Biological Approach to Eating Disorders

 

According to the biological model, disorders have a biochemical or physiological basis. There is an investigation into the functioning and structure of the nervous system, brain, production of hormones and neurotransmitters as well as inheritance of genetic material.

Reasons

Research into the biological factors that dispose and maintain eating disorders (ED) is currently at its infancy stage however the data mined is of great magnitude as this partly answers the question as to why both anorexic and bulimic patients relapse quite easily during recovery. 

A high to moderate inherited predisposition towards eating disorders has been proven to exist among patients. Genetic and familial history contribute approximately 56 percent of the risk in developing an eating disorder. Researchers have also found genetic links to physical activity, the metabolism of glucose and how the body uses fat thus supporting the view genetic factors help in the perpetuation of anorexia nervosa (AN) even after having received treatments. 

Individuals with a biological mother or sister suffering from AN are twelve times more susceptible in suffering from the same and four times more susceptible in suffering from bulimia nervosa (BN) than others. Chromosomes 1 and 10 are suspected to be linked to both BN and AN. Twin studies have shown a higher rate of eating disorders among identical twins in comparison to fraternal twins and other siblings.

In terms of gender, epidemiological studies have shown higher prevalence of AN and BN among females than males. Variations are primarily seen in ED behaviors wherein more women report purging, unhappiness with their weight and dieting and are likely, or less likely than men to report excessive exercising to maintain weight, binge eating and associated depression.

 Apart from this accidents, surgical inaccuracies or defects in prenatal developments that result in impairments in the structure or functioning of the hypothalamus seems to also contribute to the development of these disorders. There seems to exist differential alterations in the structure of brain pathways that govern taste-reward and appetite regulation. Research studies have observed among bulimics that the hypothalamus fails to activate a normal satiation response.

New research findings have suggested that the neurotransmitter serotonin (also known as the happy chemical), particularly low levels of it influences binging behavior among bulimics. Bulimics often yearn to binge food that is rich in carbohydrates which upon consumption is broken down to create tryptophan. This amino acid is used to create serotonin which in turn exerts influence on regulation of appetite and in creating the feeling of “being full”. Thus, as a response to low serotonin levels bulimics seem to binge on food. BN patients seem to also show low levels of CCK, a hormone secreted by the brain and gastrointestinal tract resulting in lack of satiation response. 

On the other hand, for AN patients’ high levels of serotonin is present which seems to produce acute stress and anxiety in them. To reduce this, they selectively consume lowered amounts of carbohydrates thus resulting in lowered serotonin levels and reduced angst.

Possible associations between dopamine (also known as the pleasure chemical) and eating disorder related behaviors seem to exist as well. In AN, there appears to be an over-production of dopamine, resulting in anxiety and the ability to resist pleasurable things like food whereas in the case of BN significantly low levels of dopamine is present, triggering binge eating so as to increase its production. 

                                        

Diagnosis

Laboratory examinations may provide an early prognosis although this must be corroborated with physical and psychological tests. In line with the biological perspective ED patients often demonstrate low triiodothyronine and thyroxine levels apart from low levels of chloride and potassium and decreased hydrogen in their blood.

Treatment

Pharmacotherapy has been extensively used to treat and/or control behaviors associated with eating disorder. For BN antidepressants of various kinds like Trycyclic antidepressant, SSRIs, SNRIs etc. have been used. These primarily aim at the imbalance of serotonin and dopamine that is present and have shown a success rate of 75 % in reducing binging and purging. Medications containing the same include Prozac, Effexor, Norpramin.

However, there has been limited success in the use of such medications for AN. Currently treatment focuses on increasing weight and appetite and in this area Olanzapine, an atypical antipsychotic drug seems to be quite effective although it is often recommended along with other therapies.

Prevention

Currently no preventive measures or programs exist to tackle biological factors that cause ED. Perhaps since genes is an important causal factor, genetic engineering for this disorder may one area of future research.

 

References

Culbert, K. M., Racine, S. E., & Klump, K. L. (2015). Research Review: What we have learned about the causes of eating disorders - a synthesis of sociocultural, psychological, and biological research. Journal of Child Psychology and Psychiatry, 56(11), 1141-1164. doi:10.1111/jcpp.12441

Davis, H., & Attia, E. (2017). Pharmacotherapy of eating disorders. Current Opinion in Psychiatry, 30(6), 452-457. doi:10.1097/yco.0000000000000358

Mayhew, A. J., Pigeyre, M., Couturier, J., & Meyre, D. (2017). An Evolutionary Genetic Perspective of Eating Disorders. Neuroendocrinology, 106(3), 292-306. doi:10.1159/000484525

Metabolic factors likely contribute to anorexia. (n.d.). Retrieved August 05, 2020, from https://www.medicalnewstoday.com/articles/325805