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Whereas the psychological construct and pathophysiological basis of craving for alcohol, a major risk for relapse in alcoholism, has been intensively evaluated in recent years, no measurable biological correlate exists.1 Neurobiological and psychological similarities between craving and appetite are well established since both are known to be influenced by the mesolimbic brain reward system and its endorphinergic inputs.2 Recently, leptin, the protein product of the obesity gene, was proposed to be a signal responsible for linking adipose stores with hypothalamic centers regulating energy homeostasis and body weight.3 In addition, leptin has been shown to alter the gene expression of corticotropin-releasing hormone and pro-opiomelanocortin in the hypothalamus, suggesting a role both in regulating the stress hormone axis and possibly in the endorphinergic modulation of the reward system.4 Leptin mutually interacts with other neuroendocrine systems involved in the regulation of appetite such as NPY (neuropeptide Y)3 or the newly discovered hypothalamic peptide CART (cocaine- and amphetamine-regulated transcript).5
Relationship between body mass–corrected plasma leptin (as the ratio of plasma leptin and body mass index [BMI], calculated as weight in kilograms divided by the square of height in meters), plasma cortisol, and self-rated craving for alcohol in a sample of 20 subjects with alcohol dependency at the first day after onset of withdrawal. Pearson product moment correlation of the leptin-BMI ratio with craving was r = 0.68 (P<.04) with no correlation of leptin with cortisol or cortisol with craving. Partial correlation of the leptin-BMI ratio with craving controlling for cortisol was r = 0.54 (P<.02). VAS indicates visual analog scale.
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