The Biochemical Foundation of Eating Disorders

by Ashley Drawal

She is standing there with her right hand on the crook of her left elbow. Her reflection in the mirror stares back at her. Emaciated. Pale. Hollow. Her cell phone vibrates violently against her dresser but she ignores it. She doesn’t want to hang out with her friends. She doesn’t want to have to eat with them.

She stares harder at the figure before her. Fat. Repugnant. But it’s a malfunction. Too many active synapses throughout the brain are causing an increase in anxiety and a decrease in appetite: her brain produces too much serotonin, an anxiety-inducer and appetite-suppressant, and not enough dopamine, a pleasure-inducer and appetite-stimulant. Serotonin is produced and released after food intake as it is synthesized from the amino acid tryptophan, which is found largely in any carbohydrate-rich diet. As part of its complex role in mood, appetite, sleep, and other behaviors, serotonin can activate 5-HT2C receptors on dopamine producing cells, blocking dopamine release. This pathway presumably indicates to the brain that the body is no longer hungry. But forced starvation and stress changes her body’s motivations; instead of proper regulation of serotonin levels in her brain, increased levels of stress and paranoia over her weight keep serotonin levels high, depleting her desire to eat even though her body is starving, reinforcing her anorexia.

She tugs her long-sleeved shirt down further over her arms to hide the lanugo, the fine white hair that’s sprouted all over her body. It’s a biological defense mechanism. She no longer has enough fat reserves to keep warm so her body compensates, causing the normally extremely fine hairs to thicken and elongate in order to trap heat to her body. She is sickened by what she sees.

She just wants to be pretty. She just wants to be thin.

She is not alone.

Another girl is eating with her friends in their college cafeteria. She is laughing with them as they head toward the dessert table. She starts piling her fourth plate with cookies and brownies and pie. She has a low number of 5-HT2C receptors in her brain, so dopamine levels aren’t blocked effectively after food intake and dopamine is consistently produced, making her constantly hungry. Every time she thinks of food, the overactive chemical release makes her believe that eating enormous amounts is making her happy. Food makes her feel better. She knows that after everyone is gone she will retreat into the bathroom, hide and purge all of the food she ate. Her throat is raw from vomiting but she doesn’t care.

She bites into the chocolate chip cookie. She just wants to be pretty. She just wants to be thin.

These girls’ stories are like those of thirteen million other men and women facing eating disorders like anorexia, bulimia, and binge-eating disorder. Just within the college student population, ten to 20 percent of females and four to ten percent of males are affected. These conditions are illnesses in which individuals use drastic methods, such as diet restriction, extreme exercising, or purging (vomiting or misusing laxatives) in order to lose weight.

Rather than being just a psychological illness, eating disorders now have a possible biological basis that current research is attributing to chemical imbalances within the brain. Now that there is a potential biological cause, treatment for victims of these “silent” disorders has become more plausible. Recent literature of bulimia nervosa shows a good potential for antidepressants, particularly selective serotonin re-uptake inhibitors (SSRIs), to be useful for treating symptoms of the disorder. SSRIs block the reuptake of serotonin, allowing more of it to stay in the synapse for chemical signaling, which would inhibit appetite. However, SSRIs have shown negative results in the treatment of anorexia nervosa, due to the already high serotonin levels found in these patients; furthermore, the upregulation of serotonin activity must be appropriately balanced to prevent any negative disturbances in mood. Pharmacological treatments for eating disorders still require further research and development, but as these conditions become better understood with increasing complexity—especially the interplay of appetite with mood and motivation—there is hope for more effective treatment.