BACKGROUND: Alcohol-related mortality and morbidity are high in socioeconomically disadvantaged populations compared with individuals from advantaged areas. It is unclear if this increased harm reflects differences in alcohol consumption between these socioeconomic groups, reverse causation (ie, downward social selection for high-risk drinkers), or a greater risk of harm in individuals of low socioeconomic status compared with those of higher status after similar consumption. We aimed to investigate whether the harmful effects of alcohol differ by socioeconomic status, accounting for alcohol consumption and other health-related factors.
METHODS: The Scottish Health Surveys are record-linked cross-sectional surveys representative of the adult population of Scotland. We obtained baseline demographics and data for alcohol consumption (units per week and binge drinking) from Scottish Health Surveys done in 1995, 1998, 2003, 2008, 2009, 2010, 2011, and 2012. We matched these data to records for deaths, admissions, and prescriptions. The primary outcome was alcohol-attributable admission or death. The relation between alcohol-attributable harm and socioeconomic status was investigated for four measures (education level, social class, household income, and area-based deprivation) using Cox proportional hazards models. The potential for alcohol consumption and other risk factors (including smoking and body-mass index [BMI]) mediating social patterning was explored in separate regression models. Reverse causation was tested by comparing change in area deprivation over time.
FINDINGS: 50 236 participants (21 777 men and 28 459 women) were included in the analytical sample, with 429 986 person-years of follow-up. Low socioeconomic status was associated consistently with strikingly raised alcohol-attributable harms, including after adjustment for weekly consumption, binge drinking, BMI, and smoking. Evidence was noted of effect modification; for example, relative to light drinkers living in advantaged areas, the risk of alcohol-attributable admission or death for excessive drinkers was increased (hazard ratio 6.12, 95% CI 4.45-8.41 in advantaged areas; and 10.22, 7.73-13.53 in deprived areas). We found little support for reverse causation.
INTERPRETATION: Disadvantaged social groups have greater alcohol-attributable harms compared with individuals from advantaged areas for given levels of alcohol consumption, even after accounting for different drinking patterns, obesity, and smoking status at the individual level.
FUNDING: Medical Research Council, NHS Research Scotland, Scottish Government Chief Scientist Office
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)