Hepatic steatosis, metabolic dysfunction and risk of mortality: findings from a multinational prospective cohort study.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS) are implicated in the aetiology of non-communicable diseases. Our study aimed to evaluate associations between NAFLD and MetS with overall and cause-specific mortality. METHODS: We used dietary, lifestyle, anthropometric and metabolic biomarker data from a random subsample of 15,784 EPIC cohort participants. NAFLD was assessed using the fatty liver index (FLI) and MetS using the revised definition. Indices for metabolic dysfunction-associated fatty liver disease (MAFLD) were calculated. The individual associations of these indices with overall and cause-specific mortality were assessed using multivariable Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (95%CIs). As a subobjective, risk associations with adaptations of new classifications of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic and alcohol-related liver disease (MetALD) were also assessed. RESULTS: Among the 15,784 sub-cohort participants, a total of 1997 deaths occurred (835 due to cancer, 520 to CVD, 642 to other causes) over a median 15.6 (IQR, 12.3-17.1) years of follow-up. Compared to an FLI < 30, FLI ≥ 60 was associated with increased risks of overall mortality (HR = 1.44, 95%CI = 1.27-1.63), and deaths from cancer (HR = 1.32, 95%CI = 1.09-1.60), CVD (HR = 2.06, 95% CI = 1.61-2.63) or other causes (HR = 1.21, 95%CI = 0.97-1.51). Mortality risk associations were also elevated for individuals with MAFLD compared to those without. Individuals with MetS were at increased risk of all mortality endpoints, except cancer-specific mortality. MASLD and MetALD were associated with higher risk of overall mortality. CONCLUSIONS: Our findings based on a prospective cohort suggest that individuals with hepatic steatosis or metabolic dysfunction have a higher overall and cause-specific mortality risk.

Role of dietary fibres in cardiometabolic diseases.

PURPOSE OF REVIEW: This review highlights recent developments in understanding the role of dietary fibre and specific fibre types on risk and management of cardiometabolic disease with a focus on the causal pathways leading to cardiometabolic diseases, namely weight management, glycaemic control, and lipid levels, as well as the latest findings for cardiovascular disease outcomes such as coronary heart disease, stroke, and mortality. Evidence for mechanisms through gut microbiota are also briefly reviewed. RECENT FINDINGS: Dietary fibre intake is associated with improved weight management, the extent of which may depend on the subtype of dietary fibre. Overall dietary fibre intake reduces blood glucose and HbA1c, however soluble fibres may be particularly effective in reducing HbA1c, fasting blood glucose and blood lipids. Individual meta-analyses and umbrella reviews of observational studies on dietary fibre, as well as major fibre types, observed inverse associations with incident coronary heart disease, stroke, and mortality due to cardiovascular disease. As different types of fibres exerted different health benefits, fibre diversity (i.e. combinations of fibres) should be further investigated. SUMMARY: Dietary fibres improve both short-term and long-term cardiometabolic disease risk factors and outcomes, and thus should be on every menu.

Adherence to the EAT-Lancet diet is associated with a lower risk of type 2 diabetes: the Danish Diet, Cancer and Health cohort.

PURPOSE: Type 2 diabetes is a global health problem. While a healthy diet lowers risk of type 2 diabetes, less is known about diets with low climate impact. This study aimed to investigate adherence to the EAT-Lancet diet and risk of type 2 diabetes in a Danish setting. METHODS: In the Danish Diet, Cancer and Health cohort, dietary data were collected using a validated 192-item food frequency questionnaire, at recruitment in 1993-1997. In total, 54,232 participants aged 50-64 years at baseline with no previous cancer or diabetes diagnoses were included in the current analyses. The EAT-Lancet diet score was used to assess adherence to the EAT-Lancet diet. Participants scored 0 (non-adherence) or 1 (adherence) point for each of the 14 dietary components of the diet score (range 0-14 points). Participants were followed through register linkage until type 2 diabetes diagnosis or censoring. Hazard ratios and 95% confidence intervals (CI) were estimated using multivariable-adjusted Cox regression models. RESULTS: During a median 15-year follow-up period, 7130 participants developed type 2 diabetes. The hazard ratio for developing type 2 diabetes was 0.78 (95% CI 0.71; 0.86) for those with highest EAT-Lancet diet scores (11-14 points) compared to those with lowest scores (0-7 points) after adjusting for potential confounders. After further adjusting for potential mediators, including BMI, the corresponding hazard ratio was 0.83 (95% CI 0.76; 0.92). CONCLUSION: Greater adherence to the EAT-Lancet diet was associated with a lower risk of developing type 2 diabetes in a middle-aged Danish population.

Adherence to the EAT-Lancet diet in midlife and development in weight or waist circumference after five years in a Danish cohort.

Purpose: The EAT-Lancet reference diet has been proposed as a healthy dietary pattern to reduce food-related climate impacts, but little is known regarding associations with bodyweight development. This study investigated adherence to the EAT-Lancet diet in midlife and development in weight and waist circumference (WC) after five years. Design: The Danish Diet, Cancer and Health cohort recruited participants in 1993-1997. At baseline, data on diet, lifestyle, and anthropometry were collected. Participants self-reported weight and WC five years later. In total, 44,194 participants were included in analyses of weight (43,678 for WC). Baseline adherence to the EAT-Lancet diet was scored 0-14 points. Multiple linear regression was used to estimate associations between the EAT-Lancet diet and development in weight and WC after five years. Poisson regression was used to estimate risk ratios (RR) of obesity (≥30 kg/m2) or elevated WC. Results: Adherence to the EAT-Lancet diet was not associated with follow-up weight, adjusting for baseline weight and confounders (11-14 vs 0-7 points ß: -0.08, 95% CI: -0.27, 0.11 kg), but was associated with lower follow-up WC adjusting for baseline WC and confounders (ß: -0.38, 95% CI: -0.69, -0.07 cm), and was associated with lower risk of obesity and elevated WC (RR 0.89, 95% CI: 0.82, 0.98, and 0.95, 95% CI: 0.93, 0.96, respectively). Conclusion: Adherence to the EAT-Lancet diet in midlife was associated with lower WC but not weight after five years follow up, taking baseline into account. Our findings suggest that greater adherence to the EAT-Lancet diet does not contribute to development of obesity.