Eating disorders are a serious problem. In the US alone, it is estimated that up to 30 million people suffer from an eating disorder, including anorexia, bulimia or binge eating. Although it can affect people of all ages, genders, and ethnicities, the incidence is highest among adolescent girls and young adult women. And even though eating disorders have the highest mortality rate of any mental illness, only a fraction of people with eating disorders receive medical treatment.

Anorexia nervosa is a very idiosyncratic mental disorder. It is characterized by a distorted body image and an overwhelming fear of gaining weight. Body-image disturbances in anorexia nervosa are complex multidimensional constructs, entailing an altered perception of oneself associated with a strong emotional reaction to self-image. This can induce severe dietary restriction behaviors, purging or excessive physical activity. The repeated, maladaptive food choices observed in anorexia nervosa can even result in starvation leading to death.

This behavioral pattern is seen as a sign of an outstanding capacity to overcome primary drives such as feeding; it’s an expression of goal-directed self-control. But this ability does not necessarily transpose to a therapeutic context: when anorexia patients enter treatment to gain weight, they still make poor food choices and continue to choose low-fat and low-calorie foods. Anorexia nervosa is therefore an example of a persistent maladaptive behavior.

Cognitive and emotional functions are deeply affected in people with anorexia. It is estimated that almost 50% of people with eating disorders meet the criteria for depression; in anorexia nervosa, nearly 75% of patients report a lifetime mood disorder, most often major depressive disorder. Also, up to 75% of patients report a lifetime history of at least one anxiety disorder. Obsessive compulsive disorder also occurs in up to 79% of anorexia patients at some point in their lives. So, psychiatric comorbidities are quite common.

Relapse is also frequent and the levels of incapacity and mortality associated with this condition are high, particularly when there is no medical intervention. In developed countries, the lifetime prevalence of anorexia nervosa is around 1% in women and less than 0.5% in men.

Medical complications associated with anorexia are plentiful. In the acute state of the disease it is common for patients to report dizziness, fatigue, or even syncope. In the chronic condition, as a consequence of malnutrition, almost every organ can be affected. Consequences can include amenorrhea (absence of menstruation) in women, cognitive deficits, dental caries, hypothyroidism , constipation, gastrointestinal bleeding, anemia, infections, compromised immunity, bone fractures, and spinal compression, just to name a few.

The causes of anorexia are variable, ranging from genetic and neurobiological factors to environmental and cultural influences. Genetics plays an important part: heritability in anorexia ranges from 28% to 74%. Research also suggests that some childhood emotional and personality traits, including anxiety, stress, fear, obsessions, and perfectionism might reflect neurobiological risk factors for developing anorexia. During puberty, hormonal changes and dysfunctions may interact with the brain’s neurochemistry and maturity, and with genetic factors, leading to the onset of the disease.

Also, sociocultural factors can’t be disregarded and are most likely the cause of the higher incidence of anorexia among women. Beauty ideals pervading the “western world” can lead to dissatisfaction with one’s body image and trigger the development of an eating disorder in a genetically and neubiologically predisposed individual.

A number of noteworthy structural and functional changes occur in the brain of anorexia patients. For example, grey matter deficits in brain areas involved in emotion, motivation, and goal-directed behavior have been reported. A neuronal system of particular impact in the neurobiology of anorexia is the serotoninergic system. Serotonin plays a role in a number of symptoms and behaviors typical of the condition, including obsessive behaviors, anxiety, impulse control, attention, and mood. Serotonin is also involved in regulating feeding behavior, including meal size and eating rate, having predominantly inhibitory actions.

Decreased grey matter volumes have also been reported in structures involved in the regulation of dopamine. Dopamine also plays an important role in eating behaviors, motivation, reinforcing behavior, and reward, which are also compromised in anorexia.

The restrictive eating behaviors associated with anorexia may therefore result from an imbalance between inhibitory and reward systems, which leads to a shift to compulsive behaviors.

These structural changes frequently observed in the brains of individuals with anorexia are generally thought to reflect the effects of malnutrition and starvation. Cerebral changes have been found to correlate with weight loss, and the reversal of these changes has also been found to correlate with the normalization of body weight. Still, some of these effects persist following weight recovery.

Therefore, a major question in anorexia research is whether these structural changes are consequence of the disease, due to the effects of starvation, or whether they are a cause that contributes to the development of the illness. Further research on the neurobiology of anorexia nervosa will be needed to clarify these issues and to establish more effective treatments.

References

Arcelus J, Mitchell AJ, Wales J, & Nielsen S (2011). Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Archives of general psychiatry, 68 (7), 724-31 PMID: 21727255

Foerde K, Steinglass JE, Shohamy D, & Walsh BT (2015). Neural mechanisms supporting maladaptive food choices in anorexia nervosa. Nature neuroscience, 18 (11), 1571-3 PMID: 26457555

Hay PJ, & Sachdev P (2011). Brain dysfunction in anorexia nervosa: cause or consequence of under-nutrition? Current opinion in psychiatry, 24 (3), 251-6 PMID: 21358334

Phillipou A, Rossell SL, Phillipou A, Rossell SL, & Castle DJ (2014). The neurobiology of anorexia nervosa: a systematic review. The Australian and New Zealand journal of psychiatry, 48 (2), 128-52 PMID: 24194589

Smink FR, van Hoeken D, & Hoek HW (2012). Epidemiology of eating disorders: incidence, prevalence and mortality rates. Current psychiatry reports, 14 (4), 406-14 PMID: 22644309

Zipfel S, Giel KE, Bulik CM, Hay P, & Schmidt U (2015). Anorexia nervosa: aetiology, assessment, and treatment. The lancet. Psychiatry, 2 (12), 1099-111 PMID: 26514083

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