Use, Abuse, and Addiction

Alcoholism

Alcoholism is equivalent to Substance Dependence on Alcohol as defined by the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, and Dependence as defined by the ICD-10, both of which are equivalent to alcohol addiction. Substance Use Disorders as defined by the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, grades the disorder as mild, moderate, and severe, and future studies will link these gradations to the commonly used terms of “addiction” and “alcoholism” (see What is Addiction?). The stages of alcoholism vary significantly and can be manifested at any time of life and take on many forms (Box 6.5). A sample time course of alcoholism in a person’s work life is shown in Table 6.5.

Figure 6.3 Influence of a meal, taken with alcohol, on blood alcohol levels, showing three different patterns of responses (A, B, and C) in a function that relates blood alcohol levels over time. Closed circles correspond to the blood alcohol level when the alcohol was taken on an empty stomach, and open circles correspond to the alcohol level after consuming the same quantity of alcohol with a meal. Each subject was tested with and without food. Units are expressed as ‰, which refers to Δ/baseline per mil. In an example of such annotation, 1.5 ‰ would be equivalent to 150 mg% (0.15 g%). (A) This “food curve” shows a large depression in relation to the fasting curve with a low maximum and a slowly descending limb. This finding is interpreted as the result of a great delay in absorption, both with regard to rate and time, with absorption continuing for 4–6 h. (B) A plateau was maintained for the 2–3 h interval after a delayed absorption period. The horizontal course was followed by a rather rapid fall, implying that absorption, distribution, and combustion balance each other. When absorption is completed, distribution is maintained which caused the rapid fall of the post-absorptive phase. (C) The post-absorptive period had a parallel course to that of the fasting curve. Absorption in this case was delayed to such an extent that the maximum appeared later, and the normal over-shooting of alcohol was prevented. The distribution phase was not reflected in the blood alcohol level as under fasting conditions, and the rate of disappearance of alcohol from the blood stream during the post-absorptive period was the same as in fasting. These data show that the ingestion of a meal delays the absorption of alcohol ingested with the meal in three different patterns (A, B, and C). However, in no case did the level of the “food” blood alcohol curve reach the values of the “fasting” curve. [Taken with permission from Goldberg L. Quantitative studies on alcohol tolerance in man. Acta Physiologica Scandinavica Supplementum, 1943, (5), 1–128.]

A strong genetic component is well established in alcoholism. Twin and adoption studies have shown that the hereditability of alcoholism may be as high as 50–60%. The phenotype of individuals with a positive family history for alcoholism is unique and suggests characteristics that can be linked to patterns of behavior that lead to excessive drinking and ultimately alcoholism. Family history-positive individuals show a low level of responsiveness to alcohol, perhaps reflecting a low sensitivity to the drug. The low response to alcohol can be seen relatively early in life and carries a similar heritability to alcoholism. This phenotypic characteristic predicts later heavy drinking and alcohol dependence but is not associated with heavy use or problems associated with substance use disorders with other drugs. The low response to alcohol as an endophenotype can enhance the risk of heavier drinking and drinking problems through environmental influences, such as associations with heavier-drinking peers, alterations in the expectations of the likely effects of drinking, and the enhanced probability of using alcohol to cope with stressors.

Figure 6.4 Alcohol metabolism. The liver has three metabolic systems that are able to oxidize alcohol. Alcohol dehydrogenase oxidizes alcohol into acetaldehyde, and acetaldehyde dehydrogenase then oxidizes acetaldehyde into carbon dioxide and water, which is then secreted in the urine. The anti-relapse medication disulfiram (Antabuse) blocks acetaldehyde dehydrogenase at therapeutic doses. Females have less of the alcohol dehydrogenase enzyme than males and a larger amount of body fat for a given weight.

TABLE 6.4

Frequency of Acetaldehyde Dehydrogenase Isozyme Deficiency in American Indians, Asian Mongoloids, and Other Populations

Population

Sample Size

% Deficient

South American Indians
 Atacameños (Chile)

133

43

 Mapuche (Chile)

64

41

 Shuara (Ecuador)

99

42

North American Indians
 Sioux (North Dakota)

90

5

 Navajo (New Mexico)

56

2

Mexican Indians
 Mestizo (Mexico City)

43

4

Asian Mongoloids
 Japanese

184

44

 Chinese Mongolian

198

30

 Chinese Zhuang

106

45

 Chinese Han

120

50

 Korean (Mandschu)

209

25

 Chinese (living abroad)

196

35

 South Korean

75

27

 Vietnamese

138

53

 Indonesian

30

39

 Thai (North)

110

8

 Filipino

110

13

 Ainu

80

20

Other populations
 German

300

0

 Egyptian

260

0

 Sudanese

40

0

 Kenyan

23

0

 Liberian

184

0

 Turk

65

0

 Fang

37

0

 Israeli

77

0

 Asian Indian

50

0

[Taken with permission from Goedde HW, Agarwal DP, Harada S, Rothhammer F, Whittaker JO, Lisker R. Aldehyde dehydrogenase polymorphism in North American, South American, and Mexican Indian populations. American Journal of Humam Genetics, 1986, (38), 395–399.]

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