Differences between Type I and Type II alcoholics
Key points
- Since the type I-type II alcoholism classification was developed, many researchers have confirmed the findings of the original studies and have further investigated differences between the two subtypes.
- Other researchers detected differences between type I and type II alcoholics not only in the age at onset and the type of alcohol-related problems, but also in certain neurobiological markers.
- Virkkunen and Linnoila (1990) also found that type I and type II alcoholics differed in their serotonin activities in the CNS.
- Type I and type II alcoholics also differed in their patterns of electrical brain waves as measured by an electroencephalogram (EEG).
Since the type I-type II alcoholism classification was developed, many researchers have confirmed the findings of the original studies and have further investigated differences between the two subtypes. In these studies, the age at onset and the type of alcohol-related problems emerged as the characteristics that most readily distinguished between the two subtypes2 (see table 2) (Babor et al. 1992; Gilligan et al. 1988; von Knorring et al. 1987a). Type I alcoholism developed during adulthood and generally was characterized by binge drinking (i.e., prolonged drinking bouts with default of responsibilities), interspersed with prolonged periods of abstinence; loss of control over drinking; excessive guilt about drinking; and rapid progression from mild to severe alcohol abuse, often accompanied by the development of alcoholic liver disease. Conversely, type II alcoholism generally commenced during adolescence or early adulthood, and alcohol consumption frequently was accompanied by fighting and arrests. In addition, alcohol abuse was moderately severe and frequently required treatment, although the severity of abuse did not change over time as it did in type I alcoholism.
Other researchers detected differences between type I and type II alcoholics not only in the age at onset and the type of alcohol-related problems, but also in certain neurobiological markers. For example, several studies found that compared with type I alcoholics, type II alcoholics exhibited lower activity levels of the enzyme monoamine oxidase (MAO) (von Knorring et al. 1987b; Sullivan et al. 1990). MAO is involved in metabolizing certain brain chemicals (i.e., neurotransmitters) that mediate signal transmission among nerve cells. One neurotransmitter metabolized by MAO is serotonin. Accordingly, reduced MAO activity could indicate a reduced turnover of serotonin in the central nervous system (CNS) (Oreland and Shaskan 1983).
Virkkunen and Linnoila (1990) also found that type I and type II alcoholics differed in their serotonin activities in the CNS. The serotonin levels were reduced in the brains of men with earlyonset alcoholism accompanied by violent behavior (i.e., type II alcoholics).
Type I and type II alcoholics also differed in their patterns of electrical brain waves as measured by an electroencephalogram (EEG). These differences existed when the subjects were resting (Cloninger 1987a), but also when they were exposed to certain stimuli. Uncommon stimuli interspersed among common stimuli (e.g., a rare green light among a sequence of red and yellow lights) elicit brain waves, called eventrelated potentials (ERP's), that are made up of several components. A commonly studied ERP component is called P300, because it occurs about 300 milliseconds after the uncommon stimulus. Branchey and colleagues (1988) found that the P300 height (i.e., amplitude) was lower in violent alcoholics (i.e., likely corresponding to type II alcoholics) than in nonviolent alcoholics (i.e., likely corresponding to type I alcoholics). The P300 amplitude also was reduced in people at risk for type II alcoholism, such as sons of type II alcoholics who were not alcohol dependent themselves (Begleiter et al. 1987).
Written and revised by
Gerald Hurowitz, M.D.
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