Aussie University’s Not-So-Surprising Finding That Our Appetite-Control Cells Head South As We Age

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Time to tack on another strong argument against the consumption of carbohydrates: A scientist at Monash University in Melbourne, Australia, says that appetite control cells in the brain degenerate as we age, leading to a sense of increased hunger and potential weight gain.

The culprits, says Dr. Zane Andrews, a neuroendocrinologist in the university’s Department of Physiology, are free radicals that attack the brain’s appetite-suppressing cells after we eat.

Even worse, he says, is that the degeneration is more significant following meals rich in carbohydrates and sugars. “The more carbs and sugars you eat, the more your appetite-control cells are damaged, and potentially you consume more.”

The attack on appetite-suppressing cells, he says, creates a cellular imbalance between our need to eat and the message to the brain to stop eating. “When the stomach is empty, it triggers the ghrelin hormone that notifies the brain that we are hungry. When we are full, a set of neurons known as POMCs kick in.”

However, he explains, free radicals created naturally in the body attack the POMC neurons. “This process causes the neurons to degenerate over time, affecting our judgment as to when our hunger is satisfied.”

The free radicals also try to attack the hunger neurons, but they are protected by a protein called UCP2, which allows them to continue signaling hunger-even if we’re not really in need of food.

A Culprit in Adult Obesity?

Dr. Andrews says that the reduction in appetite-suppressing cells could be one explanation for adult-onset obesity. “As a carbohydrate- and sugar-rich diet has become more pervasive in modern societies over the past 20 to 30 years, it has placed a strain on people’s bodies that is leading to premature cell deterioration.”

Dr. Andrews says that his next research project will focus on discovering whether a diet rich in carbohydrates and sugars has other impacts on the brain, such as increasing the incidence of such neurological conditions as Parkinson’s disease.

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