In a recent article in the American Journal of Epidemiology by Mendez et al. (Am J Epidemiol. 2011;173(4):448-458), the use of alternative approaches to the exclusion of implausible energy intakes led to significantly different cross-sectional associations between diet and body mass index (BMI), whereas the use of a simpler recommended criteria (<500 and >3,500 kcal/day) yielded no meaningful change. However, these findings might have been due to exclusions made based on weight, a primary determinant of BMI. Using data from 52,110 women in the Nurses' Health Study (1990), we reproduced the cross-sectional findings of Mendez et al. and compared the results from the recommended method with those from 2 weight-dependent alternative methods (the Goldberg method and predicted total energy expenditure method). The same 3 exclusion criteria were then used to examine dietary variables prospectively in relation to change in BMI, which is not a direct function of attained weight. We found similar associations using the 3 methods. In a separate cross-sectional analysis using biomarkers of dietary factors, we found similar correlations for intakes of fatty acids (n = 439) and carotenoids and retinol (n = 1,293) using the 3 methods for exclusions. These results do not support the general conclusion that use of exclusion criteria based on the alternative methods might confer an advantage over the recommended exclusion method.

The relationship between various diet quality indices and risk of type 2 diabetes (T2D) remains unsettled. We compared associations of 4 diet quality indices--the Alternate Mediterranean Diet Index, Healthy Eating Index 2010, Alternate Healthy Eating Index 2010, and the Dietary Approaches to Stop Hypertension (DASH) Index--with reported T2D in the Women's Health Initiative, overall, by race/ethnicity, and with/without adjustment for overweight/obesity at enrollment (a potential mediator). This cohort (n = 101,504) included postmenopausal women without T2D who completed a baseline food frequency questionnaire from which the 4 diet quality index scores were derived. Higher scores on the indices indicated a better diet. Cox regression was used to estimate multivariate hazard ratios for T2D. Pearson coefficients for correlation among the indices ranged from 0.55 to 0.74. Follow-up took place from 1993 to 2013. During a median 15 years of follow-up, 10,815 incident cases of T2D occurred. For each diet quality index, a 1-standard-deviation higher score was associated with 10%-14% lower T2D risk (P < 0.001). Adjusting for overweight/obesity at enrollment attenuated but did not eliminate associations to 5%-10% lower risk per 1-standard-deviation higher score (P < 0.001). For all 4 dietary indices examined, higher scores were inversely associated with T2D overall and across racial/ethnic groups. Multiple forms of a healthful diet were inversely associated with T2D in these postmenopausal women.

OBJECTIVETo evaluate racial and ethnic differences in the association between a dietary diabetes risk reduction score and incidence of type 2 diabetes in U.S. white and minority women.RESEARCH DESIGN AND METHODSWe followed 156,030 non-Hispanic white (NHW), 2,026 Asian, 2,053 Hispanic, and 2,307 black women in the Nurses’ Health Study (NHS) (1980–2008) and NHS II (1991–2009). A time-updated dietary diabetes risk reduction score (range 8–32) was created by adding points corresponding with each quartile of intake of eight dietary factors (1 = highest risk; 4 = lowest risk). A higher score indicates a healthier overall diet.RESULTSWe documented 10,922 incident type 2 diabetes cases in NHW, 157 in Asian, 193 in Hispanic, and 307 in black women. Multivariable-adjusted pooled hazard ratio across two cohorts for a 10th–90th percentile range difference in dietary diabetes risk reduction score was 0.49 (95% CI 0.46, 0.52) for NHW, 0.53 (0.31, 0.92) for Asian, 0.45 (0.29, 0.70) for Hispanic, 0.68 (0.47, 0.98) for black, and 0.58 (0.46, 0.74) for overall minority women (P for interaction between minority race/ethnicity and dietary score = 0.08). The absolute risk difference (cases per 1,000 person-years) for the same contrast in dietary score was −5.3 (−7.8, −2.7) for NHW, −7.2 (−22.9, 8.4) for Asian, −11.6 (−26.7, 3.5) for Hispanic, −6.8 (−19.5, 5.9) for black, and −8.0 (−15.6, −0.5) for overall minority women (P for interaction = 0.04).CONCLUSIONSA higher dietary diabetes risk reduction score was inversely associated with risk of type 2 diabetes in all racial and ethnic groups, but the absolute risk difference was greater in minority women.

Introduction Data on omega-3 polyunsaturated fatty acids in relation to cardiovascular disease are limited in women. The aim of this study was to examine longitudinal relations of tuna and dark fish, alpha-linolenic acid, and marine omega-3 fatty acid intake with incident major cardiovascular disease in women. Methods This was a prospective cohort study of U.S. women participating in the Women’s Health Study from 1993 to 2014, during which the data were collected and analyzed. A total of 39,876 women who were aged ≥45 years and free of cardiovascular disease at baseline provided dietary data on food frequency questionnaires. Analyses used Cox proportional hazards models to evaluate the association between fish and energy-adjusted omega-3 polyunsaturated fatty acid intake and the risk of major cardiovascular disease, defined as a composite outcome of myocardial infarction, stroke, and cardiovascular death, in 38,392 women in the final analytic sample (96%). Results During 713,559 person years of follow-up, 1,941 cases of incident major cardiovascular disease were confirmed. Tuna and dark fish intake was not associated with the risk of incident major cardiovascular disease (p-trend >0.05). Neither alpha-linolenic acid nor marine omega-3 fatty acid intake was associated with major cardiovascular disease or with individual cardiovascular outcomes (all p-trend >0.05). There was no effect modification by age, BMI, or baseline history of hypertension. Conclusions In this cohort of women without prior history of cardiovascular disease, intakes of tuna and dark fish, alpha-linolenic acid, and marine omega-3 fatty acids were not associated with risk of major cardiovascular disease.

Objective Adjustment for body weight and physical activity has been suggested as an alternative to adjusting for reported energy intake in nutritional epidemiology. We examined which of these approaches would yield stronger correlations between nutrients and their biomarkers. Design A cross-sectional study in which dietary fatty acids, carotenoids, and retinol were adjusted for reported energy intake, and, separately, for weight and physical activity using the residual method. Correlations between adjusted nutrients and their biomarkers were examined. Setting US. Subjects Cases and controls from a nested case-control study of erythrocyte fatty acids and CHD (N=442), and of plasma carotenoids and retinol and breast cancer (N=1254). Results Correlations between intakes and plasma levels of trans fatty acid were 0.30 (energy-adjusted) and 0.16 (weight-and activity-adjusted); for erythrocyte levels, the corresponding correlations were 0.37 and 0.25. Energy-adjusted intakes of linoleic acid and alpha-linolenic acid (ALA) were more strongly correlated with their respective biomarkers than weight- and activity-adjusted intakes, but the differences were not significant except for linoleic acid (erythrocyte). Weight-and activity-adjusted DHA intake was slightly more strongly correlated with its plasma biomarker than energy-adjusted intake (0.37 vs 0.34). Neither method made a difference for DHA (erythrocyte), carotenoids, and retinol. Conclusion The effect of energy adjustment depends on the nutrient under investigation, and adjustment for energy calculated from the same questionnaire used to estimate nutrient intakes improves the correlation of some nutrients with their biomarkers appreciably. For the nutrients examined, adjustment using weight and physical activity had at most a small effect on these correlations.

In summary, these findings suggest that caffeinated coffee, decaffeinated coffee, and caffeine are not risk factors for hypertension in postmenopausal women.

Background Hyperinsulinemia and higher insulin-like growth factors may increase breast cancer risk. We evaluated a diabetes risk reduction diet (DRRD) and breast cancer risk. Objectives We prospectively evaluated the association between adherence to a DRRD and the incidence of breast cancer. Methods We followed 88,739 women from the Nurses’ Health Study (NHS; 1980–2016) and 93,915 women from the NHSII (1991–2017). Incident breast cancer cases (n = 11,943) were confirmed with medical records, and subtypes were determined by tissue microarray data and pathology reports. Information on diet and breast cancer risk factors was repeatedly ascertained in follow-up questionnaires. A DRRD score was derived with 9 factors: lower glycemic index of diet; lower intakes of trans fat, sugar-sweetened beverages/fruit juices, and red/processed meat; higher intakes of cereal fiber, coffee, nuts, and whole fruits; and a higher ratio of polyunsaturated to saturated fat (score range: 9–45). Multivariable-adjusted hazard ratios (MVHRs) and 95% CIs were calculated with Cox proportional hazards models. Results Being in the highest compared with the lowest DRRD adherence quintile was associated with a modestly lower breast cancer risk (MVHRQ5vsQ1: 0.89; 95% CI: 0.84, 0.95; P-trend = 0.0002); this was attenuated after adjusting for weight change since age 18 y (MVHRQ5vsQ1: 0.92; 95% CI: 0.87, 0.98; P-trend = 0.01). The inverse association was strongest among women with current BMI &lt; 25 kg/m2 (MVHRQ5vsQ1: 0.89; 95% CI: 0.81, 0.98; P-trend = 0.004; P-interaction = 0.04). Among tumor molecular subtypes, the strongest inverse association was observed with basal-type tumors (MVHRQ5vsQ1: 0.67; 95% CI: 0.45, 1.01; P-trend = 0.04). Conclusions Greater DRRD-adherence was associated with lower breast cancer risk, likely mediated by less weight gain with a DRRD; however, independently of weight change, DRRD-adherence was modestly associated with lower breast cancer risk, particularly among lean women.

Background Insulin resistance has been proposed as a mediator of the increased cancer incidence and mortality associated with obesity. However, prior studies included limited cancer deaths and had inconsistent findings. Therefore, we evaluated insulin resistance and cancer-specific and all-cause mortality in postmenopausal women participating in the Women’s Health Initiative (WHI). Methods Eligible were a subsample of 22 837 WHI participants aged 50–79 years enrolled at 40 US clinical centers from 1993 to 1998 who had baseline fasting glucose and insulin levels. Baseline insulin resistance was measured by the homeostasis model assessment of insulin resistance (HOMA-IR). Cancers were verified by central medical record review and deaths verified by medical record and death certificate review enhanced by National Death Index queries. Cox proportional hazards regression models were used to calculate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for cancer-specific and all-cause mortality. All statistical tests were two-sided. Results During a median of 18.9 years of follow-up, 1820 cancer deaths and 7415 total deaths occurred. Higher HOMA-IR quartile was associated with higher cancer-specific mortality (Q4 vs Q1, HR = 1.26, 95% CI = 1.09 to 1.47; Ptrend = .003) and all-cause mortality (Q4 vs Q1, HR = 1.63, 95% CI = 1.51 to 1.76; Ptrend &lt; .001). A sensitivity analysis for diabetes status did not change findings. Among women with body mass index less than 25 kg/m2, higher HOMA-IR quartile was associated with higher cancer mortality (Fine and Gray, P = .004). Conclusions High insulin resistance, as measured by HOMA-IR, identifies postmenopausal women at higher risk for cancer-specific and all-cause mortality who could potentially benefit from early intervention.