Importance of Serotonin and Dopamine in Development of Anorexia Nervosa and Related Disorders - Essay Example

? Serotonin and Dopamine are Important Neurotransmitters in the Development of Anorexia Nervosa and Related Disorders. Noemi Meza National Abstract Anorexia nervosa is an illness associated with reduced body mass, starvation, anxiety and many other varying symptoms. It is an important disorder because there is no cure, and the biopsychology of the disease is not well understood. However, there is evidence that the dopaminergic and serotonin systems in the brain play a role in anorexia nervosa (AN) and the behaviors generally associated with suffering. Overall, the research supports an increase in levels of serotonin whilst a repression of dopamine, as well as abnormal sensitivities of the relevant receptors for these neurotransmitters. The purpose of this paper is to evaluate, using current literature, the role of these neurotransmitters in the development of AN, as well as looking at some of the current debates in biochemical research with relation to the disease. It will become evident that serotonin and dopamine are important biological contributors to the development and sustainment of AN. Serotonin and Dopamine are Important Neurotransmitters in the Development of Anorexia Nervosa and Related Disorders. Anorexia nervosa is one of the most important mental illnesses in psychology. It is the most common eating disorder, affecting up to 1% of women and 0.1% of men in some areas (Abraham, 2008). It is theorized to develop from a number of factors, including genetic and environmental (Abraham). However, one of the most important biochemical aspects of anorexia nervosa (AN) is that many sufferers share a common feature: serotonin and dopamine dysregulation (Abraham). This effect is so strong that serotonin and dopamine levels often continue to be abnormal after the individual with anorexia nervosa is seemingly recovered from their illness (Abraham). These important neurotransmitters play a role in reward and compulsion (predominantly dopamine) and anxiety and impulse control (predominantly serotonin), traits which are often linked to anorexia nervosa and a variety of other mental illnesses (Abraham). Serotonin and dopamine are, therefore, important neurotransmitters in the development of anorexia nervosa and related disorders. Serotonin is one of the most important neurotransmitters in the brain. Serotonin is a monoamine derived from tryptophan (Kalat, 2013), and has an important role in many aspects of mood and behavior (Abraham, 2008). One of the most important roles for serotonin is controlling appetite, where it has a role in regulation of blood sugar (Abraham). Additionally, it plays a role in letting the individual feel satiety (Kaye & Weltzin, 1991). Kaye & Weltzin showed, in their analysis of serotonin activity in eating disorders, that serotonin activity is much increase in patients with anorexia nervosa, and also plays a role in impulse control and obsessivity, two important aspects found in anorexia nervosa patients. Indeed, the fact that serotonin is derived from tryptophan is important because serotonin abnormalities (as well as increased or decreased sensitivity of serotonin receptors in the brain) can be caused by dietary abnormalities (Kaye & Weltzin), so this disturbance in patients with anorexia nervosa could be both cause and effect. Even in “healthy” individuals, serotonin levels in the brain are strongly influenced by diet (Kalat). Perhaps the biggest question in anorexia and eating disorder research is whether or not the effects shown on PET scans are a result of disordered eating or are the cause (Higgs, Cooper & Barnes, 2011). More specifically, serotonin dysregulation has been found in patients with AN, including especially high levels in areas of the brain with 5HT1A receptors. The 5HT1A receptor system is important in its implication in mood disorders, as it has been linked to anxiety and impulse control (Kalat, 2013). Additionally, Higgs et al (2011) have shown that stimulation of the 5HT1A receptors artificially works as an anoretic agent in mice, further implicating the role that these receptors play in the development of the disorder and its symptoms. PET studies have also confirmed the role that 5HT plays in AN brains (Abraham, 2008). Interestingly, despite the increase in 5HT1A binding in ill and recovered individuals, these patients often have reduced 5HT2A binding, suggesting specialized roles for these two types of receptor (Kaye, Wierenga, Bailer, Simmons & Bischoff-Grethe, 2013). Additionally, interactions between 5HT1A and 5HT2A receptors in the medial prefrontal cortex have shown to be important factors in the modulation of anxiety, impulse control, and attentional functioning (Winstanley et al, 2003). Another interesting factor is that differences in HTT functioning between individuals could explain why some anoretic individuals develop a restrictive type and some develop anorexia-bulimia nervosa (Bailer et al, 2007). Interestingly, 5HT1B receptors also activate osteocytes, which build up bone (Kalat, 2013), Many individuals suffering from AN also have problems with their bones, such as osteoporosis, due to the lack of nutrition in their diet. This role for serotonin may be an important protective mechanism against starvation, whether caused by AN or an outside cause. Serotonin regulation and activity in the brain does not work in a standalone system, and there are strong interactions between the serotonin and dopamine systems. In patients with AN, PET studies have shown an increased binding of DA D2/D3 receptors when compared to control subjects (Johnson & Kenny, 2010). Interestingly, this increased binding continues to be prevalent in subjects who have shown recovery from AN, supporting the fact that many individuals with the disorder have problems with relapse and may never be fully rehabilitated (Johnson & Kenny). Increased dopamine levels are also associated with increased anxiety (often co-morbid with AN [Abraham, 2011]) and studies have shown that artificially increased dopamine levels (using amphetamines) increase anxiety levels substantially in patients with AN (Bailer et al, 2011). There are suggestions that increased anxiety in patients with AN often leads to further restricted eating, perhaps furthering the problem (Kaye et al, 2013). As previously mentioned, the serotonin and dopamine systems do not work independently in the brain. There are theories that 5HT may actually have an oppositional role with DA systems (Abraham, 2008). 5HT works as a substrate for an aversive motivational system which works in contrast to DA appetitive systems (Abraham). 5HT has been shown to work as an aversive element in many animals that mediates a negative prediction error, which warns against future threats (Berridge, 2007). In contrast, the DA system is more associated with rewards, such as the rewarding feeling of having a satisfying meal (Schultz, 1997). In essence, these two systems may be working in contrast, with the DA system of reward being suppressed by 5HT. Again, it is a big debate in the neurobiology of AN and AN patients whether or not this has stemmed from disordered eating or is the major cause, and which of increased levels of serotonin and decreased levels of dopamine is the major stimulant (Kaye et al, 2013). There is strong evidence that reduced levels of dopamine in the brain are a result of calorie restriction and dieting, regardless of whether the patient has anorexia nervosa or is just a ‘typical’ dieter. This reduction occurs “in the hypothalamus, hippocampus, and the dorsal striatum” (Kontis & Theochari, 2012, p496). Additionally, this reduction in dopamine levels has been so well-documented that many studies have examined the use of dopamine and tyrosine therapies as a cure for AN. These studies have shown that dopaminergic antagonists work (in AN patients) by reducing the amount of “anorexic behaviors” (Kontis & Theochari, p496), but they do not in themselves restore a healthy body weight (Kontis & Theochari). Anorexic behaviors, as detailed by Kontis & Theochari, include obsessivity and impulse control, anxiety and mood differences, reinforcing the role of both serotonin and dopamine in AN. This suggests a route for possible temporary therapy for individuals with AN, but suggests that it is not a long-term solution to the issues. Overall, much of the literature supports a role for serotonin and dopamine in the development of anorexia nervosa and many of the behaviors associated with the disorder. The general theory suggests that serotonin levels are increased, whilst dopamine levels are decreased. This balance is perhaps a result of interactions between the neurotransmitters themselves, although they are important in their own right. Serotonin specifically shows an interaction between 5HT and receptors 5HT1A and 5HT2A, which may explain the reason why some AN patients are more restrictive and some develop binge-purge behaviors. Dopamine, in contrast, may contribute to symptoms of anorexia because it is part of a reward mechanism which is absent in patients with AN. Perhaps the biggest debate in AN research is whether these differences in neurotransmitter levels and receptor function are a result of reduced intake (and dietary levels of tryptophan) or contribute to the desire for reduced intake. Further research is needed to fully understand this debate, particularly into the interaction between serotonin and dopamine in the eating disordered brain. However, considering all the evidence outlined above, there is clearly a strong role for dopamine and serotonin in anorexia nervosa, particularly as PET imaging studies have confirmed the dysregulation of these two neurotransmitters in patients with eating disorders. Similarly, studies have also shown how these neurotransmitters may produce traits such as those found in anoretic patients, such as anxiety, impulse control and obsessivity. Taking this into account, it is evident that dopamine and serotonin are very important in the eating disordered mind. References Abraham, S. (2008). Eating Disorders. 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