1 Department of Social Medicine, University of Bristol, Bristol BS8 2PR, United Kingdom
2 Department of Epidemiology and Public Health, Queens University, Belfast BT12 6BJ, United Kingdom
We thank Dr. Phillips for his views (1). Phillips original and novel observation in a small case-control study of increased risk of myocardial infarction among men who shaved infrequently (2) was the starting point for our investigation. Our finding of very similar strengths of association between less frequent shaving and lung cancer, all-cause mortality, and cardiovascular diseases demonstrated a lack of specificity in the relation (3). Appropriate adjustment for potentially confounding factors attenuated the hazard ratios towards the null value for all causes of death, although hazard ratios for stroke events remained substantially raised among infrequent shavers.
We interpreted these findings as probably being due to confounding by smoking and social factors, whereas Phillips suggests that smoking lies on a causal pathway between frequency of shaving and coronary heart disease, mediated by hyperestrogenemia, which may be caused by smoking or may be a cause of smoking. Which is the more plausible explanation?
In our data (3), shaving frequency was strongly socially patterneda factor overlooked by Phillips in his discussion of our findings. Men who shaved infrequently were less often married and much more often employed in manual occupations, both of which are strong risk factors for cardiovascular disease mortality. It seems likely, although we do not have relevant data, that infrequent shaving is also associated with a less healthy diet and with lower levels of physical activity. Consequently, we believe that confounding by both health behaviors and socioeconomic position plays a powerful role in explaining the observed associations, since, despite statistical adjustment, residual confounding by both unmeasured variables and poorly characterized confounders remains likely.
Do our data support either a hyperestrogenemic state or a hypotestosteronemic state as an explanation? Serum levels of these hormones and of cortisol were measured but were not related to shaving frequency. However, low frequency of sexual intercourse was associated with a low frequency of shaving, which might be interpreted as supportive evidence of hypotestosteronemia. It seems more likely that this simply reflected a lack of opportunity, given the unmarried status of many of the men who shaved infrequently. We did not have strong evidence of a role for sex hormones but would not want to exclude a role on the basis of our data.
Our observation of contrasting shaving associations between coronary heart disease and stroke suggests that confounding is not a complete explanation, as we stated in our conclusions (3). It seems plausible that the inconsistency of serum testosterone associations in Phillips et al.s epidemiologic studies (4, 5) and our own reflect variation in the balance of causal factors operating and the confounding structure of the different populations studied. We agree with Phillips that further work attempting to unravel the mechanisms by which sex hormones affect propensity toward vascular thrombosis is warranted. Using the principles of Mendelian randomization (6), studies of disease risk in men with genetic polymorphisms relevant to estrogen and testosterone levels may provide more reliable and unconfounded estimates of association.
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