Addiction (1998) 93(12), 1757 ± 1759

EDITORIAL

It can be bad for the heart, tooÐ drinkingpatterns and coronary heart disease

There is now strong evidence showing that mod-

erate alcohol consumption protects from coron-

ary heart disease (CHD). Three important

papers were published last year. Although an

early report from the British Regional Heart

Study found no signi® cant association between

alcohol and CHD among men without a history

of CHD or stroke, a recent report, with a longer

follow-up period, found that regular drinkers had

signi® cantly lower CHD risk than occasional

drinkers or non-drinkers, albeit the difference

was small in absolute terms (Wannamethee &

Shaper, 1997). The huge cohort of the American

Cancer Society Study, with almost half-a-million

subjects and 46 000 deaths, provided risk esti-

mates of remarkable precision in a sample more

homogeneous than the general US population.

Mortality from CHD was, compared with non-

drinkers, 10± 30% lower among men with no

pre-existing CHD and 30± 40% lower among

men with pre-existing CHD. The respective

® gures for women were 10± 20% and 30± 40%

(Thun et al., 1997). Finally, an Australian study,

focusing on drinking patterns, found the lowest

CHD risk at the level of one to two drinks (each

10 g of alcohol) per day on ® ve or six days a

week among both men and women. In these

groups, men had 64% less coronary heart disease

than abstinent men and women 61% less than

abstinent women. However, the same study also

found signi® cantly increased CHD risk among

men who consumed nine or more drinks a day

1± 2 days a week and among men who consumed

this amount daily. Compared with life-long

abstainers, the odds ratios were 2.62 and 2.40

(McElduff & Dobson, 1997).

The Australian study is in contrast to most

epidemiological studies on CHD risk. The latter

have generally found a decreasing trend of CHD

incidence by increasing alcohol intake (Marmot

& Brunner, 1991; Rimm et al., 1996). Neverthe-

less, the Australian study is not the only one to

® nd out that alcohol can also be bad for the

heart. Earlier, The Chicago Gas Company Study

examined the 15-year survival of 1233 men,

initially free of de® nite CHD. Even after adjust-

ing for age, blood pressure, serum cholesterol,

weight, heart rate and cigarettes/day, the risk of

CHD death was 2.2-fold risk among problem

drinkers, compared with all other men (Dyer et

al., 1977). Problem drinkers had a history of

coming to work intoxicated as well as well as

other chronic alcohol-related problems. In Fin-

land, signi® cantly increased risk of CHD death

has been found in relation to heavy drinking

(Suhonen et al., 1987), frequency of intoxication

and that of hangover (Poikolainen, 1983), and

drinking six or more beers daily (Kauhanen et

al., 1997). All these studies differ from the main-

stream in that the focus is not on long-term

alcohol intake averaged on all days (including

abstinent days) but on binge or heavy drinking.

Intuition suggests an important difference

between drinking, for instance, 14 drinks in one

Saturday evening or drinking two drinks every

day, although the average intake per day is the

same. It is therefore interesting that the above

studies have found that the risk of CHD death is

clearly increased by certain drinking patterns

among middle aged and older individuals. What

could be the underlying mechanism?

First, binge drinking accelerates atherosclero-

sis. Coronary artery occlusions have been found

to be more extensive among binge drinkers than

among daily drinkers who consumed the same

total weekly amount (Gruchow et al., 1982) and

carotid atherosclerosis has been found to be

more pronounced among heavy drinkers than

0965 ± 2140 /98/121757 ± 03 $9.50 Ó Society for the Study of Addiction to Alcohol and Other Drugs

Carfax Publishing Limited

1758 Editoria l

among moderate drinkers or abstainers in a

prospective study (Kiechl et al., 1998).

In animal experiments, acute administration of

alcohol has been shown to decrease the occur-

rence of arrhythmias, while chronic exposure to

alcohol increases these (Friedman, 1992). Clini-

cally, heavy drinking increases the risk of cardiac

arrhythmias whether or not CHD is present. The

phenomenon has been called ª holiday heartº

syndrome because of its association with binge

drinking (Ettinger et al., 1978). Atrial ® brillation

is common but other supraventricular tach-

yarrhythmias, and even ventricular tachyarrhyth-

mias, may occur. It is postulated that subclinical

cardiomyopathy may produce patchy delays in

conduction, especially if there is also depletion in

magnesium and potassium, and a hyperadrener-

gic state (Koskinen & Kupari, 1992). The latter

three often go together during withdrawal from

alcohol. Heavy drinking may also cause vagal

neuropathy that restricts the variability of heart

rate, increasing the risk of CHD death (Koski-

nen & Kupari, 1992). Moreover, alcohol may

mask the chest pain of angina pectoris while

decreasing blood ¯ ow to ischaemic myocardium

(Friedman, 1992). Subclinical alcoholic car-

diomyopathy may be unmasked by CHD, which

may increase the risk of sudden death due to

either acute heart failure or fatal arrhythmias

(Fraser & Upsdell, 1981). The disturbances of

the rhythm of the heart may kill leaving no

evidence to the coroner.

The above suggests that ascertaining the

actual underlying cause of death is often

dif® cult. This could be one, at least partial,

explanation between divergent ® ndings between

various studies on alcohol and CHD. Most of

these studies have relied on the of® cial death

certi® cates, not on independent reviews of all

available documents. Accuracy may be under-

mined by low autopsy rates. Making a distinction

between cardiomyopathies, dysrhythmias, hyper-

tensive cardiovascular disease and CHD may be

problematic and be subject to diagnostic prefer-

ences in the absence of clear evidence.

Another possible explanation for the variance

of the observed shapes of associations might be

the lack of data on the drinking patterns that

actually kill. In most studies on alcohol and

CHD the highest drinking category has been

low, typically from ª three or moreº to ª six or

moreº drinks per day. This is not necessarily

high enough to uncover the adverse effects of

heavy drinking. Higher categories should be

used, whenever possible. Another dif® culty is

that the data may be too sparse to allow a more

detailed classi® cation in the wet end of the con-

sumption distribution, because the hard-core

drinkers tend to avoid participating in the

research projects. Special effort is needed to

harvest enough heavy drinkers in future projects.

More detailed mapping of drinking patterns

would also help. At least the total amount of

alcohol per a given (actual or an hypothetical

average) day should be clari® ed. Separate ques-

tions on the habitual quantity and frequency on

beer, wine and spirits consumption do not yield

this information, if the respondent drinks more

than only one beverage type on the same day.

We do not know, therefore, if the risk related to

having six or more beers daily in a Finnish study

was also in¯ uenced by additional amounts of

spirits or wine during the same day. Further

studies should take better into account variations

both in the exposure and in the host. The

exposure variables could include, whenever feas-

ible, the speed of drinking, degree of intoxi-

cation, blood alcohol levels and simultaneous

ingestion of food and other substances. The host

factors could include body weight, water con-

tent, intragastrointestinal metabolism and the

underlying condition of the heart. More thor-

ough cause-of-death examination is also needed.

Such data would help us to de® ne more precisely

the alcohol intake that is harmful. Awaiting this,

let it be widely known what has already been

observed: heavy and binge drinking is bad for the

heart.

KARI POIKOLAINEN

JaÈ rvenpaÈ aÈ Addiction Hospital,

FIN-04480 Haarajoki,

Finland

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