September 30

The Role of Epigenetics in the Obesity Epidemic

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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

Identical twins don’t just share DNA; they also shared a uterus. Might that also help account for some of their metabolic similarities? Fetal overnutrition, evidenced by an abnormally large birth weight, seems to be a strong predictor of obesity in childhood and later in life. Could it be you are what your mom ate?

A dramatic illustration from the animal world is the cross breeding of Shetland ponies with massive draft horses. Either way, the offspring are half pony/half horse, but in the pony uterus they come out much smaller (thank heavens for the poor pony). This is presumably the same reason why the mule (donkey dad and mare) is larger than the hinny (stallion and donkey mom). The way you test this in people is to study the size of babies from surrogate mothers after in vitro fertilization.

Who do you think most determines the birth weight of a test-tube baby—the donor mom who provided all the DNA, or the surrogate mom who provided the intrauterine environment? When it was put to the test, the womb won. Incredibly, a baby born to an obese surrogate mother with a skinny biological mom may harbor a greater risk of becoming obese than a baby from a big biological mom born to a slim surrogate. The researchers conclude “the environment provided by the human mother is more important than her genetic contribution to birth weight.”

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The most compelling data comes from comparing obesity rates in siblings born to the exact same mother before and after her bariatric surgery. Compared to their brothers and sisters born before the surgery, those born when mom weighed about 100 pounds less had lower rates of inflammation, metabolic derangements, and, most critically, three times less risk of developing severe obesity (affecting 35 percent of those born before the weight loss compared to 11 percent born after). The researchers conclude “these data emphasize how critical it is to prevent obesity and treat it effectively to prevent further transmission to future generations.”

But wait. Mom had the same DNA before and after surgery. She passed the same genes down. How could her weight during pregnancy affect the weight destiny of her children any differently? Darwin himself admitted that the greatest error he committed “has been not allowing sufficient weight to the direct action of the environment, like food…independently of natural selection.” We finally figured out the mechanism by which this can happen: epigenetics.

Epigenetics (literally meaning “above genetics”) layers an extra level of information on top of the DNA sequence that can be both affected by our surrounds and potentially passed on to our children. This is thought to explain the “developmental programming” that can occur in the womb depending on the weight of the mother, or even your grandmother. Since all the eggs in your infant daughters’ ovaries are already preformed before birth, a mother’s weight status during pregnancy could potentially affect the obesity risk of her grandchildren too. Either way, you can imagine how this could result in an intergenerational vicious cycle where obesity begets obesity.

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Is there anything we can do about it? Well, breastfed infants may be at lower risk for later obesity, though the benefits may be confined to exclusive breastfeeding, as the effect may be due to growth factors triggered by exposure to the excess protein in baby formula. The breastfeeding data is controversial though, with charges leveled of a “white hat bias.” That’s the concern that public health researchers might disproportionally shelve research results that doesn’t fit some goal for the greater good (in this case, preferably publishing breastfeeding studies showing more positive results)––but of course that’s coming from someone who works for an infant formula company. Breast is best regardless; its role in the childhood obesity epidemic just remains arguably uncertain.

Prevention may be the key. Given the epigenetic influence of maternal weight during pregnancy, a symposium of experts on pediatric nutrition concluded that “planning of pregnancy, including prior optimization of maternal weight and metabolic condition, offers a safe means to initiate the prevention rather than treatment of pediatric obesity.” Easier said than done, but overweight moms-to-be may take comfort in the fact that after the weight loss in the surgery study, even the moms who gave birth to kids with three times lower risk were still, on average, obese themselves, suggesting weight loss before pregnancy is not an all-or-nothing proposition.

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