CONCLUSION
The relationship between illicit drug use, abnormalities in gonadal and adrenal function and stress and depression is complex. Adrenal and gonadal dysfunction is both a cause and consequence of drug use behavior (see Fig. 1). There is, however, significant variation in the effect of opiates and cocaine on adrenal and gonadal function with both administration and withdrawal. Further, attempts to manipulate endocrine function in the treatment of addiction have had mixed results. It is possible that certain subsets of drug users are particularly vulnerable to the effects of opiates and cocaine on the HPG and HPA axes. Polymorphisms in the mu-opioid receptor, for example, have been associated with reduced HPA activation in the setting of receptor blockage with naloxone (Wand, 2002). Whether this genetic variation accounts for differences in the endocrine effects of drug administration and changes in endocrine function during withdrawal requires further study.

Studio completo: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1821355/#S10

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Adrenal dysfunction in drug use
In healthy individuals, pulsatile secretion of corticotropin releasing hormone (CRH) in the hypothalamus causes pituitary secretion of adrenocorticotropic hormone (ACTH), which stimulates cortisol synthesis and release from the adrenal cortex. Opiate administration disrupts this pathway through the inhibition of CRH release, leading to reduced cortisol production[19]. Consistent with this observation, small studies have shown a high prevalence of adrenal insufficiency in opiate dependent subjects, with a high prevalence of abnormal ACTH stimulation tests[20], low cortisol concentrations accompanied by low ACTH levels and atypical circadian production of these hormones[21]. In addition, the administration of metyrapone, a cortisol synthesis inhibitor used to test the integrity of the HPA axis, shows decreased HPA activation in heroin users[22]. An attenuated response to CRH in methadone users compared to non-users suggests that disruption of the HPA axis is at the level of the pituitary or adrenal gland.
In contrast to opiate use, cocaine administration results in enhanced HPA activity in both humans[23] and non-human primate species[24]. Interestingly, male monkeys have a more robust HPA response to cocaine use compared to females[24] however in rats, females exhibit a greater HPA response to cocaine than males. CRH antagonists block hypercortisolism observed in cocaine users across species studied[16]. However, the administration of metyrapone increased HPA activity in cocaine users, illustrating different effects of opiates and stimulants on HPA function.