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Biochemical mechanisms of anorexia and bulimia

Biochemical mechanisms

The main brain area involved in the regulation of appetite is the hypothalamus, although other brain areas and factors in the gut also infl uence hunger and satiety. The lateral hypothalamus produces hunger when stimulated; surgical damage results in dramatic reductions in food intake and weight loss. Activation of the ventromedial hypothalamus triggers feelings of satiation and reduces hunger: for this reason it has been called the satiety centre. Activity within the hypothalamus is largely mediated by two neurotransmitters: dopamine and serotonin, which initiate, maintain and then inhibit eating.


At the onset of or when anticipating eating, dopamine activity increases in both the lateral hypothalamus and the mesolimbic dopamine system – the primary reward system. Thus, the early stages of eating are both triggered and maintained by a direct effect on hunger and a feeling of pleasure. As eating continues, the dopaminergic activity is replaced by serotinergic activity, which reduces appetite and inhibits eating. Jimerson et al. suggested that people prone to binge eating may experience low levels of dopamine release (or be insensitive to the dopamine that is released) when they start eating. This may lead to binge eating as they attempt to achieve previous levels of satisfaction/reward from eating. Such speculation is supported by fi ndings of low levels of HVA (a metabolite of dopamine) in the cerebrospinal fluid of people with bulimia. Paradoxically, perhaps, people with anorexia may also have a diminished capacity to experience pleasure or reward as a consequence of low levels of dopamine in the mesolimbic system but feel less motivated to eat rather than overeating as some form of compensation. This may be re-established when they recover.

Serotonin Animal studies have shown that when serotonin is released into eithe r the ventromedial or lateral hypothalamus, animals stop eating and may starve despite the presence of food. Thus, high levels of serotonin lead to feelings of satiation and lower levels of eating – as well as improve mood. Low levels of serotonin result in excess eating and obesity – and low mood. This is not simply the result of serotonin’s infl uence on the hypothalamus – areas such as the limbic system are also involved. One explanation for the eating binges associated with bulimia has been that dieting reduces levels of tryptophan, a precursor to serotonin, leading to low mood and cravings for food high in tryptophan – carbohydrates such as chocolate, cakes and chips. Eating these restores serotonin and mood levels to normal. In support of this hypothesis, Kaye et al. found that women with bulimia typically stopped bingeing if their levels of tryptophan increased signifi cantly following an eating binge: those whose tryptophan remained relatively low continued bingeing. In a related study, Goldbloom et al. found that following release into the synaptic cleft, bulimics’ serotonin was more quickly reabsorbed by the initiating axon than that of normal controls, resulting in a reduced availability of serotonin at the receptor cells. In response to these fi ndings, Jimerson et al. suggested that periodic binge eating may cause sudden increases in serotonin levels within the brain. This causes the receptors to become less sensitive to serotonin when released. This low sensitivity to serotonin means that the individual may become less responsive to normal levels of serotonin, requiring them to take in larger amounts of tryptophan to convert to serotonin in order to maintain emotional equilibrium. Despite some supportive data, neither theory has always been supported by empirical evidence. Weltzin et al. (1995), for example, found no evidence of reduced levels of tryptophan prior to binge eating episodes in women with bulimia, and Jansen et al. found that levels of tryptophan in the foods typically eaten in a binge were actually quite low in tryptophan and were not a particularly effective means of increasing tryptophan levels. Behavioural studies also provide limited support for the hypothesis. Steiger et al. used hand-held computers to obtain repeated ‘online’ measurements of eating behaviours and mood in 21 women with bulimia. As expected, their mood was typically depressed before binge episodes. However, following bingeing, their mood deteriorated further. Some studies  have shown people with anorexia to have lower levels of serotonin metabolites in their cerebrospinal fluid than controls. Kaye  has argued that this is a consequence of anorexia rather than a cause. Indeed, Kaye, argued that anorexia may be the result of too high levels of serotonin rather than too low levels. He suggested that these high levels of serotonin may leave the individual feeling nervous and jittery, feelings that are may be reduced by reducing food intake, and thereby reducing tryptophan, and then serotonin levels. Unfortunately, even Kaye’s own work has not always supported this hypothesis, as he (Kaye et al. 2005) found lower levels of serotonergic activity during periods of both starving and recovery among people with anorexia than among ‘normal’ controls. Brain areas involved include the frontal, cingulated, temporal and parietal cortical regions – which are involved in anxiety, behavioural control and body image. Together, these data suggest that while serotonin dysregulation may be involved in both bulimia and anorexia, its exact role in either disorder is yet to be fully understood.

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