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.)
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.)