Categories · Health/Science
· Secondhand Smoke
· Pregnancy
· Women
· Diabetes
· Sex/Fertility
· Parenting / Family issues
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DOI: 10.1530/eje.1.01867, Vol 152, Issue 4, 491-499 April 1 2005, Volume 152, Issue 4 Jump to full article: European Journal of Endocrinology, 2005-04-01
Intro: Smoking has multiple effects on hormone secretion, some of which are associated with important clinical implications. These effects are mainly mediated by the pharmacological action of nicotine and also by toxins such as thiocyanate. Smoking affects pituitary, thyroid, adrenal, testicular and ovarian function, calcium metabolism and the action of insulin. The major salient clinical effects are the increased risk and severity of Graves’ hyperthyroidism and opthalmopathy, osteoporosis and reduced fertility. Smoking also contributes to the development of insulin resistance and hence type 2 diabetes mellitus. An important concern is also the effect of smoking on the foetus and young children. Passive transfer of thiocyanate can cause disturbance of thyroid size and function. Furthermore, maternal smoking causes increased catecholamine production, which may contribute to under perfusion of the foetoplacental unit. . . .
In males, the effect of smoking on androgen levels is important, given the recent interest in the association between low androgen levels and the metabolic syndrome, and coronary heart disease (90). Various studies examining the effects of smoking on serum testosterone levels have reported conflicting findings largely due to difficulties in the hormonal assays. Testosterone has a circadian rhythm with levels peaking between 0600 and 0800 h and reaching a nadir between 1800 and 2000 h. A significant proportion of the circulating total testosterone is inactive as it is tightly bound to SHBG (65–80%), whereas the biologically active fraction circulates either free (1–3%) in circulation or loosely bound to albumin (20–40%). The free plus the albumin-bound testosterone is called the bioavailable testosterone. Thus levels of total testosterone can be affected by changes in the levels of SHBG and other plasma proteins. Significantly increased (41, 91–95), decreased (96, 97) and unchanged levels of total testosterone (64, 98, 99) in male smokers have been reported in various studies. Free testosterone levels have also been found to be higher among smokers (41, 91, 92, 94, 95). However, SHBG levels have been measured only in three studies (92, 93, 95) and are reported to be higher amongst smokers. No significant differences in the levels of bioavailable testosterone have been demonstrated between smokers and non-smokers (92, 93). English and colleagues (92) demonstrated that the increase in total testosterone observed in smokers is due to the raised SHBG levels. They also reported that SHBG levels and not testosterone correlated with serum nicotine levels, a measure of cigarette smoking. However, Svartberg et al. (95) found a positive association between testosterone and smoking even after adjusting for SHBG though other plasma proteins were not taken into account. It would seem likely that the effects of smoking on testosterone levels are due to changes in plasma-binding capacity rather than a direct effect of nicotine on androgens. . . .
Smoking is an important modifier of hormones and a detailed smoking history is essential when assessing patients with endocrine disorders. The hormonal responses to smoking are responsible for the increased prevalence of several diseases in smokers. Graves’ disease and particularly Graves’ ophthalmopathy are strongly associated with smoking. Autoimmune thyroiditis and small goiters are also more commonly seen in smokers. Similarly, osteoporosis is linked to smoking through its effects on various hormones, in particular the anti-oestrogenic effect in women, which causes fertility problems and premature menopause in smokers as well. Insulin resistance is also more common in smokers and may contribute to the increased incidence of cardiovascular disease. More pronounced responses are seen in heavy smokers as compared with light smokers reflecting the direct toxicogenic effect of cigarette smoke. Maternal smoking affects the infants in a similar way to adults. It is also possible that passive smoking could also affect the growth of young children through decrease in GH, as seen in chronic smokers. The rewards of giving up smoking are thus both immediate and substantial.
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