Researchers have discovered that some people carry a genetically lower dopamine, a neurotransmitter, that motivates them to eat more, explaining why some eat to live while others live to eat.
The new study by researchers from the University at Buffalo and The State University of New York found that people with the genotype find food to be more reinforcing than their counterparts without the variant.
Leonard Epstein, PhD, a distinguished professor of paediatrics and social and preventive medicine at the university's medical school, and his team brought 29 obese adults and 45 adults who were not obese into the lab for a controlled study of the relationships among genotype, motivation to eat and caloric consumption.
Epstein differentiates reinforcing value, defined by how hard someone will work for food, from the "feel good" pleasure people get from food, saying, "They often go together, but are not the same thing."
Researchers measured participants' body mass, swabbed DNA samples from inside their cheeks, and had them fill out eating questionnaires. There were two behavioural tasks. In the first task, participants rated various foods - from chips to candy bars - for taste and personal preference. This apparent preference test disguised a task that measured how much participants ate when food was freely available.
In the second task, participants could swivel between two computer stations. Pressing specified keys on one earned points to eat their favourite food; pressing keys on the other earned points to read a newspaper. The resulting behavioural measures included calories consumed as energy in kilocalories, reflecting both amount and caloric density, and time spent earning food instead of the opportunity to read the news.
Both obesity and the genotype associated with fewer dopamine D2 receptors predicted a significantly stronger response to food's reinforcing power. Perhaps not surprisingly, participants with that high level of food reinforcement consumed more calories. The results also revealed a three-rung ladder of consumption, with people who don't find food that reinforcing, regardless of genotype, on the lowest rung. On the middle rung are people high in food reinforcement without the A1 allele. Atop the ladder are people high in food reinforcement with the allele, a potent combination that may put them at higher risk for obesity.
The reinforcing value of food, which may be influenced by dopamine genotypes, appeared to be a significantly stronger predictor of consumption than self-reported liking of the favourite food. What's more, obese participants clearly found food to be more reinforcing than non-obese participants. The authors conclude that, 'food is a powerful reinforcer that can be as reinforcing as drugs of abuse'.
Researchers still view reinforcement as one of several factors that motivate eating behaviour, but the present study highlights the genetic contribution and role of reinforcement. In theory, people producing less dopamine may, as a result, require more food to reach a certain state of reward or reinforcement that might be reached quicker, after less consumption, by those with a different genotype.
Findings such as these can help obesity experts to pinpoint people at greater risk for obesity and to develop treatments tailored to specific risk factors. "Behaviour and biology interact and influence each other. The genotype does not cause obesity; it is one of many factors that may contribute to it. I think the factors that make up eating behaviour are in part genetic and in part learning history," said Epstein.
He and his colleagues speculate that, as with other public-health campaigns, it may be better to focus behaviour change efforts on those at high risk. "A strategy for someone who is high in food reinforcement would be very different from the strategy for someone who is low in food reinforcement but higher in activity reinforcement," they wrote.
Using overweight men, the group has already found that chemically manipulating dopamine levels alters eating behaviour, a finding highly suggestive for pharmaceutical intervention. The findings appear in the October issue of Behavioural Neuroscience, published by the American Psychological Association (APA).