Squeezed between abnormally photoshopped media representations of the human form, and apocalyptically dire headlines warning us of obesity epidemics, it is hard to know where to begin when discussing human eating behaviour, how to fix it, and even if it needs fixing. Obviously, one might say, obesity is down to lifestyle choices, and maintaining a “healthy balanced diet with plenty of exercise will do the trick”. It almost sounds like a religious chant; you can almost hear the rosary beads clicking. Luckily, there is a chance for salvation, so to speak, lead by a valiant team of scientists investigating the truth behind this adage.
Recently, Dr Rapauno and her team at Dartmouth College undertook an in-depth study of the FTO gene, whose mutated form is already known to lead to childhood obesity. It has now been proposed that this mutation provides a link between genes, eating behaviour, and obesity. In other words, the mutation makes that chocolate cake even more enticing. One particular part of the brain is responsible for this cheeky trickery: the nucleus accumbens (NAcc) located in the hypothalamus. The hypothalamus is considered the brain’s control centre, silently navigating us through life in cycles of hunger, sleep and sexual desire. It is not surprising therefore, that an alteration of one structure of the hypothalamus can have effects of such impact.
The mutation of this FTO gene has the catchy name FTO rs9939609, and appears to present a greater risk of obesity in children with this mutation. Prior to this study, it was known that the NAcc activation and size is correlated with less restraint in respect food, and high adult body mass index. The NAcc is considered to be an important target of this gene mutation, causing subtle alterations in this brain structure, predisposing the individual to unhealthy eating behaviours due to changes in reward system, and thus obesity.
The group used magnetic resonance imaging (MRI) to measure the activity of the NAcc in response to food advertisements, as well as the functional size of this brain structure, in consenting nine to twelve year olds (78 children in total). To prevent biasing the results, the children were led to believe that the researchers were studying their response to television. The study reports that children with this mutation (and therefore a greater risk of becoming obese), demonstrate heightened reward responses to food cues in the NAcc, and bigger NAcc volumes, compared to children without this mutation.
Although this is just the beginning of a long pilgrimage in discovering how exactly the FTO gene is involved in altering eating-related brain structures, this study elegantly combines the ideas of self-control versus genetic predisposition, thus pacifying the masses.