Menopause Live - IMS Updates

Date of release: 02 February, 2009

Smoking and hot flushes

It is known that women who smoke tend to have an earlier menopause than non-smokers and are more likely to experience hot flushes [1]. A recent paper reports a study to test the hypothesis that cigarette smoking is associated with hot flushes through a mechanism involving levels of androgen, progesterone and sex hormone binding globulin (SHBG) or the ratio of androgens to estrogens [2].

Current smokers had significantly higher androstenedione levels, with a mean of 2.20 ng/ml (95% confidence interval (CI) 1.94-2.51 ng/ml) compared to never smokers at 1.93 ng/ml (95% CI 1.83-2.03 ng/ml; p < 0.01), and lower progesterone levels, but there was no difference in levels of serum estradiol, estrone, testosterone, SHBG or dehydroepiandrosterone sulfate between any of the groups. However, there was no correlation between hormone levels and the incidence of hot flushes.

For women who had ever smoked cigarettes, the greater number of pack-years was associated with greater odds of reporting hot flushes. Current smokers of 1–25 pack-years were 6.2 times more likely to experience any hot flushes compared with never smokers.


The hot flush is the most characteristic and often the most distressing symptom of the climacteric and yet it remains an enigma. Despite decades of research, we are still a long way from identifying the exact mechanism of the flush and few risk factors have been identified [3,4]. Androstenedione is predominantly derived from the adrenal gland and one mode of action of nicotine is to stimulate the adrenal gland. This study also suggests that smoking may permanently alter the amount of androstenedione production by the adrenal gland because the level of androstenedione was similar among current and former smokers, but was significantly lower in never smokers. Furthermore, nicotine may stimulate the pituitary gland to produce adrenocorticotrophic hormone, which also stimulates the adrenal gland to produce more androstenedione, and there is a decreased clearance of androstenedione in smokers, also leading to increased levels. But this study has not found any evidence that the raised levels of androstenedione or reduced levels of progesterone are factors in the causal pathway of hot flushes and are just another effect of cigarette smoking. Other studies have shown an increase in luteinizing hormone in smokers, suggesting another action of nicotine in stimulating the hypothalamus and pituitary. So, although this study does not provide any more information on the causation of the hot flush than is already known, it is possible that direct stimulatory action of nicotine on receptors in the hypothalamus may be a factor in the increased risk of flushes in smoking women. Advice about lifestyle is an important part of the routine counselling of women at any age, and these further data on the effects of cigarette smoking could be added to these discussions. Finally, what are the implications of permanently increased levels of androstenedione induced by smoking? More data are needed.


David Sturdee
Department of Obstetrics & Gynaecology, Heart of England NHS Foundation Trust, Solihull Hospital, Solihull, UK


  1. Gallicchio L, Miller SR, Visvanathan K, et al. Cigarette smoking, estrogen levels and hot flushes in midlife women. Maturitas 2006;53:133-43. Published January 20, 2006.

  2. Cochran CJ, Gallicchio L, Miller SR, Zacur H, Flaws JA. Cigarette smoking, androgen levels, and hot flushes in midlife women. Obstet Gynecol 2008;112:1037-44. Published November 4, 2008.

  3. Freeman EW, Sherif K. Prevalence of hot flushes and night sweats around the world: a systematic review. Climacteric 2007;10:197-214. Published June, 2007.

  4. Sturdee DW. The menopausal hot flush anything new? Maturitas 2008;60:42-9. Published May 20, 2008.