Anorexia and the Brain
Nature or nurture? That’s been the question for ages. Fascinating new research is pointing to the possibility that underlying neurobiological factors drive the behaviors exhibited by Anorexia Nervosa.
Most abide by the belief that some combination of genetics, culture, and family dynamics contributes to the development of eating disorders: society is the gun, genetics loads the gun, and the family pulls the trigger. Unfortunately, many afflicted individuals and their families have lived with a negative stigma associated with this disorder. Until recently, most research had been devoted to the sociological contributing factors to the disorder, highlighting the role that family can play in the development of eating disorders. Consequently, too much blame has been unduly placed on families. Leading research in the field is now turning towards genetic and neurobiological contributing factors.
Researchers at the University of California, San Diego Medical Center are looking at how the brain may contribute to the development of the disease Anorexia Nervosa (AN). Walter Kaye, Director of the Eating Disorders Program at UCSD, and his colleagues found that behavioral commonalities amongst those affected point to the possibility of underlying neurobiological factors: “They often become sick around the same time (early adolescence), show similar symptoms and behaviors, and are mostly females. They typically resist eating and engage in a powerful pursuit of weight loss, yet paradoxically are obsessed with food and eating rituals. Even when underweight, they tend to see themselves as fat and deny being underweight. They tend to resist treatment and lack insight about the seriousness of the medical consequences of AN.”
So is this eating disorder really a brain disorder? Anorexia patients exhibit reduced brain volume, altered metabolism of brain regions known to modulate thought and emotion, and a return to childhood levels of female hormones. These disruptions tend to normalize with weight restoration, suggesting that they are consequences of AN rather than causes. Furthermore, AN patients demonstrate that their higher brain regions, such as the frontal cortex, are able to override or ignore signals sent from the lower brain regions such as the hypothalamus which signal starvation and the need for food intake. These higher brain regions play a critical role in emotions, personality, and rewards, all important components in AN.
Genes play a huge role in causing eating disorders, contributing to certain personality traits that increase the risk of developing AN. People who develop AN tend to possess similar characteristics even in childhood, including anxiety, depression, perfectionism, people-pleasing behaviors, obsessiveness, and a drive for thinness. These traits also tend to persist after recovery. Kaye et. al. point out “they tend to be rule abiding, rigid, and anxious children who are high in harm avoidance, a personality trait characterized by a tendency to criticize and doubt past thoughts and behaviors, worry about the future, and struggle with uncertainty.” Studies have shown that these traits are heritable and found in family members of AN patients irregardless of weight. Because these personality traits persist into recovery, it is suspected that they reflect underlying traits rather than consequences of anorexia.
Appetite is regulated by a complex system of nerve signals and hormones in the brain, gut, and fat and sugar stores throughout the body. Imaging studies show that higher brain structures in those with AN are used to override signals and to cognitively control and restrict eating. Brain scans show distinct differences between the brains of those with AN and the brains of those without it. Many of these differences are found in the insula. During a sweet-perception task, people without AN are given sugar and the more they report that they enjoy the sugar, the more activity shows up in their insula, striatum, and ACC. Thus, these regions of the brain are important for sensing reward. When given the same test, people recovered from AN show less activity in these areas when given sugar.
Similarly, when looking at pictures of food, both ill and recovered anorexics show altered activity in the insula, OFC (orbitofrontal cortex), mesial temporal and parietal cortex, and the ACC (anterior cingulate cortex). Furthermore, people recovered from AN show less activity in the insula and other parts of the neural network. This suggests that the “ability to perceive palatable taste is fundamentally altered in AN, even after recovery, and that people with AN have a reduced incentive and/or motivation to approach food.” Overall, these imaging studies suggest that people with AN have a reduced drive in several systems associated with hunger and appetite, which explains how it’s possible for many to pursue emaciation even to the point of death. Unlike those without the disease who experience food as more rewarding when hungry because of neural pathways in the brain becoming more active, driving the motivation to eat, those with AN seem to received mixed messages from various parts of the brain. This may explain why food and cooking obsessions are paired with lack of motivation to eat.
Lastly, recent studies have assessed reward processing in AN. The neurotransmitter dopamine is involved in reward and affect, decision-making, and executive control. There is much evidence that alterned function of dopamine occurs in AN. Kaye and his associates conducted a study in which healthy controls and those with AN were assessed for brain activity response to winning or losing money. In controls, the neural activity for winning was very different from that of losing. But in people recovered from AN, the brain activity in the ACC and its ventral striatal target was similar whether they won or lost. “This suggests that people with AN might have trouble discriminating between positive and negative feedback and identifying the emotional significance of stimuli, which in turn could help explain why it is so tough to motivate them to go into treatment or to appreciate the consequences of their behaviors.”
Kaye et. al. also found that women who were recovered from AN showed increased activity in certain areas of the brain (DLPFC and the parietal cortex). These regions are activated when there is a perceived connection between action and outcome and when there is some uncertainty about whether the action will lead to a desired outcome. Healthy controls were able to live in the moment, make a guess, and then move on. However, those recovered from AN “tended to worry about the consequences of their behaviors, looking for “rules” when there were none, and feeling overly concerned about making mistakes.”
In conclusion, AN is a very complex disorder with etiology stemming from the interaction of genetic, biological, psychological, and sociological factors. More and more research is finding that there are actual brain and neurological changes that occur in those with AN. It is not in their head! (Well, actually it is…literally… in their brain chemistry and anatomy) It’s an actual, real life disease, and it’s my hope that those who suffer from the disorder can find some solice in knowing that they are not somehow defective and that it’s very difficult to “just get over it.” When they are feeling disconnected from their feelings, for example, there are actual neurobiological reasons for this in their brains. My hope is that as new information continues to surface, the shame and guilt can be removed from the disorder and we can respect it like we do any other disease.
Source:
Kaye, Walter H, et. al. Is Anorexia Nervosa An Eating Disorder? How neurobiology can help us understand the puzzling eating symptoms of anorexia nervosa.
http://eatingdisorders.ucsd.edu/research/biocorrelates/PDFs/Kaye2010NeurobiologyofAN.pdf
Comments