How a Pregnant Mother's Diet Could Change a Child's Brain

New research proposes an explanation for obesity based on neurohormonal changes before people are born.
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Scientists have pursued every possible avenue to try and figure out why we keep getting fatter. They’ve explored our genes, our brains, our hormones and our gut bacteria, not to mention our fatty, sugary diets and sedentary lifestyles. Now, a recent study has come out blaming our expanding waistlines and poor health on our parents’ behaviors before we were born.

The article, published in the journal Cell in January, looks at the impact a mother’s diet has on her offspring’s health. This line of research isn’t new—other studies have shown links between a woman’s health during pregnancy and her child’s weight later in life—but this is one of the first to provide a potential explanation for this phenomenon.

To explore this, researchers first fed pregnant mice a diet high in fat at varying stages during their pregnancy to figure out when the most critical period was.

It turns out that mother mice that were fed a high-fat diet while they were nursing had significantly heavier male offspring with a higher percentage of body fat than moms fed a normal diet during this time. These males also had higher insulin resistance and glucose intolerance, precursors for type-2 diabetes, even if they themselves consumed a normal diet. Interestingly, these poor health effects were only present in the female offspring if they ate a high-fat diet, but not if they ate normally.

Following this discovery, the researchers looked at what was going on in the brains of these mice that might be linked to their increase in body fat, particularly focusing on the hypothalamus, a major hormonal relay station in the brain that helps to regulate our metabolism. Two chemicals that are maintained through the hypothalamus and are key players in controlling our hunger and satiety are aGRP/Neuropeptide Y, which are released when we’re hungry, stimulating our appetites, and POMC, which is involved in triggering satiety once we’ve eaten.

In baby mice, neurons continue to develop after they’re born, but in humans, neural development is more established at birth. Therefore, the nursing stage in mice actually corresponds to the third trimester of pregnancy in humans, meaning that the most critical period for people is during the last trimester.

In the case of POMC and aGRP, the researchers discovered that there was a lower density of axon fibers—the part of the cell that connects neurons in one area of the hypothalamus to another—in mice with mothers that were fed a high-fat diet. This may then have had an effect on the processing of insulin and glucose in these mice, potentially leading to the glucose intolerance and elevated insulin levels that the scientists witnessed.

Moreover, it appears that a target of these neurons that is involved in suppressing appetite and stimulating the metabolism was also significantly affected. Specifically, the genetic expression of the thyroid-stimulating hormone TRH was significantly lower in the offspring of the high-fat mother mice. This means that there was a reduced potential for the release of this hormone, which is involved in weight-regulation.

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Dana Smith is a freelance writer based in Durham, North Carolina. She has a PhD in psychology from the University of Cambridge.

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