Physical activity and body mass index (calculated as weight in kilograms divided by height in meters squared) independently alter the risk of coronary heart disease (CHD); however, their combined effect on CHD is not established. Our objective was to study the combined association of physical activity and body mass index on CHD.
Methods
Prospective cohort study of 38 987 women free of cardiovascular disease, cancer, and diabetes at baseline in the Women's Health Study, with 10.9 mean years of follow-up. Weight, height, and recreational activities were reported on entry. Body mass index was categorized as normal weight (<25), overweight (25 to <30), and obese (≥30). Active was defined as 1000 kilocalories or more expended on recreational activities weekly. Six joint body weight–physical activity categories were defined. The main outcome measure was the occurrence of incident CHD during follow-up, defined as a cardiovascular event including nonfatal myocardial infarction, coronary artery bypass graft, percutaneous transluminal coronary angioplasty, or CHD death.
Results
A total of 948 cases of incident CHD occurred during follow-up. Higher body mass index and physical inactivity were individual predictors of CHD. In joint analyses, compared with active normal-weight individuals, the multivariate-adjusted hazard ratios (95% confidence intervals) were 1.54 (1.14-2.08) for overweight-active; 1.87 (1.29-2.71) for obese-active; 1.08 (0.84-1.39) for normal weight–inactive; 1.88 (1.46-2.42) for overweight-inactive; and 2.53 (1.94-3.30) for obese-inactive. Increasing levels of walking also resulted in significant reductions in CHD risk for overweight and obese individuals.
Conclusions
The risk of CHD associated with elevated body mass index is considerably reduced by increased physical activity levels. However, the risk is not completely eliminated, reinforcing the importance of being lean and physically active.
Background: Earlier age at menopause is associated with higher risk for cardiovascular disease, and hormonal changes are suspected to be involved. Earlier age at menarche is associated with higher risk of type 2 diabetes, but its association with CVD has been inconclusive. We investigated the association of the duration of reproductive lifespan, accounting for both age at menarche and menopause, with incident CVD. Methods: We prospectively followed 83,169 Nurses’ Health Study participants without CVD at baseline, the year of reported menopause, through 2010. CVD was defined as coronary heart disease (CHD; nonfatal myocardial infarction or fatal) and stroke (nonfatal or fatal). The duration of reproductive lifespan was generated by subtracting age at menarche from age at menopause. The relative risks were estimated using Cox proportional hazard regression with adjustment for potential confounders. Results: The median reproductive lifespan was 36 years (IQR 31-39). A shorter reproductive lifespan was associated with higher risk of incident CVD with multivariable adjustment for demographic, reproductive, and lifestyle factors, as well as prevalent and incident diabetes, hypertension, and hypercholesterolemia (RR 1.30 [95% CI 1.20-1.41] comparing duration Conclusion: A shorter duration of reproductive lifespan is associated with higher risk of CVD.
Abstract The Women's Health Initiative (WHI) postmenopausal hormone therapy (HT) trials were designed to determine the balance of benefits and risks of HT taken for chronic disease prevention by initially healthy postmenopausal women (age range, 50—79 years; mean age, 63 years). Women with an intact uterus were randomized to estrogen–progestin or placebo for a mean of 5.6 years; women with hysterectomy were randomized to estrogen alone or placebo for a mean of 7.1 years. Compared with their respective placebo‐group counterparts, women in the estrogen–progestin group were significantly more likely to experience an adverse health event, whereas women in the estrogen‐alone group were as likely to do so. Specifically, estrogen–progestin was associated with increased risks of coronary heart disease (CHD), stroke, venous thromboembolism, and breast cancer, as well as reduced risks of hip fracture and colorectal cancer. Estrogen alone was associated with an increased risk of stroke and a reduced risk of hip fracture; it had no effect on CHD risk. The results do not support the use of HT for chronic disease prevention in postmenopausal women as a whole. However, because few WHI participants were within 5 years of menopause, these trials cannot conclusively determine the risk–benefit balance of HT in recently menopausal women. Accumulating data suggest that the timing of HT initiation in relation to age or menopause onset may critically influence the relationship between such therapy and risk of CHD as well as its overall risk–benefit balance, with younger or recently menopausal women experiencing more favorable effects than older women or women further from menopause.
Abstract For primary prevention, low-dose aspirin should be considered in women aged 40 to 70 years with a 10-year cardiovascular risk of 20% or more or in women with diabetes and a 10-year cardiovascular risk of 10% or more. The risk of bleeding outweighs the benefits in low-risk women and in women aged 70 years and older.
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Chronic kidney disease (CKD) is a common complication of type 2 diabetes that can lead to end-stage kidney disease and is associated with high cardiovascular risk. Few treatments are available to prevent CKD in type 2 diabetes.To test whether supplementation with vitamin D3 or omega-3 fatty acids prevents development or progression of CKD in type 2 diabetes.Randomized clinical trial with a 2 × 2 factorial design conducted among 1312 adults with type 2 diabetes recruited between November 2011 and March 2014 from all 50 US states as an ancillary study to the Vitamin D and Omega-3 Trial (VITAL), coordinated by a single center in Massachusetts. Follow-up was completed in December 2017.Participants were randomized to receive vitamin D3 (2000 IU/d) and omega-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid; 1 g/d) (n = 370), vitamin D3 and placebo (n = 333), placebo and omega-3 fatty acids (n = 289), or 2 placebos (n = 320) for 5 years.The primary outcome was change in glomerular filtration rate estimated from serum creatinine and cystatin C (eGFR) from baseline to year 5.Among 1312 participants randomized (mean age, 67.6 years; 46% women; 31% of racial or ethnic minority), 934 (71%) completed the study. Baseline mean eGFR was 85.8 (SD, 22.1) mL/min/1.73 m2. Mean change in eGFR from baseline to year 5 was -12.3 (95% CI, -13.4 to -11.2) mL/min/1.73 m2 with vitamin D3 vs -13.1 (95% CI, -14.2 to -11.9) mL/min/1.73 m2 with placebo (difference, 0.9 [95% CI, -0.7 to 2.5] mL/min/1.73 m2). Mean change in eGFR was -12.2 (95% CI, -13.3 to -11.1) mL/min/1.73 m2 with omega-3 fatty acids vs -13.1 (95% CI, -14.2 to -12.0) mL/min/1.73 m2 with placebo (difference, 0.9 [95% CI, -0.7 to 2.6] mL/min/1.73 m2). There was no significant interaction between the 2 interventions. Kidney stones occurred among 58 participants (n = 32 receiving vitamin D3 and n = 26 receiving placebo) and gastrointestinal bleeding among 45 (n = 28 receiving omega-3 fatty acids and n = 17 receiving placebo).Among adults with type 2 diabetes, supplementation with vitamin D3 or omega-3 fatty acids, compared with placebo, resulted in no significant difference in change in eGFR at 5 years. The findings do not support the use of vitamin D or omega-3 fatty acid supplementation for preserving kidney function in patients with type 2 diabetes.ClinicalTrials.gov Identifier: NCT01684722.
Abstract Background: Observational studies and randomized trials have supported a potential role of sex hormones in colorectal cancer development in both men and women. However, data on the relationship between endogenous sex hormone levels and colorectal cancer are very limited. Methods: We prospectively evaluated plasma levels of estrone, estradiol, and testosterone in relation to colorectal cancer risk in men and postmenopausal women not using hormone therapy from four large female and male study cohorts including the Nurses’ Health Study, Women's Health Study, Health Professional Follow-Up Study, and Physicians’ Health Study II. A total of 293 female and 438 male cases along with 437 female and 719 male controls were included in the present analysis. Unconditional logistic regression controlling for matching, risk factors, and plasma c-peptide was used to estimate relative risks (RRs) and 95% confidence intervals (CIs). All statistical tests were two sided. Results: Total testosterone, sex hormone binding globulin (SHBG), and the ratio of estradiol over testosterone were associated with colorectal cancer in men after adjustment for all confounding factors including body mass index (BMI) and c-peptide levels; the RRs (95% CI) in the highest relative to the lowest quartile were 0.62 (0.40-0.96) for testosterone, 0.65 (0.42-0.99) for SHBG, and 2.63 (1.58-4.36) for the ratio (p-values for trend ≤0.02). In addition, no effect modification by BMI in men was found on the association between sex steroids and colorectal cancer (p-values for interaction ≥0.46). In women, a higher ratio of estradiol to testosterone, reflecting higher aromatase activity and likely increased estradiol production, was associated with lower colorectal cancer risk after adjustment for all factors (RR=0.43, 95% CI=0.22-0.84, p-value for trend=0.03). Specifically, the inverse association between the ratio and colorectal cancer risk was seen only among normal weight women (p-value for interaction=0.07); the multivariate RRs in the higher quartile groups were 0.26-0.72 (p-value for tend=0.03). Conversely, there was no association between the ratio and colorectal cancer in overweight and obese women (RRs=1.15-1.2, p-value for trend=0.89). Stratifying analysis by BMI for other sex steroids did not significantly change the overall association (p-values for interaction ≥0.25). Conclusion: Our data offers the first observational evidence supporting an inverse association of circulating testosterone and SHBG with colorectal cancer in men. Conversely, normal weight women with a higher ratio of estradiol over testosterone may be at a lower risk for colorectal cancer. Validation of our results in other studies will help elucidate the effects attributable to sex steroids on colorectal cancer and refine risk profiles of colorectal cancer development in both men and women. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-338. doi:1538-7445.AM2012-LB-338
