Tall men have more reproductive success

An inverse association between height and risk of coronary heart disease (CHD) has been reported in several case-control and cohort studies, but the reasons for the association remain uncertain. We evaluated this association among 22,071 male physicians, a population homogeneous for high educational attainment and socioeconomic status in adulthood. The study population was comprised of participants in the Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of low-dose aspirin and beta-carotene in the primary prevention of cardiovascular disease and cancer among US male physicians, aged 40 to 84 years, in 1982. Participants were classified into five height categories at study entry, from shortest to tallest, and were followed an average of 60.2 months to determine the incidence of myocardial infarction (MI), stroke, and death from cardiovascular disease. Men in the tallest (> or = 73 in. or 185.4 cm) compared with the shortest (< or = 67 in. or 170.2 cm) height category had a 35% lower risk of MI (relative risk, 0.65; 95% confidence interval, 0.44 to 0.99; P = .04), after adjusting for known cardiovascular risk factors. Further, a marginally significant inverse trend (P trend = .05) across the height categories was observed. Although the relationship was not strictly linear, for every inch of added height, there was an approximate 2% to 3% decline in risk of MI. In contrast, men in the tallest compared with the shortest height category had only small and nonsignificant decreases in risk of stroke and cardiovascular death. While no significant trend in risks of these end points across the height categories was observed, the numbers of events for these end points were far less than for MI, and thus the confidence intervals were wide. These data indicate that height is inversely associated with subsequent risk of MI. At this time, a few mechanisms are plausible, but none are convincing. Other epidemiological and basic research efforts are needed to explore a variety of physiological correlates of height that may be responsible for mediating the height-MI association. In the meantime, while height is not modifiable, it is easy to measure and may be useful to evaluate CHD disease risk profiles and target lifestyle interventions.

Previous studies have demonstrated that short men are at increased risk of coronary heart disease (CHD). It has been suggested that the inverse relationship between adult height and CHD risk could be attributable to the fetal origins of CHD. The hypothesis that transmissible factors could partly explain the association has been tested in the European Atherosclerosis Research Studies (I and II), in which a sample of healthy university students (cases), drawn from 18 European countries (male: n = 721; female: n = 330), whose fathers had had a documented myocardial infarction before the age of 55 years were compared to age- and sex-matched controls (male: n = 1056; female: n = 638). Information about lifestyle and birthweight was collected and a fasting blood sample was obtained from each subject. In females there was no difference in height between cases and controls but male cases were shorter than controls, on average by one cm, both in the EARS I (P = 0.02) and the EARS II studies (P = 0.01) and this difference was independent of reported birthweight and the fathers' educational attainment. In logistic regression the relationship was independent of the subjects' apolipoprotein B level, the other major biological discriminator of case-control status. In men at least, height appears to be an independent transmissible risk factor for CHD.