But what about addiction?

So many fear addiction. The former First Lady, Betty Ford, said in 1991 that alcohol was the number one addictive drug in the US. Yet the fact is that by far the majority of people who enjoy alcohol don't feel a compulsion to drink and don't suffer from withdrawal, which are the markers of an addictive drug. Roueche (1960) quotes a reformed alcoholic, the Reverend Ralph S. Pfau, in differentiating between a drunkard and an alcoholic: 'The drunkard drinks because he wants to. The alcoholic drinks because he has to.'
This is an important difference. As Harold Lovell, erstwhile clinical professor of neurology at the New York Medical College, said:

Alcoholism is a condition characterised by uncontrolled, compulsive drinking. An alcoholic is impelled to drink against his will or judgement, even if will or judgement are functioning.

Stanton Peele (1985) says: 'Addiction may occur with any potent experience.' Orford (1985) reminds us that compulsive gambling, extremes of sexual behaviour and overeating are all addictions. Might we add to these watching television, shoplifting, sur ng the Internet, shopping (notably by credit card) and work?
Alcohol is less addictive than caffeine. It was shown by Strain et al. (1984) that caffeine in coffee, tea and cola induced all of the features of psychoactive dependence, including the continued use of the material despite side effects which include anxiety, sleeplessness and gastrointestinal dif culties, as well as the displaying of withdrawal symptoms. True, it is possible to get caffeine-free versions of this type of drink - but the 'fully charged' versions of each hardly attract the same attention as alcohol in the legislature. The words 'alcohol' and 'drug' are linked in the public consciousness, not so 'coffee' or 'cola' and 'drug'.
Those over-imbibing sodas or coffee would seldom be considered generally to have a disease. Yet the majority of the public would consider alcoholism to be a disease. The medical profession (Room 1983; Fingarette 1988) no longer holds this view.
The concept of alcoholism as a disease was rst propounded in the late 1930s (Mann 1950; Jellinek 1960). The argument is that certain people are vulnerable to alcohol and will develop the disease if they start to drink. Progressively they will consume ever-increasing amounts and suffer a range of symptoms, including amnesia and blackouts, and lose control over their ability to say yes or no to another drink. There is no alternative for such a person but to abstain.
It seems, however, that there is considerable scepticism about the disease concept (Kissin 1983). As Marlatt (1983) says: 'There is no adequate empirical substantiation for the basic tenets of the classic disease concept of alcoholism.'
There is a realisation that the tendency for some to abuse alcohol is little different to other forms of compulsive behaviour, such as addictions to drugs, cigarettes, gambling, shopping and caffeine. Peele (1985) embraces all these forms of 'excessive appetite' into a 'unitary theory'.
Jellinek (1960) largely de ned the concept of alcoholism as a disease. Fingarette (1988) detailed the various aws in Jellinek's approach, to the extent of pointing out that Jellinek himself questioned the adequacy of his techniques:
In sum, Jellinek's highly in uential articles were based on questionnaires completed by 98 male members of AA (Alcoholics Anonymous). Of the 158 questionnaires returned, Jellinek had eliminated 60, excluding the data from some AA members who had pooled and averaged their answers on a single questionnaire because they shared their newsletter. Jellinek also excluded all questionnaires lled out by women because their answers differed greatly from the men's ... Even in 1960, Jellinek acknowledges the lack of any demonstrated scienti c foundation for his proposals.
There emerged diverse studies to contradict the disease concept, including the observation that those who have undertaken regular bouts of heavy drinking may very well return to a style of moderate consumption (Clark & Cahalan 1976). The reader is referred to the autobiographical confessions of Jack London in John Barleycorn (1913) for a literary example of this. As Schuckit (1984) observes, in any given month half of all alcoholics will be abstinent, with an average of four months being 'dry' in a 1- to 2-year period. Keller (1972) points out that virtually all of the alcoholics that he had encountered said that they could frequently take just 1 to 3 drinks for a period of weeks without any episodes of being unable to stop. Keller observed that if there had been an unavoidable slide towards uncontrolled drinking as a result of simply taking one drink, then that would not explain why an alcoholic would lack the self-control simply to avoid taking that rst drink. In other words, the lack of self-control exists before the drink is taken.
Several studies have presented powerful evidence that heavy drinkers do possess self-control. Mello and Mendelson (1972) (see also Heather & Robertson 1981) performed an experiment whereby heavy consumers of bourbon were allowed to earn ounces of bourbon in periods of between 5 and 15 minutes in response to their ability and preparedness to partake of simple tasks involving pushing a button according to instructions. Under conditions where they could certainly earn enough bourbon to become intoxicated, none of the subjects attempted to drink to gross excess. In fact they drank to maintain high but approximately constant blood alcohol levels, in spontaneously initiated and terminated sessions over a prolonged period as opposed to continuously. It was also concluded that the amount of alcohol consumed was related to the effort that needed to be exerted to get it - there was a bene t versus cost balance, which ies in the face of the lack of control supposition associated with alcoholism.
In another study it was shown that, when given the choice of more liquor or the ability to remain in a pleasant social environment, alcoholics mostly retrained themselves to moderate drinking (Cohen et al. 1971). Pattison et al. (1977), in a review of more than 50 clinical studies, drew the conclusion:
Within a hospital or laboratory environment the drinking of chronic alcoholics is explicitly a function of environmental contingencies.

This must mean either that there is something about non-controlled environments that impacts on drinking behaviours or that properly controlled experiments and observations made out of a clinical or laboratory setting have not been made. If the former is the case, coupled with the observations made on individuals' drinking habits in relation to reward, then this argues for the importance of a range of other motivations for heavy drinking that are not chemical based.
Indeed, a compelling study by Marlatt et al. (1973) showed that alcoholics consume beverages in response to what they are directed to believe that those drinks comprise. Thus, if given tonic water alone but told that it contained vodka, the subject consumes as much of that drink as they do of one that is genuinely a blend. However, if told that a product is pure tonic then, irrespective of whether the sample actually did contain vodka, the alcoholic would drink less of it and certainly no more of the sample that contained alcohol. This type of study ies directly in the face of arguments for a chemical-based rationale for alcoholism.
Fingarette (1988) opines that the retention of the disease concept by some in the medical profession and legislatures is one tactic for securing research funds and ensuring that those who do drink to excess seek help. As Vaillant puts it:

Calling alcoholism a disease, rather than a behaviour disorder, is a useful device both to persuade the alcoholic to admit his alcoholism and to provide a ticket for admission into the health care system. I willingly concede, however, that alcohol dependence lies on a continuum and that in scienti c terms behaviour disorder will often be a happier semantic choice than disease.
Jellinek (1960) himself said that 'A disease is what the medical profession recognises as such.'
The National Institute on Drug Abuse (Galizio & Maisto 1985) considered 43 different theories for what drives alcoholism. Fingarette (1988) says that some of them, at least, must be wrong, and that:

there is no such single 'disease' and therefore there is no cause. The very proliferation of widely diverging unsupported hypotheses is not characteristic of solid scienti c research. It is characteristic of pseudo-science and faddism.
There are, however, rm adherents to the belief that there is a gene-based inheritance of alcoholism. Studies of relative tendency towards alcoholism in adoptive children and twins have now led to the view that the risk of alcohol dependence is due to the additive or interactive impact of multiple genes (Goodwin et al. 1973, 1974; Bohman et al. 1981; Hrubec & Omenn 1981; Heath et al. 1997; Kendler et al. 1997). The question is whether children born to an alcoholic parent and put up for adoption soon after birth show a greater tendency towards alcoholism that those adoptees who were born to nonalcoholic parents. In the work of Goodwin, there were 3.6 times more alcoholic adopted children from alcoholic fathers than from non-alcoholic fathers. It is important to stress, however, that 82% of the adoptees that came from an alcoholic biological father did not become alcoholic. This may be because they did not inherit the gene(s) or that there are other impacting factors, including environmental ones. Fingarette (1988) provides a calculation to illustrate that the majority of alcoholics are not born to alcoholic parents. Indeed, in a study analogous to that reported by Goodwin, it was found that daughters of alcoholic parents were not predisposed to becoming alcoholics; indeed, there were more alcoholic women who did not have alcoholic parents (Cahalan et al. 1969).
Specic genes for alcohol dependence have not yet been identied; there may be six or so linked to alcohol sensitivity, as well as others determining personality and general predilection towards addiction (Whit eld 2001).
It is believed by some that innate resistance to intoxication increases the risk of alcohol dependence, whereas sensitivity to the impact of alcohol decreases the risk (Whit eld 2001). Seemingly 5-10% of British and Germans and twice as many Swiss have forms of the enzyme, alcohol dehydrogenase, that allow up to 30% faster elimination of alcohol (Marshall & Murray 1989). The concern is that individuals who react less intensely to alcohol may lack the inherent feedback control to prevent the negative impact of higher alcohol intake (Finn et al. 1990). Another key factor that limits the extent to which people consume alcohol is its inhibition of the synthesis of glucose in the body (gluconeogenesis). This induces hypoglycaemia (shortage of sugar) and a healthy body should respond by limiting the intake of the inhibitor, i.e. ethanol.
Alcoholism, then, is held by many to run in families (Cotton 1979; Dietrich & Spuhler 1984; Goodwin 1985), with four- fths of male and female alcoholics in treatment possessing at least one close biological relative also displaying alcohol-related problems (Hesselbrock et al. 2001). Hesselbrock et al. say that the risk of alcoholism among sons of alcoholic fathers is 3-5 times greater than for the general population. It should be appreciated that, while there may be a genetic basis for this inheritance, there may equally be an environmental in uence. This may run in a counter-indicative way; for example (if I may be permitted a qualitative observation), I know several individuals who adopt an extremely abstemious lifestyle having been raised in households where the father has been troubled by abusing alcohol.
Fingarette (1988) amply illustrates how there are undoubtedly diverse causal impacts on individuals' likelihood to take alcohol to excess. There may be no uniformity between people in this respect. While there may be some genetic contribution to the effect, there are those who believe that there may equally be a signi cant contribution of 'learning theory': some people may simply learn to deal with life's dif culties in this way. Fingarette writes:

There is no one cause of alcoholism; alcohol abuse is the outcome of a range of physical, personal and social characteristics that together predispose a person to drink to excess; and episodes of heavy drinking are triggered by immediate events in a person's life.

We are reminded, too, that there may be an economic impact. It is claimed that there is an inverse relationship between cirrhosis and the price of alcohol (Cook 1984). On this basis some rmly advocate higher taxation of alcohol to reduce alcoholism. For this to be a legitimate tool inherently assumes that an individual does indeed have total control over their environment, psychiatry, physiology and genome, and will simply not purchase alcohol if it is highly priced. On the other hand, if it is accepted that there are individuals who, for whatever reason, are predisposed to abuse alcohol, then they will surely nd the wherewithal to acquire drink by whatever means it takes. Meanwhile the vast majority who enjoy and bene t from alcohol (see later) are penalised (Chaloupka et al. 2002).
It seems that diverse psychiatric conditions tend to be found in individuals displaying alcohol dependence. Thus it was shown in one study that only one- fth of people receiving treatment for alcohol dependence failed to report other psychiatric disorders. It seems, too, that those predisposed to 'abusing' alcohol are also increasingly likely to display anxiety, affective and antisocial disorders and other substance abuse problems (Burns 1994).
It is claimed that those people with an increased tendency towards alcohol abuse metabolise alcohol in distinctive ways. Acetaldehyde levels are seemingly higher in such people (Lindros 1978). However, Lindros does not believe that acetaldehyde is directly implicated in triggering a dependence on alcohol. Males have more alcohol-related problems than females (Dawson & Archer 1992), but females tend to accumulate higher levels of alcohol in the blood, metabolising it more slowly (Frezza et al. 1990).