Endocrine Effects of Tobacco Smoking

Konstantinos Tziomalos; Faidon Charsoulis


Clin Endocrinol. 2004;61(6) 

In This Article

Diabetes Mellitus

Smoking and diabetes has recently been the focus of considerable attention. Smoking increases the risk of developing diabetes (Kawakami et al., 1997). Despite strong evidence of the epidemiological link between smoking and diabetes (Feskens & Kromhout, 1989; Rimm et al., 1993, 1995; Haire-Joshu et al., 1999), the causal basis of the association has not been explained. Clinical and population-based studies of healthy individuals have linked smoking with insulin resistance (Facchini et al., 1992; Attvall et al., 1993; Zavaroni et al., 1994; Ronnemaa et al., 1996; Eliasson et al., 1997; Daniel & Cargo, 2004). Other studies, however, have observed no effect of smoking in relation to insulin resistance (Pyöräläet al., 1985; Godsland et al., 1988; Ferrara et al., 1994; Nilsson et al., 1995; Wareham et al., 1996; Os et al., 2003). Age has been the most striking study difference as to whether a positive or negative relationship between cigarette smoking and insulin resistance has been reported; in studies showing a positive relationship, the subjects were younger. It could be hypothesized that, after an initial effect from cigarette smoking causing insulin resistance, an adverse effect on the beta cell becomes predominant after decades of exposure. In current smokers, smoking-related responses promoting insulin resistance are the androgenic state and increased secretion of anti-insulin hormones, including adrenaline and growth hormone release, as well as elevated fatty acids (Wild et al., 1990; Hautanen & Adlercreutz, 1993; Hellerstein et al., 1994; Phillips et al., 2000). Smoking-related responses that may counter insulin resistance, in normoglycaemic individuals, include elevated skeletal muscle blood flow, lower body weight and caloric intake, and enhanced thermogenesis (Weber et al., 1989). An alternate explanation for the link between smoking and diabetes might involve a direct adverse effect on the beta cell (Spector & Blake, 1988; Ostgren et al., 2000; Os et al., 2003). The impaired insulin secretion in smokers could offer an explanation for the slightly higher serum glucose levels and haemoglobin A1c (HbA1c) observed in them, despite lower body mass index and serum leptin levels (Os et al., 2003). Nevertheless, others have found only former smoking to be associated with low beta-cell function, while current smoking was related to high beta-cell function, independent of the presence of diabetes (Daniel & Cargo, 2004). It has also been reported that smoking may interfere with beta-cell function only in men (Ostgren et al., 2000).