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Annual surveys initiated in the s see Johnson et al.

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These figures too have shown no significant change since In a comparative perspective, the United States is remarkable among Western industrial nations for its proportion of adult abstainers, which is higher in the United States than in Canada or in any nation in western Europe these countries range from 3 percent to 30 percent abstainers; [NIAAA ]. There is considerable regional variation in the United States, however. The proportion is lowest in the Mid-Atlantic states 17 percent and highest in the Bible Belt states of the South 65 percent.

It is important to note that even where drinking patterns for a population appear to be stable across a number of years, there is continual flux in the drinking patterns of many individuals within the population. At the extreme, many clinically diagnosed alcoholics alternate between periods of heavy consumption and periods of abstention.

There is also a tendency for drinking to decline markedly beyond the age of 50, and there are often significant differences in drinking rates between age and sex cohorts as well as within the same cohort at different points in time. Skog has argued that these different drinking subpopulations are the primary explanation for the departure of consumption curves from Ledermann's predictions. It is one thing to know how much or how often people drink; it is another to pinpoint the effects of that drinking.

For virtually every possible consequence of alcohol use that we may be interested in, alcohol is neither a necessary nor a sufficient cause, but rather one in a series of factors that may combine in various ways to yield effects. The presence of specifiable other factors, some permanent but others subject to manipulation, is just as important as drinking per se to the production of alcohol-related effects. For example, sustained heavy alcohol use is demonstrably associated with the pathological and potentially fatal liver condition called cirrhosis.

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The data on this connection are as strong as those linking heavy smoking with lung cancer. But the mechanism by which alcohol use causes this gradual accumulation of scar tissue in the liver is still speculative. It is known that cirrhosis can occur in people who have never drunk alcohol. It is known that various nutritional deficiencies or imbalances can not only cause cirrhosis directly, but also can markedly change the vulnerability of liver tissue to alcohol-related cirrhosis.

Good nutrition probably cannot prevent alcoholic cirrhosis; but bad nutrition can certainly hasten it along.

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Another example is automobile accidents. Drunken driving is notoriously a precursor of traffic fatalities. Perhaps 1 in to 2, of legally drunk-driving episodes result in arrest—and there are far more arrests than fatalities. Moreover, an individual can hardly cause a traffic fatality, no matter how drunk, in the absence of a lethal vehicle.

This may seem trivial in a nation of million automobiles, but it is not trivial if changes in gasoline costs drastically depress people's use of cars or change the way autos are built and driven. These two examples involved the negative effects of alcohol on physical well-being.

In looking at psychological and social well-being, the difficulties do not decrease. A number of studies have found some common properties among the personalities of diagnosed alcoholics: depression, anxiety, low frustration tolerance, feelings of powerlessness, etc. But virtually the same properties have been deemed to cause alcoholism. If depression is both a cause and an effect of heavy drinking, how can one decide what part of the alcoholic's depression, or of suicides that follow from depressive episodes, is due to drinking? Similarly, attempting to pinpoint the exact part played by drinking in problematic social behavior is exceedingly difficult, compounded as it is by interaction with others during numerous situations over time.

All of these problems in attribution apply to the positive effects of alcohol use as well. They are somewhat aggravated by the disinclination of researchers to investigate positive effects, which means that less data are available for analysis. For example, the best-known study of economic effects of alcohol is on the costs of alcohol abuse and alcoholism and does not attempt to estimate effects that may yield economic positives.

Mortality studies ask how many deaths alcohol may have been at least partly responsible for and do not concern themselves with the lives alcohol may preserve, even though studies on heart disease have indicated certain advantages possibly associated with moderate drinking. There is no avoiding the difficulties in attributing the effects of alcohol use; however, it is necessary to have some scheme of accounts for these effects if we are to consider alcohol-related policy. If a central principle of any policy is to preserve and promote good effects while minimizing bad ones, then it is difficult to evaluate any policy without identifying the effects of relevance and observing how they change over time.

Since the consequences of alcohol use are manifold, it is important in the first place to identify the ones of greatest social importance, to assess the relative importance of alcohol in generating them as best we can, and then to be systematic and comprehensive in thinking about how these effects can be modified.

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A more exact feel for the difficulties of attribution may be achieved by examining recent responsible attempts to estimate the effects of drinking in the United States. Congress on Alcohol and Health. Each examines a different dimension or measure of effects: mortality deaths , economic costs dollars , and psychobehavioral problems symptoms. Table 5 , reproduced in Alcohol and Health 3 NIAAA , estimates that the number of deaths related to alcohol use in the United States in was between 61, and 95, A comprehensive study of deaths among clinical alcoholics Schmidt and Popham , also see Polich et al.

For 12, former alcoholism patients in Ontario, Canada, who were followed up at an average of 8. The authors of this study caution that alcoholics smoke cigarettes at considerably higher rates than the comparison population and, hence, that excess heart disease and cancer deaths are associated to an unclear degree with tobacco rather than alcohol exposure.

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  7. They also warn that nutritional and other life-style differences intervene in the relation between drinking alcohol and dying. But what does this mean? If we wish to determine how alcohol affects the overall death rate in the United States, i. There is some evidence, for example, that moderate drinking is correlated with decreased risk of death, particularly death involving ischemic heart disease. However, being related to or correlated with does not amount to causal proof.

    In this sense, the , figure is simply a pool within which whatever deaths might be caused by alcohol—and thus prevented by minimizing its use or misuse—are to be found. The number will be no more—it will be much less.

    How much less is not certain, but a figure in the area of 50, theoretically preventable deaths seems reasonable. This is not ,—but neither is it negligible. Table 7 is a tabulation of how much alcohol abuse and alcoholism cost the United States in This collection of dollar values is held by its authors Berry et al.

    It is difficult to assign precise significance to this result. For one thing, a large fraction of the costs tabulated here do appear to be borne by the alcohol abuser: from 25 percent to 50 percent of the total amount cited. There are implicit assumptions about the labor supply in —namely, that it was short—that are not consistent with the then-prevailing economic indicators unemployment was at 8. There are some problems raised by this approach of estimating costs in absolute, autonomous terms.

    Economic cost estimates are usually related either to a specific program of action or to a specific annual budget.

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    In the first instance, one might estimate the costs and benefits of a specific program to modify alcohol abuse. Absent from such contexts, a multibillion dollar cost figure is simply a large price tag on an empty box. It draws attention, but gives little guidance. In the original table Johnson et al. Rates of Problem Drinking Among U. Drinkers, by Drinking Population, — These data really shed little light on the relationship between alcohol use and consequences. A few categories of symptoms not the most common ones are markedly more prevalent among heavier drinkers than other drinkers.

    But this report's conglomeration and renaming of categories obscures more than it enlightens. It is impossible to attach meaning to Table 8 beyond the indication of stability across time. No single way is right for all purposes, but my concern here is to highlight the socially important effects, to examine the degree to which alcohol is a principal cause, to roughly estimate the population affected, and to note what other generative factors besides alcohol use might be important and subject to modification.

    Taking this view, I can identify five principal environments that, when combined with alcohol, produce effects. Each is best visualized as a system. First is the internal organic environment of the body, in W. Cannon's sense: its basic, enduring physiological forms and processes.

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    Our principal interests here are the organs most sensitive in the long term to alcohol exposure: the heart and the liver. The second environment is the personality. It is also internal to the person and one can even speak of it as based in an organ: the brain. But the physiological base does not suffice to complete our thinking about effects on the personality system.

    We need to use psychological concepts that we would not think of applying to hearts or livers. It is of great importance that the physical environment we touch most directly is heavily transformed by human activity. The world of moving vehicles, building elevations, and concrete and floating surfaces is no less physical for being fabricated. The fourth system, external like the last, is the system of intimate social relations, most particularly those we traditionally regard as primary and important to us: kin and coworkers or, to stress the long view, family and occupational careers.

    Finally, there is the institutional environment, the relatively impersonal social matrix of secondary relations that we can ordinarily relate to only in abstract or remote terms, although it diffusely and sometimes very directly transfigures our lives. Most particularly, we are interested here in the broad public systems of responsibility for health care, civil safety, and economic well-being. When the possibilities of sustained changes in physiological systems due to alcohol use are examined, very different effects come into view depending on whether the depth of intoxication, drinking patterns, or total consumption is considered.

    Due to the surprising capacity of the liver to rapidly convert alcohol to usable carbohydrate, the physiological effects of intoxication tend to be short-lived. The principal exception is intoxication that leads quite immediately to death. In examining drinking patterns, on the other hand, the primary effect involves physical dependence on alcohol, which induces vulnerability to the pathological syndrome of withdrawal or abstinence.

    The medical recognition and management of this syndrome, however, has relegated it to a fairly insignificant role in terms of physiological health—in contrast to the effects which physiological alcohol addiction may accentuate or support of drinking patterns on psychological and interpersonal matters.

    Finally, clear links between drinking patterns and physiological changes have been investigated most thoroughly in relation to total consumption. In this connection, rates of coronary heart disease and cirrhosis of the liver are by far the most prominent physiological aspects known at this time.

    Deaths from alcohol overdoses, alone and in combination with other drugs, account for close to 10, deaths and perhaps , episodes of medical intervention each year. The finding of BAC in excess of 0. Approximately 5, such deaths occur each year Day Since these reports indicate only measurable presence of blood alcohol and not specific BAC and do not speculate about relative mechanisms, it is difficult to know in how many of these deaths alcohol was a sufficient or necessary cause.

    The incidence of suicide within this group is not known, although in the alcohol-in-combination cases the death certificates estimate suicidal intent in about 40 percent of the cases. Cirrhosis of the liver is a disease process known to have multiple causes, that are not all well understood French Certain protein deficiencies are invariably followed by appearance of cirrhosis—the dissolution of liver cells and their replacement by scar tissue. Cytological studies on the effects of alcohol use have shown that there is a buildup of fatty yellow liver cells as a consequence of metabolizing alcohol.

    In laboratory studies of short-term high-level exposure to alcohol, mitochondria essential organelles within liver cells disintegrate. Both of these processes may contribute to liver cell death and fibrosis cirrhosis. The supply of certain amino acids in the diet also appears to have a strong influence on how well liver cells resist deterioration; but this protective effect is by no means absolute Lieber et al.

    These microbiological findings are strongly supported by macroepidemiological studies Schmidt , which show that gross rates of cirrhosis deaths track shifting rates of total consumption in a population. Among clinical alcoholic populations in which consumption of 5 ounces of alcohol daily for long stretches of time is an approximate lower limit of alcohol use, a prevalence of cirrhosis damage of 8 percent has been reported, far in excess of the general population; another 25 percent suffer acute liver inflammation, generally regarded as a precursor to cirrhosis.

    In postmortem studies of individuals identified as alcoholics in New York City Haberman and Baden , the incidence of moderate-to-severe fatty changes in the liver exceeded the rate of cirrhosis by approximately the same proportions.