The Role of Serotonin and Dopamine in Anorexia Nervosa
Amy H. Olson, LCSW
Families of individuals with Anorexia Nervosa (AN) enter the treatment room confused and afraid
of this deadly disease. Common questions include: “Why can’t she just eat, doesn’t she see how
thin she is?” and, “Did pressure from the media cause this?” An understanding of the biological
causes of AN is enormously helpful in answering such questions and in educating patients and
families about the complex etiology of the disorder. Biological abnormalities, in addition to
sociocultural, psychodynamic and familial factors contribute to the development of AN. This
multifactoral etiology complicates recovery efforts, which are often long and fraught with relapses.
Scientific research about biological risk factors, those that exist before the onset of the illness
and persist after sustaining recovery, promises to improve current psychodynamic and
pharmacological treatments. Biological risk factors include, but are not limited to, familial
transmission and genetic susceptibility (Kaye et al., 2000), personality and temperamental traits
such as obsessionality and perfectionism (Halmi et al., 2000), and abnormalities in
neurotransmitters, and neropeptides (Barbarich, Kaye & Jimerson, 2003). This paper seeks to
focus on the biological risk factors of the neurotransmitters serotonin and dopamine. A greater
understanding of premorbid abnormalities in serotonergic and dopamine activity can help
patients and families understand the chronic nature of this disorder.
The role of serotonin
Serotonin is a neurotransmitter, a group of chemical messengers that travel from one neuron
to the next, sending messages about functions such as sleep, hunger and sexual response.
Normal levels of serotonin produce feelings of general well being as well as “…stimulate satiety
and inhibit(s) the consumption of carbohydrates and lipids” (Brambilla, 2001, p. 124). Low
serotonergic activity contributes to depressed mood, and, conversely, high serotonergic activity
produces a more anxious mood.
Patients with AN have serotonin abnormalities, particularly increased serotonergic activity
(Barbarich et al., 2003, Kaye, Bailer, Frank & Wagner, 2006, Kaye et al., 2005) which “…could
contribute to restricted eating, behavioral over control, obsessive exactness, perfectionism and
negative affective states (Kaye et al., 2000, p. 801). This abnormality is not thought to be a
function of malnutrition because it persists post weight restoration and recovery (Kaye et al.,
2006). Dr. Kaye proposed in a 2006 Newsweek article that “…starvation prevents tryptophan
(present in the foods we eat), an essential amino acid that produces serotonin, from getting into
the brain…In fact, it is conceivable that people with AN might starve themselves in order to
reduce brain serotonergic activity, and in this way, temporarily make themselves feel better.”
(Tyre, 2005).
Serotonin specific medications may be very helpful in the sustained recovery for AN patients,
however, “…it is important to note that selective serotonin reuptake inhibitors (SSRI’s) appear to
have little effect on reducing symptoms and preventing hospitalization in malnourished,
underweight, AN individuals” (Kaye et al., 2000, p. 68). Such medications are associated with
reduced depressed mood, and a reduction in obsession as and compulsions when patients have
weight restored to approximately 90% of ideal body weight.
The role of dopamine
Dopamine is also a neurotransmitter, which functions to control emotional response, the
capacity to feel pleasure and pain; reinforcement and reward. The use of Positron Emission
Scans show that AN patients have overactive dopamine receptors, even post recovery. This
increased activity leads to harm avoidance and exaggerated worry about the future, and high
sensitivity to uncertainty (Guido et al., 2005).
Increased dopamine activity may explain some of the extreme self-denial of food and other
pleasures common in AN. Kaye reported to Science Daily, “Alteration in dopamine function may
affect the value of perceived rewards or perhaps make it difficult to associate good feelings with
things most people find rewarding” (2005). This inability to respond to stimuli or separate positive
and negative feedback, leaves AN patients less able to recognize and respond appropriately to
health concerns. They are not, as families complain, just being stubborn; they honestly may not
recognize their dangerous state of health.
In a presentation of his recent research findings at the National Eating Disorder Association
annual conference, Kaye hypothesized that the act of eating floods AN patients with dopamine.
This is because the brain recognizes food as pleasurable and releases a little dopamine on
already overactive dopamine receptors. He also hypothesized that this is the reason AN patients
derive pleasure from thinking about food and preparing it for others, as the brain will release a
tiny amount of dopamine from just the thought of food, an amount that does not overwhelm.
Overall, the anorexic brain maintains such high levels of dopamine that the simple pleasures in
life are too much (2006).
Abnormalities in the neurotransmitters serotonin and dopamine continue to exist post weight
restoration and recovery, leading scientists to believe that abnormalities predate the onset of AN,
and are hard wired. Pharmacotherapy may serve as an essential support to correct imbalances
and support long term recovery. AN patients and families can benefit from understanding and
learning to manage the temperamental traits and behaviors associated with neurotransmitter
imbalances during the course of psychotherapy.
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