Association of circulating vitamin D and omega 3 fatty acid with all-cause mortality in patients with rheumatoid arthritis: A large population-based cohort study.

OBJECTIVES: To assess the associations of both the level of circulating vitamin D and the ratio of omega-3 fatty acids to total fatty acids (omega-3 %) with mortality among participants with rheumatoid arthritis. STUDY DESIGN: This study included 4,293 and 1,157 adults with rheumatoid arthritis identified by self-report from the UK Biobank for the analysis of vitamin D and omega-3 %, respectively. MAIN OUTCOME MEASURES: Death outcomes were obtained from the National Health Service Information Centre (England and Wales) and the National Health Service Central Register Scotland (Scotland). Cox proportional hazards models were used to estimate hazard ratios and 95 % confidence intervals for mortality. RESULTS: The medians (25th-75th percentiles) of serum 25(OH)D and omega-3 % were 45.8 (31.4-62.9) nmol/L and 4.1 % (3.3 %-5.1 %), respectively. During 52,612 person-years of follow-up in the 25(OH)D group, 502 all-cause deaths occurred; and during 14,192 person-years of follow-up in the omega-3 % group, 122 all-cause deaths occurred. Rheumatoid arthritis patients with vitamin D levels of at least 20 nmol/L had an approximately 40-50 % lower risk of all-cause mortality than those with severe vitamin D deficiency (hazard ratio ranging from 0.51 to 0.62, all P values < 0.05). Each unit increase in natural log-transformed 25(OH)D was associated with a 22 % reduction in the risk of all-cause mortality, and a U-shaped association between serum 25(OH)D and all-cause mortality was found. However, the association between omega-3 % and mortality was not significant. CONCLUSIONS: Lower serum 25(OH)D concentration, but not omega-3 %, was significantly associated with higher all-cause mortality in patients with rheumatoid arthritis. Optimizing serum vitamin D levels may be an important factor in reducing mortality risk in this population.

Dietary phytoestrogens and total and cause-specific mortality: results from 2 prospective cohort studies.

BACKGROUND: Evidence regarding dietary phytoestrogens in relation to mortality remains limited. OBJECTIVES: The objective of the study is to examine the associations of intake of isoflavones, lignans, and coumarins with total and cause-specific mortality in US males and females. METHODS: We followed 75,981 females in the Nurses' Health Study (1984-2018) and 44,001 males in the Health Professionals Follow-up Study (1986-2018), who were free of cardiovascular disease (CVD), diabetes, or cancer at baseline. Their diet was repeatedly assessed using validated food frequency questionnaires every 2-4 y. Associations with mortality were assessed using time-dependent Cox models with adjustments for demographics, dietary and lifestyle factors, and medical history. RESULTS: During 3,427,156 person-years of follow-up, we documented 50,734 deaths, including 12,492 CVD deaths, 13,726 cancer deaths, and 24,516 other non-CVD and noncancer deaths. After multivariable adjustment, the higher total phytoestrogen intake was associated with lower risk of total CVD and other non-CVD and noncancer mortality: comparing extreme quintiles, the pooled HRs (95% CIs) were 0.89 (0.87, 0.92), 0.90 (0.85, 0.96), and 0.86 (0.82, 0.90), respectively. We did not find a significant association with cancer mortality [0.97 (0.92, 1.03)]. For individual phytoestrogens in relation to total mortality, the pooled HRs (95% CIs) comparing extreme quintiles were 0.90 (0.87, 0.92) for isoflavones, 0.93 (0.90, 0.96) for lignans, and 0.93 (0.90, 0.95) for coumarins. Individual phytoestrogens were also significantly associated with lower risk of CVD mortality and other types of mortality. Primary food sources of phytoestrogens, including tofu, soy milk, whole grains, tea, and flaxseed, were also inversely associated with total mortality. CONCLUSIONS: A higher intake of total phytoestrogens, including isoflavones, lignans, and coumarins, and foods rich in these compounds was associated with lower risk of total and certain cause-specific mortality in generally healthy US adults. These data suggest that these phytochemicals and their dietary sources may be integrated into an overall healthy diet to achieve a longer life span.

Habitual coffee consumption and subsequent risk of type 2 diabetes in individuals with a history of gestational diabetes - a prospective study.

BACKGROUND: Females with a history of gestational diabetes mellitus (GDM) are at higher risk of developing type 2 diabetes mellitus (T2D) later in life. OBJECTIVE: This study prospectively examined whether greater habitual coffee consumption was related to a lower risk of T2D among females with a history of GDM. METHODS: We followed 4522 participants with a history of GDM in the NHS II for incident T2D between 1991 and 2017. Demographic, lifestyle factors including diet, and disease outcomes were updated every 2-4 y. Participants reported consumption of caffeinated and decaffeinated coffee on validated FFQs. Fasting blood samples were collected in 2012-2014 from a subset of participants free of diabetes to measure glucose metabolism biomarkers (HbA1c, insulin, C-peptide; n = 518). We used multivariable Cox regression models to calculate adjusted HRs and 95% CIs for the risk of T2D. We estimated the least squares mean of glucose metabolic biomarkers according to coffee consumption. RESULTS: A total of 979 participants developed T2D. Caffeinated coffee consumption was inversely associated with the risk of T2D. Adjusted HR (95% CI) for ≤1 (nonzero), 2-3, and 4+ cups/d compared with 0 cup/d (reference) was 0.91 (0.78, 1.06), 0.83 (0.69, 1.01), and 0.46 (0.28, 0.76), respectively (P-trend = 0.004). Replacement of 1 serving/d of sugar-sweetened beverage and artificially sweetened beverage with 1 cup/d of caffeinated coffee was associated with a 17% (risk ratio [RR] = 0.83, 95% CI: 0.75, 0.93) and 9% (RR = 0.91, 95% CI: 0.84, 0.99) lower risk of T2D, respectively. Greater caffeinated coffee consumption was associated with lower fasting insulin and C-peptide concentrations (all P-trend <0.05). Decaffeinated coffee intake was not significantly related to T2D but was inversely associated with C-peptide concentrations (P-trend = 0.003). CONCLUSIONS: Among predominantly Caucasian females with a history of GDM, greater consumption of caffeinated coffee was associated with a lower risk of T2D and a more favorable metabolic profile.