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Are Eating Disorders Hereditary?

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Eating disorders represent a psychogenically conditioned behavioral syndrome connected with ingestion issues. There are several kinds of eating disorders, such as atypical bulimia nervosa, bulimia nervosa, atypical anorexia nervosa, anorexia nervosa, vomiting, overeating, etc. The major signs of eating disorders include considerable efforts to control weight, excessive fear of weight gain, and denial of the significance of the problem of food intake and inadequate body mass index. Recently, the views on the genesis of eating disorders have changed greatly. Previously, medical experts believed that only the social environment could trigger eating disorders. However, matching data from family and twin researches have demonstrated that these disorders have a genetic component. Although social and cultural explanation of the origin of the disease is significant, eating disorders are predominantly considered as heterogeneous disorders with a complicated multivariate etiology lying in the correlation between the environment and heredity.

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Phenotype: Disabilities of Food Behavior

The diagnosis of eating disorders represents a highly complicated problem. It is associated with the fact that the clinical picture is frequently unstable (Carvalho et al., 2013). Moreover, the symptoms can change; for example, anorexia can be replaced by bulimia. An individual may experience concomitant pathological conditions, such as depression and anxiety disorders. These diseases can have different and common risk factors, including regular diet compliance (Carvalho et al., 2013). Such a combination of dissimilar and overlapping characteristics makes it a complicated task to conduct research on prevalent risk factors, such as genetic and environmental causes.

Stable Phenotypes

Because of the temporal instability of clinical symptoms that complicates the research of such fixed markers as genes, there is a shift to the investigation of more stable properties, including neurobiological characteristics and peculiarities of the personality. These properties usually manifest themselves in childhood (Rosen, 2013). They precede the beginning of the eating disorder, which connects their origination with the development. Infant perfectionism is regarded as an especially influential risk factor in the potential development of the disease. Apparently, certain intrinsic personality traits are connected with specific kinds of eating behavior, as others are more general. People with disinhibition (bulimia) and dietary restrictions (anorexia) have a mutual personality trait, namely a high level of eschewal of harm (Rosen, 2013). Nonetheless, a personality type that strives for newness is typical for people with disinhibited eating behavior, extravagance, and impulsiveness. Rosen claims that Years of psychological and behavioral research have helped scientists better understand some signs and triggers of anorexia (2013). During episodes of overeating, impulsivity is especially perceptible in a bad emotional condition, whereas, dietary restrictions are connected with compulsiveness (Rosen, 2013). Notably, the comprehension of obsession as a part of the behavioral phenotype of anorexia nervosa can be instrumental in performing the analysis of the genetic connection to the nature of the disease. These personality features may be associated with the primary neurobiological parameters.

Compulsivity frequently relates to cognitive and perceptual rigidity. Patients suffering from anorexia nervosa do not demonstrate sufficient flexibility in a poor state of health and even after recovery (Rosen, 2013). Such behavioral pattern is not typical for people with bulimia nervosa that is connected with obsessive-compulsive manifestations in childhood. Therefore, rigidity can be an endophenotype that stems from dietary restrictions. In patients who show signs of recovery, a level of specific serotonin 5-HT2A receptors deviates from the norm (Rosen, 2013). Furthermore, this number tends to fluctuate depending on the diagnostic groups. The nature of eating disorder is responsible for the variations in the serotonin dysfunction in the central nervous system (Rosen, 2013). The fact that these modifications persist after recovery of the patient suggests that the serotonin function can be an important marker of eating disorders.


At the end of the XX century, twin researches of anorexia nervosa changed completely a traditional view on the nature of eating disorders. Previously, medical experts linked them to social and cultural factors. However, the majority of researchers now recognize the fact that eating disorders have a genetic component (Carvalho et al., 2013) . However, it is currently impossible to make a final conclusion regarding the degree of contribution of environmental and hereditary factors to the development of eating disorders (Carvalho et al., 2013) . Nevertheless, many experts presume that they account for the emergence of the eating disorder equally.

Many manifestations connected with eating disorders have a hereditary component. These are mainly self-induced vomiting, overeating, dietary requirements, and a desire for leanness (Carvalho et al., 2013) . Many of these signs are quantitative. Thus, they can be determined in any average person. Acknowledgment of the fact that eating disorders also have a genetic basis has led to the initiation of molecular researches (Carvalho et al., 2013). Their purpose was to identify the factors in the hereditary predisposition. Moreover, they focused on the detailed examination of the etiology of eating disorders. In such a way, the discovery of receptivity genes could be a significant step forward in solving this task.

The molecular genetic analysis deals with the study of candidate genes, as well as with the establishment of the linkage of genes within the genome in families with numerous cases of the disease to define gene loci in the chromosome. Eventually, the analysis of the gene linkage within the genome has not detected loci for a broad diagnostic category of bulimia and anorexia nervosa (Carvalho et al., 2013). However, the analysis of the pedigrees of one pair of relatives with a restrictive kind of anorexia nervosa has defined the adhesion to the chromosome lp34 (Carvalho et al., 2013). Thus, the findings are consistent with the view that the latter can be an individual phenotype.

With the purpose of overcoming the currently available diagnostic limitations, it is advisable to apply the methods of quantitative genetics. Obsession and an aspiration for leanness are most closely connected with anorexia nervosa becoming a reason for new genetic loci on chromosomes 1 for the mixed indicator and 13 for the desire to have a skinny body (Carvalho et al., 2013). Nervous bulimia, particularly accompanied by self-induced vomiting, is connected with chromosome 10 confirming an opinion that this form is an individual phenotype (Carvalho et al., 2013). It is also pivotal to state that this place is a known locus of the gene for obesity. Furthermore, it is consistent with the increased frequency of obesity in the family history of bulimia nervosa.

Researches on bonds focus on the study of genes connected with the specific neurochemical factors of food behavior. The HTR2A gene of the serotonin 5-HT2A receptor is one of them (Carvalho et al., 2013). In fact, the associative analysis of candidate genes established an allele of the assumed risk in this gene; this result was common for many researches. Evidently, it is possible to explain the dissimilarities between the findings of researches with the help of heterogeneity of clinical groups (Carvalho et al., 2013). It is associated with the fact that there is a hypothesis that HTR2A is related to restrictive but not to disinhibited food behavior.

The gene of the brain neurotrophic factor is also involved as a gene of receptivity in anorexia nervosa. This protein participates in the regulation of food behavior at the hypothalamus level, including the control of serotonin levels, the decline of which becomes a reason for depression (Carvalho et al., 2013). In one of the studies conducted in Europe, the scientists discovered that the polymorphism of this gene increases susceptibility to all eating disorders (Carvalho et al., 2013). Such activity is associated with its involvement in affective symptomatology.

Another approach lies in the study of various models of eating disorders in animals. Nutritional behavior in mammals is similar to that in people. Moreover, many of them, such as pigs and mice, show behavior patterns reminding eating disorders in people. For instance, the rats and mice that had free access to the food ate only several times per day, which resulted in a decrease of their body weight and the development of behavioral hyperactivity (Gura, 2008). These are typical manifestations of anorexia nervosa. This fact demonstrates the existence of fundamental types of behavior patterns in mammals, which could explicate certain phenotypes of eating disorders in people (Gura, 2008). The genetic analysis would help research them in rodents with the purpose of applying new forms of therapy and treatment.

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These days, many individuals are obsessed with the perfect body parameters. In attempt to realize an elusive body image, people tend to fail, which frequently leads to anxiety, depression, and even eating disorders. The letter presupposes an imbalanced diet that negatively affects patients' state of health. Although people have ample amount of various products, they tend to consume less than they should to satisfy the needs of their body. There are several factors determining the development of eating disorders. In the past, medical experts believed that only social and cultural factors can cause these disorders. However, these days, more studies indicate that eating disorders are complex health issues originating under the influence of both social and genetic factors. Overall, a combination of heredity and environment can trigger eating disorders.

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