Figuring this out is basically a matter of doing a literature survey, judging a few of the studies for basic sanity, and reporting the results. Being able to do this is a very important skill, and everyone should practice it at least once so that if they suddenly develop a medical condition, they know how to double check their doctor’s work. So here’s what I found in the literature:
So that’s correlation in both controlled animal tests and observational human tests, correlation in cultured human tissue, and observed mechanisms. A few names show up in a bunch of the studies, but there are also replications by unrelated research groups. There were even more studies to sort through, but I stopped there, because that’s more than enough: being infected with AD-36 makes you fatter, proven beyond a reasonable doubt. Any commenters nitpicking the statistics and sample sizes of individual studies are missing the point, because the evidence is the sum of all the studies, and they are not all flawed, or at least not flawed badly enough to seriously undermine the conclusion.
That said, there are conclusions which it is tempting to leap to, but which I could not find support for. First, it is tempting to conclude that AD-36 infection is responsible for a large fraction of the rise in obesity in the United States. However, I could not find any data on the overall prevalence of AD-36 in the US or world population, nor on factors affecting AD-36′s transmissibility; the studies I found seem to involve participants drawn from narrower geographic regions, whose exposure would be correlated and therefore not representative of the US as a whole. I also couldn’t find any sort of historical data to indicate that AD-36 prevalence has risen, rather than remain constant. Not that I would expect to find historical data in any case, since that’s very difficult to collect for recently discovered pathogens—but there are several inferential steps still not covered. The most likely conclusion, therefore, is that AD-36 accounts for some of the rise in obesity in the US, but an unknown amount, and not all. I also saw references to several other pathogens indicated to cause obesity in humans and animals, but did not research them in depth.
I stopped there, because that’s more than enough: being infected with AD-36 makes you fatter, proven beyond a reasonable doubt. Any commenters nitpicking the statistics and sample sizes of individual studies are missing the point, because the evidence is the sum of all the studies [emphasis added], and they are not all flawed, or at least not flawed badly enough to seriously undermine the conclusion.
You are the first person to actually take a firm position. I am enough of a Popper fan to applaud you, even if you end up being proven wrong. Thx.
I’m still unconvinced/neutral myself, but for the sake of argument I’ll make a few criticisms of your conclusions. I wonder how you will respond.
To begin, if you are going to sum all of the studies, you should probably include the negative ones, such as this European study or this US military study. It seems to me that rationality requires that the negative evidence somehow be explained away before the positive evidence is taken at face value. I have trouble explaining away the European study, though, of course, it might be argued that a different substrain of the virus is endemic on the European continent.
Another reason for uneasiness is the fact that the positive research is coming from so few research groups, and that the leaders of some of those groups have applied for a patent—as you yourself pointed out.
And finally, maybe it shouldn’t, but the fact that the most recent study presented such patently misleading statistics gives me a bad feeling about the whole hypothesis.
I actually missed those two negative studies—I only went through the first few pages of Google Scholar and PubMed results; I guess I should’ve been looking more closely at the preexisting discussion here. My confidence is lowered. Now for those two studies themselves -
The European one has a line in the abstract that seems to explain it: “No adenoviral DNA could be found using PCR on visceral adipose tissue.” That suggests either a significantly different strain or a significantly different (and better) immune response. I haven’t read the text of the military study (that one costs money), but the most likely confounding factor there would be military recruitment filtering out a lot of obese people; the child exposure test weakly suggests that the effect is largest on children whose adipose tissues are still growing, while the obese in the military are probably mostly those who started out fit and gained weight as they aged.
Since I posted this, two studies that I missed with negative results have been pointed out, and it’s also been pointed out that several of the studies that I thought were independent replications may actually have been subject to editorial influence by Dhurandhar and Atkinson. Additionally, serious questions have been raised about their integrity which I am not able to evaluate. Therefore, I am retracting my statement that is is proven that AD-36 causes substantial weight gain. I now assign this statement a probability of only 0.4.
EDIT: I have retracted the conclusion of this comment.
Figuring this out is basically a matter of doing a literature survey, judging a few of the studies for basic sanity, and reporting the results. Being able to do this is a very important skill, and everyone should practice it at least once so that if they suddenly develop a medical condition, they know how to double check their doctor’s work. So here’s what I found in the literature:
Literature survey of multiple pathogens indicated to cause obesity
Injecting AD-36 into rats makes them gain weight
Injecting AD-36 into monkeys makes them gain weight
Observational study showing AD-36 antibodies are correlated with obesity
AD-36 correlated with greater BMI and body fat mass, but not with greater insulin resistance and again by the same department
AD-36 makes cultured human adipose tissue accumulate more fat
AD-36 correlated with obesity in children
AD-36 increases glucose uptake by fat cells
Chemical mechanism by which AD-36 induces adipogenesis
So that’s correlation in both controlled animal tests and observational human tests, correlation in cultured human tissue, and observed mechanisms. A few names show up in a bunch of the studies, but there are also replications by unrelated research groups. There were even more studies to sort through, but I stopped there, because that’s more than enough: being infected with AD-36 makes you fatter, proven beyond a reasonable doubt. Any commenters nitpicking the statistics and sample sizes of individual studies are missing the point, because the evidence is the sum of all the studies, and they are not all flawed, or at least not flawed badly enough to seriously undermine the conclusion.
That said, there are conclusions which it is tempting to leap to, but which I could not find support for. First, it is tempting to conclude that AD-36 infection is responsible for a large fraction of the rise in obesity in the United States. However, I could not find any data on the overall prevalence of AD-36 in the US or world population, nor on factors affecting AD-36′s transmissibility; the studies I found seem to involve participants drawn from narrower geographic regions, whose exposure would be correlated and therefore not representative of the US as a whole. I also couldn’t find any sort of historical data to indicate that AD-36 prevalence has risen, rather than remain constant. Not that I would expect to find historical data in any case, since that’s very difficult to collect for recently discovered pathogens—but there are several inferential steps still not covered. The most likely conclusion, therefore, is that AD-36 accounts for some of the rise in obesity in the US, but an unknown amount, and not all. I also saw references to several other pathogens indicated to cause obesity in humans and animals, but did not research them in depth.
You are the first person to actually take a firm position. I am enough of a Popper fan to applaud you, even if you end up being proven wrong. Thx.
I’m still unconvinced/neutral myself, but for the sake of argument I’ll make a few criticisms of your conclusions. I wonder how you will respond.
To begin, if you are going to sum all of the studies, you should probably include the negative ones, such as this European study or this US military study. It seems to me that rationality requires that the negative evidence somehow be explained away before the positive evidence is taken at face value. I have trouble explaining away the European study, though, of course, it might be argued that a different substrain of the virus is endemic on the European continent.
Another reason for uneasiness is the fact that the positive research is coming from so few research groups, and that the leaders of some of those groups have applied for a patent—as you yourself pointed out.
And finally, maybe it shouldn’t, but the fact that the most recent study presented such patently misleading statistics gives me a bad feeling about the whole hypothesis.
I actually missed those two negative studies—I only went through the first few pages of Google Scholar and PubMed results; I guess I should’ve been looking more closely at the preexisting discussion here. My confidence is lowered. Now for those two studies themselves -
The European one has a line in the abstract that seems to explain it: “No adenoviral DNA could be found using PCR on visceral adipose tissue.” That suggests either a significantly different strain or a significantly different (and better) immune response. I haven’t read the text of the military study (that one costs money), but the most likely confounding factor there would be military recruitment filtering out a lot of obese people; the child exposure test weakly suggests that the effect is largest on children whose adipose tissues are still growing, while the obese in the military are probably mostly those who started out fit and gained weight as they aged.
I have the text of the military study if you want to PM an email address.
Since I posted this, two studies that I missed with negative results have been pointed out, and it’s also been pointed out that several of the studies that I thought were independent replications may actually have been subject to editorial influence by Dhurandhar and Atkinson. Additionally, serious questions have been raised about their integrity which I am not able to evaluate. Therefore, I am retracting my statement that is is proven that AD-36 causes substantial weight gain. I now assign this statement a probability of only 0.4.