Gluten intake and risk of type 2 diabetes in three large prospective cohort studies of US men and women.

AIMS/HYPOTHESIS: We investigated the association between gluten intake and long-term type 2 diabetes risk among Americans. METHODS: We followed women from the Nurses' Health Study (NHS, n = 71,602, 1984-2012) and NHS II (n = 88,604, 1991-2013) and men from the Health Professionals Follow-Up Study (HPFS, n = 41,908, 1986-2012). Gluten intake was estimated using a validated food frequency questionnaire every 2-4 years. Incident type 2 diabetes was defined as self-reported physician-diagnosed diabetes confirmed using a supplementary questionnaire. RESULT: Gluten intake was strongly correlated with intakes of carbohydrate components, especially refined grains, starch and cereal fibre (Spearman correlation coefficients >0.6). During 4.24 million years of follow-up, 15,947 people were confirmed to have type 2 diabetes. After multivariate adjustment, pooled HRs and 95% CIs for type 2 diabetes, from low to high gluten quintiles, were (ptrend < 0.001): 1 (reference); 0.89 (0.85, 0.93); 0.84 (0.80, 0.88); 0.78 (0.74, 0.82) and 0.80 (0.76, 0.84). The association was slightly weakened after further adjusting for cereal fibre, with pooled HRs (95% CIs) of (ptrend < 0.001): 1 (reference); 0.91 (0.87, 0.96); 0.88 (0.83, 0.93); 0.83 (0.78, 0.88) and 0.87 (0.81, 0.93). Dose-response analysis supported a largely linear inverse relationship between gluten intake up to 12 g/day and type 2 diabetes. The association between gluten intake and type 2 diabetes was stronger when intake of added bran was also higher (pinteraction = 0.02). CONCLUSIONS/INTERPRETATION: Gluten intake is inversely associated with type 2 diabetes risk among largely healthy US men and women. Limiting gluten in the diet is associated with lower intake of cereal fibre and possibly other beneficial nutrients that contribute to good health.

Monounsaturated fats from plant and animal sources in relation to risk of coronary heart disease among US men and women.

Background: Monounsaturated fatty acids (MUFAs) improve blood lipid profiles in intervention studies, but prospective evidence with regard to MUFA intake and coronary heart disease (CHD) risk is limited and controversial. Objective: We investigated the associations of cis MUFA intake from plant (MUFA-P) and animal (MUFA-A) sources with CHD risk separately among 63,442 women from the Nurses' Health Study (1990-2012) and 29,942 men from the Health Professionals Follow-Up Study (1990-2012). Design: Intakes of MUFA-Ps and MUFA-As were calculated by using validated food-frequency questionnaires collected every 4 y. Incident nonfatal myocardial infarction and fatal CHD cases (n = 4419) were confirmed by medical record review. Results: During follow-up, MUFA-Ps and MUFA-As contributed 5.8-7.9% and 4.2-5.4% of energy on average, respectively. When MUFA-Ps were modeled to isocalorically replace other macronutrients, HRs (95% CIs) of CHD were 0.83 (0.68, 1.00) for saturated fatty acids (SFAs; 5% of energy), 0.86 (0.76, 0.97) for refined carbohydrates (5% of energy), and 0.80 (0.70, 0.91) for trans fats (2% of energy) (P = 0.05, 0.01, and 0.001, respectively). For MUFA-As, corresponding HRs (95% CIs) for the same isocaloric substitutions were 1.04 (0.79, 1.38) for SFAs, 1.11 (0.91, 1.35) for refined carbohydrates, and 0.88 (0.77, 1.01) for trans fats (P = 0.76, 0.31, and 0.08, respectively). Given the common food sources of SFAs and MUFA-As (Spearman correlation coefficients of 0.81-0.83 between these groups of fatty acids), we further estimated CHD risk when the sum of MUFA-As and SFAs (5% of energy) was replaced by MUFA-Ps, and found that the HR was 0.81 (95% CI: 0.73, 0.90; P < 0.001) for this replacement. Conclusions: The largely different associations of MUFA-Ps and MUFA-As with CHD risk suggest that plant-based foods are the preferable sources of MUFAs for CHD prevention. These findings are observational and warrant confirmation in intervention settings. This study was registered at clinicaltrials.gov as NCT00005152 and NCT00005182.

Long term gluten consumption in adults without celiac disease and risk of coronary heart disease: prospective cohort study.

Objective To examine the association of long term intake of gluten with the development of incident coronary heart disease.Design Prospective cohort study.Setting and participants 64 714 women in the Nurses' Health Study and 45 303 men in the Health Professionals Follow-up Study without a history of coronary heart disease who completed a 131 item semiquantitative food frequency questionnaire in 1986 that was updated every four years through 2010.Exposure Consumption of gluten, estimated from food frequency questionnaires.Main outcome measure Development of coronary heart disease (fatal or non-fatal myocardial infarction).Results During 26 years of follow-up encompassing 2 273 931 person years, 2431 women and 4098 men developed coronary heart disease. Compared with participants in the lowest fifth of gluten intake, who had a coronary heart disease incidence rate of 352 per 100 000 person years, those in the highest fifth had a rate of 277 events per 100 000 person years, leading to an unadjusted rate difference of 75 (95% confidence interval 51 to 98) fewer cases of coronary heart disease per 100 000 person years. After adjustment for known risk factors, participants in the highest fifth of estimated gluten intake had a multivariable hazard ratio for coronary heart disease of 0.95 (95% confidence interval 0.88 to 1.02; P for trend=0.29). After additional adjustment for intake of whole grains (leaving the remaining variance of gluten corresponding to refined grains), the multivariate hazard ratio was 1.00 (0.92 to 1.09; P for trend=0.77). In contrast, after additional adjustment for intake of refined grains (leaving the variance of gluten intake correlating with whole grain intake), estimated gluten consumption was associated with a lower risk of coronary heart disease (multivariate hazard ratio 0.85, 0.77 to 0.93; P for trend=0.002).Conclusion Long term dietary intake of gluten was not associated with risk of coronary heart disease. However, the avoidance of gluten may result in reduced consumption of beneficial whole grains, which may affect cardiovascular risk. The promotion of gluten-free diets among people without celiac disease should not be encouraged.

The association between betaine and choline intakes and the plasma concentrations of homocysteine in women.

BACKGROUND: Elevated total homocysteine (tHcy), a risk factor for many chronic diseases, can be remethylated to methionine by folate. Alternatively, tHcy can be metabolized by other 1-carbon nutrients, ie, betaine and its precursor, choline. OBJECTIVE: We aimed to assess the association between the dietary intakes of betaine and choline and the concentration of tHcy. DESIGN: We conducted a cross-sectional analysis in 1477 women by using linear regression models to predict mean fasting tHcy by intakes of of betaine and choline. RESULTS: tHcy was 8% lower in the highest quintile of total betaine + choline intake than in the lowest quintile, even after control for folate intake (P for trend = 0.07). Neither choline nor betaine intake individually was significantly associated with tHcy. Choline from 2 choline-containing compounds, glycerophosphocholine and phosphocholine, was inversely associated with tHcy. These inverse associations were more pronounced in women with folate intake < 400 mug/d than in those with intakes >or=400 microg/d (P for interaction = 0.03 for phosphocholine) and in moderate alcohol drinkers (>or=15 g/d) than in nondrinkers or light drinkers (<15 g/d) (P for interaction = 0.02 for glycerophosphocholine and 0.04 for phosphocholine). The strongest dose response was seen in women with a low-methyl diet (high alcohol and low folate intake) (P for interaction = 0.002 for glycerophosphocholine and 0.001 for phosphocholine). CONCLUSIONS: Total choline + betaine intake was inversely associated with tHcy, as was choline from 2 water-soluble choline-containing compounds. Remethylation of tHcy may be more dependent on the betaine pathway when methyl sources are low as a result of either inadequate folate intake or heavier alcohol consumption.