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.
Finally, the researchers also found evidence of abnormalities in pancreatic cells, again suggesting an impairment in the processing of glucose and insulin release.
Now, I’m all for shifting blame away from myself and onto my parents, but I feel that, like every possible explanation behind the obesity epidemic, this is only one piece of the puzzle. Genes undoubtedly play a role in body mass, fat percentage, and metabolism, but so does what you eat and how many calories you burn through physical activity. There are absolutely individuals who gain weight easier and lose it more difficultly than others, but they still could have been born to thin or healthy parents. Additionally, in the current study, the majority of health problems seen in the offspring mice were only triggered after they themselves were fed a diet high in fat; when they were fed a normal diet, they did not display evidence of elevated body fat or insulin resistance.
The problem of obesity, like so many health and social issues we face today, is that there isn’t just a single contributor to the problem. If there were, it would have been solved by now.
We know from prior research that there are certain metabolic or genetic abnormalities that make an individual more susceptible to obesity and may explain instances of excessive eating, like leptin deficiency or Prader-Willi syndrome. However, these conditions, as well as less extreme genetic irregularities, currently only account for roughly 10 percent of cases.
A “food addiction model” has also been suggested, with some individuals having a pathology, similar to drug dependence, where they show heightened impulsivity, a flattening of reward sensitivity, and a problem with impulse control manifested through their response to food. Research has shown that a mother’s diet during pregnancy may also play a role in these types of behaviors, affecting the dopamine and opioid reward circuitry in the offspring, potentially leading them to choose more calorie-dense foods to gain the same pleasure and reward from eating.
Again though, while a flattened opioid reward system and an “addiction” to food may be appropriate in some individuals, it does not explain all of the nearly 200 million Americans who are currently overweight or obese.
One thing that does potentially contribute to all of these cases of obesity is the widespread availability of inexpensive, high-calorie food. The ubiquitous presence of cheap, convenient, tasty fast food, not to mention the barrage of advertisements we are exposed to for it, has made it very hard to resist these fatty and sugary options. This can then lead to the more extreme manifestation of the neurocognitive, genetic, or metabolic conditions that have been shown to play a role in obesity. However, without this inundation of unhealthy food, these traits might not have resulted in such an overwhelming prevalence of obesity, diabetes, and related illnesses that afflict our society.