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NEDA TOOLKIT for Parents Neurotransmitters Although eating disorders result from the interplay of a variety of cultural and biological factors, the brain is central to understanding why some people develop eating disorders, why people stay ill, and how they can recover. In recent years, scientists have made tremendous strides in understanding the brain science of eating disorders. Based on evidence from hundreds of studies, it appears that one of the factors that make a person more likely to develop an eating disorder is how their brain functions. Researchers have identified specific neurobiological differences in the brains of people with anorexia, bulimia, or binge eating disorder. These differences affect how we eat, as well as things like mood, anxiety, personality, and decision-making. This section will introduce you to the basics of eating disorder neurobiology, and how various neural systems work together in individuals with eating disorders. Neurons Neurons send signals to each other using chemicals known as neurotransmitters. The type and amount of neurotransmitters released will tell neighboring neurons whether to become active or to stay silent. The body produces an array of neurotransmitters and their receptors, which are proteins on the surface of the cell that recognize a specific neurotransmitter and relay the signal from the outside to the inside of the cell. Small variations in the shape and number of receptors, as well as the amount of neurotransmitter produced — known as polymorphisms — exist in the population, which increase or decrease the amount of neurotransmitter in the synapse (the small space between a neuron and its neighbors) and our sensitivity to it. These variations have been linked to a variety of mental illnesses, including eating disorders. For eating disorders, there are two primary neurotrans- mitters you need to know about: serotonin and dopa- mine. Each of these neurotransmitters has an influence in how we think and behave, our personalities, and even perhaps our risk for developing an eating disorder. Serotonin Given that serotonin (sometimes referred to as 5-hydroxytryptophan) helps control everything from memory and learning to sleep, mood, and appetite, researchers quickly began to look for potential relationships between polymorphisms in serotonin receptor genes and eating disorders. A variety of studies have found alterations in the serotonin system in individuals currently ill with anorexia nervosa and those recovered from the disorder. Researchers found that people who are currently suffering from anorexia have significantly lower levels of serotonin metabolites in their cerebro­ spinal fluid than individuals without an eating disorder. This is likely a sign of starvation, since the body synthesizes serotonin from the food we eat. After long-term recovery from anorexia, however, individuals have significantly elevated serotonin levels (Kaye et al., 1991). In this study, the researchers found that higher levels of serotonin correspond with levels of anxiety and obsessive behavior. Geneticists have also found that individuals with anorexia are slightly more likely to carry a particular variant of the 5HT2A serotonin receptor, which is thought to increase the amount of serotonin in the brain during the non-starved state (Gorwood et al., 2002). In an article published in 2009 in Nature Neuroscience, leading eating disorder researcher Walter Kaye hypothesizes that starvation actually makes people with anorexia feel better by decreasing the serotonin in their brains (Kaye, Fudge, & Paulus, 2009). As they continue to starve themselves, however, the brain responds by increasing the number of serotonin receptors to more efficiently utilize the remaining serotonin. So in order to keep feeling better, the person needs to starve themselves further, creating the illness’s vicious cycle. When someone with anorexia starts eating again, however, serotonin levels spike, causing extreme anxiety and emotional chaos, which makes recovery difficult without adequate support. Individuals with bulimia also have dysfunctions in their serotonin circuitry. Those with bulimia, however, appear to have somewhat different alterations than those with anorexia. When going without food for longer periods of time (such as during sleep), those with bulimia had a larger drop in serotonin levels than women without eating disorders, which led to binge eating and increased irritability (Steiger et al., 2001). Researchers also found that women with bulimia who carried a particular variant of a serotonin receptor were also significantly more impulsive (Bruce et al., 2005). Abnormalities in the serotonin system were also found to persist after recovery, hinting that these Page  | 69