A Critical Evaluation Of The Role Of Serotonin In Bulimia Nervosa

According to the DSM-V, bulimia nervosa is characterised by recurrent episodes of bingeing and purging. Binge eating involves the individual eating a larger amount of food than the average person in a shorter amount of time. Purging refers to the methods used to attempt to get rid of the food they consume. This can be achieved by vomiting or taking laxatives. These binges and inappropriate compensatory behaviours are considered a problem and diagnosed when they are occurring at least once a week for three months. Bulimia seems to be the most common eating disorder in the UK with around 40% of those with eating disorders falling into this category. However, it is hard for psychologists to get an accurate statistic as many hide their eating disorder due to feelings of shame and embarrassment which is common with eating disorders. It is also difficult to determine if an individual has this disorder by looking at them as many maintain an average body weight.

To look at the root of this particular eating disorder, a main area of focus that has received a plethora of research support, has been serotonin. Serotonin activity, or lack thereof, has been found to play a key role in bulimia nervosa. It impacts on the eating habits of these individuals including their bingeing and purging. Reviews conducted by Blundell (1984) and Leibowitz et al (1988) have shown that the central serotonin pathways in the brain play a major role in mediating postprandial satiety. Lesions caused by pharmacological antagonism of serotonin pathways have found to have led to increased meal portions with little to no effect on the latency for the start of eating or the rate of eating. This preclinical data has contributed to the hypothesis that impaired hypothalamic serotonin function in bulimic patients creates a vulnerability to recurrent episodes of large binge meals. Jimerson et al (1990) found that studies on the major serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid (CSF) provided evidence for decreased CNS serotonin activity. Furthermore, research conducted by Goldbloom et al (1990) showed that serotonin uptake was increased in patients with bulimia, meaning there was less serotonin available in their brains, therefore supporting the serotonin hypothesis. This essay will critically evaluate the role of serotonin in bulimia nervosa and how the research has impacted on how psychologists approach the disorder from a biological perspective.

By looking at serotonin levels in bulimic patients there have been major advances in treatments. The main focus in recent years has been antidepressants. The goal of antidepressants is to increase the amount of serotonin, therefore making them a good candidate for treatment in bulimia. Research has shown that they reduce the disruptive eating habits associated with the disorder. For example, Blouin et al (1989) found that antidepressants supressed bulimic tendencies in the non-depressed bulimic group. This research shows that serotonin plays a role in both depression and bulimia, but the two disorders do not always go hand in hand. The only thing that is certain is that serotonin plays a key role in both disorders. However, some researchers do argue that the two are linked, as Jimerson et al (1990) found that depressive episodes can trigger eating disorders in more vulnerable individuals. Regardless of this, there may be other underlying factors in these particular patients including their family history of mental health disorders. By focusing specifically on bulimia nervosa, researchers have shown that there is serotonin dysregulation in patients regardless of the presence of major depression (Jimerson et al 1990), and these studies have shown that bulimia can be present without depression alongside it.

To assess serotonin’s impact on bulimia nervosa, researchers have looked at the cerebrospinal fluid (CSF) of bulimic patients. Kaye et al’s (1984) study showed that bulimic patients had lower CSF 5-HIAA compared to non-bulimic anorexic patients. This provides evidence to show that low serotonin levels are specific to bulimia, rather than eating disorders in general. Kaye et al’s (1990) studies in normal weight bulimic women without anorexia suggest that those bulimic patients with the most severe symptoms have reduced CSF 5-HIAA. Thus, providing further support that lower serotonin levels can disrupt average patterns of behaviour in terms of eating. Furthermore, Jimerson et al (1988, 1992) found that bulimics in a ‘high-binge frequency’ group (bingeing more than 14 times per week) had much lower levels of CSF 5-HIAA compared to the ‘low-binge frequency’ group and the controls. In addition, lower CSF 5-HIAA levels persisted in the ‘high-binge frequency’ group after four weeks of abstinence from binge eating and purging during inpatient hospitalisation. This shows that perhaps without medication in their treatment, those with lower serotonin levels are far more likely to relapse after leaving hospital than those with higher levels. Thus, showing that their serotonin levels impact on their eating behaviours. In terms of evaluating the use of these tests, all research involving them have come to the same or similar conclusions, therefore stating their reliability. From this it can be assumed that there is a significant role being played by serotonin and it does in fact impact on the risk of bulimia.

Researchers have also used brain scans to note levels of serotonin in bulimic patients, in particular, PET scans. Tiihonen et al (2004) noted that that the increasing in binding in a wide range of areas in the brain could potentially reflect dysregulation of serotonin activity and also have an impact on impulse control, linking to the bingeing behaviours characterised in the disorder. As well as looking at those who currently have bulimia, the scans have also provided evidence to show that even after recovery, there is still serotonin dysregulation present. In the Kaye et al (2005) study, many of women participants who had recovered from bulimia still met the criteria for major depression, therefore providing evidence for the role of serotonin and that they remain at a slight risk for bulimia nervosa throughout their lives. This is shown as these same women had higher scores on the Eating Disorders Inventory. Therefore, the PET scans allow for more insight into levels of serotonin in the brains of patients with bulimia.

Following on from this, the main focus of a lot of research on bulimia is on the most detrimental eating habits that are the main criteria for the disorder; bingeing and purging. The use of antidepressants for treatment has been observed closely and studies have found that the ‘antibulimic effect’ of them may be the result of reduced appetite rather than mood elevation. This provides support for the use of antidepressants and for the hypothesis that bulimia is caused by a lack of serotonin that doesn’t necessarily coincide with depression. The research conducted by Weltzin, Fernstorm, & Kaye (1994), while supporting the serotonin hypothesis and stating that a disturbance of 5-hydroxytryptamine (5-HT) activity was present in most or all bulimic patients, did raise questions as to what extent serotonin actually had in the severity of symptoms, the potential presence of depression, or any other symptoms. That being said, by looking at the pharmacological data, they acknowledge the ‘antibulimic effect’ the antidepressants have on the patients that has been found to have a direct effect on the regulation of appetite and their other eating behaviours. Findings from Pope & Hudson (1982) found that antidepressants caused individuals to have a significant reduction in their binge eating within only a few weeks. The improvements in these specific bulimic tendencies provide further evidence for the serotonin hypothesis. It could be assumed that the antidepressants are beneficial when used in treatment for bulimia nervosa because they are in fact treating an underlying depression which does sometimes accompany the disorder. However, multiple studies, including those conducted by Blundell & Hill (1987) and Barlow et al (1988), have found that the medication decreases the bingeing and purging behaviours without any real impact on mood of the patients. This is an interesting insight as the majority of research on the impact of serotonin centres around mood and depression, but it is clear the is a significant effect on the eating habits associated with bulimia. Considering this, many researchers came to the conclusion that the effect of antidepressants in the treatment of bulimia nervosa did not depend on any underlying depression or depressive symptoms (Hughes et al 1986).

Nevertheless, many argue that there are enough non-depressed bulimic patients to conclude that the two disorders are not the cause of one another, but there is a high frequency of depression noted in patients with bulimia (Hudson et al 1983, Piran et al 1985, Walsh et al 1985). As serotonin does have an impact on individuals with bulimia, it does not seem far-fetched that they may have issues with mood on top of this. They are already vulnerable to depression because of their low serotonin levels. Family studies of those with bulimia have shown that there is significantly increased prevalence of depression if their first-degree relatives have the disorder. Suffering from the combination of depression and bulimia will have many more negative impacts on an individual as one disorder can influence the other. A study conducted by Hudson et al (1983) found that 77% of their patients with eating disorders had a diagnosis of major affective disorder. Those suffering with depression and body image issues are clearly at risk of developing an eating disorder, so the role that serotonin plays is clear in these circumstances. Earlier research on both disorders tended to link the two together because of the high rate of comorbidity (Levy et al 1989). Yet more recently, the idea to look at them separately has been more beneficial as researchers found that bulimia can be present without depressive tendencies. This is important as bulimia can lead to depression more easily than depression leading to bulimia. While it has been found that the two disorders sometimes highly coincide, it cannot be generalised to the whole population of bulimic patients. It is important to distinguish the difference in order to provide effective treatment.

In terms of recent development in this research area, the serotonin hypothesis still receives an abundance of support. Brain scans and cerebrospinal fluid tests are still being done on bulimic patients to see if there are any other neurotransmitters that play as big a part as serotonin, but serotonin still seems to be key in the development. With technology advancing and new ways of researching being developed it is important to keep observing neurotransmitters involved in certain disorders. In some cases, however, researchers have taken a different approach by looking at issues of trauma influencing the eating disorder. While this is not a revolutionary idea in terms of mental health, it gives further information on the role of serotonin. Rozenblat et al (2017) were one of the first to review the role that 5-HTTLPR (serotonin-transporter-linked polymorphic region) and trauma have on influencing bulimia. They reported that different types of abuse, physical and sexual, interacted with this s-allele and predicted increased risk of bulimia nervosa. Many researchers, including Monteleone (2015), have looked at this area of trauma and its implications on eating disorders, but there is a grey area in this particular field of study, and that is which, out of the trauma and serotonin levels, has the most impact on the development of bulimia. With all the research in this area, it could be possible to determine which plays the bigger role. Perhaps some of these individuals who experienced trauma and went on to have an eating disorder already had a predisposition of low serotonin levels. Nevertheless, it would be difficult to determine the serotonin levels before the trauma if they had not demonstrated any bulimic tendencies and were already receiving treatment. With this in mind, it can still be argued and supported that serotonin plays a major role in this disorder.

Interestingly, there has been recent research on the role of serotonin and eating in general, rather than specifying it to eating disorders. Bonnet et al (2017) found that those who had a reduced ability to control the amount they ate (e. g. eating when bored, upset etc. ) had lower levels of specific serotonin genotypes. This evidence of the impact of serotonin in eating behaviours in general shows further support to its capacity in eating disorders. When the serotonin levels get even lower, that’s when the disorders begin and cause problems for the individuals. In regard to specific eating disorder research, it has been recently established that the specific serotonin receptor, 5-HT2C, is responsible for regulating food intake. Therefore, over the many years that serotonin has been the main focus of this research, a particular receptor has been identified in bulimia nervosa, which links to the bingeing behaviour that is part of the disorder. Levels of impulsivity have also been an important factor in bulimia as it goes alongside the regulation of eating and bingeing behaviours (Culbert et al 2018). These factors have all been associated with low serotonin levels.

The vast majority of evidence points to serotonin being a key player in the development of bulimia and the behaviours that go along with it. Antidepressants have, in most cases, been shown to reduce a lot of these bulimic tendencies and eating patterns. Bacaltchuk & Hay (2003) reported that the use of these drugs was effective compared to a placebo and also had a greater remission rate. Nonetheless, these results cannot be generalised to the whole population of bulimic patients. Pilot studies conducted by Krahn & Mitchell (1985) and Mira and Abraham (1989) outlined inconsistent effects on binge frequency amongst their sample groups. From this it can be argued that there is a great deal of mixed responses regarding this type of treatment. Conclusions can be made that perhaps serotonin isn’t a prominent point in a lot of cases. However, despite these results for antidepressants, the amount of research supporting the serotonin hypothesis of bulimia significantly outweighs the amount of negative or inconsistent results and because of this, it can be established that serotonin does play a major role in bulimia nervosa and the eating behaviours that go alongside it.

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