Chemically Dependent
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Chemically Dependent

Phases Of Treatment And Recovery

Barbara C. Wallace, Barbara C. Wallace

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eBook - ePub

Chemically Dependent

Phases Of Treatment And Recovery

Barbara C. Wallace, Barbara C. Wallace

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About This Book

First published in 1992. Part I of the book covers phases of treatment for specific phases of recovery by describing key concepts and focusing on three dominant treatment modalities, inpatient, outpatient, and long-term residential therapeutic communities. Part II covers, in substantial depth, psychoanalytic/psychodynamic approaches. art III of the book examines cognitive-behavioral, self-help, and relapse prevention approaches to the treatment of the chemically dependent. Part VI mentions in all phases of treatment and recovery. Part IV of the book provides an overview of contemporary trends in research, while also discussing implications for treatment. n the therapeutic community. Part V attempts to draw the field of chemical dependency toward recognition of the importance of considering distinct population characteristics and how these characteristics may dictate modifications in treatment design. The book is suitable as a text in a course on substance abuse or as a critical reference for anyone doing clinical work or research in the field of chemical dependency.

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Publisher
Routledge
Year
2013
ISBN
9781135822835
Edition
1

PART IV

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CONTEMPORARY TRENDS IN RESEARCH AND IMPLICATIONS FOR TREATMENT

12

Neurogenetics of Compulsive Disease: Neuronutrients as Adjuncts to Recovery

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Kenneth Blum, Ph.D.
Eric Braverman, M.D.
James E. Payne
Olivia Finley, M.D.
Laurel Loeblich-Smith, Ph.D.
Daniel A. Hoffman, M.D.
Compulsive disease, particularly alcoholism, is a major and devastating health problem with an unknown etiological base. Most recently, the question of whether environment or heredity is the prime determinant for the development of compulsive disease continues to receive extensive attention worldwide. In this regard, the United States Supreme Court sided with the notion that alcoholism was not a disease (Traynor v. Turnage, 1988). On the other side, Blum and colleagues found a high association of the dopamine D2 receptor gene in alcoholism (Blum, et al. & Cook, 1990). This is the first specific gene with such a significant correlation that might confer susceptibility on at least one form of alcoholism. Although more research is required further to confirm these findings, for now this research favors the view that alcoholism is a biogenetic dis-order triggered by the environment. However, in terms of treating the neurochemistry of chemically dependent individuals as it relates to certain behavioral anomalies, therapists must begin to understand its complexity.
With this in mind, the purpose of this chapter is to develop a brief but not critical review of the neurogenetics of compulsive disease, providing a blueprint for potential prevention and treatment strategies. Let us briefly and uncritically review the progress that had been made by the beginning of 1990 in our understanding of the genetics of alcohol-craving behavior and the triggering effect of the environment. Although the goal here is to provide a concise understanding of some of the more general research in the field of alcoholism, certain of these findings can be extended to all compulsive diseases, including drug abuse and eating disorders.

PROGRESS TO DATE

Animal Models

McClearn (McClearn & Rodgers, 1959), following up leads suggested by Williams, Berry, and Beerstacher (1949), and Mirone (1957) had developed the C 57 strain of mice by 19 59 into a model that could be used as a research tool for pharmacogenetics.
In 1977, T. K. Li and his colleagues at the Indiana University School of Medicine developed the P (alcohol-preferring) and NP (nonpreferring) rat strains. The P rats met most of the requirements of an animal model of alcoholism. They voluntarily drank large quantities of an alcohol solution and would actually work to obtain alcohol by pressing a lever. Eventually, they became dependent on alcohol, developed a tolerance to it, and, if it was withdrawn, experienced the symptoms of withdrawal. These mouse and rat strains proved to be powerful tools for genetic research (Lumeng, Hawkins, & Li, 1977).
Li and his associates used these tools in an experiment of classic simplicity to answer some basic questions: Why do alcohol-preferring rats prefer alcohol? Is it the taste or smell—or is it the pharmacological effect of alcohol that the animal craves?
To eliminate the possibility that their alcohol-preferring rat strain sought alcohol because of its taste or smell, the scientists used an apparatus that automatically delivered water or an alcohol solution directly into the stomach of P and NP rats when they consumed one of two flavored-water solutions. If they drank one solution, they automatically received an injection of alcohol into their stomach. If they drank the other solution, they received an injection of plain water. The idea was to see if animals could be trained or conditioned to associate a particular flavor with the presence or absence of the pharmacological effect of alcohol.
The P rats drank up to 14 times more of the flavor linked to alcohol than the NP rats did, indicating that P rats like alcohol because of its euphoric effect on the central nervous system, and not because of taste or smell (Waller, McBride, Gaho, Lumeng, & Li, 1984).

Familial Alcoholism: The Genetic Factor

But there were troublesome questions: Can findings from research in mice or rats be generalized to humans? Because alcoholic animals can be bred, can we assume that genetics is an important factor in human alcoholism?
Affirmative answers began to emerge as early as 1972 when M. A. Schuckit, George Winokur, and D. W Goodwin at the Washington University School of Medicine mounted a study of children in which it was found that genetic predis-position might be more important than childhood environment in the development of alcoholism (Schuckit et al., 1972).
In 1973, D. W Goodwin and George Winokur and their colleagues at the Psykologisk Institut, Copenhagen, found further support for this thesis in a study based on a sample of 5,483 individuals in Denmark who had been adopted in early childhood. They found that the sons of alcoholics adopted by other families were more than three times more likely to become alcoholics than were the adopted sons of nonalcoholics, and at an earlier age (Goodwin, Schulsinger, Hermansen, Fluze, & Winokur, 1973).
Additional confirmation came in 1978 when Michael Bohman at Umea University in Sweden compared rates of alcohol abuse in 2,324 adoptees and their biological parents. The sample included 1,125 men and 1,199 women, adopted before the age of 3 years. The parents included 2,261 mothers and 1,902 fathers. Bohman found that adopted sons of alcoholic fathers were three times more likely to become alcoholic than adopted sons of nonalcoholic fathers. Adopted sons of alcoholic mothers were twice as likely to become alcoholic as those whose mothers were nonalcoholic (Bohman, Cloninger, Van Knorring, & Siguardsen, 1978).
These earlier studies came into focus in an important series of investigations of Swedish adoptees that were carried out by C. R. Cloninger and M. Bohman, and colleagues at the Washington University School of Medicine.
They sought to answer four questions:
  • What characteristics of the biological parents influence the risk of alcohol abuse in the adoptees?
  • What characteristics of the adoptive parents influence the risk of alcohol abuse in the adoptees?
  • How do genetic and environmental factors interact in the development of alcohol abuse?
  • Is the genetic predisposition to alcoholism expressed in other psychopathological ways, depending on the environment and sex of the individual?
The investigators studied 862 men and 913 women of known parentage who had been adopted before the age of 3 by nonrelatives. A total of 35.3% of the adopted children had at least one biological parent known to abuse alcohol. A careful study was made of the subjects, subdivided in terms of congenital background and postnatal home environment, and further divided into four subgroups according to their degree of alcoholism: none, mild, moderate, or severe. Characteristics of the biological parents were examined to identify those associated with a particular degree of alcoholism in the adoptees. To determine the effect of postnatal factors, the adoptive parents were also examined to identify influences that might be associated with particular degrees of alcoholism in the adoptees. Specific findings were:
  • Of the sons of alcoholic biological fathers, 22.8% were alcoholic, compared with 14.7% of the sons who did not have an alcoholic biological parent.
  • Of the sons of alcoholic biological mothers, 28.1% were alcohol abusers, com-pared with 14.7% of sons who did not have an alcoholic biological parent.
  • Of the daughters of alcoholic biological mothers, 10.8% were alcohol abusers, compared with 2.8% of daughters who did not have an alcoholic biological parent.
  • Alcoholism in the adoptive parents was not a factor in whether or not adoptees would become alcoholic, indicating that home environment and imitation of elders were not determining factors (Cloninger, 1983; Bohman et al., 1984).
Investigators identified two distinct types of genetic predisposition to alcoholism (Cloninger, Bohman, & Sigvardsson, 1981):
  1. Type I: milieu-limited alcoholism. The investigators found this to be the most common type of alcoholism. Occurring in both males and females, this type of alcoholism requires both a genetic predisposition and triggering influences in the environment. Milieu-limited alcoholism is not likely to be severe and often goes untreated. It is usually associated with mild, untreated, adult-onset alcohol abuse in either biological parent. Typically, the alcoholic parent has not been a lawbreaker. Severity may be associated with low social status or unskilled occupation of the adoptive father. Milieu-limited alcohol abuse tends to have its onset after 25 years of age.
  2. Type 2: male-limited alcoholism. The data suggested that this severe type of genetic predisposition occurs only in men. It is less prevalent than milieu-limited alcoholism and appears to be unaffected by environment. In families with male-limited susceptibility, alcohol abuse is found to be nine times greater in the adopted sons, regardless of the environment after their adoption. Male-limited susceptibility is related to severe alcoholism in the biological father, often severe enough to require treatment, and often involving law breaking, but is not associated with alcoholism in the biological mother. The onset of this particular type of alcoholism often comes early, before 25 years of age, and may be accompanied by serious encounters with the law. Postnatal influences in the adoptive family do not influence the development of alcoholism in the son, but may affect its severity. An interesting sidelight is that adoptees with male-limited alcoholism generally are not as severely afflicted as their fathers.
These classifications represent an important contribution to our understanding of the interaction of genetics and environment, but some aspects relating to sex and age differences have proved controversial. When Marc Schuckit and his group, for example, attempted to correlate age of onset with the Type I and Type II classifications, they found that age of onset correlated not with types of alcoholism, but with antisocial personality disorder.
Schuckit's data emphasize the important association between early age at onset of alcoholism and more severe clinical characteristics, including the number of alcohol-related social complications, other drug use, and childhood criminality among primary alcoholics. The Type I-versus-Type II construct did ...

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