The following studies are very interesting.
Basically, the (Finnish) authors reported acute increases in serum testosterone in both men and
women following ingestion of a moderate dose of ethanol (0.5 gm/kg) or a little more than an ounce
in a 70 kg/155 pound person. This was true in both men and women. The effect was apparently mediated
through an inhibition in catabolism (breakdown) of testosterone by the liver.
Note that this is simply an acute effect. As noted below, chronic alcohol ingestion reduces
testosterone levels through an effect on gonadal production.
But the implications of an acute rise in testosterone levels are provocative and fascinating. Not
that I would ever advocate drinking and swimming (much less drinking and more dangerous activities),
I have had a couple of occasions in my life, when, for example, I've had a beer at Silky Sullivan's
Irish Pub in Fountain Valley (to watch a Michigan game on pay per view) and then gone the one mile
over to Los Caballeros Sports Club to drown the sorrows of the Michigan loss in the pool, with, for
example, a furious 1000. I've been surprised at my level of aggression and performance. I wonder if
anyone else can, in retrospect, recall such a correlation?
- Larry
1: Alcohol Clin Exp Res. 2003 Apr;27(4):682-5.
Testosterone increases in men after a low dose of alcohol.
Sarkola T, Eriksson CJ.
Department of Mental Health and Alcohol Research, National Public Health Institute,
Helsinki, Finland.
BACKGROUND: Heavy acute alcohol drinking decreases blood testosterone in men due to an effect on the
testicular level. An acute increase in blood testosterone levels after a low alcohol dose has,
however, recently been reported in women. The objective of this investigation was to study the
effect of a low alcohol dose on testosterone in men and further elucidate the mechanism behind the
effect by using 4-methylpyrazole, an inhibitor of alcohol metabolism. METHODS: A double-blind
placebo-controlled interventional crossover trial in random order (n =
2). RESULTS: After intake of alcohol (0.5 g/kg, 10%
w/v), an acute increase in plasma testosterone (from
13.5 +/- 1.2 nmol/liter to 16.0 +/- 1.6 nmol/liter, mean +/- SEM; p < 0.05), a decrease in
androstenedione (from 5.1 +/- 0.4 nmol/liter to 4.0 +/- 0.3 nmol/liter; p < 0.05), and an
increase in the testosterone:androstenedione ratio (from 2.8 +/- 0.3 to
14.2 +/- 0.4; p < 0.01) were observed. The effects were not observed during pretreatment with
4-methylpyrazole (10-15 mg/kg orally), which inhibited the ethanol elimination rate by 37 +/- 3%.
CONCLUSIONS: Alcohol intake affects the androgen balance in men through an effect mediated by the
alcohol-induced change in the redox state in the liver.
15: J Clin Endocrinol Metab. 2001 May;86(5):1981-5.
The role of the liver in the acute effect of alcohol on androgens in women.
Sarkola T, Adlercreutz H, Heinonen S, von Der Pahlen B, Eriksson CJ.
Department of Mental Health and Alcohol Research, National Public Health Institute,
Helsinki, Finland.
The hypothalamic-pituitary-gonadal and -adrenal axes are regarded as the main sites of the actions
of alcohol on steroids. In the present study the effect of alcohol (0.4-0.5 g/kg, orally) on venous
plasma and urinary androgens was investigated in 21 premenopausal women using oral contraceptives as
well as in 10 premenopausal nonusers. After intake of alcohol, an acute elevation in plasma
testosterone, a decline in androstenedione levels, and an elevation in the ratio of testosterone to
androstenedione were observed in both groups. The effects lasted throughout the period of ethanol
elimination and were abolished during pretreatment with 4-methylpyrazole (10-15 mg/kg, orally). The
acute effects were higher in the group using oral contraceptives than in the nonusers. The
testosterone effect in plasma was reflected in the free testosterone fraction. A decline in urinary
androsterone and etiocholanolone levels, the principal catabolic products of androgens, was observed
during alcohol intoxication. In conclusion, the present acute effects on plasma and urinary steroid
hormones seem to be explained by an inhibited catabolism mediated by the alcohol-induced change in
the redox state in the liver. Our results suggests that the liver should be included as a major site
in the acute endocrinological effects of alcohol on steroid hormones in women.