Alcoholism and the Thyroid Axis

Abstract

Alcoholism, usually defined as the excessive consumption of ethanol accompanied by adverse medical, social, or psychological consequences, has received increased attention from the biomedical research community. Although ethanol is a simple molecule, it has complex effects on physiology and behavior and, as is well known, is highly toxic to cells when taken to excess over time. Understanding the biology of alcoholism, and addiction in general, is still some distance away but pieces of the puzzle are emerging. It is the purpose of this review to focus on findings linking alcoholism to disturbances within the hypothalamic-pituitary-thyroid (HPT) axis. In particular, we discuss the blunted thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) as a biological marker of alcoholism and examine the possible pathophysiological mechanisms underlying the fault. For purposes of clarity we do not include studies on alcoholic subjects with overt liver disease, gonadal dysfunction, or brain injury because findings in these populations are difficult to interpret vis-à-vis alcoholism per se. We define a blunted TSH response, at a 500-µg test dose of TRH, as Δ max TSH of under 5µU/ml. Use of this criterion results in fewer positive, i.e., blunted, results; we have found 0% of normal men and 8% of normal women to exhibit values at or below this threshold (Loosen and Prange 1982; Mayo et al., unpublished observations). For definitions of blunted TSH responses to other TRH test doses we accept the criteria as given in the original report.