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Alcohol and Alcoholism Vol. 35, No. 1, pp. 84-90, 2000
© 2000 Medical Council on Alcoholism

ACUTE EFFECT OF ALCOHOL ON ANDROGENS IN PREMENOPAUSAL WOMEN{dagger}

Taisto Sarkola, Tatsushige Fukunaga1, Heikki Mäkisalo2 and C. J. Peter Eriksson*

National Public Health Institute, Department of Mental Health and Alcohol Research, P.O. Box 719, FIN-00101 Helsinki, Finland,
1 Department of Forensic Medicine and Sciences, Mie University School of Medicine, Tsu, Japan and
2 Department of Surgery, Helsinki University Central Hospital, Helsinki, Finland

Received 1 April 1999; first review notified 21 June 1999; accepted 13 July 1999

The aim of the present study was to investigate the effect of alcohol on androgen levels among premenopausal women. Eighty-seven women in the mid-cycle phase of the menstrual cycle, 47 of whom used oral contraceptives (OC+), were included in the study. The range for reported alcohol consumption was 0–4 drinks/day. The total testosterone levels were significantly higher after alcohol intake (0.5 g/kg) than after placebo at 45 min and 90 min from the start of drinking among both OC– and OC+ subjects. This effect was also seen in the free testosterone fraction. The effect on testosterone was more prominent among OC+ subjects. Androstenedione levels were significantly lowered and the testosterone:androstenedione ratio significantly elevated by alcohol among both OC– and OC+ subjects. No effect of alcohol on dehydroepiandrosterone or dihydrotestosterone levels was observed. A positive correlation was observed between the change in testosterone levels and the change in androstenedione levels during placebo conditions. The correlation was significantly reduced during alcohol conditions among OC+ subjects, indicating an increased androstenedione to testosterone conversion. No significant dose (0.34, 0.68 and 1.02 g/kg) or time (45, 90 and 150 min) effects on total testosterone were observed in a substudy involving 10 OC+ subjects. The present results suggest that the testosterone effect is related to the zero-order mechanism of ethanol oxidation. The observed testosterone and androstenedione effects are suggested to be the result of an increased androstenedione to testosterone conversion in the liver caused by the alcohol-mediated elevation in the [NADH]:[NAD+] ratio. The present findings may be relevant in the development of hyperandrogenism and loss of female sexual characteristics associated with heavy alcohol consumption.


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