Most endocrine and reproductive function is influenced directly or indirectly by the BRAIN— specifically by the functional interactions of the brain s hypothalamus and pituitary with the target endocrine organs. The hypothalamus produces pituitary-regulating hormones; all are peptides except one (DOPAMINE). In response to each of these hypothalamic hormones, the pituitary releases a hormone, which influences the function of an endocrine or reproductive organ.

Alcohol. The anecdotal reports of changes in sexual function following alcohol consumption was the stimulus for much of the research targeting hypothalamic-pituitary relationships, since impairments here may often result in sexual dysfunction. Although acute alcohol use has been reported in public surveys to be associated with increased sexual drive and functioning, clinical and animal research have revealed major hormonal dysfunctions in chronic or heavy alcohol users.

Prolactin (PRL)—the pituitary hormone associated with preparation during pregnancy for breastmilk secretion—is increased with heavy alcohol use; however, chronic alcohol use inhibits the pituitary release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Both LH and FSH are important in regulating the sex hormones produced by the testes in males and the ovaries in females. Yet, when alcohol is administered acutely, there are no significant changes in PRL, LH, or FSH serum levels.

Heavy alcohol consumption is associated with an increase in pituitary-secreted adrenocorticotro-pic hormone (ACTH), partly explaining the

"pseudo-"Cushing's syndrome (moon faced appearance, central obesity, muscle weakness) and the increased melanocyte-stimulating hormone (MSH), which possibly leads to darkening skin pigmentation. Although there is no consistent effect of heavy alcohol use on the pituitary's release of thyroid-stimulating hormone (TSH) or growth hormone (GH), a rise in the blood alcohol level is associated with the inhibition of antidiuretic hormone (ADH) release from the posterior pituitary, resulting in increased urination.

Drugs. Complaints of derangements of libido (sex drive) and sexual functioning in OPIOID addicts (HEROIN) were among the first lines of clinical evidence to suggest the possible role of such narcotics in altering hypothalamic-pituitary functioning. Although most of what is known about drug-abuse related hypothalamic-pituitary abnormalities focuses on heroin use, the epidemic proportions of COCAINE abuse and dependency in the 1980s have brought renewed scientific interest to this area.

Studies have shown that opioid use has been associated with increased serum PRL without disturbances in serum GH or TSH levels; and cocaine use has been associated with both high and low PRL levels. The contradictory findings in the case of cocaine use might be attributable to the variations in patterns of cocaine use. Animal studies have shown that gonadotropin-releasing hormone (GnRH), released from the hypothalamus, did not stimulate PRL following acute cocaine administration, and it did not prevent acute cocaine-associated PRL suppression. Elevated levels of dopamine have been observed during acute cocaine administration, but chronic cocaine use may deplete dopa-mine.

In patients receiving METHADONE therapy for opioid addiction, some investigators have reported a normal rise in TSH released by the pituitary, in response to stimulation by the hypothalamic hormone called thyrotropin-releasing hormone (TRH). Others have observed a blunted TSH and PRL response following TRH administration in active heroin users.

Although normal basal LH secretion has been observed in cocaine abuse, opiate use is associated with decreased basal FSH and LH levels in males. In female heroin addicts, these low levels of the pituitary gonadotropins have clinical relevance, resulting in a consistently normal FSH response and a variable LH response following a GnRH challenge.

Some researchers have demonstrated normal functioning of the hypothalamic-pituitary-adrenal (HPA) axis in former heroin addicts who were maintained on methadone both long-term and only for a number of months. However, there is also evidence suggesting alteration of the normal biological rhythm of hormonal secretion.

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