Alcohol, Mortality and Cardiovascular Events in a 35 Year Follow-up of a Nationwide Representative
Cohort of 50,000 Swedish Conscripts up to Age 55
A. Romelsjö1,*, P. Allebeck1, S. Andréasson1,2,3and A. Leifman1,3
1Department of Public Health Sciences, Karolinska Institutet, Karolinska University Hospital, Norrbacka plan 2, 17176 Stockholm, Sweden,
2Swedish National Institute of Public Health, Östersund, Sweden and3Stockholm Dependency Centre, Stockholm, Sweden
*Corresponding author: Tel.: +468-52480131; E-mail: firstname.lastname@example.org
(Received 18 October 2011; accepted 4 February 2012)
Abstract — Aims: To assess the association between drinking patterns and mortality, and cardiovascular disease in a large cohort of
young- and middle-aged men and to assess whether the net balance of harm and protective effect implies protective effect or not.
Methods: Information from health examinations, psychological assessments and alcohol use background in a nationally representa-
tive birth cohort of 49,411 male military conscripts aged 18–20 years in 1969/1970, were linked to mortality and hospitalization data
through 2004. Cox regression analyses were conducted and attributable proportions (APs) calculated. Confounders (baseline social
status, intelligence, personality and smoking) were taken into account. Results: Increasing alcohol use was associated with increasing
mortality (2614 deceased) and with decreasing risk for myocardial infarction (MI). The hazard ratio (HR) for mortality was 1.42
[95% confidence interval (CI) 1.10–1.82] with a consumption corresponding to 30 g 100% ethanol/day or more in multivariate
analysis. The risk for non-fatal MI was significantly reduced at 60 g 100% ethanol/day (HR 0.37, 95% CI 0.15–0.90), not reduced for
fatal MI, and non-significantly reduced for total MI. There was a marked association between alcohol use at conscription and mortal-
ity and hospitalization with alcohol-related diagnosis. APs indicate that alcohol caused 420 deaths, 61 cases of non-fatal stroke and
protected from 154 cases on non-fatal MI. Conclusion: Many more deaths were caused by alcohol than cases of non-fatal MI
prevented. From a strict health perspective, we find no support for alcohol use in men below 55 years.
Most studies indicate that high alcohol consumption and
binge drinking is associated with increased total mortality
and low-to-moderate alcohol consumption with reduced mor-
tality in ischaemic heart disease (IHD) (Corraro et al., 2000;
Ronksley et al., 2011). This has been attributed to an
increased level of high-density lipoprotein and decreased
level of low-density lipoprotein cholesterol, a decrease in the
aggregation of thrombocytes (platelets) and a positive impact
on the fibrinogen level from alcohol (O’Brien et al., 2011).
The current knowledge has been summarized in two papers,
which however do not address the possibility of different
associations related to age (Ronksley et al., 2011; O’Brien
et al., 2011).
A possible preventive effect of alcohol may not start
until the age of ~40–50 years in men because below that
age IHD is uncommon and the atherosclerosis process has
usually not progressed far (Tolstrup and Grönbeck, 2007;
Hvitfeldt et al., 2010). However, there are few studies on
the association between alcohol and IHD before the age of
~55 years. In a follow-up to the age of 45 years of the
cohort in this study, Romelsjö and Leifman (1999) found
that alcohol consumption over 15 g 100% ethanol/day was
related to significantly elevated total mortality in multivari-
ate analysis and with a non-significantly reduced myocar-
dial infarction (MI) incidence. Hvitfeldt et al. (2010)
found, in a pooled follow-up analysis of almost 200,000
women and 75,000 men, a negative association between
alcohol and coronary heart disease (CHD) incidence but
that the reduction was smaller in men aged 39–50 years.
White et al. (2002, 2004) found in a study with aggregate
data that alcohol caused 2663 non-IHD deaths and pro-
tected from 898 IHD deaths in men aged 16–54 in Wales
and England in 1997, i.e. an overall negative effect up to
the age of 55, but they lacked data on IHD incidence.
This warranted a further 10 year follow-up, compared with
the previous study, now including many more cases of
myocardial infarction, and also analysing drinking patterns
(White et al., 2002). There is scientific support for
increased risk for haemorrhagic stroke with increases
low-to-moderate consumption, but the net effect in these
ages is unknown (Ronksley et al., 2011).
The scientific literature on alcohol, IHD and mortality is
not consistent. A few studies even report a decreasing IHD
risk with increasing alcohol consumption (McElduff and
Dobson, 1997; Ariola et al., 2009).
Variation in drinking patterns may explain differences in
estimates between studies. In one meta-analysis, binge drink-
ing was associated with a higher IHD risk than other alcohol
use, and another found that irregular heavy drinking occa-
sions were associated with a significantly increased IHD risk
of 1.45 compared with regular drinking up to 60 g 100%
alcohol/day; however, with significant between-study hetero-
geneity (Bagnardi et al., 2008; Roerecke and Rehm, 2011).
An increased risk of IHD with binge drinking might be
explained by increased coronary calcification, episodic high
blood pressure and adverse changes in the balance of fibrino-
lytic factors among binge drinkers (Puddey et al., 1999;
Pletcher et al., 2005).
The first objective in this study was to assess the associ-
ation between alcohol use, including heavy drinking and
mortality and cardiovascular events in a nationwide large
cohort of Swedish men up to the age of 55 years. The
second was to assess the population risk for mortality and
cardiovascular events to find out whether the protective or
harmful effect predominates.
for reducedrisk with
Alcohol and Alcoholism Vol. 47, No. 3, pp. 322–327, 2012
Advance Access Publication 1 March 2012
© The Author 2012. Medical Council on Alcohol and Oxford University Press. All rights reserved
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