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??? ///