Government dietary recommendations became politicized in 1980, and increasingly separated from both nutrition science and comprehensibility to the public with each 5-year revision. In 1967, the bacterium used to produce the enzyme that turns corn syrup into high-fructose corn syrup was perfected, and HFCS became available in industry. In 1983, it was confirmed as GRAS status, and started replacing sucrose sugar in foods. The food-industry had already been replacing fats with sugars as a result of popularized science suggesting that higher-fat diets were a causative factor for heart disease.
Purchasing power for below-median wage-earners has stagnated since the 1970s. Lower income levels correlate with higher obesity.
Climate-controlled buildings are now the norm. More efficient heaters and coolers make it cheaper to be in a 20 degree C environment year round. Clement climate correlates geographically with higher obesity.
Canine Distemper Virus has been shown (Lyons, 1982) to cause permanently-elevated levels of obesity in mice. Since then, other infectious diseases have been found to promote obesity in animals: RAV-7, Borna, Scrapie, SMAM-1, Ad-36, Ad-5, Ad-37. Gut parasites produced symptoms similar to metabolic syndrome in dragonflies. Obese humans have been found to have a 3 times higher incidence of evidence of past infection by adenovirus Ad-36 than the non-obese (30% vs. 11%). If twin studies, where one twin had been infected by Ad-36, and the other not, the exposed twin was fatter. Across all studies, evidence of past infection by Ad-36 always correlated with a fatter subject, with causative significance. It even works with viruses originating in nonhuman animals, that do not otherwise cause visible symptoms. A sick bird could make you fat, without ever making you sneeze.
Analyses of digestive tract microbiotic factors have discovered causative significance for obesity in some factors. Experimental fecal transplants have resulted in changes in the recipient's weight and body composition.
Studies of epigenetic DNA methylation, sibling genetics, and maternal weight suggest that children of obese mothers may have greater predisposition to obesity, creating an intergenerational feedback loop. Fat mothers make fat daughters make fat granddaughters. This could be experimentally verified by cloning/twinning a female animal embryo, applying different environmental factors to produce breeding animals of different obesity levels, and implanting each with a second set of clone embryos. The second set of clones would then be kept under identical environmental conditions. Unfortunately, cloning processes themselves introduce epigenetic regulations and deregulations that ultimately result in obesity. Cloned mice get fatter when they get older.
It seems as though older mothers bear children that grow fatter as adults. Children of moms over 30 have higher body fat percentages than children of moms under 25, by about 2.7 percentage points. Both low-birthweight and high-birthweight babies correlate to greater adult obesity, and older mothers are less likely to have middle-birthweight babies.
Sleep deprivation correlates with higher obesity.
In short:
change in foods composition \\\
wage stagnation \\\
literal adenovirus epidemics \\\
change in gut microbiota \\\ OBESITY
intergenerational epigenetics /// (complex cause)
delay in child-rearing ages ///
chronic sleep deprivation ///
other factors??? ///
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.
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This leaves us with food composition and marketing as the main causal factors.
- 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?