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Ghrelin and Bulimia Nervosa (BN)

Kalat (2007) discusses the phenomenon of increased release of the hormone ghrelin in those with BN. When compared with controls, those with BN had increased levels of ghrelin both pre- and postprandial (before and after meals)due to reduced ghrelin suppression (Jerlhag et al., 2006). According to the Journal of Clinical Investigation (2006) ghrelin assists in the balance of food intake, and energy output. Raised ghrelin increases food intake and weight gain (Kojima et al., 2005). Kalat (2007) reports that ghrelin has a role in stimulating stomach contractions upon food deprivation. Increased ghrelin is found in obese individuals with Prader Willi Syndrome, those with BN, and those with anorexia nervosa. Elevated levels of ghrelin may be associated with the oft reported feeling of loss of control during binge eating episodes (Kojima et al., 2005). It is postulated that increased levels of ghrelin boost production of dopamine, a neurotransmitter implicated in the reward system associated with addictive behavior (Jerlhag et al., 2006). Furthermore, Jerlhag et al. (2006) posited that the inhibition of nicotinic receptors by injecting nicotinic acetylcholine antagonists would decrease the effects of ghrelin. Similar to its involvement in other addictive behaviors, ghrelin may be involved in compulsive eating via neurotransmitter and hormonal pathways of the reward system (Jerlhag et al., 2006). Thus, it is proposed that psychopharmaceutical and clinical treatments might be developed to treat BN as an addiction and target symptoms when ghrelin is more clearly understood.

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