It has been known for a while that obesity can be a “legacy” passed on to succeeding generations, not only for genetic reasons but for epigenetic ones. We are born with an array of genes, but they predict our destiny only to a certain extent. The decision to switch genes on or off is often made by things that happen within our lifetimes, like exposure to toxins and consumption of certain foods.
For years, pregnant women have been warned not to smoke cigarettes, and one of the reasons is that smoking moms tend to have children with allergies. When those children grow up, even if they don’t smoke, they tend to pass along messed-up DNA to their own kids. That is called transgenerational epigenetic inheritance. It isn’t fair, but it appears to be happening anyway.
The further scientists inquire into the secrets of this new field, the stranger it becomes. As we mentioned, the sperm cells of obese men even look different from those of lean men. When a dad is obese, his kids are more likely to have metabolisms that are not correctly regulated, and even more likely to develop type 2 diabetes. One research team found evidence that women with obese fathers are more likely to get breast cancer.
The questions are so urgent because if we can figure out what is going on, as writer Bill Sullivan states, “a new wave of therapeutics could be developed that focus on reversing these changes.”
The website WhatIsEpigenetics.com covers two fronts. It is basically two websites in one, with scholarly articles for professionals, and accessible, educationally entertaining posts for the general public. Most of them contain at least one sentence or paragraph where the writer encapsulates the significance of the research in an easily absorbed package.
For that website, Bailey Kirkpatrick wrote about the work done by scientists at the Max Planck Institute and their collaborators, noting that “new research is uncovering the possibility of an epigenetic switch that is, interestingly, either ‘on’ or ‘off’.” A group of researchers from several internationally renowned institutions did mice experiments and published a report suggesting that a network of imprinted genes can act as a switch to turn obesity on or off — but only once.
One of the group, J. Andrew Pospisilik, told the journalist:
Once the switch is triggered, it is a lifelong, epigenetically-driven decision that ends in a stable, either a lean or obese phenotype. Such clearly separated phenotypes have a genetic cause; here, though we found that the effect was non-Mendelian. The effect is akin to a light switch — on or off, lean or obese.
Applied to humans, this seems to indicate how there can be a pair of identical twins where one is lean and the other obese. Because they have the same genes, that shouldn’t happen. But the difference is epigenetic, caused by “the expression levels of TRIM28,” which is the designation of a certain gene.
The researchers set out to see if the same pattern existed between obese and normal children. They teamed up with specialists in childhood obesity and analyzed adipose, or fat tissue, from children with these body types. In half of the cohort, results aligned with what they found in the mice.
This is all explained much more thoroughly in Kirkpatrick’s article, but the bottom line, as voiced by Dr. Pospisilik, is a hope that eventually “we can permanently flip the system back to lean in one shot.”
Your responses and feedback are welcome!
Source: “Epigenetics: Feeding the Obesity and Diabetes Epidemic?,” WhatIsEpigenetics.com. 03/21/16
Source: “Epigenetics Could Turn on an ‘Obesity Switch’,” WhatIsEpigenetics.com, 09/06/16
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