BACKGROUND A high body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) is associated with increased mortality from cardiovascular disease and certain cancers, but the precise relationship between BMI and all-cause mortality remains uncertain. METHODS We used Cox regression to estimate hazard ratios and 95% confidence intervals for an association between BMI and all-cause mortality, adjusting for age, study, physical activity, alcohol consumption, education, and marital status in pooled data from 19 prospective studies encompassing 1.46 million white adults, 19 to 84 years of age (median, 58). RESULTS The median baseline BMI was 26.2. During a median follow-up period of 10 years (range, 5 to 28), 160,087 deaths were identified. Among healthy participants who never smoked, there was a J-shaped relationship between BMI and all-cause mortality. With a BMI of 22.5 to 24.9 as the reference category, hazard ratios among women were 1.47 (95 percent confidence interval [CI], 1.33 to 1.62) for a BMI of 15.0 to 18.4; 1.14 (95% CI, 1.07 to 1.22) for a BMI of 18.5 to 19.9; 1.00 (95% CI, 0.96 to 1.04) for a BMI of 20.0 to 22.4; 1.13 (95% CI, 1.09 to 1.17) for a BMI of 25.0 to 29.9; 1.44 (95% CI, 1.38 to 1.50) for a BMI of 30.0 to 34.9; 1.88 (95% CI, 1.77 to 2.00) for a BMI of 35.0 to 39.9; and 2.51 (95% CI, 2.30 to 2.73) for a BMI of 40.0 to 49.9. In general, the hazard ratios for the men were similar. Hazard ratios for a BMI below 20.0 were attenuated with longer-term follow-up. CONCLUSIONS In white adults, overweight and obesity (and possibly underweight) are associated with increased all-cause mortality. All-cause mortality is generally lowest with a BMI of 20.0 to 24.9.

OBJECTIVETo examine whether day napping or short night sleeping is associated with higher risk of diabetes.RESEARCH DESIGN AND METHODSThis was a prospective study of hours of day napping and night sleeping assessed in 1996–1997 in relation to diabetes diagnosed between 2000 and 2006 (n = 10,143) among 174,542 participants in the National Institutes of Health (NIH)-AARP Diet and Health Study. Odds ratios (ORs) and 95% CI were derived from multivariate logistic regression models.RESULTSLonger day napping was associated with a higher risk of diabetes. After adjustment for potential confounders, ORs were 1.23 (95% CI 1.18–1.29) for those reporting <1 h and 1.55 (95% CI 1.45–1.66) for those reporting ≥1 h of napping compared with individuals who did not nap (Ptrend < 0.0001). For night sleeping, with 7–8 h as the referent, the OR was 1.46 (95% CI 1.31–1.63) for <5 h, 1.11 (1.06–1.16) for 5–6 h, and 1.11 (0.99–1.24) for ≥9 h. In both analyses, additional adjustment for BMI only modestly attenuated the associations. Further analysis showed a statistically significant interaction between hours of napping and sleeping on diabetes (Pinteraction < 0.0001). Among participants with no napping, only short night sleeping was associated with higher occurrence of diabetes, whereas among those with ≥1 h of napping, both long and short sleeping was associated with higher risk.CONCLUSIONSDay napping and short night sleeping are associated with higher risk of diabetes. The association between sleep duration and diabetes may be modified by napping habit.

Increased body size and lack of physical activity are associated with increased risk of several cancers, but the relations of body mass index (BMI) and physical activity to bladder cancer are poorly understood. We investigated the associations between BMI, physical activity, and bladder cancer in the NIH-AARP Diet and Health Study, a prospective cohort of 471,760 U.S. men and women, followed from 1995 to 2003. During 3,404,642 person-years of follow-up, we documented 1,719 incident cases of bladder cancer. Compared with normal weight, obesity was associated with an up to 28% increased risk for bladder cancer. The multivariate relative risks of bladder cancer for BMI values of 18.5 to 24.9 (reference), 25.0 to 29.9, 30.0 to 34.9, and z35 kg/m 2 were 1.0, 1.15, 1.22, and 1.28 (95% confidence interval, 1.02-1.61; P trend = 0.028).The association between BMI and bladder cancer was consistent among subgroups defined by gender, education, smoking status, and other potential effect modifiers. In contrast, physical activity showed no statistically significant relation with bladder cancer. After multivariate adjustment, including BMI, the relative risks of bladder cancer for increasing frequency of physical activity [0 (reference), <1, 1-2, 3-4, and z5 times a week] were 1.0, 0.85, 0.89, 0.91, and 0.87 (95% confidence interval, 0.74-1.02; P trend = 0.358), respectively. In conclusion, these findings provide support for a modest adverse effect of adiposity on risk for bladder cancer. In contrast, our results do not suggest a relation between physical activity and bladder cancer.

Background Epidemiologic data on the combined influence of several lifestyle factors on diabetes risk are rare, particularly among older adults. Objective Examine how combinations of lifestyle risk factors relate to the 11-year risk of incident diabetes. Design Population-based prospective cohort study. Setting National Institutes of Health (NIH)-AARP Diet and Health Study. Participants 114996 men and 92483 women aged 50–71 in 1995–1996 without evidence of heart disease, cancer, or diabetes. Measurements A comprehensive survey of demographic characteristics and lifestyle factors, including dietary intake, body weight and height, physical activity, smoking, and alcohol at baseline (1995–1996). Low-risk groups were formed by dichotomizing each lifestyle factor. Incident self-reported physician-diagnosed diabetes was identified with a follow-up survey in 2004–2006. Results There were 11031 (9.6%) men and 6969 (7.5%) women who developed new-onset diabetes. The odds for diabetes were 31% (odds ratio (OR): 0.69; 95% confidence interval (CI): 0.68, 0.71) lower for each 1 additional lifestyle factor in the low-risk group among men and 39% (OR: 0.61; 95% CI: 0.60, 0.63) lower among women. Men and women with a diet score, physical activity level, smoking status, and alcohol use all in the low-risk group had ORs for diabetes of 0.61 (95% CI: 0.56, 0.66) and 0.43 (95% CI: 0.34, 0.55), respectively. When absence of overweight or obesity was added, ORs for diabetes were 0.28 (95% CI: 0.23, 0.34) and 0.16 (95% CI: 0.10, 0.24) for men and women, respectively. Results did not differ by family history of diabetes and level of adiposity. Limitation The study was observational with potential for residual confounding. Conclusions Lifestyle factors, when considered in combination, are associated with a substantial reduction in risk for diabetes.

Convincing epidemiologic evidence links excess body mass to increased risks of endometrial and postmenopausal breast cancers but the relation of body mass index (BMI) to ovarian cancer risk remains inconclusive. Potential similarities regarding a hormonal mechanism in the etiology of female cancers highlight the importance of investigating associations according to menopausal hormone therapy (MHT) use. However, data addressing whether the relation of BMI to ovarian cancer differs by MHT use are very sparse. We prospectively investigated the association between BMI and ovarian cancer among 94,525 U.S. women, followed from 1996–1997 to December 31, 2003. During 7 years of follow-up, we documented 303 epithelial ovarian cancer cases. As compared with normal weight women (BMI 18.5–24.9 kg/m2), the multivariate relative risk (MVRR) of ovarian cancer for obese women (BMI ≥30 kg/m2) in the cohort as a whole was 1.25 (95%-CI=0.93–1.68). Among women who never used MHT, the MVRR for obese versus normal weight women was 1.80 (95%-CI=1.16–2.80). In contrast, no relation between BMI and ovarian cancer was apparent among women who ever used MHT (MVRR=0.96; 95%-CI=0.64–1.43; P-interaction=0.02). Exploratory analyses also suggested a positive association between BMI and ovarian cancer among women without a family history of ovarian cancer (MVRR comparing obese versus normal weight women=1.36; 95%-CI=0.99–1.85), but no relation with BMI was apparent among women with a positive family history of ovarian cancer (MVRR=0.73; 95%-CI=0.34–1.60; P-interaction=0.02). We suspect that obesity is associated with enhanced ovarian cancer risk through a hormonal mechanism.