OBJECTIVES: To investigate the association between alcohol consumption and cardiovascular disease at higher resolution by examining the initial lifetime presentation of 12 cardiac, cerebrovascular, abdominal, or peripheral vascular diseases among five categories of consumption.
DESIGN: Population based cohort study of linked electronic health records covering primary care, hospital admissions, and mortality in 1997-2010 (median follow-up six years).
SETTING: CALIBER (ClinicAl research using LInked Bespoke studies and Electronic health Records).
PARTICIPANTS: 1 937 360 adults (51% women), aged >/=30 who were free from cardiovascular disease at baseline.
MAIN OUTCOME: measures 12 common symptomatic manifestations of cardiovascular disease, including chronic stable angina, unstable angina, acute myocardial infarction, unheralded coronary heart disease death, heart failure, sudden coronary death/cardiac arrest, transient ischaemic attack, ischaemic stroke, intracerebral and subarachnoid haemorrhage, peripheral arterial disease, and abdominal aortic aneurysm.
RESULTS: 114 859 individuals received an incident cardiovascular diagnosis during follow-up. Non-drinking was associated with an increased risk of unstable angina (hazard ratio 1.33, 95% confidence interval 1.21 to 1.45), myocardial infarction (1.32, 1.24 to1.41), unheralded coronary death (1.56, 1.38 to 1.76), heart failure (1.24, 1.11 to 1.38), ischaemic stroke (1.12, 1.01 to 1.24), peripheral arterial disease (1.22, 1.13 to 1.32), and abdominal aortic aneurysm (1.32, 1.17 to 1.49) compared with moderate drinking (consumption within contemporaneous UK weekly/daily guidelines of 21/3 and 14/2 units for men and women, respectively). Heavy drinking (exceeding guidelines) conferred an increased risk of presenting with unheralded coronary death (1.21, 1.08 to 1.35), heart failure (1.22, 1.08 to 1.37), cardiac arrest (1.50, 1.26 to 1.77), transient ischaemic attack (1.11, 1.02 to 1.37), ischaemic stroke (1.33, 1.09 to 1.63), intracerebral haemorrhage (1.37, 1.16 to 1.62), and peripheral arterial disease (1.35; 1.23 to 1.48), but a lower risk of myocardial infarction (0.88, 0.79 to 1.00) or stable angina (0.93, 0.86 to 1.00).
CONCLUSIONS: Heterogeneous associations exist between level of alcohol consumption and the initial presentation of cardiovascular diseases. This has implications for counselling patients, public health communication, and clinical research, suggesting a more nuanced approach to the role of alcohol in prevention of cardiovascular disease is necessary.
Registration clinicaltrails.gov (NCT01864031)
BACKGROUND: We investigated four factors, height, weight gain since age 20, physical activity, and alcohol drinking, for associations with risk of breast cancer (BC) according to menopausal status, using the latest data of the Japan Collaborative Cohort Study (JACC Study).
MATERIALS AND METHODS: We confined the analysis to 24 areas available of cancer incidence information, excluding women with a previous diagnosis of BC. Baseline data were collected from 38,610 (9,367 premenopausal, and 29,243 postmenopausal) women during 1988 and 1990. The study subjects were followed-up at the end of 2009, and 273 (84 premenopausal, and 189 postmenopausal) cases of BC were newly diagnosed in 501,907 person-years. The Cox model was used to estimate a hazards ratio (HR) and its 95% confidence interval (CI) of BC risk.
RESULTS: As a result of the multivariate analysis adjusting for age at baseline survey, age at menarche, number of live births, and, age at first delivery, weight gain since age 20 of 6.7 kg-9.9 kg, and >/=10.0 kg were significantly associated with increased risk for postmenopausal BC (HR=2.48, 95% CI 1.40-4.41, and, HR=2.94, 95% CI 1.84-4.70, respectively). Significantly increased trend of BC risk was also observed in weight gain since age 20 (p for trend, p<0.001). Amount of ethanol intake per day>/=15.0 g was significantly associated with increased risk for postmenopausal BC in the multivariable-adjusted analysis (HR=2.74, 95% CI 1.32-5.70).
CONCLUSIONS: Higher weight gain in adulthood and larger amounts of ethanol intake were significantly associated with increased risk of BC in Japanese postmenopausal women. None of the investigated factors were significantly associated with BC risk in Japanese premenopausal women.
Effects of Alcohol Consumption on Hepatocarcinogenesis in Japanese Patients With Fatty Liver Disease
BACKGROUND & AIMS: The effect of ethanol consumption on hepatocarcinogenesis in patients with fatty liver disease (FLD) is not clear. We aimed to investigate the influence of alcohol consumption on hepatocarcinogenesis and determine the risk factors for hepatocellular carcinoma (HCC) in a large number of Japanese patients with FLD without viral hepatitis.
METHODS: This multicenter, retrospective cohort study was conducted at a specialized center for hepatology in Japan and included 9959 patients with FLD without viral hepatitis, diagnosed by ultrasonography from January 1997 through December 2011. The patients' level of ethanol consumption was divided into 4 categories: /=70 g/day (n = 946). The primary endpoint was the onset of HCC. Statistical analyses performed included the Kaplan-Meier method and Cox proportional hazard analysis. The median follow-up period was 5.4 years.
RESULTS: Of the study cohort, 49 cases (0.49%) developed HCC during the follow-up period. The annual incidence rate of HCC was 0.05% in patients with FLD and a daily ethanol consumption /=70 g/day ethanol consumption (HR, 10.58; 95% CI, 5.06-22.13), compared with patients with ethanol consumption /=40 g/day was an independent risk factor for HCC: for 40-69 g/day the HR was 2.48 (95% CI, 1.01-6.05; P < .047) and for >/=70 g/day the HR was 12.61 (95% CI, 5.68-28.00; P < .001).
CONCLUSIONS: Based on a multicenter, retrospective analysis of almost 10,000 patients with FLD, ethanol consumption >/=40 g/day is an independent risk factor for HCC.
BACKGROUND: Sipping alcohol is common during early adolescence, but research has ignored the distinction between sipping and drinking whole alcohol beverages, conflating the 2, or else simply classifying "sippers" as abstainers. Research has not addressed whether sippers are different to drinkers, in relation to variables known to be associated with adolescent alcohol consumption, or considered whether sipping and drinking behaviors may have quite different associations.
METHODS: Parent-child dyads (N = 1,823) were recruited in 3 states from Australian grade 7 classes. Multinomial logistic analyses compared adolescents who had only had a sip/taste of alcohol (sippers) with adolescents who had consumed at least a whole drink (drinkers) in the past 6 months. The multivariate model assessed a broad range of demographics, parenting practices, peer influences, and adolescent externalizing and internalizing behaviors, and controlled for school clustering.
RESULTS: Compared to drinkers, sippers were less likely to come from 1-parent households (odds ratio [OR] = 0.59, 95% confidence interval [CI]: 0.35 to 0.98); less likely to come from low-socioeconomic status (SES) households (OR = 0.54, 95% CI: 0.31 to 0.94); more likely to come from families where parents provide stricter alcohol-specific rules (OR = 1.21, 95% CI: 1.11 to 1.32), stricter monitoring of the child's activities (OR = 1.10, 95% CI: 1.04 to 1.16), more consistent parenting practices (OR = 1.13, 95% CI: 1.05 to 1.23), and more positive family relationships (OR = 1.56, 95% CI: 1.02 to 2.43); and report having fewer substance-using peers (OR = 0.80, 95% CI: 0.70 to 0.91) and greater peer disapproval of any substance use (OR = 1.30, 95% CI: 1.19 to 1.42). After adjustment for confounders, the associations with household composition and SES were no longer significant, but the familial and peer associations remained significant in the multivariate analysis, chi2 (40) = 1,493.06, p < 0.001.
CONCLUSIONS: Sipping alcohol has different associations with known predictors of adolescent alcohol use than drinking whole beverages, and sipping may be a distinct or separable behavior. Future research should better define quantities of early consumption and assess the relationship between early sipping and drinking on long-term outcomes separately.