correspond to the AIDS epidemic. Deusberg’s 2003 paper has more on this, but it’s in the data you linked. From the emergency room data it looks like cocaine use was still growing up to 2001, but my point was with the rise. AIDS peaked in the mid 90′s from your data link.
This much at least is something that should be relatively easy to confirm to a reasonable level of satisfaction. It would seem to require only a microscope, as syringe and a sufficient sample of people with AIDS. Has anybody ever founds someone with AIDS who did not have HIV? If not is that because nobody has bothered to take a close look? If so then I would certainly support your questioning of the standard of research supporting the mainstream position.
According to skeptics, yes, in all but name. The standard skeptical argument is that AIDS, as it is currently defined, includes HIV+ as a necessary diagnostic criterion, and that this is a circular definition: if someone presents with all the symptoms of AIDS, but tests HIV-, then they are defined to not have AIDS. This means that 100% of diagnosed AIDS patients will be HIV+, just by definition, not due to a meaningful correlation.
The skeptical position here is that you can’t actually see a virus with an optical microscope (which I believe is true), and “HIV tests” are actually just testing for HIV antibodies (or substances alleged to be HIV antibodies), not HIV itself.
I’m not endorsing these positions, just passing them along, btw.
Thankyou. I’m not familiar with the subject and wanted the information.
Yes, unless one defines AIDS as a collection of symptoms plus HIV. I forget the name, but any definition of AIDS which does not include HIV has some HIV-.
Now on the other hand, AIDS is a syndrome of immune supression, not a disease, so there of course could be other things that cause a similar syndrome.
If you are interested in venturing down that rabbit hole, read a little Duesberg:
(warning: reading his papers may result in general increased skepticism about the medical establishment)
http://www.duesberg.com/papers/chemical-bases.html
Now that is a familiar mistake—and a negligence that does real damage. I’m more familiar with the mental side of the medical establishment so have seen, for example, ADD symptoms lumped together and medicated presuming there is only one distinct etiology. Looking at a brain scan could tell them the difference easily enough.
That would be surprising—purely because my existing skepticism is already significant. All the more so after I spent some time involved in medical research myself. Scary stuff. “Hang on, wait. you want me to do what with the data?”
I find denialism in all forms simply fascinating. I wonder if you could indulge my curiosity.
You find your arguments completely convincing. Yet they are based on publicly available statistics and rather obvious and common-sense kinds of reasonings. So, I have to wonder, what do you think is wrong with the cognitive apparatus of all those medical and research professionals who believe that HIV == AIDS and is an STD?
Why don’t they reach the same conclusions as you? Are they stupid? Just haven’t thought of the train of thinking you use? What are your guess as to where they are all going wrong? Why none of them has realized the simple truth and shared it with colleagues?
Incidentally, I have a hypothesis as to what is wrong with your reasoning, which I will share on request, but I really want to understand how you reconcile your own certainty with the opposing certainty of people who (on paper) seem far better qualified on this subject.
I will indulge your curiosity in a moment, but I’m curious why you use the politically loaded term “denialism”.
As far as I can tell, it’s sole purpose is to derail rational dicussion by associating one’s opponent with a morally perverse stance—specially invoking the association of Holocaust Denialism. Politics is the mind-killer. In regards to that, I have just been spectating your thread with Vladimir M, and I concur wholeheartedly with his well-written related post.
There is no rational use of that appelation, so please desist from that entire mode of thought.
Firstly, I don’t think nearly as many quality researchers believe HIV == AIDS as you claim, at least not internally. The theory has gone well past the level of political mindkill and into the territory of an instituitionalied religion, where skeptics and detractors are publically shamed as evil people. I hope we can avoid that here. Actually, I think most intelligent researchers, if they could afford to be honest, would admit that HIV is the major indirect causitive factor, but this is not the same as saying HIV == AIDS. Likewise, I think most would admit that HIV is not quite an STD, not really at all.
Finally, even though I just said what I think is “wrong [with] the cognitive apparatus of all those medical and research professionals”, namely that it is more an issue of politically charged public positions; I should also point out that even by the standard of your implied criteria—which seems to consist of counting up scientists for or against, it is even less clear that HIV == AIDS can be supported on that criteria. (which I do not favor as a rational criteria regardless). There are a large number of skeptics on public record for that hypothesis even considering the huge social stigma associated with adopting such a position in public. The HIV==AIDS hypothesis has far more skeptics on record than String Theory, for comparison.
But regardless, counting scientists is not a good rational criteria.
If you want to get into a discussion about rationality and reasoning in highly politicized issues such as this, that is an interesting side topic. But otherwise don’t stoop to the moral high ground of politicized orthodoxy—just provide your hypothesis.
This is Less Wrong, not Mere Mainstream.
Actually, though you may not believe me, Holocaust denialism hadn’t even occurred to me. In the portion of the blogosphere that I follow, it applies most frequently to AGW denialism, with the AIDS denialists second, evolution denialists third, and the anti-vaccination crowd getting an honorable mention.
The wikipedia article on HIV that you reference has a section entitled “AIDS Denialism”.
But now that you mention it, why do you consider Holocaust denialism morally perverse? I thought that questioning PC conventional wisdom was considered a Good Thing here.
No, I don’t believe I do. I wouldn’t want to further offend you.
My hypothesis is pretty simple. You are using the wrong numbers.
When I Googled, the first few hits I found suggested 0.3% per coital act as a lower bound on heterosexual transmissibility with the risks increasing by 1-2 orders of magnitude in case of genital ulcers and/or high viral loads. I don’t think that it is particularly difficult to understand the epidemic spreading in Africa as an STD when these higher numbers are used.
I did look at this study providing smaller numbers and this paper critiquing it, as well as this abstract mentioned in the wikipedia article. It was pretty clear to me that the kinds of low numbers you were using to argue against HIV being an STD are actually based on monogamous couples who are regularly examined by physicians and have been instructed in the use of condoms to prevent transmission. Those numbers don’t apply to the most common cases of transmission, in which ulcers and other factors make transmission much more likely.
That is the hypothesis I was going to offer. When you suggested that you only had a 20-30% level of doubt of the orthodox position, I simply had no idea that it was such a strong and assured 30%.
Please see my response below concerning the perjorative “Denialist”, and why such perjoratives have no place here.
You haven’t offended me.
The google hits you mention are just websites, not research papers—not relevant. There is no reason apriori to view the ~0.3% per coital act transmission rate as a lower bound, it could just as easily be an upper bound. You need to show considerably more evidence for that point.
The data on wikipedia comes from the official data from the CDC1, which in turn comes from a compilation of numerous studies. I take that to be the ‘best’ data from the majoritive position, and overrides any other lesser studies for a variety of reasons.
This may be ‘clear to you’, but the Wikipedia data comes from a large CDC sponsored review considering aggregates of other studies to get overall measures of transmission. This is the orthodox data! I highly doubt it has the simple methodological errors you claim. And even if you did prove that it does have those errors, then you are only helping the skeptic case—by showing methodological errors in the orthodox position, and the next set of data should then come from the heterodox camp.
If I can take the liberty of butting in...
Here’s the table of data I believe you’re referring to:
It cites references 76, 77 & 79, all of which turn out to be publicly available online. That’s good, because now I can check the validity of Perplexed’s claim that the studies backing your CDC data used samples of relatively healthy, well-off people who lack some risk factors.
I took ref. 76 first. It reports data from the “European Study Group on Heterosexual Transmission of HIV”, which recruited 563 HIV+ people, and their opposite-sex partners, from clinics and other health centres in 9 European countries. (Potential sampling bias no. 1: HIV+ people in European countries are more likely to have access to adequate healthcare than many Africans and Americans.) It also says:
That fits Perplexed’s claim that the study’s couples were “regularly examined by physicians” and “instructed in the use of condoms to prevent transmission”. It’s not clear whether they were “monogamous”, but the study did exclude “[c]ontacts reporting other risks of HIV infection and those with other heterosexual partners with major risks for HIV infection”. I also see another sampling bias: if the man & the woman in a couple disagreed on their questionnaires, that couple was blocked from the study. I would think that such couples have a higher risk of transmitting HIV (as I’d guess they’re more likely to be couples where someone’s lying about their sexual history); if so, the study’s more likely to lowball HIV transmission risks.
What about refs. 77 & 79? Where did their data came from? It’s pretty clear that they used the same European Study Group data. From 77:
And 79:
To be explicit: the three studies you’re citing (via the CDC) are based on one data set, and Perplexed’s characterization of that data is essentially accurate. That adds credence to his claim that the transmission rates you’re citing don’t represent HIV transmission rates in other situations.
Incidentally, tables 2 & 3 of ref. 76 suggest that HIV transmission risk is not only associated with type of sex act, but also with the HIV+ partner’s infection stage, especially (I did not expect this!) for male partners of HIV+ women. Maybe more evidence that there’s more to HIV transmission risk than who’s putting which organ in which orifice?
By all means. While you were writing this I was reading 76 and writing my own reply.
Ah I hope he wasn’t claiming this, because they certainly were anything but healthy, with around 20% being hardcore IV drug users, 23% transfusion recipients, 10% hemophiliacs, and overall high rates of STD’s.
I noticed the discrepancy about sexual history part but I didn’t see how to factor it. They are relying on self-reporting to make any of these links.
Err, no, because his characterization is based on the idea that these couples were using condoms frequently, but the study specifically shows that is not the case—see my reply to Perplexed.
If you want to characterize this study, fine, but don’t pretend that these are “regular couples regularly using condoms”—that is not what the study claims.
And finally this is the orthodox data. I mean if you want to reject … ok .. and then we move to searching for other data which supports our relative positions . . . to the extent we have positions.
Perhaps it would be best to agree what the ideal study would be and precommit to that ideal in a sense? And then we could look for other studies that may be closer. Of course in the real world they will rarely be clear cut.
I quite agree that they weren’t healthy in absolute terms; I just meant that they were relatively healthy for people with HIV. Compared to HIV+ people in much of the rest of the world, especially sub-Saharan Africa, I’d expect this European study’s subjects to have (on average) better nourishment, better healthcare, stronger immune systems, less exposure to infectious disease, much less exposure to parasites, and a far lower rate of promiscuity & prostitution. I should’ve been more explicit that that was the sort of comparison I had in mind.
Looking at your reply, I think we disagree about whether or not Perplexed was hinting that the couples were consistently using condoms. I didn’t think Perplexed was implying anything more than that most cases of HIV transmission involve people who weren’t regularly reminded to use condoms. So I took his statement at face value, in which case it’s surely true (unless European doctors have come up with a way of counselling couples “about the risk of HIV infection and safer sex practices” that doesn’t involve advising condom use!).
I don’t believe Perplexed or I are pretending that these are normal couples who continually use condoms. I think it goes without saying that these weren’t “regular couples” — after all, “regular couples” don’t visit hospitals and clinics to get HIV infections checked out. Whom are you quoting?
I reject your interpretation of the data, rather than the data. The study probably gives a fair idea of transmission risks among faithful Western couples living in the 1980s/90s who regularly see doctors...but for that reason (among others) it’s likely to underestimate transmission risks in other demographics.
I think you’re probably right on that point. I suspect that looking at per-sex act transmission risks isn’t going to be very enlightening about whether or not HIV causes AIDS. It would be better to have data from
previously healthy people
who were accidentally infected with HIV
and don’t engage in risky behaviour
and are followed up regularly
for at least 20 years
(each bullet point getting more restrictive). I don’t know if there are such data, but it would get us closer to the original question than big-picture arguments about transmission risks.
I generally agree with most of this except perhaps the last part—I doubt that promiscuity and prostitution varies that much from 3rd and 1st world.
I think he was implying that the reminders led to condom use, but this was in fact not the case according to the study itself (possibly because they excluded many of the condom users, some aspects of the study’s design are not all that clear to me).
Not quoting, just paraphrasing. He was implying that the heterosexual couples receiving counseling were not indicative of a typical HIV hetero population, but the study designers of course realized that and were at least attempting to gather representative data.
Ok, whether HIV causes AIDS is a larger topic. My original point was just about the orthodox claim that HIV is sexually transmitted, which I believe is rather obviously bogus according to the orthodox’s own data. I hope you can see how the orthodox could go wrong there and some of the political factors at work.
As to the larger HIV == AIDS issue, I largely agree with your ideal data criteria, but one potential issue is whether we are comparing HIV to the null hypothesis or to some other hypothesis. I don’t think any reasonable skeptic claims that HIV is not at least correlated with AIDS—Richard Gallo may be many things, but he is probably not stupid nor a charlatan.
So it would be better to compare the orthodox HIV hypothesis vs the Drug/Lifestyle Hypothesis (which predated HIV). Some immediate concerns are that one must take care to then define AIDS reasonably without circular reference to HIV (which precludes some data)
The next concern would be that either way, previously healthy people don’t get HIV or AIDS, in reality or according to either theory. The risk groups are all unhealthy in various ways.
All that being said, Duesberg does indeed provide data very close to what you are proposing. There are some groups of HIV+ who, for whatever reason, have refused mainstream treatment. There aren’t many such people, but he cites a study about a group in Germany—they are called long term non-progressors (which is kind of funny when you think about it—AIDS is progress?).
Anyway, this study is small, only 30-40 people IIRMC, but it is long lasting and only a handful have died. He calculates their death rate as measurably lower than the death rate of HIV+ treated patients, and uses this as a major piece of evidence.
here .. that part is on page 402 (it’s a large journal excerpt or something—not really that long)
An interesting read overall, would like to read a good rebuttal.
Quite possibly, but note that I was comparing the subjects in the European study with the rest of the world, rather than all of the 1st world. The study’s screening procedures probably cut out quite a few people who have a lot of sex.
I think I do. (I hope I do!) Still, I do see the orthodox belief that HIV can be transmitted sexually as being compatible with the CDC numbers. The CDC transmission rates are surely below the average real-world HIV transmission rate (due to the nature of the European study sample), and there are features of the data that are easier to explain if we acknowledge that HIV’s sexually transmitted: the condom-using couples had lower HIV transmission rates than the non-condom users, men who (claimed to have) had period sex with HIV+ women were at higher risk of transmission than men who (claimed to have) avoided period sex, and so forth. So I continue to disagree that the HIV-is-an-STI view is “obviously bogus according to the orthodox’s own data”.
It might even preclude the Duesberg/Koehnlein data you link. Page 402 says the study’s of “AIDS patients”, and it’s not clear from the immediate context what definition of “AIDS” was used for the study. All 36 of the patients (you were right about the study’s size!) are listed as being HIV+, which suggests to me that the AIDS diagnoses were made (at least partly) based on HIV+ status, as is standard practice.
I would have thought that healthy people are capable of getting HIV? Getting pricked with an HIV-infected needle works, as does sexual transmission. A lot of people in high-risk groups are unhealthy, of course, but there are surely unlucky people who get HIV without prior major illness.
I looked up long-term nonprogressors on Wikipedia (not the most reliable source, but anyway), and it looks like many long-term non-progressors have genetic traits that make them better able to resist HIV, or have a weaker form of HIV.
I also saw that the group in Germany Duesberg’s talking about all come from Kiel, a relatively small city (population about 240,000). I’m wondering whether the people living there could be more likely to have HIV-resistant genes. Or maybe the form of HIV circulating there is less virulent? (Or both?)
I should say upfront that there’s no way I’m rebutting all 30 pages of the article (I really doubt the game’s worth the candle), but I can comment a bit more on the little German study.
The first thing that jumps out at me is the lack of detail. I’m curious about how Koehnlein discovered the subjects for the study (personal contact?) and whether they included all of the eligible patients they found. I also wonder how Koehnlein followed up patients, and how regularly. How rigorously do they track the patients to make sure they’re staying off HIV drugs & illicit drugs? How often do they check on them to see whether they’re still alive? When was the last follow-up? The article’s dated mid-2003, but it looks like Koehnlein’s added no new subjects to the study since 2000, and the latest update is from 2001 (when the 3 dead patients died). It would be very interesting to know how many of the remaining 33 patients are still alive 7-9 years on. I looked for later publications by Koehnlein on his study and didn’t find any (which is a bit of a red flag in itself).
I’m also not sure that some of these “AIDS patients” had AIDS in the first place. This looks like the CDC’s definition of AIDS: typically, you have to HIV, and either a CD4 count below 200 (“or a CD4+ T-cell percentage of total lymphocytes of less than 15%”) or one of a list of AIDS-defining illnesses. (You might dispute using HIV+ status as part of the definition of AIDS, but it makes no difference with Koehnlein’s subjects because they all had HIV.) The table doesn’t offer enough information about CD4 T-cell percentages to check whether they’re less than 15%, but it does give CD4 counts and list what appear to be the patients’ “initial AIDS-indicator symptoms”.
So I look at case 1. His CD4 count is 256. His initial symptom was “Herpes zoster”. The Wikipedia/CDC list of AIDS-defining diseases does not include herpes zoster, only chronic ulcers due to herpes simplex. It’s not clear that the patient actually had AIDS when Koehnlein included him in the study. Moving on to case 2, she’s marked as asymptomatic and no CD4 count is given. What was the basis for her AIDS diagnosis?
I sorted the 36 cases into 3 groups: a “questionable diagnosis” group (patient was asymptomatic/had symptoms clearly not on the AIDS-defining illness list, and their CD4 count was explicitly given as >200), a “definite AIDS” group (patient had an illness clearly on the AIDS-defining list, and/or a CD4 count explicitly <200), and an “unsure” group (cases that didn’t fit the other two groups). I put cases 1, 8, 9, 17, 19, 20, 23, 24, 25, 27 & 35 in the “questionable” group; cases 3, 4, 6, 12, 13, 21, 30, 31, 32 & 36 in the “definite AIDS” group; and cases 2, 5, 7, 10, 11, 14 (they had pneumonia, but only recurrent pneumonia and/or PJP is AIDS-defining), 15, 16 (they had toxoplasmosis, but it’s not said whether it was in the brain), 18, 22, 26, 28, 29, 33 & 34 in the “unsure” group.
So the Koehnlein’s study’s effective sample size & death rate seems to be sensitive to how rigorously one defines AIDS. As I see it, only 10 of the 36 cases unambiguously have AIDS, and counting deaths in that subgroup leads to a death rate of 20% as opposed to “only 8%”. I think Koehnlein’s data are interesting, but there are a multitude of reasons not to take Duesberg’s 8% vs. 63% comparison at face value.
I would have given more creedence to this view at the beginning of this whole inquiry, but in another branch several other posters found some large meta-analysis studies, and low and behold they confirm and agree with the old CDC European study. I discuss that here
Of note is that the infection rate in 1st world countires agrees with the original CDC European Study, and the infection rate in Africa/3rd world appears to be 3-6 times higher. Metastudies which mix 1st and 3rd world results get rates somewhere in between.
Some of these metastudies were of thousands of individual studies, and say what we will about them, I think they nail down the real world transmission rates, and the 1st world rates are just as low as I originally quoted (or lower)
Effects like this surely can increase transmission rates in specific instances, but for epidemilogical modelling we are interested in the average rates—and note as I analyzed elsewhere, the original CDC European study does attempt to control for condom use—it intends to show infection rates for unprotected sex. I don’t think you can so easily dismiss all these studies and the work that has gone into computing these transmission rates.
This is certainly a possibility and fits what we know with viruses—variable genetic resistance is to be expected.
However, what is important is how one samples and when. If you take a sampling of survivors years later, then sure you can expect to be finding survivors due to genetic resistance.
But if you sample a subset based only on the criteria that they refuse medication after testing seropositive, then that is a very different sampling, and you should expect it to be largely uncorrelated from genetic resistance (unless you want to argue that people with genetic resistance are strongly expected to resist medication!, but I hope you won’t take that route)
You do bring up a potentially valid criticism:
Possibly, but I don’t find a reason why we should expect this without specific evidence—from what I understand the HIV-1 virus variants spread diffusely in specific at-risk subgroups. It would help the case if the study had more widely distributed patients, and maybe there are other such studies, but it isn’t strong evidence against. We can’t expect many patients to have resisted medicating, and those that did would tend to be clustered geographically in regions where some cluster of doctors were allowed to hold that view and resist medication for a long period of time and study the patients. From what I understand, this was not allowed to happen in the states.
You raise some further methodological questions:
I don’t know, and yes these are interesting questions, and it would be useful if there was a meta-study of all long-term survivors/non-progressors.
Yes, this would be interesting, but note that we shouldn’t expect these people to have full life expectancy, in either theory—as seropositive status is clearly a marker for ill-health. The bigger question is does refusing medication increase lifespan? That is the central point.
Even if they all died after 12 years on average, that still may be better than typical, for example.
A follow up would be interesting, but lack thereof isn’t necessarily a red-flag. They are going to die at some point, and probably much earlier than seronegatives. The question is one of statistics.
As to your questioning of whether these are “AIDS patients”, I find that is rather irrelevant—we are only concerned with the fact that they tested positive for HIV. If HIV doesn’t strongly cause AIDS, but medication does, then of course we shouldn’t expect these medication refusers to progress into AIDS and become AIDS-patients, which is exactly what the study is showing. So I dont’ understand why you are trying to show that they are not AIDS patients—that’s the whole point! You may be unknowling arguing for the opposition (or perhaps I am confused on your position or you have none).
All of this is consistent with the CDC statistics underestimating the general transmission rate. You write that the rate estimated from the European study “agrees with” meta-analyses of 1st world data, and that the 3rd world rate estimated by meta-analysis is higher still. So pooling the two meta-analytic results gives a global average rate greater than the 1st world average rates, i.e. averages greater than the CDC rates.
I don’t think I am dismissing these studies and the work. The bit of my comment you’re quoting refers, after all, to secondary analyses in one of those studies. The point I’m trying to make by drawing attention to those analyses isn’t something like “look, the transmission rates are higher if you don’t use condoms, clearly they’re high enough for HIV to spread through the population”, but instead “associations between condom use and transmission rates, and between sex during menses and transmission rates, have a far higher likelihood in a model where HIV is an STI than in a model where it’s not”. It’s much easier for me to explain why having sex with a woman at particular times in her menstrual cycle would correlate with HIV transmission if I presume HIV’s sexually transmitted, which I interpret as evidence for [edited: I had a brain fart and originally wrote “against”] the view that HIV’s an STI.
Don’t worry, I’m not. I’m suggesting that because the sampled people all come from the same small geographic region, it’s possible that genetic resistance and/or weaker HIV variants are more common among them.
The specific evidence I have in mind is the geographic restriction of the sample. A group of people from one place will tend to be more genetically similar than a worldwide sample, and will be more likely to share strains of a disease. I expect HIV-1 variants do spread diffusely in subgroups, but I don’t think that rules out my point. Particular alleles of genes spread throughout humanity, but spatial proximity still correlates with genetic similarity among people. Sure, geographic restriction is hardly strong evidence of these things — a sample of people who live on the same street could quite easily contain just as much variety in genes that affect HIV resistance (or variety in HIV substrains) as a wider sample. But with geographic restrictions, the variance is likely to be less. (Notice also that the sample seems to be relatively racially homogeneous — only one of the 36 cases is described as black. That’s more evidence of less genetic variance, though very weak evidence, as racial groupings don’t represent much genetic variance.)
Yes, but you originally presented the study as “data very close to what [I am] proposing”, and part of my proposal was that the study’s subjects “are followed up regularly” for 20+ years. Koehnlein’s study started in 1985, most of the subjects entered it in the 1990s or later, the latest update is from 2001, and the published report is from 2003. So most subjects don’t seem to have had anything like a 20-year (or more) follow-up.
The bigger question we’re looking at is whether HIV causes the complex of conditions we recognize as AIDS (and, before that, HIV transmission rates).
True, but the question is how much better than average their lifespan was, and the causes of death also matter. If the patients lived for many post-HIV years more than average, but most of them died of Kaposi’s sarcoma, I would strongly suspect AIDS.
It doesn’t mean the study is somehow wrong, but I see it as a warning sign. It’s very unusual for someone to spend 16+ years on a unique, systematic study of untreated HIV patients, and then not publish it anywhere except as a one-page summary in the middle of a review article that I suspect was mostly written by someone else. I have a hunch that Koehnlein’s unable to get the study published in full.
I can think of two reasons why it’s very relevant. First off, if most of the subjects didn’t have AIDS, that might well explain why their death rate’s less than that of AIDS patients (and Duesberg & Koehnlein quite explicitly compare the sample’s death rate to that of “German AIDS patients”) — one dies of AIDS instead of HIV per se, and it normally takes years to go from being HIV+ to having AIDS. Secondly, Duesberg & Koehnlein say the study is of “AIDS patients”; if it turns out that there are people in the study who didn’t have AIDS, D&K have made a specious comparison, and a false claim about the nature of the study. That would raise questions about how much I should trust their report of it.
Agreed, with the proviso that one would have to wait a long time to be sure that HIV didn’t eventually progress to AIDS.
Disagreed. If you’re agreeing with my suspicion that some of the people in Koehnlein’s study didn’t have AIDS, you’re implicitly accepting my guess that the clinic symptoms and CD4 counts in the table are those observed for each subject when they entered the study, because that forms the basis for my suspicion. And if you believe that, it follows that you can only infer whether a subject had AIDS when they entered the study, and not whether they later developed AIDS.
Well, it’s possible I am. But see above!
For a variety of reasons, I find it useful to separate the two, and the 1st world rates are the most important—the virus outbreak started in San Francisco essentially (following the end tail of the massive hippie/drug liberation social experiment). Also, the 3rd world rates are suspect in general, as one of the meta-studies notes, for a variety of reasons. And regardless, even the 3rd world rates are 30 times lower than typical STD’s, even if they were accurate (which is dubious).
Yes, but as you admit,
So at this point I think it is more time profitable to switch gears and spend a little effort investigating other LTP reports other than this single study. And just a little google searching shows that there appears to be now a number of other LTPs from across the world that are similar to the Koehnlein group—and avoiding traditional treatment appears to be a common link. You can google it as well, but here are some links:
from an article in Health Care Industry (older − 2000):
A 2005 NYT story about a LTNP:
And finally here is a compilation of another dozen studies or cases of untreated LTNPs (older hasn’t been updated recently)
So it doesn’t look like the Koenhnlein study is an isolated incident. I am still looking for more recent studies or follow ups.
From everything I know so far, the vast majority of patients were treated, so if treatment has a beneficial effect at all, then it follows that the ratio of treated LTNPs to untreated LTNPs must be equal or greater to the original treatment ratio. I understand that in the west that treatment ratio was very high, probably > 95%
And as far as I can tell, we aren’t seeing anything like that ratio in LTNPs, so this could be very strong support indeed for at least part of the Deusberg hypothesis: that the treatment can itself cause the disease.
Edit: I completely guessed on that 95%, and later found this telling quote in the NYT article (I am reading these as I go):
But what it would really need is a big long term study with the sampling precommitted early based only on choice of treatment strategy. Actually, this should be how our entire medical system works in general. If the drug companies produce a treatment like AZT, doctors and patients get to choose treatment strategies, and overall mortality data is collected slowly over time. Survival of the fittest strategy.
I should have said here “what the study intends to show”
I was under the impression they tested them when they entered the study and then periodically thereafter just as you’d expect. The overall concern is the long term result—the death rate. I thought the entire point Deusberg was making was that overall mortality was lower in this untreated group than in the general treated population, and the medications themselves were actually causing AIDS progression.
As I understand things, HIV jumped into the human population in Africa decades before hippies and the 1960s counterculture, and that only after being established in West/Central Africa did it reach the US. As such, the 3rd world transmission rates have just as big a role to play as 1st world transmission rates. With an external pool of infected people established, it became possible for HIV to be reintroduced to the US over & over again until it landed in US subpopulations that spread it with needle sharing & frequent anal sex.
Without being more specific about what’s wrong with the rates, I’m not sure why this means the 3rd world rates are necessarily about equal to (or less than) the 1st world rates. At any rate, HIV is not a “typical STD”, and a lower transmission rate than other STDs doesn’t mean much as long as HIV’s rates are sufficient to enable its spread. Also, Wei_Dai suggested that the P/V sexual transmission rate for HIV is comparable to that of genital herpes, a point you didn’t seem to dispute in your reply. Do you believe that genital herpes has too low a transmission rate to be an STD?
But here’s the thing: the lone fact that a case report or study has some LTNPs doesn’t necessarily mean much in terms of questioning the HIV-AIDS link. For example, the studies in the 2000 Research Initiative/Treatment Action! article (I think “Health Care Industry” is just the name of the section on findarticles.com where the article’s mirrored) seem to focus on gathering together people already known to be treatment-refusing LTNPs, and finding out what makes them LNTPs. Simply observing that treatment-refusing LTNPs exist doesn’t convince me. Even if 99% of HIV+ people progress to AIDS within some time frame, with so many HIV+ people there are going to be a lucky few who turn out to be treatment-refusing non-progressors.
By contrast, Koehnlein’s methodology seemed to be different, which was why I initially thought that work might be compelling. I’d assumed that Koehnlein systematically recruited people into the study when they originally tested HIV+, not later, which would prevent Koehnlein gaming the study by excluding non-LTNPs. (Of course, with all the questions I now have about the study, I’m questioning even that. D&K don’t say when the subjects were recruited into the study, only when they were diagnosed HIV+. Possibly Koehnlein recruited subjects years after their HIV+ diagnoses.)
The catch with those 14 reports (the last of which is just a second-hand anecdote) is the same as for the other ones you linked: the page listing them doesn’t say what their sampling strategies were, and I think it’s likely that a lot of the reports’ authors deliberately sought out treatment-refusing LTNPs instead of representative samples. (The list is probably also a selective one, considering the website hosting it.) For example, the first report in the list is “based on 10 HIV+ people” who didn’t use antiviral drugs. I find it unlikely that doctors would bother publishing a study of only 10 LTNPs if those people had taken antiviral medication; it wouldn’t be very informative. It’d effectively be a tiny drug trial, and there are already far bigger trials of anti-HIV drugs. So I’d guess the doctors’ aim was to deliberately search for as many treatment-refusing LTNPs as they could find, because other doctors have something to learn from how their bodies work. If so, it wouldn’t be surprising that they found a handful.
That only follows if there aren’t any confounding factors associated with treatment status. If (making up an example here) HIV+ people being treated use treatment as an excuse to resume risky behaviour, and the treatment is only marginally effective, we might well end up with relatively few treated LTNPs. (I haven’t looked into this. Maybe it turns out that there aren’t any major confounding factors, but I wouldn’t want to assume them away without evidence.)
If you’re basing this on counting reports of LTNPs, you might be getting a skewed picture, since treatment-refusing LTNPs are much more newsworthy than LTNPs who accept treatment, and the latter probably don’t get so many of their own journal articles and magazine profiles. To count them, you’d probably have to locate reports of HIV drug trials that happen to have data on how the testees progress.
It usually takes several years for HIV to progress with AIDS, with or without treatment. So it wouldn’t be that surprising if there’s a large minority of people who don’t develop AIDS within a decade of HIV infection, and a fair few of them are probably, yes, medicine-free. (Plus, of course, we’re looking at a newspaper’s paraphrase of something a scientist said, so I’m inclined to exercise caution.)
To be honest, I think D&K are confused themselves about what the study’s meant to show. D&K call it “a study of AIDS patients”, but then they write “our relatively small sample supports the hypothesis that without anti-HIV drugs and/or recreational drugs HIV fails to cause AIDS.” But if the subjects were all AIDS patients, how could the study show that they failed to progress to AIDS? They would already have had AIDS!
If you’re correct that Duesberg’s intent was to make the point “that overall mortality was lower in this untreated group than in the general treated population, and the medications themselves were actually causing AIDS progression”, then he’s trying to have it both ways. He can’t infer the first thing (lower mortality) unless the study subjects are AIDS patients, because other AIDS patients are his comparison group, and he can’t infer the second thing (medications causing AIDS) unless some of the subjects aren’t AIDS patients.
Also, I doubt Koehnlein did systematically test the subjects periodically for AIDS. CD4 counts are missing for some of the asymptomatic patients, and to test them for AIDS, they would have needed CD4 counts. So either Koehnlein didn’t have their CD4 counts (which implies that Koehnlein wasn’t periodically testing them for AIDS), or Koehnlein’s selectively withholding CD4 counts (and something funny’s going on).
Whew. The more I go over this study, the more worrying it gets.
Ah, unfortunately this got too long, so I had to split it.
I think this was a confusion of terminology, and “AIDS patient” in the general sense was used to just refer to all HIV+ patients he was treating. It did not refer to only a subset that had later stage ‘AIDS’ symptoms. At least, that’s how it read to me.
From what I understand, Koehnlein somehow found a way to treat patients without antivirals legally, so patients seeking non-antiviral treatment came to him. His ‘study’ is just a record of all such patients, when they first came under his care, their backgrounds, and eventual prognosis (a couple of deaths out of thirty or so patients so far).,
Koehnlein may subscribe to the Duesberg hypothesis, and as such wouldn’t place any special value on persistent tracking of CD4 counts.
It might be for the best! This splits the Koehnlein study discussion and the general HIV discussion into their own separate subthreads.
Yes, we initially read the phrase differently. I originally interpreted it at face value, figuring that in a review article about HIV & AIDS, D&K would take care to avoid confusing having AIDS with being HIV+. I now think I might’ve given them too much credit.
Nonetheless, at one point, D&K must be using “AIDS patients” with its narrow meaning (patients with AIDS proper) and not its informal one (patients with HIV who may or may not also have AIDS), because the statistics they quote for German AIDS patients match the Robert Koch Institut’s AIDS statistics, but not the organization’s HIV+ headcount.
Whatever D&K’s intentions or confusions, my earlier point that the study can’t provide strong, simultaneous support of all the conclusions drawn from it still stands.
If so, Koehnlein’s testing his (her?) own definition of AIDS, not an orthodox one, and all bets are off.
That’s a theory, but it has some critical flaws. Namely one must wonder why did it not spread via prostitutes, needle sharers and blood transfusions earlier? Condom use dropped with the adoption of the pill in the 1960′s and the sexual liberation opened up a hetero transmission channel which has about the same net transmission rate (always limited by the insertive step).
AIDS became an epidemic in San Francisco in the early 80′s, and it grew quickly from a handful of cases to effect a large portion of the gay population, and was closely correlated with a diverse number of fundamental lifestyle differences. It is this phenomena, this quick sudden outbreak in a very specific subgroup, which I find extremely difficult to reconcile with the transmission data. Tops and bottoms tend to specialize so the rate-limiting factor for expansion in the gay community would be closer to the insertive A rate, at around 0.06% vs receptive at 0.5%. Needle sharing is about 10 times more effective, and blood transfusion is around 1,000 times more effective.
But all the early cases are in this one specific group, which is not even the highest risk group. I mean, the transmission rates for insertive V and A are about the same, and there are far more heteros than homos, so it just doesn’t make any sense. And don’t tell me the homos are having all the sex—they may be having more individually, but not when considering prostitutes and sexually liberated women in the 60′s and 70′s, the fact that heteros have anal as well, and the 100 to 1 hetero to homo ratio. The overall hetero transmission channel is much much larger, especially after considering needle sharing and transfusions, and yet the disease only appears in the homo subgroup, time and time again. Why?
Ignore for a second all high level conceptions about HIV. Don’t privilege the orthodox HIV hypothesis, instead compartmentalize and consider just this evidence concerning transmission rates, and how that evidence should cause one to update from an initial 50⁄50 split between two alternate hypotheses:
HIV spreads primarily horizontally and is novel in homo sapiens
HIV spreads primarily vertically and has been in homo sapiens for a long time
The transmission rates clearly favor 2 - the virus can barely spread sexually, but can spread fairly easily antenatally.
Also, if you actually read into the depths of these studies, it becomes clear that there is a strong framing bias to favor the default sexual transmission theory. The actual sexual transmission rates are not known with certainty, and all of these studies depend on the orthodox HIV model. The actual horizontal transmission rate may be . .. zero.
One of the more interesting hetero sero-discordant studies is the Padian 10 year study. Trying to isolate for hetero sexual transmission, they actually strictly eliminated all drug users by using actual drug tests—something that others have not done to my knowledge. They then did the typical questionnaire analysis trying to determine how each seropositive index member in the couple actually caught HIV—which is more or less just a random guessing game, and then they applied regression techniques to look for risk factors.
The risk factors they found are more or less random, and do not point to a sexually transmitted disease. For instance:
So large amounts of unprotected sex did not appear to be a very significant risk factor. The highest risk factor was just anal sex as a practice, not the number of contacts.
But what was really interesting in this group of some 600ish hetero non-drug users was that during the length of the study, there was not a single seroconversion, even though condom use in these couples was imperfect:
There is zero evidence that non-drug using heterosexuals acquire the disease sexually, and studies such as this are evidence favoring a vertically transmitted virus.
Why does it only spread laterally into gay men and drug users, even though this is extraordinarily unlikely if it truly is horizontally transmitted?
I haven’t analyzed genital herpes and know very little about it, and regardless it is irrelevant. If the data says that HIV can not be sexually transmitted, and another disease has the same epidemologial data and is also called an STD, that somehow doesn’t magically change the data. It just makes both classifications wrong.
Simply observing that treatment-refusing LTNPs exist doesn’t convince me. Even if 99% of HIV+ people progress to AIDS within some time frame, with so many HIV+ people there are going to be a lucky few who turn out to be treatment-refusing non-progressors.
There is no ‘luck’ and it all depends on the ratios. If only 1% of HIV+ people refuse treatment, but even just 10% of all “long-term non progressors” refuse treatment, then clearly treatment itself is part of the problem.
It is strange and interesting that you think the cofactors only could work in favor of your privileged hypothesis. There is also the placebo effect to consider, and in a drug trial that is not double blind (as the AZT trials could not be) those who found out they were getting placebo believed they were going to die, and that encouraged wreckless behavior, not the other way around. Also, all the reports on LTNPs I have read are unanimous on lifestyle change being a distinguishing factor- reduction in drug use and bathouse type partying, general increase in healthier behavior. However, they still die at accelerated rates, and some eventually get AIDS.
Overall though it is pretty clear that even with some placebo benefit in it’s favor, AZT had no net benefit. If one could factor in the placebo bias, I expect it actually increases mortality a little on the whole. However, the data on the original AZT trial and later the more extensive concorde trial show that AZT has little effect or a small net negative effect. I think it is difficult to pin all of the modern deaths on AZT, and clearly AZT was not the main killer during the trials, but the fact of the matter is we simply do not have a control group to compare to in the long term.
This is the first cohort to basically be on sustained chemotherapy for life. It’s hard to imagine that this could not have negative long term effects.
Looks like I have to split a comment too!
I’m not sure which specific time period you’re referring to with “earlier”. If you’re talking about the 1970s, I’d guess it’s because HIV simply hadn’t been introduced to those subpopulations often/early enough to stick. If you’re talking about the early 1980s, well, it looks like HIV did spread, at least among needle sharers and people who had blood transfusions. (I haven’t seen data on prostitutes.) According to this 1985 Science article, 12,932 AIDS sufferers were reported to the CDC by August 30, 1985. 1.5% of them had received blood transfusions within 5 years of diagnosis, and 17% were heterosexuals who’d used IV drugs. (Also, 12% of the homosexual & bisexual men diagnosed were IV drug users.)
Although I’m sure tops & bottoms “tend to specialize”, I doubt men with dozens of sexual partners are completely picky about which role they play. If men are inconsistent about being the top/bottom, the insertive anal transmission rate is going to be an underestimate. In fact, it’s likely to be an underestimate twice over, because preexisting STIs make transmission more likely, and promiscuous men will have more STIs on average. You’ve also got the handful of IV drug users among these men. If I’d had to bet on where HIV would rear its head first, the bathhouse subculture would’ve been a great choice to put my money on.
But neither of those can have an impact until HIV’s introduced to the subpopulations of needle sharers/blood donors, and even after that, their effect will depend on when HIV reached those subgroups, and how many people in those subgroups start off with HIV.
Only if you define “early” as really early: the first reports of IV drug users with AIDS came out in the same year as the first reports of AIDS in gay men. And again, risk isn’t everything. Even if group X has much higher transmission risks than group Y, if the virus reaches group Y first, the earliest infections are likely to emerge in group Y.
While the receptive A rate is higher than the receptive V rate.
Ease of person-to-person transmission within a subgroup matters more to how quickly a disease spreads through that subgroup than the subgroup’s absolute size.
Which increases the ease of transmission.
Which doesn’t much matter if there’s hardly any HIV among those women to start off with. I’d also guess that the proportion of “sexually liberated women” having as much sex and injecting as much drugs as gay men in the 1970s/1980s bathhouse culture is relatively small.
As often as promiscuous gay men?
See above about subpopulation size.
To extend your own metaphor, the “hetero” channel was wider than the “homo” channel, but the “homo” channel had faster flow. Plus, again, there were gay men who engaged in IV drug use, and if gay men were among the first US citizens exposed to HIV, as is very possible, that would’ve given them a head start.
Not sure what that means specifically.
It’s the hypothesis favoured by the medical establishment and the scientific mainstream on the basis of evidence that is at least circumstantial, and at best definitive, which suggests it’s a good starting point. I’m not plucking an arbitrary hypothesis to defend out of thin air.
I really disagree with how you’re framing things here. It’s screwy to split horizontal transmission & vertical transmission into separate hypotheses, since both processes are happening right now throughout the human race, and both processes happen at different rates across time & place. I don’t understand why the mode of transmission corresponds to how long HIV’s been circulating in humanity, either.
Mother-child HIV transmission rates per child (without anti-HIV prophylaxis) are generally higher than sexual transmission rates per sex act, sure. But there’re a lot more sexual acts happening than childbirths. So there’s more to the situation than raw transmission rates.
There are several documented cases of early AIDS where we have stored tissue that later tested positive for HIV, such as the gay teenager who died in St Louis in 1969. This poses a serious problem for the standard theories that HIV is transmitted horizontally (unlike any other retroviruses) and presumably came out of Africa. So how did it get into this teenager? You would need some world travelling gay subculture at the time to link the disease to Africa, but not a big enough subculture to create an epidemic. Since only a small portion of men are gay, we should expect that if it came out of Africa the first vectors would have been heterosexual, not homosexual. And as there are several of these strange early cases, it would have had to come over from Africa multiple times, but always only in gay men. This theory is just not salvageable.
Also, consider that the different genetic subtypes are closely associated with particular risk groups—subtype M appears in MSM and IV drug users but not others, which doesn’t make any sense for a horizontally transmitted viral vector. Most of the subtypes are linked to particular geographical regions in Africa, which points to a long history in humans (with M representing a novelty linked to novel behaviour).
Also consider that all other primates have naturally occurring lentivirus family retroviruses very similar to HIV. Consider that the entire family of retroviruses are more symbionts than parasites—humans are ‘infected’ with thousands of different retroviruses, many of which are integrated into our genome, and they have functional roles in gene expression and even the formation of the placenta.
So if all other primates have naturally occurring lentiviruses, why don’t humans? There is a clear evolutionary niche for a lentivirus in mammals, and it seems odd that homo sapiens somehow lost their naturally occurring lentivirus at some point in our evolutionary divergence, only to re-acquire it very recently in the last one hundred years. It just doesn’t make any sense at all.
Retroviruses generally are not horizontally transmittable, and there is no evidence that HIV is an exception. The Padian study in the other thread branch directly shows that HIV is probably not sexually transmittable.
But most of the earliest confirmed AIDS cases were retracted (David Carr) or have a direct connection to Africa (anonymous Congolese adults & Arvid Noe). It’s only Robert R. (the “gay teenager” you refer to) who didn’t have a direct African connection, but that doesn’t mean there wasn’t one, and such a connection wouldn’t even be necessary with Haiti available as a closer source of HIV.
This is one teenager. He only had to be unlucky once when having sex with just one infected man.
I’m confused. This PNAS paper presents good phylogenetic evidence that the HIV strains causing the North American epidemic came from Haiti, and that Haiti’s HIV came from Africa in the 1960s, which “suggests its arrival in Haiti may have occurred with the return of one of the many Haitian professionals who worked in the newly independent Congo in the 1960s”. So it’s Haitian economic migrants who would’ve been the “first vectors” to carry HIV out of Africa in any real number, and I have no reason to think they were disproportionately homosexual.
If by “strange” you mean that all those cases are inexplicable, I disagree.
Not at all.
I’m not an epidemiologist (or a geneticist), but couldn’t that just be a founder effect perpetuated by MSM and IV drug users transmitting HIV much better amongst themselves than they transmit it to everyone else?
I’m not seeing why this would be evidence for/against orthodox theories of HIV & AIDS. (And if I were being pedantic, again I’d suggest the relative insularity of MSM and injecting drug users as why subtype M’s linked with them, rather than the novelty of their behaviour as such.)
I’ll pass on commenting on your last three paragraphs, since what I know about retroviruses would fit on the back of a postage stamp. I will try checking Padian et al. again, though.
Yes, I don’t know any other studies that used direct drug tests. There is this Madrid study of heterosexual transmission that used indirect testing of “markers related to drug addiction (e.g., hepatitis C serology)” to check for drug use in addition to questionnaires, and its recorded transmission rate is quite high: 26%, out of 38 couples. However, it looks like a retrospective study.
Although quantity of sex doesn’t seem to have made much difference, the unadjusted odds ratio associated with not using condoms bordered on statistical significance with a confidence interval of 0.95 to 3.01. After adjusting for the number of sexual contacts, that odds ratio went up to 2.1, becoming significant and equal to the adjusted odds ratio associated with anal sex. I notice too that after adjustment, STI history — a risk factor elsewhere associated with HIV transmission — was the risk factor with the highest odds ratio.
It would be more interesting if the relevant sample did contain 600 heterosexual non-drug users followed for the length of the study. However, the “no seroconversions” result comes from the study’s prospective part, which involved only “175 HIV-discordant couples over time, for a total of approximately 282 couple-years of follow-up [...] attrition was severe”. That’s a mean follow-up time of only 19 months per couple. Most couples probably got less follow-up time than that, because severe attrition would tend to negatively skew the follow-up time distribution, depressing the median.
That’s not all. The investigators didn’t just counsel the couples on safe sex, but also set up a 24-hour telephone support line, a newsletter and regular meet-ups. These measures were very effective in changing the couples’ behaviour: by the final follow-up, 15% of the 175 couples abstained from sex and 74% used condoms. So, at final follow-up, only 11% of the couples — nineteen in absolute terms — were at substantial risk of HIV transmission. The study’s statistical power to detect the small (in absolute terms) risk of heterosexual HIV transmission wouldn’t have been that great, especially given “the lack of incident STDs during the course of the study” (page 355).
You’re exaggerating. Even ignoring all other work on HIV’s epidemiology, there’s evidence of heterosexual HIV transmission in this very study! Its prospective aspect is just half of the research; there’s also the cross-sectional sample, which includes 230 couples recruited after the researchers began screening subjects for drug use in 1990. HIV transmission occurred in this subgroup, and after adjusting for estimated number of sex acts across the entire cross-sectional sample, there was no association between being enrolled before 1990 and HIV transmission (adjusted odds ratio = 1.0, 95% confidence interval = 0.98-1.0), so the transmissions in the cross-sectional group can’t just be attributed to the pre-1990 (i.e. unscreened) subgroup. (And again, recall the higher odds ratio for failing to use condoms and having a history of STIs. That sounds like more evidence of sexual transmission to me!)
But...it doesn’t only spread laterally into gay men and drug users?
That’s true!
Or your definition of an STI too restrictive.
I think you have some implicit assumptions there to unpack.
Do you have references for this?
Well, I expect that helps. (Which is not to say that switching to a healthy lifestyle halts the progression into AIDS.) I can’t imagine doing poppers and having casual sex is a good thing for anyone with HIV. (Come to think of it, isn’t it possible for someone who already has HIV to reinfect themselves with other substrains and make their infection worse?)
Makes sense.
I think I’ll hold off on commenting on the last couple of paragraphs about AZT since (1) I really don’t know much about AZT, and (2) this discussion is becoming quite extensive and too much of a time sink for my liking.
Ok, so concerning the Padian study, I believe you have misread it, and I am to blame because I originally mislabeled it when I said:
I was wrong—it was not in fact a study of sero-discordant couples, and I apologize for that mistake, for it seems to have mislead you. This is evident in the abstract and is explicitly clarified elsewhere:
So they recruited non-drug using heteros of either sex who had steady partners, and some fraction of those partners were already infected—specifically 19% of the female partners and 2% of the male partners. They explicitly state there were no new infections in the abstract:
And again later:
The last part happens to be in the ‘prospective results’ portion (where they switched focus to only serodiscordant couples), but should not be interpreted to somehow only apply to the post 1990 time period—as it says “after entry into the study”, and agrees with the “no new infections” in the abstract.
So I believe you have misinterpreted when you say:
There was not a single new infection (seroconversion) during the entire ten years across all couples.
You are correct that they were counseled on condom use, but this does not seem to have influence actual reported condom use, even though the percentage of couples using condoms upon entry increased from around 50% to 75%, a significant fraction reported inconsistent usage:
So the key of this study and really all of the heterosexual transmission studies is that it is all just guess work. The 19% female and 2% male seropositive partners were just assumed to have acquired HIV sexually, but as this occurred prior to the study, the drug controls were not in place (and testing didn’t start until 1990). They are just assuming sexual transmission in these cases based on the strong unfounded assumption that HIV is sexually transmittable, they really have no idea.
What they did show, was that over about 4000 couple years, there was not a single new transmission in this drug-screened hetero sample. Using the 75% consistent condom use number, lets say then 1000 couple years of inconsistent usage, and perhaps then taking that to conservatively imply 80% condom usage on average for ‘intermittent’ users, you still have 200 couple years of unprotected sex, and not a single transmission. Remember that most of the partners (80%) are female, some practise anal, and that condom usage was reported as highest only for female index patients (male partners—paradoxically). Also, condoms are not at all 100% effective, even when used properly.
If there had been just a single seroconversion, that would correspond to a rate of transmission of 1 per 200 to 1000 years of sex, or perhaps a rate of 1 in 20,000 to 1 in 100,000 sex acts − 0.01 to 0.05%. But that single seroconversion did not happen. The actual transmission rate was exactly zero. As this study actually controlled for drug use cofactors it is the most accurate data I’ve seen for actual sexual transmission, and it shows that most studies grossly overestimate sexual transmission—the reality is there is no M->F transmission or it involves iv drug use.
The problem is simple—as untreated HIV presumably leads to death in 5-10 years, it needs to infect more than one person on average in that timespan just to maintain HIV population rate. To achieve a doubling in 10 years, it would need to infect 3 new people on average in that time.
To explain the growth rate in the early 80′s requires an absurdly faster doubling rate. This is not an STD. It is something else.
Agreed. I need to stop thinking about this.
Alright, I’ve had another look at Padian et al.’s paper. I did follow your lead in thinking the study was solely of sero-discordant couples, and I agree with you now that it actually wasn’t. However, the relevant part of the study is the prospective sample, which was solely of HIV-discordant couples, so my overall interpretation of the study’s nominally zero transmission rate remains unchanged.
Right, but Padian et al. refer to the retrospective part of the study as the “cross-sectional” part (see page 351: “the retrospective nature of the cross-sectional aspect of our design”), implying there was no follow-up in that part. Without follow-up, they couldn’t have detected seroconversion after entry into the study, so the retrospective method wouldn’t pick up on post-entry transmissions however often they actually happened. So it’s a mistake to argue that no transmission happened in the retrospective group on the grounds that no transmission was observed, because the retrospective method can’t detect new transmissions.
So, although it’s technically true that the “no seroconversions” result applies to the whole period of the study, it would’ve been disingenuous for me to say so, because the researchers could only spot new seroconversions from 1990 onwards.
The study’s non-prospective part was incapable of detecting post-recruitment seroconversions, so the basis for the “no seroconversions” result is indeed the prospective part.
Well, there might’ve been new infections between 1985 & 1996 among the retrospective sample, but the study wouldn’t have detected those. The retrospective method would only detect those that happened in a couple before they entered the study.
The fact that a minority of the couples still didn’t use condoms consistently at their final follow-up doesn’t mean the counselling had no influence!
Only for the retrospective sample.
The calculations you do in the next couple of paragraphs seem to be based on both the retrospective & prospective subsamples, which exaggerates the number of couples in which new HIV transmissions could have been observed. New transmissions would only be observable among the couples in the prospective group.
So let’s run the numbers again for just that group. That group had 282 couple-years of follow-up, just 7% of your starting point of 4000 couple-years. Multiplying your final unprotected sex estimates by 0.07 gives me just 14 to 70 couple-years of unprotected sex.
Following on from that, how likely was a seroconversion for some hypothetical transmission rate? Let’s take 0.05%; 0.1% is unusually high for heterosexual couples, if I remember rightly, and 0.01% feels too low. Supposing the couples had 100 sex acts a year, we have (with a lot of simplifying assumptions) 1400 to 7000 sex acts. With 7000 acts at 0.05% a time, I get a 3% chance of no seroconversions. With 1400 acts, I get a 50% chance. This suggests that the likelihood of no seroconversions was not insignificant, so inferring a transmission rate of zero is likely to be a type II error. I also haven’t accounted for the 15% of prospective subgroup couples who became abstinent during the study.
Not with this lack of statistical power it doesn’t.
Whaaa?! Wouldn’t that imply that every female partner who became seropositive in the other studies got infected from secret lesbian sex or injecting drugs?
I don’t see that as a prohibitively high barrier. Especially because there’s not really just one transmission rate for each kind of sex act: transmission rate is moderated by other factors like stage of HIV infection, being infected with other STIs, and so forth.
The early 80s growth rate wasn’t just driven by heterosexual sex.
There was follow up starting in 1990. Basically they started the study by recruiting in 1985 and were originally focused on the retrospective aspect. Couples come in, fill out a questionairre and they attempt to screen out drug users and look for patterns in infected partners (couples where both are seropositive). Then in 1990, they began bringing couples in for examinations and follow up tests—“Physical examinations for both partners were initiated in 1990.” This is the beginning of the prospective part, but it doesn’t mean it is only valid for couples starting after that date, which comes from the very first sentence of the abstract:
The prospective part was not limited to only couples enrolling after 1990. That is only the beginning of the biannual checkups.
Technically yes, but immediately in 1990 on the first follow-up they would have spotted any new seroconversions in any serodiscordant couples currently in the study. And they would have clearly mentioned any such detected seroconversions, and indeed they clearly mentioned that they detectected exactly zero.
But regardless, yes I did botch the total couple-years. The text implies that the 175 couple group with follow up was the total set of persistent couples:
Abstenence was between 0 and 14.5%, consistent condom use betwen 32% and 74%, and anal between 37 and 8%. We should probably also factor in that condoms are not 100% effective. Lets ignore that for a second and assume midpoints of the above numbers, with around 100 sex acts per year, or 10 per month. If ‘inconsistent’ means ~50%, I get ~2 unsafe acts per month, or ~6,000 unsafe acts. The majority of these couples (80%) are male seropositive, so the higher M->F numbers apply 0.1% to 0.5%.
The infection rate for P->V is supposedly 10 in 10,000, or 0.1% according to the CDC from the European study. The infection rate for P->A is supposedly 50 in 10,000, or 0.5%.
Sure it would have been better with 10,000 couples over many years, but how much specific negative evidence for sexual transmission does one require? Is there any specific positive evidence?
There is a larger set of data Deusberg points to for lack of sexual transmission, which is the hemophiliac population, around 75% of which tested positive for HIV in the 80′s. There were about 5,000 wives of HIV+ hemophiliacs, and the CDC reports 131 were diagnosed with miscellaneous AIDS diseases between 1985 and 1992. However, the particular diseases were age-related opportunistic infections, including 81% pneumonia—no KS, demantia, lymphoma, or wasting syndrome generally characteristic of typical AIDS. The 131 / 5000 appears to just be regular background rates for those illnesses. If AIDS was sexually transmitted, we should have seen evidence in this population of wives. Many of these couples were having sex for years before the blood was tested. This strongly contradicts any theories of a sexually transmitted etiological agent.
And if it is not sexually transmittable, then it is either only vertically transmittable or the entire theory is hopelessly flawed at a deeper level. I suspect the latter because the measured vertical transmission rates are not high enough to sustain plausible viral population.
Not at all—the data just shows that seropositivity is not sexually transmittable. A great deal of other evidence, combined with this clear lack of sexual transmission shows that seropositivity is clearly linked to risk groups with immunosuppression in general.
What you’re saying about Padian et al. just clicked for me. I’d got it into my head that they were allocating each recruited couple to either a retrospective track or a prospective track, with couples switching from the retrospective track to the prospective track after 1990, but without their data being carried over. But you’re saying the couples already enrolled in the study pre-1990 were automatically entered into the prospective part with their earlier questionnaires & lab work retained, right? That’d make more sense than how I first interpreted the paper. (Serves me right for skipping the abstract and diving straight into the methods section. Twice.)
Alright, let’s crunch some numbers.
Using the midpoints of the ranges is a good first guess in the absence of other information. However, I think there’s a good reason to use estimates much closer to the follow-up percentages (14.5%, 74% & 8%) than the baseline percentages (0%, 32% & 37%). The prospective results section says that “approximately 97 percent of behavior change was reported between baseline and the first follow-up visit”. That is, when couples started/stopped using condoms consistently (or abstaining, or having anal sex), they almost always did so before their first follow-up visit, suggesting the couples changed their behaviour shortly after counselling, not gradually. If so, then the baseline percentages only represent the couples’ behaviour distribution for a few weeks; after that, the distribution would be much better represented by the rates at final follow-up.
This could have a big impact on the surprisingness of the zero seroconversions result. Switching from the midpoint rates to the final follow-up rates boosts the abstinence rate to 14.5% and the consistent condom use rate to 74%, while cutting the “[a]ny anal intercourse” rate from 22.5% to 8%. So the neither-abstinent-nor-consistently-condom-using rate sinks from 39.7% to 11.5%. Carrying that forward, I get an unsafe act count ≈1600 instead of ≈5600 (assuming 50% condom use in that 11.5% of couples).
That of course makes a big difference: with a 0.1% risk per act (and I’d peg the risk as being far closer to 0.1% than 0.5%, given the low rate of couples admitting to any anal sex, let alone repeated anal sex), 1600 sex acts have a 20% chance of not causing any transmissions, but 5000 sex acts have only a 0.03% chance. Evidently the unlikeliness of getting no seroconversions under a hypothesis of low-but-nonzero transmission rates hinges on the numerical assumptions made about sexual behaviours. (And there are yet more tweaks one could make to the numbers: whether to adjust for the couples that were female HIV+ instead of male HIV+, how much to adjust for condom unreliability, how much to adjust for the time lag between HIV infection and showing up as HIV+ on a blood test, and so on.) A claim that HIV isn’t an STI is a hefty claim to hang on this single result.
If I’m remembering correctly, the only pieces of specific negative evidence I’ve seen cited here were the transmission rates’ small sizes (which I don’t see as evidence that HIV isn’t an STI, because the fact that a number is small doesn’t mean I can safely assume it’s nil), and the zero seroconversions result from Padian et al., the strength of which is arguable.
I think the other studies of heterosexual transmission are at least suggestive. Explaining away the hundreds of female HIV seroconversions detected in those studies by assuming that each case of male-to-female transmission “involves iv drug use” does not seem credible to me. IV drug use is more common that it once was, but surely it’s not that common!
My scepticism is stronger still because a few of the studies have methodological features that would make transmission via needle sharing even less likely. I mentioned this Madrid study before. There’s also this ingenious study, which used sequence analysis on the subjects’ HIV samples to confirm that transmission was within pairs, making it less likely that non-index partners who seroconverted caught HIV from sharing needles with strangers.
It’s not as if these are the only studies that’re informative, either. This meta-analysis finds that male circumcision reduces HIV transmission risks, a conclusion bolstered by this randomized trial, a second randomized trial, and a third randomized trial. I’m not sure how I could explain these results without invoking sex as a way to transmit HIV.
Immunosuppressed or not, a person won’t get infected by a virus unless that virus makes it into their body. Even with immunosuppression as a cofactor for HIV transmission, it can’t substitute for HIV transmission.
I almost forgot to ask for a reference for this:
I’m unwilling to take Duesberg’s synopsis of these data on trust, and would want to see where he got his numbers from, and which methodological issues he might’ve glossed over. I can think of a few issues already, without even looking. The fact that the couples were having sex for years before getting tested in the 1980s wouldn’t mean much if HIV hadn’t been circulating in the blood supply for long. Different AIDS risk groups often have different constellations of AIDS-defining illness: Haitians often present with diarrhoea & TB, whereas US gay men often present with KS, for example, so I would guess haemophiliacs & their wives might have their own distinct AIDS-associated illnesses. Counting AIDS cases would underestimate HIV transmissions, because only some HIV+ wives would have progressed to AIDS. And so forth.
Also note this ‘ingenious’ study has an important point of evidence that does agree with the Padian study and points to a non-sexually transmitted etiology:
The circumcision studies from Africa don’t tell us much either, as circumcision is associated with ethnic/cultural groups and thus drug use and other factors.
There are other more parsimonious explanations that don’t rely on a ‘virus’ at all, and HIV—as far as it exists as a rather arbitrary collection of DNA/RNA sequences, may not be a virus at all. It could just as easily be trash RNA being secreted in exosomes tagged for immune system garbage collection. It could be regulatory RNA exosome messages intended for other cells. It could be a mutant form of an endogenous regulatory RNA exosome. It could be an endogenous ‘virus’ that forms as a cancer-like mutation of normal endogenous regulatory RNA exosome communication. And yes, it could actually be a true exogenous RNA virus that just happens to be remarkably similar to sequences embedded in the human genome (such as the so called “HERV” sequences) - and just happens to look like typical RNA exosomes in the microscope.
But even if it is a true exogenous virus that can jump between cells and that is a huge if, there is astonishingly little evidence it causes much harm.
There is a mountain of evidence that drug use causes harm, and specifically that particular drugs linked especially to the gay community cause specific types of chronic accumulated immune damage.
Methanphetamine (speed) and its derivatives for example is tightly correlated with HIV/AIDS, it is endemic in the “party and play” gay community, and we have a large amount of evidence that Meth does significant long term harm.
Firstly, Meth is a hyper-stimulant of the “flight or fight” stress response. This stress response essentially temporarily shuts down the immune system and digestion to focus the body on a temporary threat. A lion may kill you in a matter of minutes, while your body’s normal symbiotes/parasites such as fungal candida are not going to do much in this time frame—so stress is bad for the immune system, but this is ok because stress normally is temporary.
What happens when go on a multi-day meth binge and hyper-stimulate your stress response? Well, we don’t entirely know, but it appears to be pretty bad for your immune system. And finally, the drug itself has potential DNA damaging effects through oxidative free radicals. This is a particular problem for any drugs that are often heated up and burnt in either the consumption or production phases, resulting in oxidative byproducts. The typical crack-cocaine ‘cooking’ procedure is especially bad in this respect.
The ‘immune system’ - which really should be called the ‘regulatory system’, is second only to the brain in complexity. It is responsible for not only protecting the body from foreign invaders, but also for general regulation of symbiotes/parasites in the gut, identification and control of rebellions (cancer), as well as normal tissue generation and regeneration (healing).
The CD4 cell pathway in particular is especially complex, and these cells are responsible for identification and long-term memory of particular antigens. They go through an extensive selection process to eliminate possible identification errors (auto-immune disorders). This system is especially sensitive to DNA damage, which is happening all the time—and these cells are expected to stick around for many years to hold antigen memory. They also use a random DNA shuffling process early on to generate their antigen recognition system, and these cells are bouncing around constantly in the blood in such a way that makes essential complex DNA repairs—double strand break repairs—much more difficult.
Consider the insults that AIDS patients are inflecting on this system: known potent stress inducing immuno-suppressants such as Meth and Cocaine type drugs, and oxidized byproducts of cooked drugs directly injected or smoked. Also consider that the rectum is second only to injection as a route into the bloodstream, and associated with anal sex are lubricants which can be absorbed. Has anybody seriously evaluated the long-term health effects of anal lubricants? I haven’t seen such a study. Consider that earlier in the AIDS era more toxic oil based lubricants, possibly containing benzoprene deriatives, were more common. Fortunately presumably safer water based lubricants are more common today, as the oil-lubricants can destroy condoms. All of this stuff goes—right up into the bloodstream.
And finally we should look at gay related intestinal disorders—as most of the CD4 cells are actually in the gut, and gut problems are endemic in gay men. Whether it’s semen absorption, lubricants, or anal douching is unclear, but it appears to cause some chronic gut problem—and possibly leaky gut syndrome, allowing more foreign antigens to pass directly into the blood. Exposure to all these strange antigens may simply confuse the immune system. Now combine that with chronic meth use and you have a clear recipe for AIDS which doesn’t require a virus. Overall, the gut/immune system is designed for forward entry.
The hetero groups that get AIDS in the west tend to be hardcore drug users. The other known group is hemophiliacs. The “AIDS” each of these groups gets are quite different and really only have the low CD4 count and blood reaction test in common—which really are just general markers of a dysfunctional immune system. Hemophilliacs have a genetic disorder of the blood and never lived long until the AIDS era anyway, and injecting foreign protein for the clotting agent is immuno-suppressive in itself.
AIDS, like cancer, is something that anybody can get—but most will not progress to AIDS or cancer until they are already quite old, and will usually die of something else well before that. AIDS is really just a common immune disorder—the elderly often have it to some degree—lower CD4 counts and opportunistic infections. You can accelerate the aging of your immune system and progress to AIDS faster by chronic use of immune supressing hyper-stressors such as Meth/coke drugs and or direct toxic DNA damage through injecting or absorbing (anally) foreign matter into the blood.
None of this causes much immediate damage, but like smoking it ages particular vulnerable systems, probably through accumulated DNA damage, and this is why many people who quit eventually will progress to AIDS anyway a decade later or so—the damage has already been done, just as many smokers who quit will still progress to lung cancer at an accelerated rate.
But the insults that these risk groups are doing to their blood and lymph are considerably worse than smoking. Although notice there is a huge amount of overlap—someone who chronically smokes crack cocaine is much more likely to die of some lung infection than say karposi’s sarcoma.
Flicking to page 354 of Padian et al. I see this: “the practice of anal sex and lack of condom use have remained strong predictors of transmission since the beginning of the study”. And table 2 of the paper suggests that not using condoms is a statistically significant transmission risk factor, after adjusting for number of contacts (as I previously mentioned). I would not interpret that as agreement with a finding of “no significant difference”.
This argument might go through for observational studies, although even there I’d want a quantitative argument for why I should expect those confounders to have as strong (or stronger) an effect as circumcision’s apparent effect. But I also referred to three large randomized trials, and randomization reduces the association between confounders and treatment effects to statistical noise — that’s why people conduct randomized trials. So I still regard the trials as strong evidence for circumcision having an effect on HIV transmission; confounders don’t have a substantial effect on the results of randomized trials unless the randomization process was faulty.
(Incidentally, my original links to the 2nd & 3rd trials are now broken. Here are alternative links, although they may be paywalled.)
I’m skipping over the paragraphs on whether or not HIV is a virus since what HIV is specifically doesn’t bear on the point I was trying to make, which is that cofactors can’t subtitute for exposure to HIV (whatever one thinks HIV is).
Agreed.
Even if I grant you that, it doesn’t mean much to me unless one of those “specific types” of immune damage is the massive reduction in CD4 cell counts characteristic of AIDS. There are different kinds of immunosuppression, and it won’t do to presume that because something causes one kind of immunosuppression, it causes the kind of immunosuppression associated with AIDS.
At any rate, I suspect properly accounting for HIV+ status eliminates the link between whichever drugs you have in mind and AIDS. (Note that I am not denying any association between drug use and some form of immunosuppression — just non-spurious associations between drug use and substantial depletion of CD4 counts.) This 1993 Nature report describes results from the Multicenter AIDS Cohort Study. Check out the graph: there is a clear difference in CD4 count between seronegatives & seropositives, and only the seropositives suffer a downward slide in CD4 counts over the years, whereas differing levels of drug use show only meagre effects on CD4 count trajectories.
But how much does it affect CD4 counts?
But how much do they affect CD4 counts?
Skipping the background commentary on the immune system and the speculation about lubricants & intestinal disorders.
CD4 counts below 200-400 are AIDS’ key feature. The Nature paper I linked refers to “CD4+ T-lymphocyte depletion” as “the primary pathognomonic feature of AIDS”. Opportunistic infections of course vary in prevalence across subpopulations, but that doesn’t somehow negate the common symptom that allows them to get a foothold: low CD4 counts.
Do you have references for this?
But how much does it affect CD4 counts?
If they have HIV. Or idiopathic CD4+ T-lymphoctyopenia, come to think of it. Other than that...?
Hedging with the phrase “to some degree” makes that statement too vague for me to get a handle on, and it’d help to put a number on it. At any rate, CD4 counts don’t appear to be much lower among the elderly than among younger adults. A quick poke around for CD4 reference counts brings up this Mayo Medical Laboratories page, which gives a range of 424-1509 for people aged 18-55, and a range of 430-1513 for people aged 55+.
You can probably anticipate what I’d say/ask for the rest of the parent post, so I’ll save you the repetition.
You people are still going at it on the HIV thing?
This thread is now at 4.5*10^4 words (counted by copying into a text editor, and find/replacing to delete words that’re actually headers or vote/navigation links). I believe it should have been taken off-line at approximately the 5*10^3 word mark, if not sooner.
I admit I’m obsessively addicted. The more I look into it, the more I have found that HIV science has gone horribly, horribly wrong, and ‘HIV’ - whatever it is—if it even exists—is neither necessary nor sufficient to cause AIDS.
Considering that we have spent hundreds of billions of dollars on this hypothesis, this has larger implications for rationality and the scientific establishment in general.
This is absolutely true, and is a very good point. However, keep in mind that seropositivity is not a direct measure of HIV, and isn’t even especially correlated with HIV (see my reply in the other thread). Seropositivity is a rather good measure of CD4 cell decline—simply glance at that graph in the Nature paper and you can see that. Although I should point out I’m not sure if it’s actual cell loss that is measured or simply more CD8 expressing T-cells vs CD4.
Also note that there was no body of non-users of nitrates in the homo risk group in this study—they were split simply into ‘light’ and ‘heavy’, and the heavy users were twice as likely to get KS—I’d say that is a rather significant correlation.
This study has some flaws for looking at toxological causes though, as it was only looking at rather recent drug use (24 months), which is not quite the same as use history overall.
I’m not sure about Meth’s effects on CD4 counts in particular, but heavy cocaine use has a strong depleting effect on CD4 counts. First google result
But there are other factors in the homosexual risk group, the most important of which is simply semen. Semen is loaded with immunosuppressants that are designed to temporarily and locally deactivate the female immune system in the vaginal tract. One of those components are the prostglandins. It appears that evolution has struck a balance between semen’s need to disable immunity and the female’s need to regulate opportunistic microbes in the vagina (namely candida) - this balance sometimes fails and yeast infections result.
AIDS is in general associated with candidiasis—yeast infections—which overgrows in the rectal tract and eventually in the blood, and some of the seminal components absorb into the blood. Large-scale overuse of antibiotics to combat STD’s in the gay community is another significant cofactor, but semen itself may be a major part of the problem.
Many papers about semen’s immune suppression effects are a simple google search away—here is one typical example.
One of the most interesting though was this study of semen’s effects on rats from 1985.
They found that just seven daily rectal semen insertions had a marked immune suppression effect, but only in male rats, female rats didn’t seem to be particularly effected.
You seem to think that the CD4 count decline is somehow completely explained by HIV theory. It is not. The CD4 count decline is the defining feature of AIDS, but HIV’s role, if any, is theoretical and not well understood. So it makes sense to look at all the factors involved—for there are many independent immune suppressing factors in the primary AIDs risk groups—homosexuals and injection drug users.
In the original AIDS defining population of homosexuals, AIDS is associated with a tightly bundled set of cofactors:
passive anal sex
drug use
a history of a large number of past sexual partners and STD’s
a history of heavy antibiotic treatment
More on all the known immune suppressing factors in the gay cohort here. All of this needs to be taken into consideration before one starts chasing some new ‘virus’.
The drugs have changed over time (meth and MDMA being more popular now), but the correlation has remained.
The second significant risk group of AIDS patients appears to be injection drug users—really crack cocaine injectors in particular, and cocaine is known to deplete CD4 cells and cause AIDS all by itself.
I don’t know. Do you know? Do you want to investigate this? How? Keep in mind that before the AIDS era, hemophiliacs didn’t live all that long. We simply didn’t have much data on their longer term health problems. Then in 1985 the HIV panic mania spread, and the hemophiliac population was tested with Gallo’s “HIV’ test—which really is just a CD4 decline surrogate test. And we found that a big % of this population had declining CD4 counts and somewhat AIDS-like blood. What does this really mean?
And their wives don’t get it, btw. Neither do non-drug using prostitutes. Porn actresses in general do not appear to be at an elevated risk of developing AIDS either. None of this makes any sense for a sexually transmittable viral theory, but it makes perfect sense if AIDS is caused by primarily toxological chronic immune suppression.
I’m not so sure about that. I’m not sure that low CD4 counts in particular is common in the elderly, but compromised immune function is a typical problem of the elderly:
from the CDC: Opportunistic Infections in Immunodeficient Populations
“Opportunistic infections occur with greater frequency or severity in patients with impaired host defenses. Growing numbers of HIV-infected persons, transplant recipients, and elderly persons are at increased risk.”
“Elderly persons have defects in T-cell immunity that result in increased incidence and death from TB”
?
I won’t reply to this comment in full, but there’s a little loose end of my own making here, and I should tie it up:
“But how much does it affect CD4 counts?” (In response to the references to meth, cocaine, direct DNA damage due to injection and rectal absorption of foreign matter, and smoking.)
Strong claims shouldn’t hinge on a single study, but this study can be used to update probabilities for certain theories. You can think of it as eliminating possibilities.
Namely it eliminates or vastly reduces any hypotheses involving a typical STD transmission route. It allows for a very small possible horizontal transmission rate, but the most likely cluster is centered around zero. That doesn’t prove it is zero, it is just that this evidence strongly favors zero transmission rate theories over all others.
The what? I don’t think there is a single “female HIV seroconversion” to be “explained away” in any of those studies. From what I understand, and what Padian et al claim, the Padian study is the only properly controlled prospective study of heterosexual transmission. The other studies are just observational guesswork that are all circularly dependent on the notion that seropositivity is transmissible—they see a couple where both test positive and they just assume it was sexually transmissible—hardly anything resembling evidence for the theory—just circular logic.
First of all, in the other theories, there is no transmission to explain—and it certainly doesn’t have to involve iv drug use.
You have to understand what exactly seropositivity actually means. It is a blood test that was specifically designed to classify “aids-like” blood. Gallo developed it by comparing and testing a large amount of antibody combinations (biological IDs essentially), until he found a combination which successfully partitioned the AIDS-like and pre-AIDS-like blood from the normal blood. There are a host of other conditions that can cause full or partial seropositivity—think of it as a semi-general measure of CD4 immune malfunction. And actually, ‘malfunction’ is not even the right term, as one can test positive under some normal circumstances as well—such as pregnancy or during the course of some illnesses.
Testing positive multiple times, for no other apparent reasons, is a clear sign of some persistent CD4 immune malfunction which is highly correlated with full-blown AIDS in the future.
I glanced at the Madrid study and find it largely worthless compared to the Padin study. It is small, not properly controlled, and not prospective. They found higher “viral load” in couples that were both positive vs couples where only one partner was positive? That makes sense simply because as viral load loosely correlates with degree of sickness, we expect that to be correlated in couples. More sick people are more likely to not have partners at all or have sick partners.
You would see the exact same effect in smokers, and keep that analogy in mind when looking at any of this data.
Your “ingenious study” is not well controlled for drug use, and in fact barely even mentions it. As HIV/AIDS is highly correlated with drug use in all the epidemological data I have seen in the west, I don’t think this study allows us to differentiate much of anything.
For example, if you want to determine if lung cancer is predominantly caused by a sexually transmittable virus or toxicological effects of smoking, you need to design studies that carefully differentiate between the two. If you don’t screen for drug use (or smoking) you won’t learn much. Smoking (and drug use) are both highly correlated in long-term couples. If you just simply assume from the get go that the sexually transmitted viral theory is correct, you would naturally see an apparent low rate of transmission proportional to the length of time the couple is together (because this correlates with the smoking behavior ‘catching’.)
So to show that lung cancer is caused by a sexually transmitted vector, you would need to focus on non-smokers. That is why the Padian study is useful, and this African study you point to is not useful.
The part that you seem to think is ingenious—the so called “sequence analysis”, I do not find necessarily ingenious or able to “confirm that transmission was within pairs” in the slightest.
If you want to get into the side discussion on “viral load” and viral DNA comparison based on PCR techniques, it’s critical that you understand Kary Mullis’s objection. Kary Mullis won the nobel for inventing PCR, and he is a strong critic of the whole HIV theory, and the entire interpretation of genetic data based on the technique he invented.
Basically, PCR-like techniques allow you to detect DNA sequences that match a partial fragment, and they allow you to massively amplify those matches—allowing one to find a needle in a haystack by duplicating the needle into a new haystack, so to speak. It’s more useful for qualitative vs quantitative results. The problem with the whole idea of using PCR to test for “HIV DNA” is multi-fold. First, HIV-DNA is allowed to be any of a vast set of sequences—presumably because of it’s massive “mutation” potential. The human body is floating in a sea of RNA and DNA sequences, most of which we know little about—large amounts of various types of RNA that is used to control gene expression, regulatory computation, and regulatory signaling between cells.
So out of that sea of DNA/RNA you get in a tube, a huge set of 10bp-ish sequences are rather arbitrarily determined to be “HIV”, and then one tests many partial sequences and usually finds some similar-ish matches. If you use this PCR test on anybody you will always get some positive results—everybody has some amount of “HIV-ish” genetic material circulating in their blood normally. Comparing sequences in this way is fraught with methodological problems—if you pick some random sequence you will probably find something similar in someone else’s blood, so there is a huge amount of potential sample bias—somewhat like looking for pictures of crystals in ice patterns or looking for coded messages in the bible. There is so many random sequences that it is easy to find some that match, focus on those, and then ignore all the non-matches. A real true similarity comparison would involve a tremendous amount of sequencing on a scale that is—as far as I can tell—never done or not even feasible today. It is not as if PCR gives us some complete snapshot pictureof all the DNA/RNA floating around.
And finally, keep in mind that any way you slice it—we should expect to see sequence similarities in these couples, as they are genetically related—from the same area in africa and much more related on average than two random samples of homo sapiens.
That’s my issue — I don’t think Padian et al.’s zero seroconversions result is sufficiently strong to outright eliminate a possibility, unless one’s already assigned a low prior to that possibility. Personally, I walked into this discussion with a very high prior (something like 99%) for HIV being sexually transmissible to some nontrivial (more than, say, once in every million unsafe sex acts) extent, and the Padian et al. result is not a strong one, so my prior is essentially unchanged.
Since the prior estimates for sexual transmission I’ve seen are already very small (on the order of 0.01% to 0.1%), the Padian et al. result doesn’t really clash with them that much. I also doubt “the most likely cluster” is centred on zero if one accounts for all of the evidence in the study, rather than focusing exclusively on the zero seroconversions result.
It favours a zero transmission rate strongly only if one makes particular strong assumptions about the sexual behaviour of the study’s subjects, and disregards the evidence of risk factors.
Let’s return to one of the papers that kicked off this discussion, as it has a few examples. From page 810: “seroconversions occurred in three male and seven female contacts after enrolment in the study” (that’s not even counting whatever seroconversions had to have occurred in those subjects already HIV+ at the start of the study). There must be some explanation for those seven seroconversions.
Whether or not one believes HIV is sexually transmitted, seroconversions occurred. What were their causes, if not HIV infection due to sexual transmission?
Where does the HIV come from if not an external source?
I’m having difficulty squaring some of your comments on seropositivity and HIV testing with the high reported sensitivity & specificity of properly conducted HIV tests.
I do not see the Madrid study as “largely worthless”, though I’d give it less weight than the Padian et al. study for the reasons you give. (I should emphasize that I’m talking about the Padian et al. study as a whole there; I maintain my reservations about the zero seroconversions result.) Still, the Madrid study sample’s not particularly small compared to the number of Padian et al. couples who consistently had unprotected sex and were followed up prospectively.
Yes. The point I was making was that with the sequence analysis confirming the source of the transmission, the probability of any given seroconverter having been infected by IV drug use with strangers is less than if the researchers hadn’t done the sequence analysis (although of course still more than zero). So, to have me agree that the HIV infections are due to IV drug use, I would have to be convinced that the seroconverters had been sharing needles with their partners. And...
...as the study took place in Uganda, I find it very unlikely that even half of the seroconverters were infected by sharing needles (especially since none of the subjects reported injection drug use). Unless you are now arguing that seroconversion doesn’t actually indicate HIV infection (and I can’t tell whether you are or not), I expect you can see why I’d want alternative explanations for each of these seroconversions.
The African study, I’d say, is weaker evidence than the Padian study. At the same time, I think it’s absurd to write it off as “not useful”. At the risk of repeating myself, my reasoning goes like this: some number of subjects acquired HIV during the Ugandan study; exposure to HIV is necessary for infection; it is not credible to suppose that every HIV exposure that led to seroconversion is attributable to IV drug use. If there were only four or five seroconversions, I’d say it was statistically possible. In fact, the study reports that out of 239 monogamous couples that were initially HIV-discordant, 72 “acquired HIV during follow-up”. The probability that all 72 of these Ugandans acquired HIV by IV drug use is surely astronomically small.
Not especially, to be honest.
I’m not much impressed by Mullis’s Nobel credentials. There are quite a few Nobelists who got the prize and promptly started dabbling in crankery. (Including, as it happens, Luc Montagnier, so this isn’t just an issue for people who downplay the links between HIV & AIDS.) Jim Watson co-discovered DNA’s structure, but I’m not about to take all his proclamations about genetics at face value.
Anyway, I haven’t seen anything in the Uganda study report to suggest they used PCR in so sloppy a way as you’re suggesting, and I doubt they’d have much to report if they had. As such, it’s hard for me to avoid the feeling that your remarks about PCR are something of a fully general counterargument against HIV sequencing.
Right, but two samples of virus from a couple where one member infected the other will nonetheless be far more genetically similar on average than two samples of virus from randomly selected infected people in Rakai.
First off, before we get into anything else, we need to understand and agree on what seropositivity actually means. Seropositivity means a positive result on an antibody test such as western blot, to some combination of antigens identified by Gallo in 1985 in his large scale blood screening tests. He did a large number of tests on transformed (immortalized) cell lines derived from AIDS patients and found a combination of antigens that could screen blood—separating AIDS and pre-AIDS blood from regular blood.
The problem is he (like Motagnier) failed to isolate the ‘virus’, and most or all of the antibodies in the test react or cross-react with antigens to opportunistic microbes (candida namely) and cellular debris. The p24 protein in particular is essentially just a normal cellular wall or microvescile component—so the ‘HIV’ test is really just a general test of opportunistic infection and apoptosis or immune directed killing of CD4 cells (possibly due to widespread viral parasite burden). It is not a measure of ‘HIV’, it is a direct measure of declining CD4 cells and AIDS or pre-AIDS.
more on this
and a longer, more detailed analysis of cross-reactivity for the different ‘HIV’ proteins
The antibody tests are not standardized geographically or temporarily, so it also makes it very difficult to compare across studies—“seropositivity” means different things in different places and times.
As just one random example—most dogs typically have a mix of ‘HIV’ antigens, and are HIV ‘seropositive’ in whole or in part:
from this paper
You post a link to a paper which supposedly shows the ” high reported sensitivity & specificity” of HIV tests. This is not actually what that paper is about, but it references several other papers for this claim—the first I investigated being this. The important quote:
So they are just using Western blot as ‘confirmation’. So they are just using one antibody test to confirm another antibody test—which of course is rather ridiculous.
To actually compute the sensitivity and specificity for a “HIV” test, one needs a gold standard such as viral isolation or perhaps a DNA test. Unfortunately HIV can not be isolated, either because it doesn’t exit or it exists in only minute quantities.
But one can attempt to use the presumed viral DNA as a gold standard, and the result is extremely poor sensitivity and specificity:
Poor sensitivity, specificity, and reproducibility of detection of HIV-1 DNA in serum by polymerase chain reaction. The Transfusion Safety Study Group.
Poor sensitivity is perhaps a gross understatement—the study actually shows that around 18-25% of the population at large test positive for ‘HIV DNA’, and this is only weakly correlated with seropositivity.
You completely dismiss Mullis’s argument based solely on an ad hominem “not much impressed by Mullis’s nobel credentials” without seeming to acknowledge or understand the argument itself.
Seroconversion in the west is closely correlated with AIDS or pre-AIDS. This does not appear to be as true in Africa, so we are generally talking about two different worlds. Part of this may be genetic (black americans have amazingly higher seropositvity in general), the other part may relate simply to higher precedence of opportunistic infections and antigens that seropositivity measures. KS for example is vary rare in the west and along with systemic candidaisis was part of the original AIDS definition, but it is one of the most common cancers in Africa.
I am arguing that.
Seropositivity does not strongly correlate with ‘HIV’ infection (by DNA test), which is why it is better to discuss AIDS itself as being sexually transmittable or not.
The Gallo blood test is tightly correlated with AIDS (at least in the west) - simply because that is what it was designed to do, so you can use that as data for AIDS transmission discussions.
OK. At this point, I’m going to have to disengage and walk away from this debate. I’m realizing that the inferential distance between us is far bigger than I originally thought, and trying to bridge it would need me to considerably ramp up the effort I’m already putting into this. (Even then I can imagine this going on indefinitely, which isn’t a very appealing prospect to me, nor to other Less Wrong posters, by the looks of it.)
I’d still like to respond briefly to one part of your comment, which comments on my own words rather than HIV/AIDS:
It’s wholly legitimate for me to respond to someone citing Mullis’s credentials (as if I didn’t know about them already) by explaining why I give them little weight, and my next paragraph was meant to summarize why I gave “your remarks about PCR” (that is, those you paraphrased from Mullis) short shrift. In other words, I acknowledged the argument by rejecting it.
I’m glad you can walk away, I have a harder time initiating that. I’m curious though about the direction of the inferential distance you see—do you have a biology background?
The dissidents point to a rather surprising pile of evidence that the serological HIV tests are based on rather general, cross-reactive antibodies, and this is essentially a fundamental flaw in HIV science which has never been corrected. Now it may be that the orthodoxy has a really good counter to this, but if they do I have yet to find it. The orthodox position on this, from papers linked to wikipedia, points to studies which measure the sensitivity of various HIV antibody tests by comparing them to . . other HIV antibody tests.
The few large double-blind meta-studies that compare the different antibody tests to PCR tests show terrible sensitivity and specificity between the two, and I haven’t seen the orthodox counter to this. So something is wrong with the antibody tests, the PCR tests, or the whole thing. I imagine it’s a little bit of both—the antibody tests are cross-reactive (hence many dogs test positive), and PCR tests are difficult and subject to experimenter bias.
Perhaps the orthodox counter is that there are a whole big host of HIV related viruses, and the antibody tests are cross-reactive across these related species. This seems to then just beg more questions than it answers, and doesn’t circumvent some of the specific non-viral cross-reactions the dissidents point to.
My paraphrase of Mullis’s argument may actually be a mix of other dissident positions. I just rechecked that part of his book and he covers the difficulty of PCR and the confirmation bias but largely in regards to the OJ trial. On HIV he mainly rehashes Deusberg’s argument.
All right, enough.
None at all. (I expect the inferential distance would be even greater if I did. If I had personal experience of working with retroviruses, for instance, I reckon my prior probabilities for claims like “HIV can not be isolated” or “HIV doesn’t exist” would be far, far less than they are. And they are already very low.)
So those electron microscope pictures are fakes?
Which electron microscope pictures?
When ‘HIV’ was first ‘discovered’ in the original papers by Gallo and Montagnier, they had difficulty isolating and didn’t publish pictures from what I understand—that didn’t happen until years later. Gallo’s great discovery for HTLVIII was based on running a lager number of antigen/antibody tests with an immortalized cell line to find an antibody test that could screen AIDS and pre-AIDS blood from regular blood. That is the basis of all the current HIV tests.
The first published pictures came more than a decade later, and they showed that “HIV isolate” really consists largely of cellular debris and microvesciles. In these EM photos, they do find some occasional particles of roughly the right size and label them as “HIV”, but they could also just be any of a number of other things, and for all intents and purposes, HIV ‘particles’ look like regular microvesciles.
The titles of the papers say it all:
“Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations”
“Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations”
more on HIV ‘pictures’
I have lost the link, but there are better more recent pictures taken with ATM, and they show that for all intents and purposes, it’s impossible to distinguish ‘HIV’ from regular microvesicles that bud from the cell wall naturally. If HIV can be said to exist at all as a unique exogenous virus, it is only because of unique RNA content in the microvesicle, and in this sense is very much unlike all other known viruses.
Of course, the part of HIV’s genome which is supposed to code for the outer envelope is pretty much the same as the endogenous sequences that already exist in the human genome—the HERVs.
Huh. While I still think that the HIV explanation is the most likely one for AIDS, I am slightly less convinced.
Well the best cure for doubt is to actually read the papers referenced. For example, following the links from your reference to the abstract of the actual paper which generated the numbers brought me to this abstract. I think you should read it.
The issue isn’t methodological errors in the studies—the studies clearly describe the methodologies used and their limits. The issue is trying to use the numbers in ways that they are not designed to be used. It is not the orthodox folks that are doing that. It is you that is doing that.
Ah, so do the numbers come with little instruction manuals that say “CAN ONLY BE USED TO SUPPORT ORTHODOX POSITION”? Haha sorry, couldn’t resist.
OK, I’m game, I will now look into the CDC studies, but let’s be clear on the trace ..
it starts with the wikipedia chart which has the ref note 80 linked here, which points to this, which in turn lists refs 76, 77, and 79 for P/V sex, which are (in order):
76: Comparison of female to male and male to female transmission of HIV in 563 stable couples
77: Reducing the risk of sexual HIV transmission: quantifying the per-act risk for HIV on the basis of choice of partner, sex act, and condom use
79: European Study Group on Heterosexual Transmission of HIV. Heterosexual transmission of HIV: variability of infectivity throughout the course of infection
I’ll comment more after I have read these.
You will find that #77, the Varghese et al paper, can be found online by Googling the title, and that it gets its 0.1% number for heterosexual transmission from the paper whose abstract I recommended.
I’m pretty sure you will find that all of these papers involve monogamous couples. If you give it some thought, you will realize that there is just about no other way to come up with a solid empirically-based number. And I again urge you to read that abstract—particularly the bottom third.
Haha ok this is kinda funny, but the abstract you linked to which is the source of the data in Varghese(77), is just 76! - the couple comparison from the European Study Group which I linked to and have been trying to parse. 79 appears to be another chapter from that same book, but I haven’t looked at it yet.
So before we get into 76 - the source of the stat you don’t like in 77, I need to backup and remember your original claim about the data:
Your implied point appears to be that couples in this study use condoms frequently. Surprisingly, this is not the case—only a surprisingly small number of couples reported consistent condom use (out of 500+),
Contraceptive behaviour:
No regular contraceptive 12 (10/86) 20 (43/212) Oral contraceptive 18 (7/40) 23 (26/114) Intrauterine device 10 (1/10) 28 (7/25) Condom* 0(0/11) 18 (6/33)
These people were using other methods of birth control more than condoms.
and they further removed consistent condom users from the data:
No, it is not. The reference leading to the abstract is the absolute risk described in the first paragraph of page 40 of Varghese. It is reference 28 of Varghese.
You are apparently following the references (21) appearing in Table 1 of Varghese. But these are relative risks (relative to felatio). Not at all what I meant.
My point about condom use came from an earlier reference that I had supplied which discusses a study that took place in Uganda in 2005. And I didn’t say that they used condoms frequently, I said that they were monogamous couples who got regular medical inspections and had been counseled regarding condoms. And in this study, as I recall, there was no exclusion of condom users.
I’m confused—the table says “assuming no condom use”. So you’re talking about other data, or they were able to filter the data.
What table in what document says that?
I’m talking about the data I said I am talking about: this paper and this piece of primary research which states
The original table in the top-level comment. I guess you’re off on a tangent then.
I repeat. What table in what top-level comment? WTF is a “top-level comment?”
The top-level comment of this thread. Comments are nested. Click parent enough times and you’re at a top-level comment. I’m surprised the name is confusing to you.
As for the table, it’s linked in the top-level comment:
I can see how you would have missed this link.
The linked table is clearly labeled and indicates that the risk is supposed to be for not using a condom. The table has the same figures as the “Table 1” appearing as an image in a nested comment by satt, which has the same indication. I doubt you missed that.
Given that you appear to be discussing the cites referenced in the table, I’m puzzled as to why you think condom use is implied. Are you saying the table is wrong, or are you talking about some other part of the cite than was used to build it?
Well, what do you know. You do know how to provide links to what you are talking about.
I don’t know why you are doubtful. Have I responded to anything on that branch before now?
You know something, you are a very effective troll. You have me boiling with fury right now. However, now that I know what is happening, I can become relatively calm, with effort.
If you want to know what I was talking about when I discussed condom use, I would refer you to what I said I was talking about when I discussed condom use.
Have a good day.
Pro tip: When everything you say seems to get downvoted into oblivion, the other guy is probably not the troll in the thread.
I’m sorry. I really thought you understood that the papers you were discussing are exactly those that were used to build the table:
This entire conversation is definitely mostly a mistake. Nobody can possibly care enough about the answer to my original question, which was: “is the table misrepresenting the studies it’s built out of, or are you mistaken?”, in order to justify reading this crap.
Ah no I haven’t even read Varghese(77) yet. You looked at that one and posted a link to an abstract—this abstract, which comes from the same European Study Group and has the same numbers (563 couples) as 76. So the abstract you wanted me to look at is just 76, it’s all the same source.
Satt also pointed this out in another reply here.
I’m not really concerned (at the moment) with what may or may not be happening in Uganda. The CDC data comes from this European Study Group, that is the original data in question - (the data you questioned).
Oh please. Stop trying to pretend you have the rationalist high ground here. You don’t.
It didn’t occur to me either, and seemed strange. That word does have strong negative connotations in my mind, but only because I associate it with stupid people denying true things and refusing to update on evidence. I thought the comment that referred to was incorrect, but it seemed more like honest confusion of the sort that clarification would dispel than denialism.
Some history then of exactly why the word conjures strong negative correlations is in order.
Look at the wikipedia entry for “denialism”. It originates with holocaust denialism, was then applied to skeptics of HIV==AIDS, and then later to other areas.
Peter Duesberg, the leading HIV==AIDS skeptic, is a German of non-Jewish descent raised in Nazi-era Germany, so it’s use against him and his followers adds extra moral angst. It is just about the deepest insulting connotation one can use. It is a signal of stooping to the ultimate low, that, in running out of any remaining rational argument, one must invoke deep moral revulsion to stigmatize one’s opponent.
In my view, the term is a serious Crime of Irrationality, it is an empty ad-hominem and should be seen as a sign of great failure when one stoops to using it as a name-calling tactic against one’s opponents.
That being said, I don’t think Perplexed has this view, and that wasn’t his intention. I am just giving background on why the word should not be used here.
Those who don’t subscribe to HIV==AIDS, should just be called skeptics.
Do we call proponents of quantum loop gravity String Theory Denialists? It’s ridiculous.
Should we call those who subscribe to HIV==AIDS to be Inquisitors, Mcaurthy-ists, or Witch-hunters?
I do.
Oh, I certainly was aware that I wasn’t complimenting you in using that term. But I don’t see any reason to waste the perfectly good word “skeptic” on someone who imagines that scientists who disagree with him are mostly doing so out of fear of being attacked by their politically powerful colleagues. I think that “denialist” does the job just fine.
Now, if you told me that several of your scientist friends had confided in you that they are living in fear, well, then that would be the kind of evidence that just might justify the label of skepticism.
So you are actually advocating the use of such perjoratives, even though they have no rational purpose and only serve to incite moral revulsion? Their only purpose is to exploit irrational cognitive bias.
“AIDS denialism” has become the standard term for this view.
It seems to be a reasonable-enough phrasing to me.
I think that applying the term AIDS denialist to someone who irrationally denies the validity of the scientific consensus on HIV/AIDS is entirely appropriate. It is certainly the standard term for the phenomenon.
As for moral revulsion, I would strongly suggest that you actually read some of the references regarding AIDS denialism that exist in that wikipedia article that you recommended. You will find that moral revulsion for your position is relatively common.
I would say that the purpose of using this terminology would be to signal to the person so labeled that he has stepped over an important line and that many people will disagree that that person deserves to be called a rationalist.
Rationality is a methodology, not a position, and name-calling goes against it’s core principles.
To quote Vlad M:
I don’t think that’s right. “AIDS denialism” is usually used to mean this:
http://en.wikipedia.org/wiki/AIDS_denialism
I’m not sure what your point is. Jacob_cannell has denied that HIV is the cause of AIDS. What is worse, to my mind, he has offered the opinion that many scientists who say that HIV is the direct cause of AIDS are doing so dishonestly—out of fear of retribution. Read the wikipedia article on denialism. He fits the pattern.
Nobody thinks that HIV == AIDS. HIV is a virus, and AIDS is a syndrome, that may—or may not—subsequently develop in individuals infected with HIV.
That HIV != AIDS is not even remotely controversial:
http://en.wikipedia.org/wiki/HIV
I think you’re reading this in an excessively literalistic manner. “HIV==AIDS” as it’s being used here is just shorthand for “AIDS is caused exclusively and entirely by HIV infection”
That thesis shouldn’t be controversial either.
For instance, a person obtaining two mutated CCR5 genes will be virtually immune to the HIV virus.
The chance of developing AIDS is probably also associated with age of HIV infection, the use of antiretroviral drugs—and other genetic and environmental factors.
Does the non-mutated CCR5 gene do anything important that the mutation disrupts? (In the sort of way the mutation for malaria resistance causes sickle cell anemia if you have two of them.)
That is the way I understand it and the way I assume jacob_cannell is using it. I’m pretty sure all concerned know the difference between viruses and diseases.
The question is whether HIV-1 is the cause of AIDS. Sure, there may be other factors that contribute, but I am claiming “no AIDS without HIV” and “HIV infection if untreated by anti-virals, leads almost inevitably to the diagnosable disease AIDS”. Jacob_cannell is apparently disputing this.
I’m basically agnostic on the HIV/AIDS question, but my layman’s understanding is that even mainstream thought on AIDS would not support this second statement. I believe it’s well understood that there are nontrivial numbers of people who are HIV+ and do not develop AIDS, decades after infection. This may be the gene mutation(s) referred to by timtyler, or it may be something else (I’m not well-read on the specifics)
You may be right that some people infected with HIV will never develop AIDS. Thx for the correction.
First I should point out that even the mainstream, as far as I understand, does not claim that HIV-1 is the sole cause of AIDS, unless one takes AIDS to be a very specific form of immune suppression only caused by HIV, but so far there is little scientific support for that—other causitive factors can mimic AIDS-like immune supression, and I believe this knowledge and view is mainstream.
As to your 2nd point, kodos96 addresses that, and again it’s not even the mainstream position.
So first off, I am not disputing what you are claiming—firstly because it’s not even the mainstream position, but secondly because what I am disputing is something of a meta nature. I am disputing the certainty in the mainstream position.
I hold a range of beliefs about HIV and AIDS, and distribute probabilities amongst them. I naturally tend to simultaneously consider multiple viewpoints. In this case they are:
(orthodox) HIV is the prime cause of a progressive immune deregulation, although riskgroup specific co-factors contribute
(moderate) HIV, like the other exogenous retroviruses, has health negative effects, but is hardly outright lethal. It exists in an evolutionary limbo—it was once more lethal, but is evolving into more of a harmless vertically transmitted symbiote. Other exogenous retroviruses have been implicated in cancers, but not strongly. They are somewhere between epidemic viruses and harmless exogenous retroviruses that long ago were neutered and intergrated into our DNA. Furthemore, there are several genetic variations, and they have differential individual effect—picking up novel retroviruses from someone else’s blood is not good for one’s health. .. .
Deusberg’s fully harmless passenger retrovirus theory.
I assign highest creedence to 2 atm. Note that it is very difficult to distinguish between these 3 theories. About the only specific differentiator would be koch’s postulate—isolating the virus and then infecting it into new hosts, observing the symptoms, and then reisolating the virus from infected cells. HIV has not been shown to cause AIDS under that criteria—it fails in any animal models.
Went googling and found that “Idiopathic CD4+ T-lymphocytopenia” is thought to cause AIDS as well as HIV.
See a company here and a scientific paper
Hmm, the scientific paper has only been cited 8 times, so I’m not sure how mainstream the view is.
The author is published for other more highly cited work, including nature.
Yes, that’s the term. Idiopathic just means “crap we have no idea what causes this”, so basically low CD4 counts and weak immune function is usually associated with HIV antibodies, but not always. I’ve seen that term used elsewhere, I think it is mainstream. I don’t think mainstream researchers are claiming HIV is the only thing that can cause low CD4 counts and AIDS-like symptoms—AIDS is not a specific set of symptoms at all, so it’s bound to have many classification errors.
Stop playing dumb—everyone who uses the word “denialist” knows exactly what it’s supposed to connote. Godwining has no place in a rationalist community.
Believing that other people knew (or should have known) how angry they were going to make you is exactly what makes outrage-driven discussions blow up.
Malice and spite exist, but I think they’re very rare compared to incompetence.
“Should have known better” is a very tempting stance to take, but it strikes me as unreasonable.
Also note that doing things even when you know that they will make other people angry is not necessarily malicious or spiteful. In most cases it will be because healthy individuals place limits on how much responsibility they assume for other people’s emotions. Doing things because they will cause another person could be spiteful. (Although even then that is not necessarily the case. See, for example, the recent Star Trek movie in which time-travelled Spock tells Kirk to provoke an emotional response in the young Spock, allowing Kirk to save everyone including Spock.)
So I guess what you’re trying to say is that he didn’t intend for the word “denialist” to conjure up images of the Holocaust in the minds of readers. Of course this is possible, but I think it’s pretty unlikely. The modern revival of the word (in the context of climate change) was specifically intended to have that connotation, and this was discussed openly by those who popularized its use in that arena.
Now I suppose it’s possible that he just picked the word up from context and started using it, without realizing that it was designed to provoke an emotional response and shut down rational debate… but based on his tone and overall approach, that’s not what it seems like to me.
That’s it.
Generalizing from the inside of my head, I think “denialist” has a stench from “Holocaust denialist”—it implies refusal to accept a true, important, and morally obligatory mainstream belief.
Perhaps such a word should be tabooed in a rationalist forum.
However, precisely because “denialist” became commonly used for such purposes as “global warming denialist”, the connection to the Holocaust got weakened.
The connotations of words shift, and as Holocaust denial has become less of a public issue (this is called “winning”), ‘denialist’ has acquired other default meanings.
This is a truly impressive bit of sophistry. You have succeeded in phrasing your objection in a manner such that a casual observer, unfamiliar with the topic under discussion, would think that you were being completely sincerely intellectually curious, while at the same time employing a coded epithet unmistakable to those already inclined to agree with you. This is a very common tactic, but I have rarely seen it done so skillfully. Bravo sir!
Now leave and go do it someplace else. This is lesswrong, not realclimate
Mr Hanson on “asexual” AIDS transmission: “Africa HIV: Perverts or Bad Med?”.
As I say in my comment there, it looks as though there are probably good reasons why this is not a very common perspective.