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Reduction is supported by other studies
EDITOR In 1995 we reported a significant reduction in Lp(a) lipoprotein
concentration in a prospective study of 20 healthy volunteers (men and
women) given 21 g of alcohol daily for 10 days in the form of red wine
(median (range) 186 (15-1420) mg/l v 132 (10-1210) mg/l,
P<0.001).5 This reduction was not repeated when the same subjects were given white wine, raising the issue of potential differences between various alcoholic drinks. Interestingly, we found
no changes in high density lipoprotein cholesterol concentrations.
We have conducted a larger unpublished crossover trial in 50 men
comparing the effects of 3 units (24 g) of alcohol a day as red wine or
vodka for 14 days on Lp(a) lipoprotein concentrations. Each period of
alcohol consumption was preceded by two weeks' abstinence. Both drinks
produced a 10-12% decrease in Lp(a) concentration (geometric mean 153 mg/100 ml v 135 mg/l after vodka, P<0.001; 151 mg/l
v 136 mg/l after red wine, P<0.01). These results
suggest that moderate alcohol consumption results in changes in Lp(a) lipoprotein which are independent of the type of alcoholic drink consumed. In conclusion, we agree with Paassilta et al that lower Lp(a)
concentrations may be one factor conferring lower mortality and
cardiovascular benefit in social drinkers.
No effect seen in Australian drinkers
EDITOR Current alcohol intake was assessed by personal interview and
classified as nil, 10-70 g/week, 80-140 g/week, 150-280 g/week, and
>280 g/week (the last group in men only). The third and fourth groups
correspond most closely with the middle and highest third of alcohol
intake described by Paassilta et al.1 Lp(a) lipoprotein concentration was assessed by a sandwich enzyme linked
immunosorbentassay (ELISA) with polyclonal sheep antibody raised
against purified human apo(a) (TintElize Lp(a) Biopool, Sweden). The
table shows median (interquartile range) Lp(a) lipoprotein and mean
high density lipoprotein cholesterol concentrations by sex and alcohol
intake.
There was no significant relation between Lp(a) lipoprotein
concentration and alcohol intake in either sex. We drew similar conclusions when the data were examined in those below or above 70 years of age. The usual positive relation between alcohol intake and
high density lipoprotein cholesterol was confirmed. Paassilta et al
examined only 259 men aged 40-60 years. The median Lp(a) lipoprotein
concentration in 37 teetotallers seemed high at 206 mg/l, and this may
have been a spurious result. Surprisingly, they found no relation
between alcohol intake and high density lipoprotein cholesterol
concentration. Though we have reported that any alcohol intake in our
cohort is associated with reduced coronary risk3 and
raised Lp(a) lipoprotein concentration is associated with increased
coronary risk,2 any link between alcohol intake and Lp(a)
lipoprotein concentration seems unlikely.
Reduction is not found in women
EDITOR The groups were similar regarding body mass index and total cholesterol
concentrations. The mean age of former drinkers was higher than that of
men in the other groups (analysis of variance P<0.0001). We therefore
adjusted for age in all other analyses. Lp(a) lipoprotein concentration
decreased with increased alcohol consumption in men except in former
drinkers (table). Fibrinogen concentrations fell with increasing
alcohol consumption
(P<0.05).
For women the geometric mean Lp(a) concentrations were 148 mg/l in
non-drinkers, 144 mg/l in former drinkers, 144 mg/l in lowest third,
136 mg/l in middle third, and 138 mg/l in highest third. There was no
significant association between Lp(a) lipoprotein concentration and
alcohol consumption (P=0.27). Fibrinogen concentrations decreased with
increasing consumption (P<0.0001).
Our analysis shows a negative relation between alcohol consumption and
and Lp(a) lipoprotein concentrations in men but not in women. These
results support Paassilta et al's study and confirm our previous
qualitative analysis.
We agree with Paassilta et al that there may be a relation
between moderate alcohol consumption and lower Lp(a) lipoprotein concentrations.1 The relation between alcohol consumption
and cardiovascular mortality is U shaped, with the lowest mortality at
an alcohol consumption of 2-4 units (16-32 g) a day.2
Several mechanisms contribute to this cardioprotective effect including beneficial increases in high density lipoprotein
cholesterol3 and inhibition of platelet
aggregation.4 However, other factors may be involved.
Lp(a) lipoprotein is a recognised independent risk factor for the
development of atherosclerosis and, as stated by Paassilta et al,
little attention has been directed to the effects of alcohol on Lp(a)
lipoprotein.
Ian S Young
Department of Clinical Biochemistry, Queens University of
Belfast and Royal Hospitals Trust, Belfast BT12 6BA
Alun E Evans
Division of Epidemiology, Queen's University of Belfast
the evidence for a protective effect.
Clin Chim Acta
1996;
246:
59-76[Medline].
Paassilta et al suggest that a moderate intake of alcohol in
Finnish men is associated with a roughly 50% reduction in median Lp(a)
lipoprotein concentration.1 We have published relevant
data from a large Australian cohort participating in an ongoing
prospective study of cardiovascular disease (2805 subjects
60 years,
average age 70 years).
2 3
Judith Simons
University of New South Wales, Lipid Research Department, St
Vincent's Hospital, Darlinghurst, NSW 2010, Australia
Paassilta et al showed a quantitative association between social
alcohol consumption and low Lp(a) lipoprotein concentrations in middle
aged men.1 As they indicated, we reported a negative qualitative association between drinking habits and Lp(a) lipoprotein concentrations in men.2 We report here the results of a
quantitative analysis of the association between alcohol intake and
Lp(a) lipoprotein concentration in the Jichi Medical School cohort
study. During 1992-5 we collected population based data in rural
districts in Japan. The 9532 subjects (3658 men and 5874 women), which
included all subjects in our previous report, were divided into five
categories by drinking status; non-drinkers, (963 men), former drinkers
(140 men), drinkers in the lowest third of alcohol intake
(<107 g/week; 711 men), drinkers in the middle third
(107-224 g/week; 942 men), and drinkers in the highest third
(>224 g/week; 902 men). Serum Lp(a) lipoprotein concentrations were
measured with an enzyme linked immunosorbent assay (ELISA) and Lp(a)
lipoprotein and triglyceride concentrations were calculated as
geometric means. We used SAS software for statistical analysis.
Tadao Goto
Naoki Nago
Department of Community and Family Medicine, Jichi Medical
School, Minamikawachi, Kawachi, Tochigi, Japan
© BMJ 1998
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