23 November 2022 In General Health

BACKGROUND: Alcohol is a discretionary, energy dense, dietary component. Compared to non-drinkers, people who consume alcohol report higher total energy intake and may be at increased risk of weight gain, overweight, and obesity, which are key preventable risk factors for illness. However, accurate consumer knowledge of the energy content in alcohol is low. To inform future behaviour change interventions among drinkers, this study investigated individual characteristics associated with changing alcohol consumption due to energy-related concerns.

METHODS: An online survey was undertaken with 801 Australian adult drinkers (18-59 years, 50.2% female), i.e. who consumed alcohol at least monthly. In addition to demographic and health-related characteristics, participants reported past-year alcohol consumption, past-year reductions in alcohol consumption, frequency of harm minimisation strategy use (when consuming alcohol), and frequency of changing alcohol consumption behaviours because of energy-related concerns.

RESULTS: When prompted, 62.5% of participants reported changing alcohol consumption for energy-related reasons at least 'sometimes'. Women, those aged 30-44 years, metropolitan residents, those with household income $80,001-120,000, and risky/more frequent drinkers had increased odds of changing consumption because of energy-related concerns, and unemployed respondents had reduced odds.

CONCLUSIONS: Results indicate that some sociodemographic groups are changing alcohol consumption for energy-related reasons, but others are not, representing an underutilised opportunity for health promotion communication. Further research should investigate whether messaging to increase awareness of alcohol energy content, including through systems-based policy actions such as nutritional/energy product labelling, would motivate reduced consumption across a broader range of drinkers.

23 November 2022 In Cancer

There is evidence that diet and nutrition are modifiable risk factors for several cancers, but associations may be flawed due to inherent biases. Nutritional epidemiology studies have largely relied on a single assessment of diet using food frequency questionnaires. We conduct an umbrella review of meta-analyses of observational studies to evaluate the strength and validity of the evidence for the association between food/nutrient intake and risk of developing or dying from 11 primary cancers. It is estimated that only few single food/nutrient and cancer associations are supported by strong or highly suggestive meta-analytic evidence, and future similar research is unlikely to change this evidence. Alcohol consumption is positively associated with risk of postmenopausal breast, colorectal, esophageal, head & neck and liver cancer. Consumption of dairy products, milk, calcium and wholegrains are inversely associated with colorectal cancer risk. Coffee consumption is inversely associated with risk of liver cancer and skin basal cell carcinoma.

22 September 2022 In General Health

We aimed to investigate whether alcohol intake contributes to lung function levels and which beverage type may have an effect. We investigated 3742 participants from the Wuhai-Zhuhai Cohort and 12,526 participants from the Dongfeng-Tongji Cohort, and they were followed up for 3 and 5 years, respectively. Information on the type and daily amount of alcohol intake was collected through face-to-face interviews. Lung function was measured by trained physicians using electronic spirometers. Compared with nondrinkers, moderate alcohol intake was significantly associated with a 70.03 and 74.92 mL increase in FEV1 and FVC, respectively (P < 0.05), after adjusting for covariates. With regard to beverage type, red wine was associated with a 105.31 and 98.91 mL increase in FEV1 and FVC, respectively (P < 0.05). Moderate alcohol intake was also associated with a 53.37 and 66.17 mL increase in FEV1 and FVC for liquor, respectively, and a 106.90 and 103.62 mL increase for red wine (all Ps < 0.05). In the longitudinal analyses, moderate alcohol intake and red wine were associated with a 67.77 and 103.77 mL increase in FVC, respectively (P < 0.05). Moderate alcohol intake is associated with increased lung function, especially for red wine. Further studies are needed to investigate the potential mechanism.

15 June 2022 In Diabetes
AIMS: We examined associations of baseline alcohol drinking with incident type 2 diabetes (T2D) or impaired fasting glucose (IFG), and explore whether the associations were modified by genetic polymorphisms of aldehyde dehydrogenase-2 (ALDH2) and alcohol dehydrogenase-1B (ADH1B). MATERIALS AND METHODS: All participants were aged 50+ (mean = 60.45; standard deviation = 6.88) years. Information of alcohol consumption was collected at baseline from 2003 to 2008. Incident T2D was defined as fasting glucose >/=7.0 mmol/L or post-load glucose >/=11.1 mmol/L at follow-up examination (2008-2012), self-reported T2D and/or initiation of hypoglycaemia medication or insulin during follow-up. Impaired fasting glucose was defined as fasting glucose >/=5.6 mmol/L and <7 mmol/L. RESULTS: Of 15,716 participants without diabetes and 11,232 participants without diabetes and IFG at baseline, 1624 (10.33%) developed incident T2D and 1004 (8.94%) developed incident IFG during an average 4 years of follow-up. After multivariable adjustments, compared with never drinking, occasional or moderate alcohol drinking was not associated with risk of incident hyperglycaemia (T2D + IFG) (odds ratio (OR) = 1.10, 95% confidence interval (CI) 0.95-1.27, and 0.90 (0.69-1.18), respectively), whereas heavy alcohol drinking was associated with a higher risk of incident hyperglycaemia (T2D + IFG) (OR = 1.82, 95% CI 1.24-2.68). No interactions of sex, overweight/obesity and genetic polymorphisms of ADH1B/ALDH2 genes with alcohol drinking on incident T2D and/or IFG were found (P for interaction from 0.12 to 0.85). CONCLUSIONS: Our results support a detrimental effect of heavy alcohol use on IFG and T2D. No protective effect was found for those carrying lower risk alleles for ADH1B/ALDH2 genes.
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