BACKGROUND: The identification of effective dementia prevention strategies is a major public health priority, due to the enormous and growing societal cost of this condition. Consumption of a Mediterranean diet (MedDiet) has been proposed to reduce dementia risk. However, current evidence is inconclusive and is typically derived from small cohorts with limited dementia cases. Additionally, few studies have explored the interaction between diet and genetic risk of dementia.
METHODS: We used Cox proportional hazard regression models to explore the associations between MedDiet adherence, defined using two different scores (Mediterranean Diet Adherence Screener [MEDAS] continuous and Mediterranean diet Pyramid [PYRAMID] scores), and incident all-cause dementia risk in 60,298 participants from UK Biobank, followed for an average 9.1 years.
The interaction between diet and polygenic risk for dementia was also tested. RESULTS: Higher MedDiet adherence was associated with lower dementia risk (MEDAS continuous: HR = 0.77, 95% CI = 0.65-0.91; PYRAMID: HR = 0.86, 95% CI = 0.73-1.02 for highest versus lowest tertiles). There was no significant interaction between MedDiet adherence defined by the MEDAS continuous and PYRAMID scores and polygenic risk for dementia. CONCLUSIONS: Higher adherence to a MedDiet was associated with lower dementia risk, independent of genetic risk, underlining the importance of diet in dementia prevention interventions.
PURPOSE: Previous observational studies have shown that alcohol and coffee were associated with colorectal cancer (CRC) risk, but the causal relationships have not been adequately explored. This study aimed to assess the potential causal associations of alcohol and coffee with CRC risk using Mendelian randomization (MR) analyses in an East Asian population.
METHODS: Publicly available summary-level genome-wide association studies data on ever/never alcohol drinker (n = 165,084), alcohol consumption (n = 58,610), coffee consumption (n = 152,634), and CRC (7062 cases and 195,745 controls) were obtained from the BioBank Japan (BBJ). Single-nucleotide polymorphisms (SNPs) that were significantly related to the exposures were identified as instrumental variables.
Five, two, and six SNPs were used for ever/never alcohol drinkers, alcohol consumption, and coffee consumption, respectively. The inverse variance weighted method was used as the main MR method to calculate the odds ratios (ORs) and 95% confidence intervals (95% CIs) of CRC risk per one-unit change in exposures.
RESULTS: Genetically predicted ever/never alcohol drinkers (OR: 1.08; 95% CI 1.06, 1.11; P < 0.001) and alcohol consumption (OR: 1.39; 95% CI 1.21, 1.60; P < 0.001) were positively associated with CRC risk. Conversely, genetically predicted coffee consumption was inversely related to CRC risk, with an OR (95% CI) of 0.80 (0.64, 0.99) (P = 0.037). CONCLUSION: Genetically predicted alcohol use and consumption were risk factors for CRC while genetically predicted coffee consumption was a protective factor.
Our findings highlight the effectiveness of keeping healthy dietary habits to prevent CRC. Further studies with more valid SNPs and CRC cases are needed. Validation of our findings is also recommended.
PURPOSE: To examine whether higher levels of cardiorespiratory fitness are related to increased alcohol consumption and dependence among a large sample of adults attending a preventive medicine clinic. METHODS: A cross-sectional study of 38,653 apparently healthy patients who visited the Cooper Clinic (Dallas, TX) for preventive medical examinations (1988-2019) and enrolled in the Cooper Center Longitudinal Study. The primary independent variable was cardiorespiratory fitness, based on a maximal treadmill test, and the dependent variables were alcohol consumption and dependence (self-reported).
The relations between fitness category (low, moderate, high) and alcohol consumption (low, moderate, heavy) and suggested alcohol dependence (Cut down, Annoyed, Guilty, Eye opener score ≥2) among women and men were estimated via multivariable regression while adjusting for covariates (e.g., age, birth year cohort, marital status, and body mass index).
RESULTS: Women within the moderate and high fitness categories had 1.58 (95% confidence interval [CI], 1.32-1.91) and 2.14 (95% CI, 1.77-2.58) greater odds of moderate/heavy alcohol consumption, respectively, in comparison to their low fitness counterparts. Similarly, moderate and high fit men had 1.42 (95% CI, 1.30-1.55) and 1.63 (95% CI, 1.49-1.80) times greater odds of moderate-to-heavy alcohol consumption, respectively, in comparison to the low fitness group. In addition, among men who were heavy drinkers (but not women), higher fitness levels were related to lower rates of suggested alcohol dependence. Specifically, these men had 45.7%, 41.7%, and 34.9% proportions of clinically relevant alcohol problems across low, moderate, and high fitness categories (adjusted P for trend <0.001).
CONCLUSIONS: Higher fitness levels are significantly related to greater alcohol consumption among a large cohort of adult patients. Interventions focusing on increasing fitness (via physical activity promotion) might consider concurrently aiming to reduce alcohol consumption.
Alcohol use and metabolic syndrome are highly prevalent in the population and frequently co-exist. Both are implicated in a large range of health problems, including chronic liver disease, hepatocellular carcinoma, and liver-related outcomes (i.e. decompensation or liver transplantation). Studies have yielded mixed results regarding the effects of mild-moderate alcohol consumption on the risk of metabolic syndrome and fatty liver disease, possibly due to methodological differences.
The few available prospective studies have indicated that mild-moderate alcohol use is associated with an increase in liver-related outcomes.
This conclusion was substantiated by systems biology analyses suggesting that alcohol and metabolic syndrome may play a similar role in fatty liver disease, potentiating an already existing dysregulation of common vital homeostatic pathways. Alcohol and metabolic factors are independently and jointly associated with liver-related outcomes. Indeed, metabolic syndrome increases the risk of liver-related outcomes, regardless of alcohol intake. Moreover, the components of metabolic syndrome appear to have additive effects when it comes to the risk of liver-related outcomes. A number of population studies have implied that measures of central/abdominal obesity, such as the waist-to-hip ratio, can predict liver-related outcomes more accurately than BMI, including in individuals who consume harmful quantities of alcohol.
Many studies even point to synergistic interactions between harmful alcohol use and many metabolic components. This accumulating evidence showing independent, combined, and modifying effects of alcohol and metabolic factors on the onset and progression of chronic liver disease highlights the multifactorial background of liver disease in the population. The available evidence suggests that more holistic approaches could be useful for risk prediction, diagnostics and treatment planning.