One such breakthrough is a study found in the American Journal of Human Genetics. The researchers who performed this study found strong biological evidence of a genetic linkage on chromosome 1 for Anorexia Nervosa. These findings support that Anorexia is caused, at least in part, by genetics. University of Pittsburgh psychiatrist Walter Kaye, M.D., believes that scientists are going down the same path that they did twenty years ago when researching schizophrenia-a psychiatric disorder with genetic susceptibilities (Monitor on Psychology).
Thirty-seven families with two or more anorexic relatives were tested, and researchers found a strong susceptibility gene or genes on chromosome 1. Kaye makes sure to note that they have not found a specific gene that causes Anorexia Nervosa, but more of a group of genes that predispose someone to it. The goal of researchers is to narrow down the search and hopefully one day conduct gene replacement therapy (Monitor on Psychology).
Lena and colleagues proposed that certain etiological factors exist before, during, and after the onset of an eating disorder like Anorexia Nervosa. These researchers also propose that there are neuropsychological deficits that preexist in all women who will eventually fall victim to Anorexia. Conclusions such as these were drawn after completing a series of neurocognitive tests on both individuals with eating disorders, and a normal control group.
"Using standardized neuropsychological test, deficits in executive functioning, visual-spatial ability, divided and sustained attention, verbal functioning, learning, and memory have been observed in eating disordered individuals" (Lena, et al. 2004).
Although those results are concrete, many of the authors of the study do not correlate eating disorders and these cognitive deficits. They say that the deficits are merely a result of poor nutrition and probable starvation. This can be countered, however, by the fact that these cognitive deficits are found in bulimics as well, ruling out starvation and possibly poor nutrition (Lena, et al. 2004). Therefore, it can be surmised that these deficits were there before the eating disorder began.
In addition to deficits in behavior and in the cognitive functioning of the brain, there are also abnormalities in the brain chemistry of patients with Anorexia Nervosa. There are frequent changes in the levels of serotonin in the brain, a neurotransmitter in the Central Nervous System (CNS) responsible for appetite and mood, among other vital functions. The changes in levels of this neurotransmitter may contribute to depression, impulsiveness, Obsessive Compulsive Disorder, or other mood disorders in patients with Anorexia Nervosa. In addition, if an anorexic purges, he or she may be depleting tryptophan, which is an amino acid necessary in the production of serotonin, thus causing further imbalances (University of Maryland Medical Center, 2007).
Thankfully, much work is being done to hopefully someday understand eating disorders like Anorexia. In one study, twenty-six female participants with eating disorders (ten with Bulimia Nervosa, and sixteen with Anorexia Nervosa) were matched comparatively by age and education with nineteen healthy female participants. Each of the women was presented with pictures of food, and with pictures of particularly aversive emotional images. The activity of each woman's brain was scanned with an fMRI (Uher, Murphy, Brammer, & Dalgleish, 2004). fMRI, or functional magnetic resonance imaging, refers to the use of an MRI to measure the changes in blood flow or blood oxygenation related to neural activity in the brain (Radiology Info, 2007). It is used in many experiments to see how and where blood in the brain is flowing.
The results of the study showed that women with eating disorders constantly identified the images of food as threatening and disgusting. There was greater activation in the left medial orbitofrontal and anterior cingulated cortices of the eating disordered women (Uher, et al. 2004). The orbitofrontal cortex is primarily involved in decision making, especially in regard to reward and punishment (Journal of Cognitive Neuroscience, 2007). The anterior cingulate cortex functions in error detection, task anticipation, and motivation (Oxford Journals, 2007). There was less activation, however, in the lateral prefrontal cortex, inferior parietal lobule, and cerebellum of the eating disordered women (Uher, et al. 2004). The lateral prefrontal cortex is chiefly involved in memory and organization (Barde & Thompson-Schill, 2002). The inferior parietal lobule is involved in the function of attention, perception, and visuospatial processing (Frederikse, Lu, Aylward, Barta, Sharma, & Pearlson, 2000). Lastly, the cerebellum is involved in coordinating fine and gross motor movements.
Walter Kaye, M.D. of University of Pittsburgh, led another study in 2005 along with Guido Frank, M.D. of University of California, San Diego using Positron Emission Tomography (PET) imaging to examine the activity of dopamine receptors in the brain. Dopamine receptors are a neurotransmitter system that are known for controlling movement, and also weight and feeding behaviors, and responses to rewards and reinforcement-involved heavily in learning behaviors (University of Pittsburgh Medical Center).
The research was conducted with ten women who had recovered from Anorexia Nervosa at least a year prior, and twelve normal control women. The doctors found increased dopamine receptor binding in the basal ganglia's antero-ventral striatum in the previously anorexic women. This part of the brain is responsible for reinforcement and rewards as well, and is important in learning from experience. Another interesting finding was increased dopamine D2/D3 receptor activity in the basal ganglia's dorsal caudate, related to responses and avoidance of harm. This can possibly account for the worried attitude of many anorexic patients (University of Pittsburgh Medical Center).
Another change in the brains of patients with Anorexia Nervosa is ventricular enlargement, as is the case with many psychiatric disorders. The dilation was found using Computerized Tomography (CT) scans and Magnetic Resonance Imaging (MRI) primarily in the third and lateral ventricles than in control patients. It is surmised by researchers that this is because of the patients' protein malnutrition. The third ventricle is located in close proximity to the hypothalamus, was more enlarged than the lateral ventricles. This is consistent with the findings of hypothalamic dysfunction in patients with Anorexia Nervosa (Golden, Ashtari, Kohn, Patel, Jacobson, Fletcher, & Shenker, 1996).
References
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the Process Model. Journal of Cognitive Neuroscience, 14(7), 1054-1063.
Frederikse, M., Lu, A., Aylward, E., Barta, P., Sharma, T., & Pearlson, G. (2000). Sex
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Golden N.H., Ashtari M., Kohn M.R., Patel M., Jacobson M.S., Fletcher A., & Shenker I.R.
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Lena, S.M., Fiocco, A.J., & Leyenaar, J.K. (2004). The Role of Cognitive Deficits in the
Development of Eating Disorders. Neuropsychology Review, 14(2), 99-111.
Monitor on Psychology (2007). A Genetic Link to Anorexia. Retrieved November 9, 2007 from
http://www.apa.org/monitor/mar02/genetic.html.
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