It seems that many people if asked for their opinion on eating disorders say that they are caused by all the media, the culture, the skinny models, the glossy magazines with dieting tips and pictures of impossible to achieve body types. Perhaps, the biological side to them is a bit neglected. Especially as we have to remember that as with everything in psychology, it’s both nature AND nurture, never just the one (I will be writing about probabilistic epigenesis soon).
A little bit of introduction:
Eating disorders refer to a wide range of problems characterised by abnormal eating behaviours and beliefs about eating, body weight and shape (Grilo, 2006). Eating Disorders include anorexia nervosa (AN), bulimia nervosa (BN), and eating disorders not otherwise specified (EDNOS).
The etiology of eating disorders is largely unknown. Grilo (2006) reports that it is likely that eating disorders have complex multi-factorial causes. Current research continues to investigate the role of biological factors as culprits in the development of eating disorders. Genetics research and investigations into hormonal and neurotransmittal links are the most frequently explored areas of biological explanations for eating disorders, research into hereditary personality types is also being conducted (Mitchell, 2004).
Research indicates that, as with many psychiatric disorders, there is evidence that there are genetic and familial components to eating disorders. Genetic contribution is considered significant in the development of both AN and BN, as genetic susceptibility to eating disorders may cause a person to feel the influence of risk factors in the environment more strongly (Bulik, 2005).
Family studies and twin studies have demonstrated the familial aggregation of eating disorders (Bulik, 2005). Grilo (2006) reports available twin studies to show higher concordance rates for monozygotic (MZ) twins than for dizygotic (DZ) twins. Twins showed tendency to share specific eating disorders. Bulik (2005) reports consistent findings across samples and across countries, despite different assessment and diagnostic strategies, supporting the observation that there is indeed some critical genetic component influencing risk for these disorders.
However, twins who are brought up together also share substantial degree of environmental similarity, called shared or common environment. Additionally, shared environment is believed to be greater for MZ twins (Hamilton, 2007). It is argued, however, that being presumed to be similar and being treated similarly (i.e. being dressed alike) has no causative relevance to the disorder. Additionally, even MZ twins do not share all of their environment. There are no adoption studies of eating disorders, those would provide crucial information and important information about the genetic factors (Grilo, 2006).
Grice as reported by Collier and Treasure (2004) reported suggestive evidence for the presence of an AN-susceptibility locus on chromosome 1p in molecular genetic analysis. Furthermore, Collier and Treasure (2004) reported a study by Bulik which identified bulimia nervosa, in particular the form with self-induced vomiting, to be linked to chromosome 10. Those findings provide strong support for the notion of genetic linkage to the development of eating disorders.
Additionally, Gratacos et al. (2004) found evidence that polymorphism in the brain-derived neurotrophic factor (BDNF) gene increases susceptibility to all eating disorders. BDNF is involved in regulating feeding behaviour in the hypothalamus, including the regulation of serotonin.
Inherited vulnerabilty personality traits.
Further in the favour of genetic explanation, research indicates that there are certain heritable psychological traits, known as vulnerability traits that predispose certain individuals to development of eating disorders. Those include personality traits such as perfectionism, obsession or anxiety. Hewitt et al. (1995) reported that self-oriented perfectionism was related to anorexic symptoms. While social facets of perfectionism, especially socially prescribed perfectionism and the perfectionistic self-presentation dimensions, were related to eating disorder symptoms as well as body image avoidance and self-esteem among female college students.
Study by Anderluh et al. (2003) revealed that childhood perfectionism appears to be a particularly strong antecedent risk factor. The study concluded childhood obsessive-compulsive personality to be important risk factor for the development of eating disorders, as it showed a high predictive value. Some enduring personality traits, such as depression, persistence, harm avoidance, and self-transcendence appear linked to specific types of eating behaviours (Karwautz et al, 2002)
Moreover, it has been documented that some personality types, or sometimes personality disorders, are much more susceptible to eating disorders than other types. Obsessive-compulsive personality disorder is common in restricting anorexics but not in bulimic anorexics, while normal-weight bulimia was associated with histrionic personality disorder (Goodman et al. 2006). Additionally, novelty-seeking personality is linked specifically to those who show dis-inhibited eating behaviour, as is exploratory excitability, impulsiveness and extravagance (Audenaert et al, 2004). Hereditary, or the genetic transmission of characteristics from parents to offspring, determines personality to a certain extent; it can be said that they are biological factors contributing to, if not certainly causing, eating disorders. It could be argued, however, that there is more to one’s personality than genetics. As much as this is a valid notion, the genetic influence cannot be ignored. Ultimately, the old argument of nature vs. nurture has never really been resolved.
Physiological disturbances of patients suffering from anorexia nervosa and bulimia nervosa led to speculation that the abnormal behaviour is caused by biological abnormalities (Walsh, 1998). Pharmacological studies have more precisely characterised the nature of the inhibitory effect of brain serotonin (5-hydroxytryptamine) on feeding behaviour (Leibowitz, 1990). Serotonin has effects on appetite, sleep and general metabolism, it is believed to activate satiety neurons localised in the medial hypothalamus (Leibowitz, 1990). Therefore, it has been postulated that disruptions of the gastrointestinal tract, the pituitary, the hypothalamus, and various neurotransmitters could be causal factors in the development of eating disorders. Increase in brain serotonin function leads to reductions in food intake, while decrease in brain serotonin function is associated with depression. Low serotonin levels are also associated with impulsive behaviour. The lower the serotonin levels of the bulimic individuals, the more likely they were to binge and purge. Furthermore, individuals recovering from eating disorders showed higher than normal levels of serotonin. High serotonin levels are associated with anxiety, perfectionism, ritualistic behaviour and obsessive thinking, all of those behaviours are characteristic of individuals suffering from eating disorders. Therefore, researchers believe serotonin could play important role in the development of eating disorders, additionally selective serotonin re-uptake inhibitors (SSRIs) have been proven helpful in treatment of bulimia nervosa.
Research has also been undertaken to determine if hormones could be a cause of eating disorders. Some studies have shown that disturbances to the hypothalamus and anterior pituitary gland can be linked to eating disorders. Brambilla et al. (1981) demonstrated derangement of anterior pituitary to hypothalamic neurohormones in patients with anorexia nervosa presuming it to reflect a primary alteration in brain neurotransmitter function.
Studies suggest that hormone leptin, secreted by fat cells also plays important role in the development of eating disorders. Leptin plays a key role in regulating appetite and metabolism. It is secreted by fat cells and consistent with reduced mass of fat tissue, individuals suffering from AN show low levels of leptin (Walsh, 1998). Additionally, studies show that fasting and low calorie diet lowers leptin levels (Weigle, 1997).
Zinc, an essential nutrient has been found to contribute to eating disorders. Responsible for many crucial physiological functions, including immune and antioxidant function, growth and reproduction, zinc also regulates appetite. Many aspects of zinc deficiency-induced anorexia have been studied in experimental animals, such as rats. There is evidence that suggests zinc deficiency may be intimately involved with anorexia in humans: if not as an initiating cause, then as an accelerating or aggravating factor that may deepen the pathology of the anorexia (Mangian, 2000). Investigation of the link between zinc and anorexia nervosa continues. Birmingham and Gritzner (2006) reported that low zinc levels create dynamics in the brain that are similar to those seen with anorexia nervosa. Additionally zinc administration has been proven to significant improve body mass index of anorexia nervosa patients compared to a group of anorexic persons not receiving zinc (Birmingham and Gritzner, 2006). Deficiency of other nutrients such as tyrosine, tryptophan, and vitamin B1 could contribute to development of eating disorders induced by already existing malnutrition (Mangian, 2000). Nonetheless, more research needs to be conducted to establish the causal link for sure.
For decades culture, society, and family were blamed and held responsible for eating disorders (Bulik, 205). Bulik (2005) reported that genes and environment can interact in several ways, i.e. genes may influence how sensitive one is to the effects of environment such as culture. This type of explanation is supported by probablisitc epigenesis.
Although there is no doubt that these do influence the development of eating disorders, they do not on their own cause them (Bulik, 2005). Eating disorders are very complex conditions that arise from a combination of long-standing behavioural, biological, emotional, psychological, interpersonal, and social factors. Scientists and researchers are still learning about the underlying causes of these emotionally and physically damaging conditions. Currently it is argued that no one component is to be blamed for the development of eating disorders. Neurobiologic research has provided deeper understanding of eating disorders, beyond the socio-cultural exposure explanation. It is believed that ultimately, this research will allow to create a model that will explain how genes and environment interact to influence this vulnerability (Bulik, 2005).
It seems that inherited vulnerabilities, hormonal imbalances, cultural and societal pressure, individual and family experiences all appear to play part in onset and in perpetuating the disorder. The aetiology seems to be a typical example of nature – nurture debate. A comprehensive understanding of the causes of eating disorders must take into account genetic, cultural and environmental factors and their interplay. Further understanding of this complex interplay will allow to further understand risk factors, as well as perpetuating factors, and therefore treatment.
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