Department of Medicine, Columbia University College of Physicians and Surgeons, St. Lukes-Roosevelt Hospital Center, New York, NY 10019
In a recent prospective study, Ebrahim et al. (1) reported the striking finding that men who shaved less often than daily (infrequent shaving) had a 52 percent higher risk of cardiovascular disease (CVD) mortality over 20 years than men who shaved daily (frequent shaving), after adjustment for age. They concluded that the association of infrequent shaving with CVD mortality was "probably due to confounding by smoking and social class" (1, p. 238); however, they found a significantly increased risk of stroke events among infrequent shavers compared with frequent shavers even after adjusting for these and other variables. Furthermore, they reported similar relations of infrequent shaving with CVD mortality and stroke events in nonsmokers.
In both the study by Ebrahim et al. (1) and my study (2), in which I reported infrequent shaving among men under 44 years of age who had had a myocardial infarction, the infrequent shaving was accompanied by evidence of hormonal aberrations, including breast tenderness (2), gynecomastia (2), and a decreased sex drive (1, 2). Given the strong relation between beard growth and sex hormone status (3), these findings suggest a possible role of sex hormones in the relation between infrequent shaving and CVD mortality. Although Ebrahim et al. did not find a relation between hormone levels and shaving frequency, they suggested that hormones might play a role. In addition to the possibility that infrequent shaving could be a prospective marker at an early age for CVD, the interrelations of infrequent shaving, smoking, hormones, and mortality have etiologic implications that invite speculation and warrant further investigation. I suggest that sex hormones may underlie these relations.
Which sex hormone alteration might underlie the infrequent shaving is not entirely clear. The relation of reduced or absent beard growth with testicular feminization, 5--reductase deficiency, and hypogonadism (3) indicates the critical role of testosterone, or more specifically dihydrotestosterone, in beard growth. However, it seems likely that hyperestrogenemia, even in the presence of a normal or elevated testosterone level, could also be responsible for infrequent shaving. Estradiol level has been reported to be inversely related to sperm count in men with a normal mean testosterone level (4). Administration of estrogen to men has been reported to produce breast tenderness, gynecomastia, and a decrease in sex drive (5)signs seen among the infrequent shavers (1, 2). From the data in my study (2), calculations (not reported) show that the infrequent shavers had higher mean estradiol (p = 0.005) and estrone (p < 0.004) levels than those who had to shave twice per day when going out at night; the mean testosterone and dihydrotestosterone levels were not significantly different, although these relations could have been confounded by past smoking and by a myocardial infarction 4 months to 10 years previously in all of the infrequent shavers.
A relation of hyperestrogenemia with an elevated or normal testosterone level has also been reported in male smokers (4, 6). Consistent with this finding are the reported associations of estrogen administration (5) and smoking (7) with impotence. Hyperestrogenemia, then, could explain the association between smoking and infrequent shaving.
The possibility that hyperestrogenemia and smoking might be related to coronary heart disease through a common mechanism raises the possibility that hyperestrogenemia could also link both smoking and infrequent shaving with CVD mortality. While smoking is a risk factor for myocardial infarction and sudden death, it does not appear to be a risk factor for stable angina (8). This finding and the finding of a positive association of smoking with fibrinogen level (8) suggest that smoking may lead to myocardial infarction by provoking thrombosis. The fact that hyperestrogenemia in men was found to be related to myocardial infarction but not coronary artery disease suggests that it too may underlie the thrombosis of myocardial infarction (9). Supporting this possibility is the relation of estrogen to hemostasis (9) and the observation that administration of estrogen to men led to myocardial infarction and venous thrombosis (5). Thus, hyperestrogenemia could provide a common link between infrequent shaving, smoking, and CVD mortality.
Because the studies of sex hormone levels in smokers were not randomized and prospective, they did not determine which came first, the smoking or the hormonal alteration. If smoking leads to infrequent shaving by raising the estrogen level, which in turn may link the infrequent shaving to CVD mortality, what then might lead to infrequent shaving and link it to CVD mortality in nonsmokers? Although hyperestrogenemia may be implicated here as well, it is also possible that in nonsmokers hypotestosteronemia is the predominant link. Not only does testosterone appear to be necessary for normal beard growth (3), it has also been reported in men to correlate inversely with the degree of coronary artery disease (10), as well as with risk factors for myocardial infarction (11). Thus, if smoking leads to hyperestrogenemia, hyperestrogenemia could be the predominant factor leading to infrequent shaving in smokers and hypotestosteronemia could be the predominant factor leading to infrequent shaving in nonsmokers, and both hormonal alterations could be links between infrequent shaving and CVD mortality.
However, it is possible that rather than smoking leading to hyperestrogenemia, hyperestrogenemia in men may lead to smoking and to difficulty in stopping, as well as to infrequent shaving and coronary heart disease. This hypothesis does not preclude the possibility that smoking could also induce a change in sex hormone levels or that smoking leads to CVD independently of sex hormone levels. In support of the hypothesis that the smoking may not be primary is the fact that 75 percent of the smokers in the study by Ebrahim et al. (1) shaved daily. In addition, smoking in men was found not to affect the level of estradiol acutely (12). The genetic tendency to smoke (13) could be based on elevated estrogen levels. One mechanism for this relation could be depression. Hyperestrogenemia has been found to be associated with depression in men (14), and depression in adolescence has been found to be a predictor of daily smoking 9 years later (15). Therefore, hyperestrogenemia could precede the smoking in men.
Whether or not in men hyperestrogenemia leads to smoking, smoking leads to hyperestrogenemia, or both mechanisms obtain, the interrelations of infrequent shaving, smoking, CVD mortality, and hyperestrogenemia suggest that hyperestrogenemia should be considered as a possible common link. A clue to the answer of whether hyperestrogenemia or smoking is primary might be obtained by determining by history whether smoking is prospective for infrequent shaving or vice versa.
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