Table 2 presents the baseline characteristics of men with and without prevalent CHD at study induction. As expected, men with CHD had less favourable characteristics. Thus, they were older, had higher cholesterol concentration and blood pressure, and poorer lung function than their disease‐free co‐workers. Men with CHD were also more likely to be physically inactive, smoke cigarettes, be without a partner, and to report having experienced unintentional weight loss in the preceding year, although differences according to CHD status were not substantial. They were also more likely to carry a morbid load other than CHD as evidenced by the increased prevalence of blood pressure lowering medication use and impaired glucose tolerance.
Table 2Baseline characteristics* of men with and without prevalent CHD at baseline
In table 3 we present the relation (age‐adjusted) of obesity and overweight with baseline characteristics in men with and without CHD. Men with obesity and overweight constituted 4.2% (n
711 men) and 41.5% (n
7048 men) of the analytical sample, respectively. In general, unfavourable levels of most characteristics were apparent in the higher weight categories in both men with and men without CHD at induction. The prevalence of morbidity of overweight and obese men—according to disease at entry, glucose intolerance, and diabetes—was generally raised in comparison with their normal weight colleagues. In comparison with the obese, leaner men were also younger, had lower plasma cholesterol concentration and blood pressure, were more active, and were less likely to be employed in a low grade job. By contrast, the prevalence of smokers was reduced in the overweight and obese groups.
Table 3Obesity and overweight in relation to baseline characteristics*
Table 4 shows the relations of obesity and overweight to five mortality end points in men with and without baseline CHD. A total of 10
845 men (64%) had died (8886 without baseline CHD; 1959 with baseline CHD) during a maximum of 35 years' follow up. After age‐adjustment in men with CHD, a modest raised risk in the overweight groups relative to the normal weight was apparent for all‐cause (hazard ratio 1.10, 95% CI 1.00 to 1.20), cardiovascular disease (1.27, 95% CI 1.13 to 1.43), and CHD mortality (1.28, 95% CI 1.11 to 1.47) but not for non‐cardiovascular disease (0.88, 95% CI 0.77 to 1.02) or stroke (1.01, 95% CI 0.73 to 1.40). The number of cases in the stroke analyses was low, however. In general, for men with CHD, the point estimates were similar in the obese and overweight groups. Hazard ratios for these outcomes were similar for men with obesity.
Table 4Mortality rates and hazard ratios (HRs) (95% confidence intervals) for selected mortality outcomes in relation to obesity and overweight in men with and without prevalent CHD at baseline in the original Whitehall study
In men with no evidence of baseline CHD, weight was positively associated with each outcome in an age‐adjusted analysis. The magnitude of these relations was typically higher than in analyses featuring men with baseline CHD. The raised risk was largely evident in obese men for all causes (hazard ratio for obese compared with normal weight: 1.53, 95% CI 1.39 to 1.69), stroke (1.64, 95% CI 1.17 to 2.28), and non‐cardiovascular disease (1.24, 95% CI 1.08 to 1.44), whereas for cardiovascular disease and CHD an incremental effect was suggested across the weight categories. On comparing gradients across mortality outcomes according to baseline CHD status, these differences did not reach significance at conventional levels in any of the analyses (p value for interaction
0.24). In both men with and men without CHD, with the exception of non‐cardiovascular disease, the relation of each end point with weight was partially attenuated after adjustment for covariates. In general, control for potential mediating variables (for example, systolic and diastolic blood pressures and plasma cholesterol) rather than potential confounding variables (for example, employment grade and physical activity) was responsible for this attenuation.
Our definition of CHD comprised both positive responses to items on the Rose questionnaire and ECG measurement. That the Rose questionnaire is self reported raises concerns about validity. We therefore examined the effect on our results, if any, of confining our analyses to men with only positive ECG findings. A similar pattern of association was seen to that apparent when the all inclusive definition was used. Given that some men in the normal weight group may have experienced weight loss because of existing medical conditions other than CHD, we first re‐computed our analyses after dropping deaths occurring within the first 10 years of mortality surveillance. In so doing we reasoned that men with serious illness would have died during this time frame. We hypothesised that this approach would have the effect of lowering the mortality in the normal weight group and therefore strengthen the overall positive relation between weight and mortality. In addition, we fitted interaction terms for the BMI categories with the logarithm of the follow up time, expecting the positive weight–mortality relation to increase in magnitude with follow up time. Both these hypotheses were supported in men with and without CHD at study induction, although the interaction terms were significant at conventional levels (p
0.05) only for the overweight category in men without baseline CHD for all cause and non‐cardiovascular disease mortality (data not shown).