Supports Chapter 20: Healthy eating is fattening
Carbs may destroy appetite regulation over time
People who eat diets high in carbs and sugar may lose their natural ability to regulate their appetite, researchers warned today. The ability to regulate appetite may decline with age depending on what is eaten, new research suggests.
A team from Monash University in Victoria, Australia, say that appetite-suppressing cells are attacked by free radicals after eating. This degeneration is more significant after meals high in carbohydrates and sugars.
People who consume more carbohydrates and sugars experience more damage to their appetite-control cells, which could result in over-eating and weight gain, the researchers believe.
Dr Zane Andrews, the lead author, says that the damage to appetite suppressing cells creates a cellular imbalance between our need to eat and signals to the brain to stop eating. "People in the age group of 25 to 50 are most at risk," he said. "The neurons that tell people in this crucial age range not to over-eat are being killed-off.
"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, free radicals created naturally in the body attack the POMC neurons. This process causes the neurons to degenerate overtime, affecting our judgement as to when our hunger is satisfied."
It could therefore play an important role in adult-onset obesity. Dr Andrews said. "A diet rich in carbohydrate and sugar that has become more and more prevalent in modern societies over the last 20-30 years has placed so much strain on our bodies that it's leading to premature cell deterioration."
These findings were published in the journal Nature. The team are now looking at whether carbohydrates and sugars affect the brain in other ways, including risk of neurological conditions such as Parkinson's disease.
Andrews ZB, et al. UCP2 mediates ghrelin's action on NPY/AgRP neurons by lowering free radicals. Nature 454, 846 - 851 (30 Jul 2008), doi: 10.1038/nature07181,