25 August 2020 In General Health

The beneficial association of the Mediterranean diet (MedDiet) with longevity has been consistently demonstrated, but the associations of MedDiet components have not been accordingly evaluated. We performed an updated meta-analysis of prospective cohort studies published up to 31 December 2017, to quantify the association of adherence to MedDiet, expressed as an index/score (MDS) and of its components with all-cause mortality.

We estimated summary relative risks (SRR) and 95 % CI using random effects models. On the basis of thirty studies (225 600 deaths), SRR for the study-specific highest/lowest and per 1sd MDS increment were 0.79 (95 % CI 0.77, 0.81, Iota 2=42 %, P-heterogeneity 0.02) and 0.92 (95 % CI 0.90, 0.94, Iota 2 56 %, P-heterogeneity <0.01), respectively. Inversely, statistically significant associations were evident in stratified analyses by country, MDS range and publication year, with some evidence for heterogeneity across countries overall (P-heterogeneity 0.011), as well as across European countries (P=0.018).

Regarding MDS components, relatively stronger and statistically significant inverse associations were highlighted for moderate/none-excessive alcohol consumption (0.86, 95 % CI 0.77, 0.97) and for above/below-the-median consumptions of fruit (0.88, 95 % CI 0.83, 0.94) and vegetables (0.94, 95 % CI 0.89, 0.98), whereas a positive association was apparent for above/below-the-median intake of meat (1.07, 95 % CI 1.01, 1.13).

Our meta-analyses confirm the inverse association of MedDiet with mortality and highlight the dietary components that influence mostly this association. Our results are important for better understanding the role of MedDiet in health and proposing dietary changes to effectively increase adherence to this healthy dietary pattern

25 August 2020 In Cancer

Estimates of the future breast cancer burden preventable through modifications to current behaviours are lacking. We assessed the effect of individual and joint behaviour modifications on breast cancer burden for premenopausal and postmenopausal Australian women, and whether effects differed between population subgroups.

We linked pooled data from six Australian cohort studies (n = 214,536) to national cancer and death registries, and estimated the strength of the associations between behaviours causally related to cancer incidence and death using adjusted proportional hazards models. We estimated exposure prevalence from representative health surveys. We combined these estimates to calculate Population Attributable Fractions (PAFs) with 95% confidence intervals (CIs), and compared PAFs for population subgroups.

During the first 10 years follow-up, there were 640 incident breast cancers for premenopausal women, 2,632 for postmenopausal women, and 8,761 deaths from any cause. Of future breast cancers for premenopausal women, any regular alcohol consumption explains 12.6% (CI = 4.3-20.2%), current use of oral contraceptives for >/=5 years 7.1% (CI = 0.3-13.5%), and these factors combined 18.8% (CI = 9.1-27.4%). Of future breast cancers for postmenopausal women, overweight or obesity (BMI >/=25 kg/m(2) ) explains 12.8% (CI = 7.8-17.5%), current use of menopausal hormone therapy (MHT) 6.9% (CI = 4.8-8.9%), any regular alcohol consumption 6.6% (CI = 1.5-11.4%), and these factors combined 24.2% (CI = 17.6-30.3%).

The MHT-related postmenopausal breast cancer burden varied by body fatness, alcohol consumption and socio-economic status, the body fatness-related postmenopausal breast cancer burden by alcohol consumption and educational attainment, and the alcohol-related postmenopausal breast cancer burden by breast feeding history. Our results provide evidence to support targeted and population-level cancer control activities.

26 June 2020 In Cancer

Introduction: Alcohol is a carcinogen for human cancer. This contribution summarizes the relationships between alcohol use and gastrointestinal cancers, and implications for prevention.

Methods: Comparative risk assessment and narrative literature review.

Results: The following gastrointestinal cancer sites were found to be causally impacted by alcohol use: lip and oral cavity, pharynx other than nasopharynx, esophagus, colon and rectum, and liver. Globally, 368,000 deaths (304,000 men and 64,000 women) and more than 10 million disability-adjusted life years (DALYs) lost (10.1 million; 8.4 million men and 1.6 million women) in 2016 were attributable to alcohol use, making up about 10% of all deaths and DALYs lost due to these cancers, respectively.

There are effective and cost-effective alcohol control policies available to reduce this burden, namely the best buys of increasing taxation, reducing availability, and banning advertisement. In addition, public knowledge about the alcohol-cancer link should be increased. Discussion: There are a number of assumptions underlying these estimates, but overall all of them seem to be conservative.

04 May 2020 In Cardiovascular System

AIMS: To investigate associations of life-time hazardous and binge drinking with biomarkers of cardiometabolic health, liver function, cardiovascular disease (CVD) and mortality.

DESIGN: Prospective cohort study with median follow-up time to CVD incidence of 4.5 years.

SETTING: London, UK: civil servants within the Whitehall II Study.

PARTICIPANTS: A total of 4820 drinkers aged 59-83 years with biological measurements during the 2011-12 survey.

MEASUREMENTS: Hazardous drinking was defined as having an AUDIT-C score >/= 5 calculated at each decade of life, forming the following groups: never hazardous drinker, former early (stopping before age 50), former later (stopping after age 50), current hazardous drinker and consistent hazardous drinker (hazardous drinker at each decade of life).

FINDINGS: More than half the sample had been hazardous drinkers at some point during their life-time, comprising former early (< age 50) (19%), former later (>/= age 50) (11%), current (21%) and consistent hazardous drinker (AUDIT-C >/= 5 across life (5%). After adjusting for covariates, waist circumference was larger with more persistent hazardous drinking (e.g. compared with never hazardous drinkers, former early had increased waist circumference by 1.17 cm [95% confidence interval (CI) = 0.25-2.08]; former later by 1.88 cm (CI = 0.77-2.98); current by 2.44 cm (CI = 1.50-3.34) and consistent hazardous drinker by 3.85 cm (CI = 2.23-5.47). Current hazardous drinkers had higher systolic blood pressure (2.44 mmHg, CI = 1.19-3.68) and fatty liver index scores (4.05 mmHg, CI = 2.92-5.18) than never hazardous drinkers. Current hazardous drinkers [hazard ratio (HR) = 2.75, CI = 1.44-5.22) had an elevated risk of stroke, and former later hazardous drinkers had an elevated risk of non-CVD mortality (HR = 1.93, CI = 1.19-3.14) than never hazardous drinkers. Life-time binge drinking was associated with larger waist circumferences and poorer liver function compared with never binge drinkers.

CONCLUSION: Hazardous drinking may increase cardiometabolic risk factors; this is made worse by persistent hazardous drinking throughout life, particularly in relation to weight gain, suggesting benefits of early intervention.

Page 7 of 169

Disclaimer

The authors have taken reasonable care in ensuring the accuracy of the information herein at the time of publication and are not responsible for any errors or omissions. Read more on our disclaimer and Privacy Policy.