The present study elucidates the association of intrinsic sugars and free sugars (FS) from all relevant sources with all-cause mortality in the prospective UK Biobank cohort. Sugar intake was assessed in 186,811 UK Biobank participants who completed at least one web-based 24-h dietary recall (Oxford WebQ). Cox proportional hazard regression models for all-cause mortality were used with sugar intake from different sources included as penalized cubic splines to allow non-linear predictor effects. Over a mean follow-up of 12.3 years, 8576 (4.6 %) deaths occurred. FS but not intrinsic sugars were significantly and dose-dependently associated with hazard ratio (HR) for all-cause mortality. The association with all-cause mortality was significant and dose-dependent for FS in beverages, but not in solids with the mean (confidence interval) HR at 50 g/d versus 0 g/d consumption at 1.10 (1.07 to 1.14) and 1.01 (0.98 to 1.03), respectively. Within the beverages subcategories, a significant dose-dependent association with mortality was detected for FS in soda/fruit drinks and milk-based drinks whereas this relation was not significant for FS in pure juice and tea/coffee. FS in four different subtypes of solids, i.e., treats, cereals, toppings, and sauces, were not positively associated with all-cause mortality. Major findings were robust in sensitivity analyses. In conclusion, only some FS sources were associated with all-cause mortality. Interventions targeting FS subtypes might be most effective concerning mortality if focused on the reduction of soda/fruit drinks and milk-based sugary drinks; however, the present results need to be confirmed by independent studies.

Purpose The impact of gluten intake on metabolic health in subjects without celiac disease is unclear. The present study aimed to assess the association between gluten intake and body fat percentage (primary objective), as well as a broad set of metabolic health markers. Methods Gluten intake was estimated in 39,927 participants of the UK Biobank who completed a dietary questionnaire for assessment of previous 24-h dietary intakes. Multiple linear regression analyses were performed between gluten intake and markers of metabolic health with Holm adjustment for multiple comparisons. Results Median gluten intake was 9.7 g/day (male: 11.7 g/day; female: 8.2 g/day; p < 0.0001). In multiple linear regression analysis, association between gluten intake and percentage body fat was negative in males (β = − 0.028, p = 0.0020) and positive in females (β = 0.025, p = 0.0028). Furthermore, gluten intake was a negative predictor of total cholesterol (male: β = − 0.031, p = 0.0154; female: β = − 0.050, p < 0.0001), high-density lipoprotein cholesterol (male: β = − 0.052, p < 0.0001; female: β = − 0.068, p < 0.0001), and glomerular filtration rate (sexes combined: β = − 0.031, p < 0.0001) in both sexes. In females only, gluten intake was positively associated with waist circumference (β = 0.041, p < 0.0001), waist-to-height ratio (β = 0.040, p < 0.0001), as well as body mass index (β = 0.043, p < 0.0001), and negatively related to low-density lipoprotein cholesterol (β = − 0.035, p = 0.0011). A positive association between gluten intake and triglycerides was observed in males only (β = 0.043, p = 0.0001). Conclusion This study indicates that gluten intake is associated with markers of metabolic health. However, all associations are weak and not clinically meaningful. Limiting gluten intake is unlikely to provide metabolic health benefits for a population in total.

The present study examines how alcohol intake from wine and non-wine alcoholic beverages (non-wine) in g/d, as well as cups of coffee and tea included as continuous covariates and mutually adjusted are associated with all-cause, cancer, non-cancer and CVD mortality. Consumption was assessed in 354 386 participants of the UK Biobank cohort who drank alcohol at least occasionally and survived at least 2 years after baseline with 20 201 deaths occurring over 4·2 million person-years. Hazard ratios (HR) for mortality were assessed with Cox proportional hazard regression models and beverage intake fitted as penalised cubic splines. A significant U-shaped association was detected between wine consumption and all-cause, non-cancer and CVD mortality. Wine consumption with lowest risk of death (nadir) ranged from 19 to 23 g alcohol/d in all participants and both sexes separately. In contrast, non-wine intake was significantly and positively associated in a dose-dependent manner with all mortality types studied except for CVD in females and with the nadir between 0 and 12 g alcohol/d. In all participants, the nadir for all-cause mortality was 2 cups coffee/d with non-coffee drinkers showing a slightly increased risk of death. Tea consumption was significantly and negatively associated with all mortality types in both sexes. Taken together, light to moderate consumption of wine but not non-wine is associated with decreased all-cause and non-cancer mortality. A minor negative association of coffee consumption with mortality cannot be excluded whereas tea intake is associated with a consistently decreased risk of all mortality types studied.

Background Gluten has been linked to adverse effects on metabolic and vascular health. Objectives The present study determines the association between dietary gluten intake and all-cause (primary objective), as well as cause-specific, mortality in people without celiac disease. Methods Gluten intake was estimated in 159,265 participants of the UK Biobank which is a large multicenter, prospective cohort study initiated in 2006. Cox proportional hazard regression models were used and HRs were determined for all-cause and cause-specific mortality. All models were adjusted for confounders and multiple testing. Results Median (IQR) age was 57 (49–62) y with 52.1% of participants being female. Gluten intake was 8.5 (5.1–12.4) g/d with significantly higher consumption in males [10.0 (6.3–14.1) g/d] than in females [7.2 (4.6–10.7) g/d] (P &lt; 0.0001). During a median follow-up of 11.1 (10.6–11.9) y and 1.8 million person-years, 6259 deaths occurred. Gluten intake was not significantly associated with all-cause mortality after adjusting for confounders (HR: 1.00; 95% CI: 1.00, 1.01; P = 0.59). Dietary gluten was not significantly associated with cancer (HR: 1.00; 95% CI: 1.00, 1.01; raw P = 0.24) or noncancer (HR: 1.00; 95% CI: 0.99, 1.01; raw P = 0.56) mortality. However, gluten intake was positively associated with ischemic heart disease mortality (HR: 1.02; 95% CI: 1.01, 1.04; raw P = 0.003, Holm-adjusted P = 0.04). Conclusions Gluten intake is not significantly associated with all-cause and cancer mortality in adults without celiac disease. The findings support the hypothesis that limiting gluten intake is unlikely to provide significant overall survival benefits on a population level. The positive association between gluten intake and ischemic heart disease mortality requires further study.

The prevalence of dementia is increasing globally and is linked to obesity and unfavorable dietary habits. The present study analyses the association of alcohol intake from wine and non-wine alcoholic beverages (non-wine) in g/d, as well as coffee and tea in cups/d, with incident dementia. Over 4.2 million person-years, 4270 dementia cases occurred in 351,436 UK Biobank participants. Hazard ratios (HRs) for incident dementia were defined with Cox proportional hazard regression models in which beverage intake was fitted as penalized cubic splines. Wine intake showed a significant U-shaped association with the lowest risk for incident dementia (nadir) ranging from 21 to 23 g alcohol/d in all participants and in males. In contrast, non-wine consumption was significantly and dose-dependently associated with incident dementia, and the nadir was found at 0 g alcohol/d. Coffee consumption was not related to dementia risk, while moderate-to-high tea intake was negatively associated with incident dementia. Taken together, the current study shows on a population level that moderate consumption of wine and moderate-to-high tea intake is associated with a decreased risk of incident dementia. In contrast, non-wine is positively related to dementia risk in a linear fashion, and no clear association is found for coffee.