- Marita Paassilta, research fellowa,
- Kari Kervinen, consultant physiciana,
- Asko O Rantala, consultant physiciana,
- Markku J Savolainen, associate professora,
- Mauno Lilja, consultant physiciana,
- Antti Reunanen, head of laboratoryb,
- Y Antero Kesäniemi, professor of medicine ()a
- a Department of Internal Medicine and Biocenter Oulu, University of Oulu, Kajaanintie 50, FIN-90220 Oulu, Finland
- b National Public Health Institute, Mannerheimintie 166, FIN-00300, Helsinki, Finland
- Correspondence to: Professor Kesäniemi
- Accepted 24 June 1997
Light or moderate alcohol consumption decreases the risk of coronary heart disease.1 Beneficial changes in high density lipoprotein cholesterol concentrations are, however, observed at quite high levels of alcohol consumption—that is, ≥20 units per week, 1 unit being 10-12 g.2 Therefore, other factors may be responsible for decreasing the risk of coronary heart disease when alcohol is consumed in social amounts. We studied the relation between light and moderate alcohol intake and Lp(a) lipoprotein concentrations. Lp(a) lipoprotein is an independent risk factor for coronary heart disease3 and is affected by alcohol misuse.4
Subjects, methods, and results
We performed a population based cross sectional study of 300 men aged 40-60 years selected randomly by age stratification; 259 (86%) participated in the study. Subjects were divided into four groups by alcohol consumption: abstainers (mostly lifetime teetotallers; 37 men) and three groups of drinkers. Drinkers in the lowest third consumed <39 g alcohol/week (74 men), those in the middle third 39-132 g/week (75), and those in the highest third >132 g/week (73). Alcohol intake was ascertained from a questionnaire on the amount and quality of alcoholic beverages consumed during the previous two weeks. Plasma Lp(a) lipoprotein concentrations were determined by a two site immunoradiometric assay that showed a close correlation with two different enzyme linked immunoassays (r≥0.96). Liver function was assessed by measuring lipid and enzyme concentrations in fasting blood samples using standard techniques. Statistical analysis was carried out with the SAS software package. The groups were similar for age and smoking habits. The body mass index, waist to hip ratio, systolic and diastolic blood pressure, and alanine aminotransferase values were highest in subjects in the third drinking >132 g/week compared with those in the two lower thirds and with non-drinkers (P<0.001 for each parameter, analysis of variance). The mean concentrations of serum γ-glutamyltransferase increased with increasing alcohol intake—that is, 34, 33, 49, and 64 U/l respectively for teetotallers, and the lowest, middle, and highest third of drinkers (P<0.001). Blood glucose and serum insulin values did not differ between the groups. Lp(a) lipoprotein concentrations were higher (median, 206 mg/l) in the teetotallers than in the drinkers. Lp(a) lipoprotein concentrations for the lowest, middle, and highest alcohol thirds were 137, 109, and 94 mg/l (P<0.05, Kruskal-Wallis test) (figure). As noted in other white populations, we observed a highly skewed distribution of Lp(a) lipoprotein concentrations and a wide range within the population. The ranges were similar in the study groups (figure). Lp(a) lipoprotein concentrations showed a weak but significant correlation with body mass index, waist to hip ratio, and insulin concentrations (Pearson's correlation coefficients −0.15, −0.14, and −0.15 respectively, P<0.025 for each correlation). There were no significant differences in high density lipoprotein (means for the teetotallers, and the lowest, middle, and highest thirds of alcohol consumption 1.19, 1.19, 1.23, and 1.27 mmol/l respectively) or low density lipoprotein cholesterol concentrations between the groups.
Our report shows that social drinking—that is, <39 g alcohol/week or 1-4 units/week—is associated with low Lp(a) lipoprotein concentrations in middle aged men. No changes were observed in high density lipoprotein cholesterol or low density lipoprotein cholesterol concentrations, blood pressure, or liver enzyme concentrations.
Other studies of alcohol consumption and Lp(a) lipoprotein cholesterol concentrations have dealt with differences between men and women, analysed alcohol intake qualitatively,5 and compared heterogeneous groups—that is, non-drinkers together with those who drink regularly on three or less days a week. To our knowledge, ours is the first study to show a relation between moderate alcohol consumption and Lp(a) lipoprotein concentrations. We conclude that low Lp(a) lipoprotein concentrations may be one factor explaining low mortality and retarded progression of coronary artery disease in social drinkers.
We thank Ms Saija Kortetjärvi, Ms Anna-Riitta Malinen, and Ms Liisa Laine for technical and secretarial support, and Markku Linnaluoto for help with the statistics.
Contributors: MP participated in data analysis, writing the paper, and a discussion of the core ideas. KK discussed the study hypothesis and core ideas, and participated in data analysis and writing the paper. AOR participated in the study design, patient investigations, and data collection. MJS discussed the study hypothesis and core ideas, and participated in writing the paper. ML participated in the study design, data collection, and writing the paper. AR participated in the study design, statistical analysis, and writing the paper. YAK was the principal investigator; he initiated and coordinated the formulation of the primary study hypothesis, designed the protocol, discussed core ideas, and participated in data interpretation and writing the paper. YAK will act as guarantor of the study.
Funding: This study was supported by grants from the Finnish Foundation for Alcohol Studies, the Finnish Foundation for Cardiovascular Research, and the Medical Council of the Academy of Finland.
Conflict of interest: None.