[pygy_]

Lots of correlates, Let's untangle that a bit...

- Poverty can't be causal here, since it doesn't match either the timing nor the geography of the epidemics.

- Intergenerational epigenetics is a secondary factor, but it can't be causative in the first generation.

- While the adenovirus study is interesting I'd be surprised its spread mapped with the time/space patterns of the obesity epidemics worldwide.

I mention geographical spread because the epidemics seems to spread along with industrialization, e.g. urban China is affected, while rural China isn't (yet?). The spread of the epidemics seems to map well with the spread of Western junk food. The following parameters could somehow make sense if Japanese folks weren't so lean

- delay in child rearing (where the effect size is minor)

- chronic sleep deprivation (and wow, 1/3 US adults sleeps less than 6 hours per night whereas 1/3 gets more than 8 hours).

- Microbiota is interesting, but known to be influenced by diet. So a problematic microbiota could be a maladaptative change consecutive to a bad diet, that perpetuates the issue.

These factors also apply to Japan, which has resisted the junk food onslaught for cultural reasons. Japan has ~3% of obese folks, and that was the case before they started aggressively monitoring belly fat in middle aged folks. Japanese folks who migrate to the US and adopt the local diet grow fat, so the difference isn't genetic.

————

This leaves us with food composition and marketing as the main causal factors.

[logfromblammo]

- Why can't poverty be causal? An essential part of food composition and marketing is price. As your disposable income decreases, the composition of items on the McDonald's value menu becomes more relevant to you, and the quality of the produce at Whole Foods markedly less so.

- Intergenerational epigenetic influence means that factors that are no longer overtly visible may have a lasting effect. If, for example, leaded gasoline exhaust fumes made grandma fat, that contributory cause could then invisibly propagate to a later generation via epigenetic regulation attached to gametes and occurring in utero.

- In 2011, someone suggested that Ad-26 and Ad-35 be used in an Ebola vaccine, to work around preexisting Ad-5 immunity in targeted populations. The anti-vaxxer nonsense notwithstanding, the hypothesis that an unknown obesity vector has been spread via routine vaccination, without any other adverse symptoms or side effects, has not yet been tested. Better fat than dead, though.

Several hypotheses regarding decrease in dietary quality have been tested, and found to be unsupported by evidence. The corn lobby has quite a vested interest in proving that HFCS is not significantly different from cane sugar sucrose in prepared foods, so you can find a lot of very narrow studies comparing HFCS to sucrose that all conclude they are the same dietarily, without going anywhere near price, or politics, or comparisons with the fats that both sucrose and HFCS have been replacing over the years. I foresee future studies declaring (cheap) palm oil to be dietarily equivalent to other (more expensive) oils, without ever noting the impact of prices on recipes and diets. Broader studies likely have a harder time getting funding.

Microbiota are also influenced by location--even temporary changes in location. Montezuma's Revenge and Delhi Belly and trail trots can all cause rapid change in one's gut constitution.

Observing Japanese who migrate to the US and preserve their previous diet could be elucidative. If they don't change anything about their lives other than their location, would they grow fatter?

[pygy_]

> - Why can't poverty be causal?

Because most poor people around the world are not fat and have never been until recently. In the countries affected by the obesity epidemics, it may be causal, but it doesn't explain why obesity struck somewhere and not elsewhere.

> - Intergenerational epigenetic influence means that factors that are no longer overtly visible may have a lasting effect.

Agreed 100%, it has an impact in the long run, but as a secondary factor, not as a trigger.

> - vaccines

I don't understand the point you're tying to make (beside "fuck anti-vaxxers", and I couldn't agree more). Specifically, I don't understand the link between these specific anti-Ebola vaccines and the possibility that vaccines could cause obesity.

> - HFCS...

A high fructose diet causes non-alcoholic fatty liver disease (a close cousin of metabolic syndrome), and that is well established. In general I have little trust studies that are privately funded. Too much room for bias.

IIRC the Japanese who migrate and keep their traditional diet don't grow fat. This is purely out of memory though, from something I read or heard a long time ago, and I could be wrong.

[logfromblammo]

In vaccines, viruses that are related to the target virus that present similar external structures may be used to train the immune system to target those structures. Immunity to the lesser virus confers immunity to the dangerous one. The specific suggestion was to change the viruses used in the Ebola vaccine, because too many people already had exposure and immunity to Ad-5. This implies that Ad-5 had been used in an earlier iteration of the vaccine. And Ad-5 is one of the adenoviruses that cause obesity.

Cowpox conferred immunity to smallpox--the similarity that led to the invention of vaccination in the first place.

It might be possible that some routine vaccination employs a virus that has always been considered completely harmless, with no visible symptoms beyond a little soreness and nasal sniffle, and that virus actually causes epigenetic changes that impact appetite and satiety, just like Ad-36, Ad-37, and Ad-5. There are about 50 known human adenoviruses, and less than 10 are believed to cause additional obesity. There are also viruses that are mainly pathogenic in other species, which cause no obvious symptoms whatsoever in humans--and in other species that are not the main host species--other than an increase in body fat. There are a lot of viruses out there. Only a small fraction have been studied extensively. Few would care to fund a test for antibodies to a virus that no one is afraid of, and that's what is needed to establish a correlation between exposure and obesity. The only reason adenoviruses were studied for this at all is because the avian virus that caused chickens to die fatter was denied an import license, and the researcher had to find something else that was already endemic.

Sometimes, a virus can be added as an adjuvant. It doesn't even have a direct impact on the targeted dangerous virus, it just makes the vaccine more effective by stirring up the immune system a little.

So it is entirely possible that vaccines that use live viruses that are traditionally considered harmless have never even tried to evaluate whether those viruses have impact on weight gain 10 to 20 years later. Those kids of anti-vaxxers that somehow survive to middle age might just end up with a lower average BMI than their vaccinated peers. It might be the only way we'd ever know. Usually, people who are not vaccinated live in a completely different culture, that would confound all the variables. An American anti-vaxxer living the same lifestyle (aside from the addled parents) as an immunized American would be a more apt comparison. The only other way to test would be to change the composition of the vaccine (an act that has an ethical impact) and wait a few decades to weigh people and caliper their back fat.

[pygy_]

That's fascinating, thanks a lot! I have a medical background, so I was familiar with how vaccination works, but not with the specifics of adenovirus!

[logfromblammo]

Adenoviruses are just scraping the surface, too. We have very little knowledge so far on how viruses, bacteria, fungi, and parasite animals can impact epigenetic regulation and deregulation in ways that are not immediately obvious. And obesity isn't exactly something that shows up in measurable quantities a few days after initial exposure. You wait decades, and the difference attributable to the variable under study might be a 2% difference in body fat. That's something you would only find if you already sort of knew where to look.

We're only finding this stuff now because the problem has grown to the point where researchers are specifically asking "why the heck are we so much fatter now?" They are finding multiple answers.

It turns out that real viruses can hack your body and change your persistent settings, just like software viruses can get into your computer and install a botnet rootkit. Some of those settings aren't even accessible to users. (I know if I had a slider bar to change my own body's preference for fat percentage, I'd drag it to 20% and tap the lock icon.)

Learning about this stuff, I now look at fictional plot devices like the super soldier procedure from "Captain America" in a new way. The machine demethylated all the DNA in Steve's body, and the serum injection targeted some specific genes to be re-regulated. Rather than chopping up the genes as CRISPR/Cas9 would do, an epigenetic regulator nondestructively tuned them, and set up positive feedback loops to keep them tuned to the "maximize Nazi-punching" profile. That's still far beyond our current abilities, but it makes it all seem more plausible.

[pygy_]

Tangentially, I remember reading a paper that was linking an auto-immune reaction to some hormone-like protein produced by e. coli and both anorexia and bulimia. Are you familiar with the subject? Has it been confirmed?