Brain circuits involved in drug addiction are also activated by the desire for food, say researchers this week, claiming that the mere display of food - the smelling and tasting of favourite foods without actually eating them - causes increases in metabolism throughout the brain. An event that could contribute to the 'globesity' epidemic, they add. The findings confirm the power of advertising and the food maker's widely known belief that food needs to look good to sell.
According to scientists at the US Department of Energy's Brookhaven National Laboratory, increases in metabolism in the brain region that controls pleasure were strongly linked to the desire for food in the study participants.
"These results could explain the deleterious effects of constant exposure to food stimuli, such as advertising, sweet machines, food channels, and food displays in shops," said Gene-Jack Wang , the study's lead author. "The high sensitivity of this brain region to food stimuli, coupled with the huge number and variety of these stimuli in the environment, likely contributes to the epidemic of obesity in this country."
In previous studies Brookhaven scientists found that food stimulation increases levels of dopamine, a neurotransmitter involved in pleasure and reward, in the brain's dorsal striatum. Additionally, to better understand the relationship of the dopamine system to obesity, they looked at the brain circuits of obese individuals and found that, like drug addicts, these individuals had fewer dopamine receptors than normal control subjects.
For the new study the scientists looked at how 12 food-deprived, normal-weight study volunteers responded to their favourite foods by using positron emission tomography (PET), a brain-scanning technique, to measure brain metabolism during food stimulation.
Each volunteer was given an injection containing a radiotracer, a radioactive chemical 'tag' designed to 'light up' activated areas of the brain. Study subjects' brains were scanned twice over a two-day period, with and without food stimulation. Subjects were asked not to eat for 17 to 19 hours prior to the study.
Volunteers were presented with foods that they had reported as their favourites on a pre-study questionnaire. The food was warmed to enhance its smell and the subjects were allowed to view and smell it, as well as taste a small portion placed on their tongues with a cotton swab. They were also asked to describe the foods as they tasted them.
As a control, during scans when food stimulation was not used, subjects were asked to describe in great detail their family genealogy while they were presented with non-food related items. They were allowed to smell these items and they had a cotton swab dipped in water placed on their tongues to mimic the food-stimulation condition.
Study participants were also instructed to describe, on a scale of one to ten, whether they felt hungry or desired food at the start of the study and at five-minute intervals for a total of 45 minutes.
The researchers found that food stimulation significantly increased whole brain metabolism. Metabolism was higher in all regions of the brain examined, except for the occipital cortex, which controls vision and would not be affected.
The areas most affected were the superior temporal, anterior insula, and orbitofrontal cortices. Food stimulation also resulted in increases in self-reports of hunger and desire for food. Increases in metabolism in the right orbitofrontal cortex were the ones most significantly correlated with increased reports of hunger, report the researchers.
Full findings of the study are published in the April 2004 issue of NeuroImage.
According to the London-based Food Advertising Unit overall budgets from food firms devoted to food advertising (including fast food retail products) in the UK have been decreasing since 1984 - from 15 per cent of total advertising to 9 per cent in 2002. Total food advertising expenditures have also dropped - from £652 million in 1989 to £430 million in 2002.