You may be aware that a lot of the mechanisms that control our weight are genetic ones, but did you know that the expression of our genetic code itself can be influenced by aspects of our environment? The process by which this occurs is called epigenetics, and it usually involves something called gene methylation.

When genes are "methylated" or "unmethylated," an extra methyl group attaches itself to or detaches itself from the end of that gene's DNA code. This in turn can alter how the gene functions, effectively turning it "on" or "off."

Epigenetics is one possible explanation for the fact that a lot of the seemingly heritable variance in human body weight cannot be explained by the direct inheritance of mutations or by lifestyle factors alone. While the sheer speed at which the epidemic of obesity and related conditions like type 2 diabetes has taken hold means that traditional evolutionary mechanisms couldn't have caused it, some scientists suspect that epigenetic mechanisms may have indeed have played a part.

Since metabolic syndrome limits the amount of glucose that can be used by the muscles and liver, people who suffer from it store more of their calories as fat, thus theoretically making them more likely to survive times of famine. However, since the typical diet of an obese person is as low in actual nutrients as it is high in calories, it makes sense that obesity in a parent could "turn on" the "thrify genes" that would better enable their child to make it through times of scarcity, thus predisposing that child to obesity.


In other words, simply by eating a poor diet, you may be elevating your offspring's chances of experiencing the kind of metabolic dysregulation that can predispose them to obesity, thus putting them at an increased risk for the same chronic obesity-related illnesses that may be threatening your own health.

For example, mothers who were obese during pregnancy were three times more likely to have a child with type 2 diabetes. Meanwhile, eating a high-nutrient "mediterranean diet" during pregnancy and getting an adequate intake of nutrients like folate, vitamin B12, vitamin B6, riboflavin, methionine, choline, and betaine has been shown to have a protective effect against these genetic alterations. Interestingly, these protective effects seem to work synergistically; you can't protect your offspring by supplementing just one or two nutrients, only by eating an overall healthy diet.

Now, none of this means that if you have a Y chromosome, you're off the hook. The nutritional status of a baby's father prior to a child's conception has been associated with changes in gene expression as well. For example, one mouse study showed that obese mice tended to have daughters who had impaired insulin sensitivity. However, if the father had been put on a diet and exercise regime prior to his daughter's conception, these effects started to disappear.

This, too, makes sense when you think about it; exercise "signals" to your genes that your muscles need easy access to glucose, a process that insulin resistance could impair.

Of course, while many studies have found that changes in DNA methylation were associated with obesity, its not always clear whether these changes are a cause of obesity or a consequence of it. Either way, the association is dependable enough that a scientist could use your methylation profile to strongly predict your BMI!


The good news, however, is that these indicators are not a life sentence. While you can't change your genes, you can change the expression of those genes, and living a healthy lifestyle can help normalize your genes. Dieters who have successfully lost weight and kept it off were found to have similar epigenetic profiles to people who had never been overweight.

Another study showed that a group of overweight men who undertook aerobic exercise only twice a week experienced changes in the expressions of the genes that controlled their fat storage, thus reducing their risk of obesity and type 2 diabetes. In this case, epigenetics might be best understood as the mechanism by which some of the lifestyle changes that can contribute to health and weight loss take effect.

It's also fascinating that while some of the epigenetic changes associated with obesity seem to involve complex interactions between many different genes and many variations in gene expression, others seems to act more like simple light switches; in lean people, they are turned off, and in obese people, they are turned on.

It's horrifying to think that the modern obesity epidemic could be setting the stage for the next generation to experience the same struggles we do. However, the existence of such light-switch genes have made some scientists hopeful that more effective drug treatments for obesity could one day be developed, or that people predisposed to be overweight could be identified early on and taught appropriate prevention strategies. Until then, though, diet and exercise are the best weapons we've got.

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