Per capita alcohol consumption and all-cause mortality in 14 European countries

Aims. (1) To estimate the relationship between per capita alcohol consumption and male all-cause mortality in 14 European countries. (2) To compare the estimates with predictions from the U -shaped curve at the aggregate level. Data and method. The outcome measures comprised annual data, after 1950, on male mortality (all-cause mortality and mortality from diseases) for the following age groups: 15 +, 15-29, 30-49, 50-69 and 70 + years. Female mortality was included as a control variable. Alcohol sales were used as proxy for per capita consumption. The data were analysed using the Box-Jenkins technique. The estimated alcohol effects were pooled within low-, medium- and high-consumption countries. Results. For all-cause mortality (15 +), the effect estimates were significantly positive in eight of the 14 countries. The effect on mortality of a 1-litre increase in consumption tended to be stronger in low-consumption countries (3% per litre) than in medium- and high-consumption countries (1%). This pattern deviates from that predicted from the U -shaped curve. No significant impact of alcohol was found in the youngest age group when mortality from diseases was used as the outcome. Conclusions. Increases in overall consumption seem to be associated with increases in total mortality. Differences in drinking patterns are discussed as a possible explanation for the variation between country groups in alcohol effect.     

Per capita alcohol consumption and sickness absence

AIM: The purpose of the study was to assess the relationship between aggregate alcohol consumption and sickness absence in Sweden. DATA AND METHODS: Two indicators of sickness absence were used, one based on sickness insurance data, the other on data from the labour force surveys. Alcohol consumption was gauged by sales of pure alcohol (100%) per inhabitant 15 years of age and older. Because changes in the economy may affect alcohol consumption as well as sickness absence, two macroeconomic indicators were included as control variables: unemployment and real wages. The study period was 1935-2002. The data were analysed through the Box-Jenkins method for time-series analyses. FINDINGS: A 1-litre increase in total consumption was associated with a 13% increase in sickness absence among men (P < 0.05). The relationship was not statistically significant for women. CONCLUSIONS: Previous research has documented that aggregate alcohol consumption is related to a large number of harm indicators, such as cirrhosis and accident mortality. The present findings add yet another indicator to this list.     

Per capita alcohol consumption and ischemic heart disease mortality in a panel of US states from 1950 to 2002

Aims To estimate the overall impact of alcohol on ischemic heart disease (IHD) mortality in the United States using aggregate‐level models and to consider beverage‐specific effects that may represent more effectively the changes in drinking patterns over time that are related to both harmful and protective impacts of alcohol consumption on IHD. Design Several model specifications are estimated, including state‐specific autoregressive integrated moving average (ARIMA) models and generalized least squares (GLS) panel models on first‐differenced data. Setting US states from 1950 to 2002. Participants US general population. Measurements Per capita alcohol sales and cigarette sales, age‐standardized IHD and cirrhosis mortality rates. Findings Apparent consumption of total alcohol was associated with a significant overall increase of IHD of about 1% mortality per litre of ethanol. Beverage‐specific models found that spirits consumption was significantly positively related to IHD mortality overall, for both genders and in three regions defined by drinking culture (or ‘wetness’), while beer was found to have a significant protective relationship overall and in the wet region. The results for wine also suggest a protective relationship, but only marginally significant effects were found. Cirrhosis mortality rates were consistently positively related to IHD mortality. Combined results from state‐specific ARIMA models including both cigarette sales and cirrhosis rates were generally consistent with the GLS results. Conclusions Population‐level models confirm individual‐level findings of both harmful and protective relationships between alcohol use patterns and ischemic heart disease mortality. However, an overall harmful impact of per capita alcohol consumption on IHD mortality was found.     

Per capita alcohol consumption and liver cirrhosis mortality in 14 European countries

Aim. To estimate the effects of changes in per capita alcohol consumption on liver cirrhosis mortality rates in various demographic groups across 14 western European countries. Method. Yearly changes in gender- and age-specific mortality rates from 1950 to 1995 were analysed in relation to corresponding yearly changes in per capita alcohol consumption, employing the Box-Jenkins technique for time series analysis. Country-specific estimates were pooled into three regions: northern, central and southern Europe. Measurements. Cirrhosis mortality data for 5-year age groups were converted into gender-specific mortality rates in the age groups 15 +, 15-44, 45-64 and 65 + and expressed as the number of deaths per 100 000 inhabitants. Alcohol sales were used to measure aggregate consumption, which were calculated into consumption (litres 100% alcohol) per year per inhabitant over 14 years of age and weighted with a 10-year distributed lag model. Findings. The country-specific analyses demonstrated a positive and statistically significant effect of changes in per capita consumption on changes in cirrhosis mortality in 13 countries for males and in nine countries for females. The strongest alcohol effect was found in northern Europe, due mainly to a large effect in Sweden. Moreover, when different age groups were analysed significant estimates were obtained in 29 of 42 cases for males and in 20 of 42 cases for females. Most of the non-significant estimates were found in older age groups. Conclusions. The results suggest clearly that a change in the overall level of drinking as a general rule affect cirrhosis mortality in different drinking cultures as well as among different demographic groups. Moreover, the findings correspond with what is expected from the collectivity theory of drinking cultures.     

Per capita alcohol consumption and total mortality: an analysis of historical data

Since total mortality is a classical proxy for the overall health status of the population, its degree of association with per capita alcohol consumption is of great interest. Existing evidence, based on historical data from the turn of the century, is mostly in graphical form. These data arc analysed using modern statistical tools. The results suggest a significant alcohol effect; a 1-l increase in consumption is expected to increase mortality (middle-aged men) by about 1 %. This effect might seem fairly modest but it is noted that it may well be locally substantial because of its concentration to specific categories of the population. The alcohol effect is also compared with the impact of a factor that is a surrogate for a large number of etiological agents, namely real wages. Although the latter factor seems to be the more important one the difference is not overwhelming. The shift in the cause of the death panorama during this century, with an increasing share of CHD-mortality, may well have attenuated the aggregate relationship between alcohol and mortality.     

Per capita alcohol consumption and all-cause mortality in Canada, 1950-98

AIMS: To estimate the relationship between per capita alcohol consumption and male all-cause mortality in Canada. DATA AND METHOD: The outcome measure comprised annual data on male all-cause mortality for the period 1950-98. Alcohol sales (in litres 100% alcohol) were used as proxy for per capita consumption. The data were analysed using the Box-Jenkins technique. Two models were estimated, one including only female mortality as control, the other in addition cigarette sales. RESULTS: The first model yielded a significant alcohol effect that implied a 2.9%[standard error (SE) = 0.6%] increase in mortality given a 1-litre increase in consumption. This estimate coincides with that obtained for northern Europe in previous research. When cigarette sales were included in the model the alcohol effect was still statistically significant but markedly reduced, to 1.7% (SE = 0.6%). CONCLUSIONS: Total mortality is a classic indicator of the general health status of the population. Its relationship with per capita consumption of alcohol supports the view that total consumption is a concern for public health.     

The cardioprotective association of average alcohol consumption and ischaemic heart disease: a systematic review and meta-analysis

Aims Most, but not all, epidemiological studies suggest a cardioprotective association for low to moderate average alcohol consumption. The objective was to quantify the dose–response relationship between average alcohol consumption and ischaemic heart disease (IHD) stratified by sex and IHD end‐point (mortality versus morbidity). Methods A systematic search of published studies using electronic databases (1980–2010) identified 44 observational studies (case–control or cohort) reporting a relative risk measure for average alcohol intake in relation to IHD risk. Generalized least‐squares trend models were used to derive the best‐fitting dose–response curves in stratified continuous meta‐analyses. Categorical meta‐analyses were used to verify uncertainty for low to moderate levels of consumption in comparison to long‐term abstainers. Results The analyses used 38 627 IHD events (mortality or morbidity) among 957 684 participants. Differential risk curves were found by sex and end‐point. Although some form of a cardioprotective association was confirmed in all strata, substantial heterogeneity across studies remained unexplained and confidence intervals were relatively wide, in particular for average consumption of one to two drinks/day. Conclusions A cardioprotective association between alcohol use and ischaemic heart disease cannot be assumed for all drinkers, even at low levels of intake. More evidence on the overall benefit–risk ratio of average alcohol consumption in relation to ischaemic heart disease and other diseases is needed in order to inform the general public or physicians about safe or low‐risk drinking levels.     

The association of alcohol consumption with coronary heart disease mortality and cancer incidence varies by smoking history

OBJECTIVE: To evaluate the effect of alcohol on coronary heart disease (CHD), cancer incidence, and cancer mortality by smoking history. DESIGN/SETTING: A prospective, general community cohort was established with a baseline mailed questionnaire completed in 1986. Participants: A population-based sample of 41,836 Iowa women aged 55-69 years. MEASUREMENTS: Mortality (total, cancer, and CHD) and cancer incidence outcomes were collected through 1999. Relative hazard rates (HR) were calculated using Cox regression analyses. MAIN RESULTS: Among never smokers, alcohol consumption (> or =14 g/day vs none) was inversely associated with age-adjusted CHD mortality (HR, 0.40; 95% confidence interval [CI], 0.19 to 0.84) and total mortality (HR, 0.71; 95% CI, 0.55 to 0.92). Among former smokers, alcohol consumption was also inversely associated with CHD mortality (HR, 0.45; 95% CI, 0.23 to 0.88) and total mortality (HR, 0.78; 95% CI, 0.62 to 0.97), but was positively associated with cancer incidence (HR, 1.25; 95% CI, 1.03 to 1.51). Among current smokers, alcohol consumption was not associated with CHD mortality (HR, 1.05; 95% CI, 0.73 to 1.50) or total mortality (HR, 1.07; 95% CI, 0.92 to 1.25), but was positively associated with cancer incidence (HR, 1.30; 95% CI, 1.10 to 1.54). CONCLUSIONS: Health behavior counseling regarding alcohol consumption for cardioprotection should include a discussion of the lack of a decreased risk of CHD mortality for current smokers and the increased cancer risk among former and current smokers.     

The combined influence of leisure-time physical activity and weekly alcohol intake on fatal ischaemic heart disease and all-cause mortality.

AIMS: To determine the combined influence of leisure-time physical activity and weekly alcohol intake on the risk of subsequent fatal ischaemic heart disease (IHD) and all-cause mortality. METHODS AND RESULTS: Prospective cohort study of 11 914 Danes aged 20 years or older and without pre-existing IHD. During approximately 20 years of follow-up, 1242 cases of fatal IHD occurred and 5901 died from all causes. Within both genders, being physically active was associated with lower hazard ratios (HR) of both fatal IHD and all-cause mortality than being physically inactive. Further, weekly alcohol intake was inversely associated with fatal IHD and had a U-shaped association with all-cause mortality. Within level of physical activity, non-drinkers had the highest HR of fatal IHD, whereas both non-drinkers and heavy drinkers had the highest HR of all-cause mortality. Further, the physically inactive had the highest HR of both fatal IHD and all-cause mortality within each category of weekly alcohol intake. Thus, the HR of both fatal IHD and all-cause mortality were low among the physically active who had a moderate alcohol intake. Conclusion Leisure-time physical activity and a moderate weekly alcohol intake are both important to lower the risk of fatal IHD and all-cause mortality.     

Regional variations in mortality from ischaemic heart and cerebrovascular disease in Britain

In middle-aged men and women, mortality from ischaemic heart disease and cerebrovascular disease is highest in the north and west of Britain. The worst region is West Central Scotland. Statistical analysis using a linear logistic model shows that the differences between the regions are significant and the yearly fluctuation in numbers of deaths contributes little to the overall variation.     

The association between mortality from ischaemic heart disease and mortality from leading chronic diseases.

AIMS: Coronary risk factors raise the risk of other chronic disorders. We therefore tested the hypothesis that the geographic distribution of ischaemic heart disease mortality is associated with that of other chronic diseases with which it shares risk factors. METHODS AND RESULTS: For the 50 provinces of Spain, we collected mortality data for the period 1980-1995 from the national vital statistics. We calculated age-adjusted mortality rates for the leading causes of death in quintiles of provincial distribution of ischaemic heart disease mortality, and correlation coefficients with respect to provincial ischaemic heart disease mortality. As expected, because they share risk factors with ischaemic heart disease, mortality from cerebrovascular disease, malignant tumours, lung cancer, respiratory diseases, chronic obstructive pulmonary disease, diseases of the digestive system, cirrhosis of the liver and all causes, increase with the rise from lower to higher quintiles of ischaemic heart disease mortality. Ischaemic heart disease mortality registered correlations over 0.5 (P<0.001) with mortality from many of the above diseases in the periods 1980-1984 and 1991-1995. Expectations were similarly borne out for disorders not sharing risk factors with ischaemic heart disease, in that mortality from prostate and breast cancer, injury and poisoning, traffic accidents and ill-defined causes in most cases did not show a provincial association with ischaemic heart disease mortality. In general, these results were observed for both sexes and across all age groups. CONCLUSION: Ischaemic heart disease mortality is associated with mortality from chronic diseases which share coronary risk factors, across provinces of Spain over the period 1980-1995. This suggests that the geographic variation in such chronic diseases is due to common factors, potentially susceptible to similar preventive interventions.     

Meta-analysis of the relationship between alcohol consumption and coronary heart disease and mortality in type 2 diabetic patients

Aims/hypothesis This systematic review examines the relationship between alcohol consumption and long-term complications of type 2 diabetes. Meta-analyses could only be performed for total mortality, mortality from CHD, and CHD incidence, because the availability of articles on other complications was too limited. Materials and methods A PubMed search through to September 2005 was performed and the reference lists of relevant articles examined. Among the relevant articles there were six cohort studies reporting on the risk of total mortality and/or fatal and/or incident CHD in alcohol non-consumers and in at least two groups of alcohol consumers. Results Statistical pooling showed lower risks in alcohol consumers than in non-consumers (the reference category). The relative risk (RR) of total mortality was 0.64 (95% CI 0.49–0.82) in the <6 g/day category. In the higher alcohol consumption categories (6 to <18, and ≥18 g/day), the RRs of total mortality were not significant. Risks of fatal and total CHD were significantly lower in all three categories of alcohol consumers (<6, 6 to <18 and ≥18 g/day) than in non-consumers, with RRs ranging from 0.34 to 0.75. Conclusions/interpretation This meta-analysis shows that, as with findings in the general population, moderate alcohol consumption is associated with a lower risk of mortality and CHD in type 2 diabetic populations.     

How does variability in alcohol consumption over time affect the relationship with mortality and coronary heart disease?

Objective To examine the relationship between alcohol consumption and risk of mortality and incident coronary heart disease (CHD), taking account of variation in intake during follow‐up. Method Prospective cohort study of 5411 male civil servants aged 35–55 years at entry to the Whitehall II study in 1985–88. Alcohol consumption was reported five times over a 15‐year period. Mortality, fatal CHD, clinically verified incident non‐fatal myocardial infarction and definite angina were ascertained during follow‐up. Results We found evidence that drinkers who vary their intake during follow‐up, regardless of average level, have increased risk of total mortality (hazard ratio of high versus low variability 1.52: 95% CI: 1.07–2.17), but not of incident CHD. Using average consumption level, as opposed to only a baseline measure, gave slightly higher risk estimates for CHD compared to moderate drinkers at the extremes of the drinking range. Conclusions Multiple repeated measures are required to explore the effects of variation in exposure over time. Caution is needed when interpreting risks of exposures measured only once at baseline, without consideration of changes over time.     

Hypercoagulability and ischaemic heart disease

Thrombogenesis is increasingly recognised as an immediate cause of most major clinical episodes of ischaemic heart disease (IHD) and the haemostatic system makes a significant contribution to the development of atheroma. It is therefore important to consider how far concepts of increased thrombotic tendency and hypercoagulability can be demonstrated in reality. A number of general observations do suggest that characteristics of the circulating blood influence the course of events in IHD--for example, the occurrence of IHD or stroke in young women using oral contraceptives in whom advanced arterial wall changes are not a feature. Epidemiologically, the coagulation system has been more rewarding than the study of platelets. The Northwick Park Heart Study (NPHS) has demonstrated a strong relationship between the level of factor VII activity and the later incidence of IHD. Several biochemical characteristics of factor VII suggest that this relationship may well be one of cause and effect. There is growing evidence that high levels of factor VII activity lead to high levels of thrombin production. In addition to NPHS, three other prospective studies have shown an association between high levels of plasma fibrinogen and IHD incidence. Again, there are several reasons for believing that this association, too, is of pathogenetic significance. Dietary fat intake is a major determinant of the factor VII activity level, and smoking of the fibrinogen level. Hypercoagulability determining IHD is best defined, on present evidence, as over-activity of procoagulatory influences (whereas hypercoagulability leading to venous thrombosis is predominantly manifested as underactivity of natural defence mechanisms).(ABSTRACT TRUNCATED AT 250 WORDS)