SummrrrIn this paper u it mgucd that LcdmMrm's so-cakd singlcdishibwwn theory is not based on substanrial hypotheses about human drkking behaviour, and that u t h m f m fads to explain anything. An ahnative theory of the disnibhm of alcohol UmsUmpLion is owlincd. The themy is folcndcdon basic hypothaws about human drinking beiraoiolrr. The thaory it usted against ~l p c y data from diffacnt colmrritt, and u is concluded that a snvng c o k t i v e componou ncins in human drinking ?iabits. As a main rule, the popularion unds to moac in c o t u m up and doum the scak of connmption. IlltlUdUCtionLedarmnn's theory of the distribution of alcohol consumption [ 11 has caused heated controversy during the last IS years. According to this socalled singledistribution theory, a high degree of lawfulness should exist in the drinking bthnviour of members of a culture. In fact, the theory postulates that the distribution of the population along the scale of consumption can be described mathanatidy by a special variant of the socalled log-normal distribution function.The debate on the Ledamam theory has partly been concaned with the validity of its basic hypotheses, and partly with its implications for primary prevention of alcohol related problems. The points of vim have varied strongly. Some have argued that the theory contains important insights, and haw used it as a basis for rccommendations to the health authorities [2-4]. others have been much more critical and have maintained that the results have few or no conscquu~xs at d for prevention [5-7]. This disagreement reflects in part dissimilarities in the understanding of what the available data actually have shown, and in part divergencies in the casual interpretations and the gamplity of the result. In the present paper I will try to clarify some of thcse questions. I shall argue that the Ledcrmann theory in its original form is untenable, strictly spmking. However, the theory *Resented at the 29th International Institute of the Prevention and Treatment of Alcoholism, Zagreb 27th June-1st July 1983.still seems to contain some truth even though it does not explain the phcnomcnn it predicts. The theory should therefore be replaced by a less rigid one, which is in agrument with the data. In an attempt to obtain this, two hypotheses, describing the genesis of individual d r i n h g habits, will be formulated. Thcse hypotheses can be tested against the data present on hand, and the hypotheses give predictions about several important charpcteristics of the distribution pattern for alcohol consumption. The Ledcmpnn theoryLedumann's theory of the distribution of alcohol consumption is based on two hypotheses. Firstly, Ledamann hypothesized that the annual intake of lations, and that thesc variations can be described mathematically by a so-called lognormal distribution function. This implies that each population should be distributed according to the well-known gaussian normal distribution, if one uses a logadmtic consumption scale. On a hear consumption scale, the distribution wou...

This supplement includes a collection of papers that aim at estimating the relationship between per capita alcohol consumption and various forms of mortality, including mortality from liver cirrhosis, accidents, suicide, homicide, ischaemic heart disease, and total mortality. The papers apply a uniform methodological protocol, and they are all based on time series data covering the post-war period in the present EU countries and Norway. In this paper we discuss various methodological and analytical issues that are common to these papers. We argue that analysis of time series data is the most feasible approach for assessing the aggregate health consequences of changes in population drinking. We further discuss how aggregate data may also be useful for judging the plausibility of individual-level relationships, particularly those prone to be confounded by selection effects. The aggregation of linear and curvilinear risk curves is treated as well as various methods for dealing with the time-lag problem. With regard to estimation techniques we find country specific analyses preferable to pooled cross-sectional/time series models since the latter incorporate the dubious element of geographical co-variation, and conceal potentially interesting variations in alcohol effects. The approach taken in the papers at hand is instead to pool the country specific results into three groups of countries that represent different drinking cultures; traditional wine countries of southern Europe, beer countries of central Europe and the British Isles and spirits countries of northern Europe. The findings of the papers reinforce the central tenet of the public health perspective that overall consumption is an important determinant of alcohol-related harm rates. However, there is a variation across country groups in alcohol effects, particularly those on violent deaths, that indicates the potential importance of drinking patterns. There is no support for the notion that increases in per capita consumption have any cardioprotective effects at the population level.

The results lend support to the public health perspective in that the increased accessibility to alcohol rendered by Saturday opening also seems to have increased consumption. On the other hand, we could not detect any increase in alcohol-related harm. The question of whether this may be due to insufficient statistical power is discussed, together with some other methodological complications that were highlighted by the study.

The contribution of heavy and moderate drinkers, respectively, to the rate of alcohol problems in society is evaluated for different types of risk functions. It is demonstrated that if the risk function is linear, the moderate drinkers will be responsible for the bulk of the problems. When the risk function is curved upwards, the heavy drinkers contribute a larger share of the problem. However, the risk function needs to be quite strongly curved before the majority of the problems can be attributed to the heavy drinkers. These calculations are based on certain empirically motivated assumptions about the distribution of the consumers along the consumption scale. The results suggest that the validity of the prevention paradox depends very much on the shape of the risk function, and hence that the role of the moderate drinkers may vary a lot across the spectrum of alcohol-related disabilities. For disabilities where the risk curve has a pronounced threshold-like form, the prevention paradox cannot be expected to apply. However, the role of the moderate drinker could be expected to be more significant for disabilities with a smoother and less convex risk curve. Accidents and social problems seem to fulfil the latter qualification, because the causal mechanism underlying such problems are connected to rates of acute intoxication, rather than to annual intake per se.

Both survey data and liver cirrhosis mortality data demonstrate the existence of a relationship between per capita consumption of alcohol and the prevalence of heavy alcohol use. The present paper reviews some of the explanations given for this relationship, and the so-called “contagion between persons” explanation is further developed. The empirical evidence for the basic assumptions of this theory is reviewed, and some predictions are derived and related to empirical facts.