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.