A wonderful example debunking the favorite line of all allopathic doctors – i.e. that our risk of chronic diseases is largely written in our genes, confirmed by the strong hereditary link in said diseases. Well, as has been known for at least a decade, traits of the parents (including personality, habits, body composition, and even memories) can be passed onto the next generation in non-genetic manner. Perhaps the most (in)famous study to question the genetic dogma recently was the rodent study demonstrating that adults males and females taught to fear a predator they are never exposed to in nature do pass onto their offspring an inborn fear of said predator. The study below now extends this epigenetic heritability to the most prevalent chronic diseases. Namely, metabolic syndrome, obesity, and type II diabetes. The study found that accumulation of microplastics (ubiquitous in our environment) in the male’s body damages his sperm and as a result a significant portion of his offspring go on to develop diabetes II in their adulthood. It just so happens that most plastic residues/particles are highly estrogenic, so another way to capture the study findings is to say that chronic estrogen exposure damages a male’s sperm and causes a heritable disease phenotype that only manifests in offspring, so that it would be very hard to legally link to the poor environmental quality the father experienced. Since there are many other estrogenic endocrine disruptors (e.g. bisphenols, heavy metals, etc) we are routinely exposed do, I think the study findings can be safely extended to those as well.
https://doi.org/10.1210/jendso/bvaf214
https://scitechdaily.com/microplastics-can-rewire-sperm-triggering-diabetes-in-the-next-generation/
“…Microplastics (MPs) are extremely small plastic fragments, measuring less than 5 millimeters, that form as consumer products and industrial materials break down. Metabolic disorders describe a group of conditions that include elevated blood pressure, high blood sugar, and excess body fat, all of which raise the risk of heart disease and diabetes. To uncover metabolic effects in F1 offspring, the researchers placed them on a high-fat diet. This strategy helps expose the impacts of paternal MP exposure that might otherwise be subtle under standard dietary conditions. The high-fat diet reflects common unhealthy eating patterns, such as the Western diet, and increases metabolic stress. Because the fathers consumed a normal diet, the obesity observed in the offspring was driven by diet rather than inherited eating behavior. The team found that female offspring of male mice exposed to MPs were far more prone to metabolic disorders than offspring of unexposed fathers, even though all offspring received the same high fat diet.”
