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Eating disorders hardly qualify as a new phenomenon, as documented cases date back to the Middle Ages; however, these disorders have become a prevalent and unique healthcare problem in the United States. Eating disorders prove difficult to conquer due to the social stigma surrounding the affected individuals, preventing open discussion, acknowledgement, and treatment of the conditions. Both women and men undergo extreme measures to hide their eating disorders in fear of societal condemnation, even from peers and family. This stigma originates from the socially learned tendency to misconceive the affected persons’ conditions and attribute blame and character generalizations to these individuals. They are often viewed as high-strung, overachieving people with low self-esteem who have taken extreme measures in order to conform to society’s ideal body type (UNC-Chapel Hill, 2008). When making judgments about affected individuals, society rarely acknowledges the genetic aspects of eating disorders. Research indicates a genetic predisposition that makes individuals more susceptible to an eating disorder, and when triggered by certain environmental cues, a predisposition will develop into a full-blown disease. The goal of researching the genetic and biological basis of the etiology of eating disorders is to decrease the negative stigma attached to individuals with these conditions. By integrating biological research, a complete biopsychosocial model for anorexia and bulimia can be created to dispel the myth that eating disorders are solely brought about by sociocultural influences.
The term “eating disorder” encompasses a wide range of illnesses including restrictive dieting, binge eating, chronic overeating, and even peculiar food fetishes. The two most common eating disorders are anorexia nervosa and bulimia nervosa. Anorexia nervosa is characterized by caloric restriction that generally leads to severe malnutrition and physical wasting, a condition called cachexia. Bulimia nervosa describes the condition of binge eating accompanied by purging, usually by self-induced vomiting or the abuse of laxatives. In both disorders, the affected individual possesses a distorted body image, unhealthy eating habits, and medical complications as a direct result of the exhibited behavior. Sometimes the diseases can be comorbid, and an individual can go through bouts of deprivation, binging, and purging with long periods of healthy eating habits in between. These disorders also vary in severity, ranging from a short period of obsessive dieting to a lifelong, daily struggle with eating habits.
In addition to comorbidity among eating disorders, research initiatives have shown a correlation between eating disorders and other mental disorders, leading scientists to investigate the biological basis for this connection. Bulimia nervosa has been linked to drug-use disorder, and anorexia has been linked with much evidence to obsessive-compulsive disorder (OCD). Correlation between these eating disorders and other mental illnesses reveals a genetic component acting as a link between the two. One study addressing the genetic and environmental influences of bulimia analyzed a group of mono- and dizygotic twins, as well as average participants who suffered from bulimia, drug-use disorder, or both. Three factors were identified as common characteristics of both disorders: depression, neuroticism, and childhood sexual abuse. Genes for depression, neuroticism, bulimia, and drug-use disorder were subsequently investigated, and results showed that shared genetics play a large role in the inheritance of these diseases. The most common shared genetic influence was a gene coding for a predisposition to neuroticism. The authors of this paper support what they call the “personality hypothesis,” suggesting that people are born with neurotic tendencies that can then lead to the development of various disorders (Baker et al., 2007).
Anorexia and obsessive-compulsive disorder (OCD) also share an important correlation, and recent research suggests that anorexia may develop as a reaction to OCD because individuals are fearful of contaminated food. A common symptom of OCD is the need for complete cleanliness and control, which is a common personality characteristic of individuals with anorexia (Jarry et al., 1996). The article, “Eating Disorder and Obsessive-Compulsive Disorder: Neurochemical and Phenomenological Commonalities,” confirms by surveying personality traits of affected individuals that people with OCD and anorexia share common characteristics relating to fear and avoidance, (Jarry et al., 1996). The overall trend shown by the research demonstrates that genetics give individuals a predisposition to eating disorders. A predisposition is an inherited peculiarity in a person’s genome that increases his or her likelihood of developing certain characteristics or disorders, and no individual can control the acquisition of a genetic predisposition, as it is inherited and present at birth. If one has a predisposition to anorexia, he or she has a heightened susceptibility to the disorder due to the biological construction of his or her genome and not because of environmental influences. This does not mean that developing the disorder is inevitable, but it states that some individuals are more susceptible when coupled with environmental factors (Ogilvie, 2008).
Because of the established connections between anorexia, bulimia, and other mental illnesses and diseases, scientists have turned to neurochemical explanations. Serotonin, estrogen, monoamine oxidase A, and brain-derived neurotrophic factor are all chemicals undergoing extensive research, with serotonin yielding the most evidence. These investigations identify neurochemicals that contribute to abnormal brain functions, which would provide a genetic causation of eating disorders since neurochemical regulation is ultimately controlled by genetic factors, such as regulating proteins. Brain-derived neurotrophic factor (BDNF) is a protein acting in the brain that influences food intake. Levels of BDNF correspond with weight gain, weight loss, and appetite, prompting researchers to investigate its correlation with eating disorders. Variants of the BDNF gene, specifically the Met66 variant, have been associated with restricting-type anorexia nervosa shown through familial studies (Klump et al., 2007). Another hormone widely studied in regard to eating disorders is estrogen.
Abnormal serotonin levels have been identified in both anorexia and bulimia and carry a strong association with anxiety. The paper, “Eating Disorder and Obsessive-Compulsive Disorder: Neurochemical and Phenomenological Commonalities,” explains an in-depth study of serotonin and its function in regard to anorexia, bulimia, and OCD, presenting an analogy of a continuum to relate the three disorders. One end of the continuum is characterized by avoidance, as people with anorexia tend to avoid food just as people with OCD might avoid germs. These types of people have been found to have abnormally high levels of serotonin in their brain. On the other end of the continuum are the uninhibited-a bulimic who binge eats or an OCD-sufferer with violent tendencies, both of whom are characterized by lowered serotonin levels (Jarry et al., 1996). This continuum helps clarify the correlation between anorexia, bulimia, OCD, and serotonin. High levels of serotonin correspond with anorexia, and low levels correspond with bulimia, with OCD on both ends of the continuum.
Since it is clear that eating disorders and OCD share associations with serotonergic irregularities, serotonin has been established as an important neurotransmitter associated with eating disorders, and much research today surrounds the mechanisms by which it is inherited and functions abnormally. The heritability of serotonin and its power in predisposing individuals to anorexia was studied by investigating how it is regulated. Monoamine oxidase A (MAOA) is the protein responsible for clearing serotonin from synapses, or neuronal connections, in the brain. High or low levels of serotonin can be credited to the action of this enzyme. If the enzyme does not function properly due to a genetic mutation, individuals will be at increased risk or predisposed to developing anorexia. Mutated MAOA proteins leave either too high or too low of levels of serotonin in the brain, which increases or decreases serotonin’s effect. People with inherited abnormalities in the gene coding for MAOA are more likely to develop anorexia because they are more likely to have increased serotonin levels in the brain, leading to behavioral tendencies such as perfectionism and anxiety which are both common to anorexia (Urwin et al., 2005).
Familial and twin studies have commonly been published supporting the argument for the heritability of anorexia and bulimia because differing regions on specific chromosomes have been associated with higher frequencies of eating disorders. In familial studies, scientists map genomes and analyze regions that are linked to heritability, and significant findings have been made with respect to chromosomes 1 and 10p, furthering the “personality hypothesis” that certain individuals can be born more susceptible to eating disorders (Baker et al., 2007). One genomic study, “Significant Linkage on Chromosome 10p in Families with Bulimia Nervosa” aimed to find regions within the human genome correlating with bulimia. Specific loci on chromosomes were identified as exclusive to bulimia by studying twins (both mono- and dizygotic), siblings, parents, and children who had some history of bulimia. The main regions identified were between markers D10S1430 and D10S1423 on chromosome 10 and a smaller region on chromosome 14. A higher frequency of purging corresponded with a higher genomic linkage, meaning that within this region affected individuals had more similar DNA than unaffected individuals. This supports the notion that self-induced vomiting is highly heritable. Chromosome 10 showed a “double peak” region, where genomic linkage was very high, and researchers suggest that these peaks may code for personality characteristics common in bulimia, such as impulsivity. Finally, certain loci on chromosome 10p have also been linked to alcoholism, which may explain bulimia’s connection with drug-use disorder (Bulik et al., 2003). In all, this study supports the genetic basis for the heritability of bulimia, and leads to the next steps in researching certain serotonergic regulators (Bulik et al., 2003).
Anorexia has also been established as a disease influenced heavily by genetics. When a linkage analysis was performed, similar to the analysis performed for bulimia, significant evidence pointed to regions on chromosome 1 that may be responsible for inherent anorexia precursors, such as perfectionism and neuroticism. In a mono- and dizygotic twin study researchers were able to distribute causation between environment and genetics, since only monozygotic twins have identical DNA. None of the dizygotic twins were concordant for anorexia; however, 29-50% of monozygotic twins were concordant, with the range accounting for the severity of anorexia. 74% of the difference between developing an eating disorder and maintaining healthy eating habits was attributed to genetics, suggesting certain people are born with a predisposition and that genetics play a larger role than most other factors in the development of anorexia (Klump et al., 2001).
Often well-informed citizens believe that eating disorders are caused by influences such as images from the media and familial or peer pressure to be thin. While these factors do play a very strong role in the development of an eating disorder, individuals cannot be wholly blamed for falling prey to these influences since the origination of the disorder lies in their genome. In a study performed at the University of North Carolina- Chapel Hill, nursing students were found to project blame onto patients with anorexia, completely disregarding professional objectivity. A class of nursing students was divided into two groups: one group was given information about social and cultural aspects of the disorders, and the other studied information regarding the biological basis of anorexia. All of the participants were given the same questionnaire regarding causation of anorexia, and results showed that nursing students given genetic and biological information placed less blame on the affected individual for their condition than those solely given sociocultural aspects (UNC-Chapel Hill, 2008). It is especially alarming that nursing students and not just uninformed citizens are neither fully informed nor objective with regard to eating disorders, which can be potentially damaging to patients. If even medical practitioners fail to refrain from judgment and perpetuating the social stigma, little chance exists that the general public will remove their own condemnation of the affected individuals.
Individuals with eating disorders will often attempt extreme measures to conceal their condition from parents, doctors, etc because they are afraid of societal and personal condemnation. Individuals struggling with anorexia and bulimia often lie to their friends and family about skipped meals, avoid social events surrounding food, and deceive their doctors by saying they have been sick and without appetite. All of these fabrications are constructed to avoid judgment and awkward and difficult conversations about their conditions. The world’s largest pro-anorexia website community claims to be a safe place where people affected by anorexia can discuss their eating disorder without judgment, “without being exposed to the constant “just eat more”, “fasting is dangerous” and “purging is dangerous” that causes them to withdraw from society in the real world.” If the general public would accept the genetic basis of eating disorders and remove the surrounding stigma, then affected individuals will feel more comfortable seeking help within the medical community and among close friends and family rather than anonymous and potentially detrimental websites.
Today’s research is creating a better-rounded approach toward the understanding of eating disorders. Associations with other diseases and certain neurochemicals lead scientists to study causation of related mental disorders and regulation of neurochemicals. Also, certain regions within the human genome have been pinpointed as “hotspots” where variability in genes leads to variability in eating patterns. Research shows that individuals do inherit genes that make them more likely to be affected by an eating disorder, and that these genetic differences lead to chemical imbalances in the brain. It is important to remember that genetics and biology do not guarantee an eating disorder. An environmental trigger must be present to yield a full-blown eating disorder; however, genetics provide the predisposition to be affected by the environment.
Environment has persisted as the winner in the nature versus nurture debate in the recent past, especially with regard to eating disorders, primarily because scientific research has only boomed within the last 30 years. However, because of the recent success in finding substantial evidence for the heritability of genetic predispositions for anorexia and bulimia, society’s perception of affected individuals with eating disorders should become more educated and reflect the validated research. Society cannot rightfully stigmatize an individual for factors beyond that person’s control, which expands beyond eating disorders to other mental illnesses, and is part of the reason why the nature via nurture paradigm is currently so ubiquitous in psychology and biology. In addition to the necessity of social acceptance and application of these scientific findings, society must promote different forms of beauty and encourage women to value their self worth, therefore reducing environmental factors that could trigger underlying predispositions. When genetic factors are accepted by society and subsequent preventative measures are taken in combination with a societal embrace of “loving the skin you’re in,” eating disorders will hopefully cease to exist as a major threat in current United States healthcare.
Baker, Jessica H., Suzanne E. Mazzeo, and Kenneth S. Kendler. “Association Between Broadly Defined Bulimia Nervosa and Drug Use Disorders: Common Genetic and Environmental Influences.” International Journal of Eating Disorders 40 (2007): 673-78.
Bulik, Cynthia M., B. Devlin, Silviu-Alin Bacanu, Laura Thornton, Kelly L. Klump, Manfred M. Fichter, Katherine A. Halmi, Allan S. Kaplan, Michael Strober, D. Blake Woodside, Andrew W. Bergen, J. Kelly Ganjei, Scott Crow, James Mitchell, Alessandro Rotondo, Mauro Mauri, Giovanni Cassano, Pamela Keel, Wade H. Berrettini, and Walter H. Kaye. “Significant Linkage on Chromosome 10p in Families with Bulimia Nervosa.” The American Society of Human Genetics 72 (2003): 200-07.
Henry, Molly C., Susan J. Perlmutter, and Susan E. Swedo. “Letters to the Editor.” Journal of American Academy of Child and Adolescent Psychiatry 38 (1999): 228-29.
Jarry, Josee L., and Franco J. Vaccarino. “Eating Disorder and Obsessive-Compulsive Disorder: Neurochemical and Phenomenological Commonalities.” Journal of Psychiatry and Neuroscience 21 (1996): 36-48.
Klump, K. L., K. B. Miller, P. K. Keel, M. McGue, and W. G. Iacono. “Genetic and Environmental Influences on Anorexia Nervosa Syndromes in a Population-Based Twin Sample.” Psychological Medicine 31 (2001): 737-40.
Klump, Kelly L., and Kristen M. Culbert. “Molecular Genetic Studies of Eating Disorders.” Current Directions in Psychological Science 16 (2007): 37-41.
Ogilvie, Megan. “How Biology Trumps Image as Cause of Anorexia.” The Toronto Star 13 Apr. 2008: A01.
“UNC-Chapel Hill; People With Anorexia Less Likely to be Blamed When Biology, Genetics Explained.” NewsRx Science 28 Jan. 2008: 112.
Urwin, Ruth E., and Kenneth P. Nunn. “Epistatic Interaction Between the Monoamine Oxidase A and Serotonin Transporter Genes in Anorexia Nervosa.” European Journal of Human Genetics 13 (2005): 370-75.
World’s Largest Pro Anorexia Site – 24 hr Posting. LiveJournal. <http://community.livejournal.com/proanorexia>.
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