From: Engs, Ruth C. [Ed.]. Contoversies in the Addition's Field. Donald W. Goodwin, Chapt 2: "Evidence for a Genetic Factor in Alcoholism."
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CHAPTER 2 Evidence for a Genetic Factor in Alcoholism
Donald W. Goodwin, M.D.
Three types of evidence support the possibility that heredity may contribute to alcoholism: family studies, adoption studies, and twins studies. Each will be reviewed briefly, followed by some comments about etiology.
Family Studies. Alcoholism runs in families. An estimated 20-25% of sons of alcoholics become alcoholic and about 5% of the daughters (Cotton, 1979). Estimates of the rate of alcoholism in the general population vary widely, but the rates for first degree relatives of alcoholics are several fold higher than most population estimates. A family history of alcoholism represents the strongest known risk factor for alcoholism.
Similarly, about 20-25% of male siblings of alcoholics become alcoholic and about 5% of female siblings. The observation that alcoholism runs in families dates to classical times and is one of the most documented facts in the field of substance abuse.
Not everything that runs in families is inherited. Languages, for example, run in families. For many years it was believed that alcoholism was "learned" in the way that languages were learned: largely emulation. Twin and adoption studies tend to challenge this belief.
Adoption Studies. Studying adoptees is one way to separate nature from nurture. If there is alcoholism in the biological parents and the disorder has a partial genetic basis, one would predict that children of alcoholics adopted in infancy to nonalcoholics would still have a relatively high rate of alcoholism. Four such studies have been conducted.
The first by Roe (1944) found no difference between children of alcoholics and children of nonalcoholics when both groups had been raised by adoptive parents who presumably were not alcoholic. There were no alcoholics in either group. The sample size was small and it was not clear that the biological parents would be classified as alcoholic today. Many had a history suggestive of antisocial personality. Also, the adoptees were young at the time they were studied and may had not entered the age of risk for alcoholism.
The 1970s saw a renewed interest in biological factors in alcoholism. Three adoption studies were conducted in three countries: Denmark (Goodwin et al.. 1973), Sweden (Bohman, 1978) and the United States (Cadoret, Cain, and Grove, 1979)Although methologically dissimilar, the three studies came to similar conclusions:
1. Grown up children of alcoholics raised by nonalcoholic adoptive parents continued to have a high rate of alcoholism—about as high as that found in children of alcoholics raised by alcoholic parents.
2. Having an alcoholic biological parent apparently did not increase the risk of the adopters having other psychiatric disorders.
In the Danish study, four groups of individuals were interviewed: sons and daughters of alcoholic parents who were adopted out and raised by nonalcoholic, unrelated, adoptive parents, and their brothers and sisters raised by the alcoholic parent. No difference in alcoholism rates in same sex siblings were found. Nor did the adopted-out children of alcoholics have elevated rates of other psychiatric pathology compared to controls (adopted-out children of nonalcoholics). Alcoholism ran true to type. Having an alcoholic parent did not even increase the chance of the adopted-out offspring being classified as heavy drinkers.
The Swedish and Iowa studies initially reported similar findings. In the Swedish study, criminality in the biological parents did not predict criminality in the offspring, nor did alcoholism predict criminality. The data were later reanalyzed by Cloninger (Cloninger, Bohman, and Sigvardsson, 1981) who identified environmental factors (e.g., income) as important in one group of adoptees but not in the other. In the first group (called Type I alcoholism) both sexes were susceptible to what seemed a rather mild form of alcoholism and heredity seemed relatively unimportant. In Type II alcoholism, men were mainly susceptible and there was a strong history of alcoholism in the biological parents. Also, Cloninger reported that Type II alcoholism was associated with antisocial personality.
Originally, the Iowa study also found that alcoholism ran true to type; that is, a family history of alcoholism in the biological parents did not increase the likelihood of other psychiatric illnesses occurring in the adopted-out offspring. Further study found a tendency for the adopted-out children to misuse drugs and also found that alcoholism in the adoptive parents somewhat raised the chance of alcoholism occurring in their adopted children (Cadoret et al., 1984). At present, the issue remains unclear about whether alcoholism in parents increased the chance of other psychiatric disorders occurring in their adopted-out offspring.
Twin Studies. Single egg monozygotic twins share the same DNA and presumably have identical susceptibility to genetic illnesses. Twinegg dizygotic twins share a familial susceptibility to genetic illnesses to the extent to which they share the same genes.
Four twin studies have examined drinking patterns and alcohol dependence. ASwedish study (Kaij, 1960) found that identical twins were more concordant for alcoholism than fraternal twins. A large Finnish study (Partanen, Brunn, and Markkanen, 1977) found similarities of drinking pattems, but no difference between identical and fraternal twins regarding "loss of control" (believed by some to be the sine qua non of alcoholism). However, there was a discrepancy in concordance rates for younger twins, with young identical twins more likely to be concordant for alcoholism than young fraternal twins. A review of Veterans Administration records in the United States lent support to a genetic factor (Hrubec and Omenn, 1981), finding that identical twins were more often concordant for alcoholism than fraternal twins. Finally, an ongoing study in England has failed so far to find differences between identical and fraternal twins with respect to alcoholism (Murray and Gurlin, 1983).
Like the adoption studies, most of the twin data are consistent with the presence of genetic factors in alcoholism, but there are exceptions, and the relative importance of environmental and genetic factors remains to be ascertained.
What is Inherited?
To the extent that alcoholism is influenced by heredity, what is inherited? The answer is that nobody knows. The cause of alcoholism is unknown.
Nevertheless, there is much speculation. Often the word multifactorial is used. What is meant by this?
Multifactorial is a mathematical-sounding word usually uttered in tones which suggests that our ignorance about alcoholism may be total, but that we at least agree that it is "multifactorial." When we do not know the cause of alcoholism (which means that it could just as easily be unifactorial as multifactorial), I believe we should admit it and not disguise our ignorance with big words.
One reason why alcoholism is called multifactorial may be that it seems a nice thing to say—politic, diplomatic. Meetings on alcoholism are attended by people from a variety of specialties: medicine, psychiatry, psychology, social work, etc. When alcoholism is attributed to multiple factors—biologic, sociologic, psychologic—everyone feels useful. There is a kind of unspoken agreement that, because experts form diverse backgrounds study alcoholism, alcoholism must have diverse origins.
In one sense this is obviously true. Genes give us the enzymes to metabolize alcohol; society gives us the alcohol to metabolize; and our psyches respond in wondrous ways to these combined gifts. Nevertheless, beyond this obvious level, the evidence for multiple causes of alcoholism is no better or worse than the evidence for a single cause.
The etiology of alcoholism may actually involve a single cause—a single chemical "switch." If someone ever finds the switch, the next step will be to learn how to turn it off. This is relatively easy once a switch is found (as has been done in other illnesses). Lewis Thomas says the same thing about cancer (Thomas, 1979). When people interested in cancer get together at meetings, they also use terms like multifactorial. But Thomas believes cancer may also involve a single switch:
"The record of the past half century has established. I think, two general principles about human disease. First. it is necessary to know a great deal about underlying mechanisms before one can really act effectively..."
"Second, for every disease there is a single key mechanism that dominates all others...This generalization is harder to prove... but I believe that the record thus far tends to support it. The most complicated, multicellular, multitissue, and multiorgan disease I know of are tertiary syphilis, chronic tuberculosis, and pernicious aniema... Before they came under scientific appraisal each was thought to be what we now call a "multifactorial" disease, far too complex to allow for any single causative mechanism. And yet, when all the necessary facts were in, it was clear that by simply switching off one thing—the spirochete, the tubercle bacillus, or a single vitamin deficiency—the whole array of disordered and seemingly unrelated pathologic mechanisms could be switched off, at once..."
"I believe that a prospect something like this is the likelihood for the future of medicine. I have no doubt that there will turn out to be dozens of separate influences that can launch cancer...but I think there will turn out to be a single switch at the center of things. ..I think that schizophrenia will turn out to be a neurochemical disorder, with some central, single chemical event gone wrong. I think there is a single causative agent responsible for rheumatoid arthritis...I think that the central vascular abnormalities that launch coronary occlusion and stroke have not yet been glimpsed, but they are there, waiting to be switched on or off."
Thomas did not include alcoholism in his list of potential single-switch disorders, but I suspect he would have, had he attended a few multidisciplinary conferences on alcoholism. (In the case of cancer, single switches were found, called oncogenes, long afterThomas wrote the above words.)
Two possible switches might turn on alcoholism. One involves producing too little of something. The second involves producing too much of something.
To illustrate the former: Let's assume that some alcoholics lack the gene(s) for optimal production of Substance H (H for happiness). They are bom, so to speak, unhappy. Sometime in their teens they discover that having two or three beers or drinks makes them happy. Someone once said that you never feel better than when you feel good after feeling bad, and, for some alcoholics—those who start life feeling bad drinking alcohol feels so good it becomes habit-forming. But all is not bliss. Ten minutes or so after the H-deficient person has a drink, he wants another. He is feeling unhappy again—unhappier than before he had the drink. The unhappiness now has a special quality sometimes called craving. A drink relieves this new special unhappiness and even restores the original happiness, but just briefly. Another drink, and another, is needed to overcome the unhappy feeling produceed by the same drug that produced the happy feeling— alcohol. "It lifts you up and puts you down," as the saying goes, and some people are lifted up and put down more than others, possibly because of genes.
Substance H (if it exists) has not been identified. Let's assume, for the sake of speculation, that it is serotonin. Perhaps the pre-alcoholic has too little serotonin. Alcohol brings his serotonin level to normal and even above nominal, making the act of drinking highly reinforcing. Alcohol does this by releasing serotonin from brain cells. Brain cells contain limited amounts of serotonin and, after a short time, they run out of serotonin. Now the pre-alcoholic who had low levels of serotonin to begin with has even lower levels, and because drinking, for him, is so strongly reinforced and habit-forming, he wages a desperate battle to overcome his serotonin deficiency by drinking more and more alcohol. It is a battle he will inevitable lose; his cells cannot keep up with the demand for serotonin. As a result, there is considerable stress and strain on the organism. Stimulant chemicals like epinephrine pitch in to help, but ultimately make matters worse by leaving the drinker in a hyperstimulated state when he stops drinking (as he eventually must).
A second chemical possibility involves overproduction. Alcohol produces substances in the brain that resemble morphine. Conceivably, alcohol produces more morphine-like substances in some brains than in others—again because of genes. The pre-alcoholic is the person whose brain overproduces morphine when he drinks alcohol—or overproduces something that makes drinking unusually rewarding, habit-fomming, addictive. Chemical mediators of addiction (if they exist) may not be like morphine at all, but the overproduction model is a good one to pursue.
In summary, alcoholism runs in families. It runs in families even when the children are raised by nonalcoholic adoptive parents. Thus the transmission of alcoholism cannot be attributed entirely to conditions of upbringing. This is as far as our knowledge goes. Terms like multifactorial merely disguise our ignorance. But knowing that alcoholism involves a biological susceptibility—possibly genetic—is new and important information. It has led to some biochemical theories that deserve pursuing.
Bohman, M. (1978). Some genetic aspects of alcoholism and criminality: A population of adoptees. Archives of General Psychiatry, 35 269-276.
Cadoret, R.J., Cain, C.A., and Grove, W.M. (1979). Development of alcoholism in adoptees raised apart from alcoholic biologic relatives. Archives of General Psychiatry, 37 561-563.
Cadoret, R.J., O'Gorman, T.W., Troughton, E., and Heywood, E. (1984). Alcoholism and antisocial personality: Interrelationships, genetic and environmental factors. Archives of General Psychiatry, 42 161-167.
Cloninger, C.R., Bohman, M., and Sigvardsson, S. (1981). Inheritance of alcohol abuse: Cross-fostering analysis of adopted men. Archives of General Psychiatry, 36 861-868.
Cotton, N.S. (1979). The familial incidence of alcoholism: A review. Journal of Studies on Alcoholism, 40 89- 116.
Goodwin, D. W., Schulsinger, F. , Hermansen, L., Guze, S .B . , and Winokur, G. (i973). Alcohol problems in adoptees raised apart form alcoholic biological parents. Archives of General Psychiatry, 28 238-242.
Hrubec, A. and Omenn, G. (1981). Evidence of genetic predisposition to alcoholic cirrhosis and psychosis: Twin concordances for alcoholism and its biological end points by zygosity among male veterans. Alcoholism Clinical and Experimental Research, 5 207-215.
Kaij, L. (1960). Studies on the Etiology and Sequels of Abuse of Alcohol. University of Lund: Lund, Sweden.
Murray, R.M. and Gurlin, C.C. (1983). Twin and alcoholism studies. Recent developments in Alcoholism, edited by M. Galanter,Volume 1, Chapter 5, Gardner Press: New York.
Partanen, J., Bruun, K. and MarEkanen,T. (1977). Inheritance of dnnking behavior: A study on intelligence, personality, and use of alcohol in adult twins. Emerging Concepts of Alcohol Dependence, edited by E.M. Pattison, M.B . Sobell, L.C. Sobell, Chapter 10. Springer Publishing Co., Inc.: New York.
Roe, A. (1944). The adult adjustment of children of alcoholic parents raised in fosterhomes. Quarterly Journal of Studies on Alcohol, 5 378-393.
Thomas, L. (1979). The Medusa and the Snail. Viking Press: New York.
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