Hannibal Lecter likes to eat brains for dinner, but your brain has more control over how much we eat than we think, writes Kate Purcell
Comfort-eating is a well established phenomenon. You would be hard pressed to locate a single person who hasn’t overindulged on ice cream and chocolate at some point to mask their sorrow. The reasons behind comfort-eating have never been completely understood, but recent studies have shown that anxiety and depression are intricately linked to our eating habits.
Garret Stuber of the University of North Carolina has shown a crucial link between fear and anxiety in the stimulation of over eating in rats. By focusing on the effect these emotions have on the lateral hypothalamus, the hunger centre of the brain, his research has shown that perhaps there is more to the endemic rise of obesity and eating disorders in society than merely the physical need for food and the neurological experience of hunger.
This wider interpretation of destructive eating habits may well prove a means of controlling such behaviour in years to come. For more than fifty years prior to this study, the control of food intake was hypothesised to lie in two areas of the brain, the lateral hypothalamus and the ventro-medial hypothalamus, the centres for hunger and satiety respectively.
Known as the dual-centre hypothesis and developed by Elliot Stellar, scientists believed that damage to these areas would provoke over or under eating. Essentially this concept derived from the idea that these two areas work in balance with each other.
When blood sugar levels dropped, receptors in the blood send a message to the lateral hypothalamus leading to the feeling of hunger. Once these levels returned to normal, a similar message would be sent to the ventro-medial hypothalamus, causing the satisfaction that fullness creates. This is essentially your brains way of telling you to stop shoving Doritos down your neck.
In a historical study conducted by Anand and Brobeck in 1951, lesions were made in both the lateral and ventro-medial areas of the hypothalamus of rats in an effort to discover how this would affect their eating habits. Their results showed that lesions in the ventro-medial hypothalamus resulted in the rats being unable to feel full leading them to excessively overeating.
Conversely, when the lateral hypothalamus was damaged, their inability to feel hunger culminated in a dramatic decrease in food intake. While the dual-centre hypothesis has in some ways been debunked and it is now thought that the pathways of hunger and satiety are ultimately more complex.
The original idea behind the study still rings true, that the process is ultimately a neural and hormonal balancing act. Perhaps this can go some way to explaining why we comfort eat so much, as once hormones become involved, all bets are off.
Stuber’s study agrees that eating disorders and obesity have a neurological basis and that the disruption of circuits to the lateral hypothalamus could indeed contribute to such problems. Rather than drawing attention to this previously accepted chemical see-saw, however, his work instead focuses on how the hunger centre is affected by the bed nucleus of the stria terminalis (BNST), a band of fibers running along the brain that are commonly interpreted as the area that controls anxiety.
A large portion of the inhibitory neurons associated with the BNST transmit to the lateral hypothalamus, and the results of Stuber’s research of its interaction with this sphere of the brain were, according to Hans-Rudolf Berthoud, a neurobiologist attached to Pennington Biomedical Research Centre, “completely unexpected.”
Stuber used a technique called optogenics to influence the neurons within the BNST in such a way that they would turn on and off the blocks located on the neurons of the lateral hypothalamus. Once the cells within the hunger centre were suppressed by stimulating the BNST, mice ate uncontrollably no matter how well fed they were prior to the experiment.
In fact, when given the choice between healthy foods and those with a high fat content, the rats showed a clear preference for the latter. As soon as the optogenic switch was turned off, the gorging ceased. Similarly, by halting activity in the stria terminalis, the rats involved under ate or didn’t eat at all.
This research is contradictory to studies that have come before it, which may revolutionize the way society understands eating disorders and obesity and may indeed lead to more effective therapies for these diseases.
Stuber states that “[the] BNST is really important for affective behaviour state in response to emotionally relevant stimuli, and the results show the output of those cells can actually directly modulate feeding behaviour.”
Although this is not a new idea, and it has shown true in patients with anorexia in previous studies, there has yet to be a foray into developing therapies for obesity or eating disorders based on the pathways of the brain. That said, there is a clear connection between anxiety and eating disorders such as anorexia and, indirectly, obesity.
A study published in General Hospital Psychiatry in 2008 showed that people who suffer from anxiety are 30% more likely to be obese than their calmer counterparts. The understanding of anxiety and mental health as a whole has come along in leaps and bounds in recent years, with a menagerie of therapies available, from pharmaceuticals to cognitive behavioural therapy to mindfulness.
SSRI’s (Specific Serotonin Re-uptake Inhibitors) are one type of drug which has proved successful in the regulation of anxiety, and hopefully with time neuroscientists will find a way of helping patients control their eating habits in a similar manner in conjunction with treating anxiety.
While these experiments have yet to be repeated on people, there is little doubt that Stuber’s study holds hope for the future of comfort-eaters everywhere. On the other hand, Ben & Jerry’s will be disappointed by the study, as the news surely predicts a massive drop in their share price in the near future.