Scientific evidence for the optimal number, timing, and size of meals is lacking. We investigated the relation between meal frequency and timing and changes in body mass index (BMI) in the Adventist Health Study 2 (AHS-2), a relatively healthy North American cohort. The analysis used data from 50,660 adult members aged ≥30 y of Seventh-day Adventist churches in the United States and Canada (mean ± SD follow-up: 7.42 ± 1.23 y). The number of meals per day, length of overnight fast, consumption of breakfast, and timing of the largest meal were exposure variables. The primary outcome was change in BMI per year. Linear regression analyses (stratified on baseline BMI) were adjusted for important demographic and lifestyle factors. Subjects who ate 1 or 2 meals/d had a reduction in BMI per year (in kg · m · y) (-0.035; 95% CI: -0.065, -0.004 and -0.029; 95% CI: -0.041, -0.017, respectively) compared with those who ate 3 meals/d. On the other hand, eating >3 meals/d (snacking) was associated with a relative increase in BMI ( < 0.001). Correspondingly, the BMI of subjects who had a long overnight fast (≥18 h) decreased compared with those who had a medium overnight fast (12-17 h) ( < 0.001). Breakfast eaters (-0.029; 95% CI: -0.047, -0.012; < 0.001) experienced a decreased BMI compared with breakfast skippers. Relative to subjects who ate their largest meal at dinner, those who consumed breakfast as the largest meal experienced a significant decrease in BMI (-0.038; 95% CI: -0.048, -0.028), and those who consumed a big lunch experienced a smaller but still significant decrease in BMI than did those who ate their largest meal at dinner. Our results suggest that in relatively healthy adults, eating less frequently, no snacking, consuming breakfast, and eating the largest meal in the morning may be effective methods for preventing long-term weight gain. Eating breakfast and lunch 5-6 h apart and making the overnight fast last 18-19 h may be a useful practical strategy.

Associations between the 'Meat' and 'Nuts & Seeds' protein factors and cardiovascular outcomes were strong and could not be ascribed to other associated nutrients considered to be important for cardiovascular health. Healthy diets can be advocated based on protein sources, preferring low contributions of protein from meat and higher intakes of plant protein from nuts and seeds.

Background Associations between soy, dairy intakes and breast cancer risk are inconsistent. No studies exist with large numbers of dairy consumers and soy consumers to assess mutual confounding. Methods The study cohort contains 52 795 North American women, initially free of cancer, followed for 7.9 years (29.7% were Black). Dietary intakes were estimated from food frequency questionnaires and, for 1011 calibration study subjects, from six structured 24-h dietary recalls. Incident invasive breast cancers were detected mainly by matching with cancer registries. Analyses used multivariable proportional hazards regression. Results The participants (mean age of 57.1 years) experienced 1057 new breast cancer cases during follow-up. No clear associations were found between soy products and breast cancer, independently of dairy. However, higher intakes of dairy calories and dairy milk were associated with hazard ratios (HRs) of 1.22 [95% confidence interval (CI): 1.05–1.40] and 1.50 (95% CI 1.22–1.84), respectively, comparing 90th to 10th percentiles of intakes. Full fat and reduced fat milks produced similar results. No important associations were noted with cheese and yogurt. Substituting median intakes of dairy milk users by those of soy milk consumers was associated with HR of 0.68 (95% CI: 0.55–0.85). Similar-sized associations were found among pre- and post-menopausal cases, with CIs also excluding the null in estrogen receptor (ER+, ER-), and progesterone receptor (PR+) cancers. Less biased calibrated measurement-error adjusted regressions demonstrated yet stronger, but less precise, HRs and CIs that still excluded the null. Conclusions Higher intakes of dairy milk were associated with greater risk of breast cancer, when adjusted for soy intake. Current guidelines for dairy milk consumption could be viewed with some caution.

Scope Phytosterols are bioactive compounds in plants with similar cholesterol-lowering properties as vegetarian diets. However, information on phytosterol intake and plasma plant sterols among vegetarians is sparse. Methods and results We examined dietary intake and plasma concentration of plant sterols and cholesterol across five dietary patterns in the Adventist Health Study-2 Calibration Sub-study (n=861, 66% females, average age 61 y). To measure intake and plasma concentration of these compounds, we used 24-hour dietary recalls and gas-liquid chromatography-flame ionization detection, respectively. Mean (SD) total phytosterol and cholesterol intake were 363 (176) mg/d and 131 (111) mg/d; plasma β-sitosterol, campesterol, and cholesterol were 3.3 (1.7) μg/mL, 4.2 (2.3) μg/mL, and 1.9 (0.4) mg/mL, respectively. Total phytosterol intake was lowest among non-vegetarians (263 mg/d) and highest among vegans (428 mg/d) (P < 0.0001). Cholesterol intake was lowest among vegans (15.2 mg/d) and highest among non-vegetarians (124.6 mg/d) (P < 0.0001). Plasma plant sterols and cholesterol did not differ by diet. Cholesterol-adjusted plasma β-sitosterol and campesterol were significantly higher in Blacks than Whites, though no ethnic differences were observed in dietary intake of these plant sterols. Conclusion Dietary intake but not plasma concentration of plant sterols and cholesterol varies across distinct plant-based diets.

Associations of low-to-moderate consumption of red and processed meat with mortality would add to the evidence of possible adverse effects of these common foods. This study aims to investigate the association of red and processed meat intake with mortality. The Adventist Health Study-2 (AHS-2) is a prospective cohort study of ~96,000 Seventh-day Adventist men and women recruited in the US and Canada between 2002 and 2007. The final analytic sample after exclusions was 72,149. Cox proportional hazards regression was used and hazard ratios (HR) and confidence intervals (CI) were obtained. Diet was assessed by a validated quantitative food frequency questionnaire (FFQ), calibrated using six 24-h dietary recalls. Mortality outcome data were obtained from the National Death Index. During a mean follow-up of 11.8 years, there were 7961 total deaths, of which 2598 were Cardiovascular diseases (CVD) deaths and 1873 were cancer deaths. Unprocessed red meat was associated with risk of all-cause mortality (HR: 1.18; 95% CI: 1.07–1.31) and CVD mortality (HR: 1.26; 95% CI: 1.05–1.50). Processed meat alone was not significantly associated with risk of mortality. The combined intake of red and processed meat was associated with all-cause mortality (HR: 1.23; 95% CI: 1.11–1.36) and CVD mortality (HR: 1.34; 95% CI: 1.12–1.60). These findings suggest moderately higher risks of all-cause and CVD mortality associated with red and processed meat in a low meat intake population.