18 May 2018 In General Health

OBJECTIVES: The primary goal was to examine the relationship between alcohol use and frailty, a variable characterizing late-life decline, in a national, longitudinal survey of older adults living in the United States.

METHODS: The sample drawn from the Health and Retirement Study included 9,499 stroke-free participants over age 65 in 2000. The sample was 59.1% female, and had a mean age of 74.25 years (SD = 6.99). Follow-up data was from 2004, 2008, and 2012. Frailty was defined phenotypically using the Paulson-Lichtenberg Frailty Index (PLFI). Alcohol use was measured via self-report. Control variables included age, race, education, socio-economic status (SES), depressive symptomatology, medical burden score, body mass index (BMI), and partner status. With abstinent participants as the reference group, logistic regressions were conducted to determine prevalent frailty at 2000, and Cox's proportional hazard models were utilized to determine time to incident frailty over a 12-year period.

RESULTS: Results revealed that age, depressive symptomatology, and medical burden score were significant positive correlates of prevalent and incident frailty (p < .05) for both males and females. Logistic regressions revealed that consumption of 1-7 alcoholic drinks per week was associated with reduced prevalent frailty (OR = .49, p < .001) for females. Survival analysis results reveal that compared with nondrinkers, males and females who reportedly consumed 1-7 drinks per week had a decreased probability of incident frailty (HR = .78-081, p < .05).

CONCLUSIONS: Findings suggest that moderate alcohol use confers reduced frailty risk for both older men and women. Future research should examine the mechanism(s) relating alcohol consumption and frailty.

CLINICAL IMPLICATIONS: Findings support extant literature suggesting some healthcare benefits may be associated with moderate drinking.

18 May 2018 In General Health

BACKGROUND: We examined the associations of alcohol consumption and liver holidays with all-cause mortality and with mortality due to cancer, heart disease, cerebrovascular disease, respiratory disease, and injury using a large-scale prospective study in Japan.

METHODS: We followed 102,849 Japanese who were aged between 40 and 69 years at baseline for 18.2 years on average, during which 15,203 deaths were reported. Associations between alcohol intake and mortality risk were assessed using a Cox proportional hazards model, with analysis by the number of liver holidays (in which a person abstains from drinking for several days a week).

RESULTS: A J-shaped association was observed between alcohol intake and total mortality in men (nondrinkers: reference; occasional drinkers: hazard ratio [HR] 0.74; 95% confidence interval [CI], 0.68-0.80; 1-149 g/week: HR 0.76; 95% CI, 0.71-0.81; 150-299 g/week: HR 0.75; 95% CI, 0.70-0.80; 300-449 g/week: HR 0.84; 95% CI, 0.78-0.91; 450-599 g/week: HR 0.92; 95% CI, 0.83-1.01; and >/=600 g/week: HR 1.19; 95% CI, 1.07-1.32) and in women (nondrinkers: reference; occasional: HR 0.75; 95% CI, 0.70-0.82; 1-149 g/week: HR 0.80; 95% CI, 0.73-0.88; 150-299 g/week: HR 0.91; 95% CI, 0.74-1.13; 300-449 g/week: HR 1.04; 95% CI, 0.73-1.48; and >/=450 g/week: HR 1.59; 95% CI, 1.07-2.38). In current drinkers, alcohol consumption was associated with a linear, positive increase in mortality risk from all causes, cancer, and cerebrovascular disease in both men and women, but not heart disease in men. Taking of liver holidays was associated with a lower risk of cancer and cerebrovascular disease mortality in men.

CONCLUSIONS: Alcohol intake showed J-shaped associations with the risk of total mortality and three leading causes of death. However, heavy drinking increases the risk of mortality, which highlights the necessity of drinking in moderation coupled with liver holidays.

18 May 2018 In General Health

BACKGROUND: Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease.

METHODS: We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose-response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12.5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5.6 years [5th-95th percentile 1.04-13.5]) from 71 011 participants from 37 studies.

FINDINGS: In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5.4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around or below 100 g per week. Alcohol consumption was roughly linearly associated with a higher risk of stroke (HR per 100 g per week higher consumption 1.14, 95% CI, 1.10-1.17), coronary disease excluding myocardial infarction (1.06, 1.00-1.11), heart failure (1.09, 1.03-1.15), fatal hypertensive disease (1.24, 1.15-1.33); and fatal aortic aneurysm (1.15, 1.03-1.28). By contrast, increased alcohol consumption was log-linearly associated with a lower risk of myocardial infarction (HR 0.94, 0.91-0.97). In comparison to those who reported drinking >0-100-200-350 g per week had lower life expectancy at age 40 years of approximately 6 months, 1-2 years, or 4-5 years, respectively.

INTERPRETATION: In current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week. For cardiovascular disease subtypes other than myocardial infarction, there were no clear risk thresholds below which lower alcohol consumption stopped being associated with lower disease risk. These data support limits for alcohol consumption that are lower than those recommended in most current guidelines.

FUNDING: UK Medical Research Council, British Heart Foundation, National Institute for Health Research, European Union Framework 7, and European Research Council.

18 May 2018 In Cancer

Importance: Inflammation is important in colorectal cancer development. Diet modulates inflammation and may thus be a crucial modifiable factor in colorectal cancer prevention.

Objective: To examine whether proinflammatory diets are associated with increased colorectal cancer risk by using an empirical dietary inflammatory pattern (EDIP) score based on a weighted sum of 18 food groups that characterizes dietary inflammatory potential based on circulating levels of inflammation biomarkers.

Design, Settings, and Participants: Cohort study of 46804 men (Health Professionals Follow-up Study: 1986-2012) and 74246 women (Nurses' Health Study: 1984-2012) followed for 26 years to examine associations between EDIP scores and colorectal cancer risk using Cox regression. We also examined associations in categories of alcohol intake and body weight. Data analysis began January 17, 2017, and was completed August 9, 2017.

Exposures: EDIP scores calculated from food frequency questionnaires administered every 4 years.

Main Outcomes and Measures: Incident colorectal cancer.

Results: We documented 2699 incident colorectal cancer cases over 2571831 person-years of follow-up. Compared with participants in the lowest EDIP quintile (Q) who had a colorectal cancer incidence rate (per 100000 person-years) of 113 (men) and 80 (women), those in the highest Q had an incidence rate of 151 (men) and 92 (women), leading to an unadjusted rate difference of 38 and 12 more colorectal cancer cases, respectively, among those consuming highly proinflammatory diets. Comparing participants in the highest vs lowest EDIP Qs in multivariable-adjusted analyses, higher EDIP scores were associated with 44% (men: hazard ratio [HR], 1.44; 95% CI, 1.19-1.74; P < .001 for trend), 22% (women: HR, 1.22; 95% CI, 1.02-1.45; P = .007 for trend), and 32% (men and women: pooled HR, 1.32; 95% CI, 1.12-1.55; P < .001 for trend) higher risk of developing colorectal cancer. In both men and women, associations were observed in all anatomic subsites except for the rectum in women. In subgroups (P </= .02 for all interactions), associations differed by alcohol intake level, with stronger associations among men (Q5 vs Q1 HR, 1.62; 95% CI, 1.05-2.49; P = .002 for trend) and women (Q5 vs Q1 HR, 1.33; 95% CI, 0.97-1.81; P = .03 for trend) not consuming alcohol; and by body weight, with stronger associations among overweight/obese men (Q5 vs Q1 HR, 1.48; 95% CI, 1.12-1.94; P = .008 for trend) and lean women (Q5 vs Q1 HR, 1.31; 95% CI, 0.99-1.74; P = .01 for trend).

Conclusions and Relevance: Findings suggest that inflammation is a potential mechanism linking dietary patterns and colorectal cancer development. Interventions to reduce the adverse role of proinflammatory diets may be more effective among overweight/obese men and lean women or men and women who do not consume alcohol.

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