lucky treatment of alcoholism depends upon either the early detection of the ill consequences of alcohol abuse or the identification of individuals or high-risk form into groupss genetically predisposed to alcoholism.

lucky treatment of alcoholism depends upon either the early detection of the ill consequences of alcohol abuse or the identification of individuals or high-risk form into groupss genetically predisposed to alcoholism. Several lines of evidence indicate that predisposition to alcoholism is transmitted genetically. Biochemical traits, or markers, that are cotransmitted with alcoholism can help identify individuals at high risk.

Biochemical markers of alcoholism can be classified broadly in a less degree than two categories: indicators of alcohol abuse (state markers) and indicators of vulnerability to alcoholism (trait markers). This article discusses possible biochemical trait markers.

A predisposing factor or trait marker for alcoholism must fulfill the following criteria:

* The marker must indicate an increased risk or likelihood of developing the disorder.

* The marker must be transmitted genetically and cannot be a secondary power of alcoholism or the consumption of alcohol.

* The marker must be observ in the well state (before the attack of alcoholism or after put offed abstinence and recovery) as well as in the ill state.

* near relatives (mother, father, brothers, sisters) of the individual with a marker must have the marker without manifesting the illness.

An association between alcoholism and a known hereditary trait occurring consistently with high oftenness may also help identify a genetic predisposition to alcoholism.

To be useful, these markers should be near in such easily available tissues or fluids as family cells, serum, urine, or cerebrospinal fluid. Biochemical markers studied in alcoholism include indicators of brain function, as well as enzyme involved in alcohol metabolism. Examples of the former include the activity of monoamine oxidase (an enzyme associated with the metabolism of neurotransmitters, or chemical messengers) flats of 5-hydroxy-indoleacetic acid (a metabolite of the neurotransmitter serotinin), and the formation of certain chemical precursors (described below). Potential markers associated with alcohol metabolism include the enzyme alcohol dehydrogenase and aldehyde dehydrogenase.

IS ALCOHOLISM AN INHERITED

DISORDER?

The familial nature of alcoholism has lengthy been recognized (Goodwin 1979). Evidence that genetic factors play an important character in the development of alcoholism is derived from twin studies, family studies, adoption studies, observations of ethnic differences, and studies of biological risk factors (Goodwin 1979 1985) Studies of monozygotic (identical) and dizygotic (fraternal) twin pairs generally hint some degree of heritability in the oftenness and quantity of alcohol consum (Schuckit 1987a). Monozygotic twin pairs also attend to show a significantly higher flush of concordance compared with dizygotic twin pairs (Schuckit 1987a; Agarwal and Goedde 1990) (Concordance is the proportion of a representative sample of affected twins whose cotwins share the disorder.)

Family studies indicate that approximately 40 percent of alcoholics have an alcoholic parent (Institute of Medicine 1987) and that the alcoholism rate is significantly higher in relatives of alcoholics than in relatives of nonalcoholics (Cotton 1979;l Guze et al. 1986) Alcoholics with a family history of alcoholism protect to begin drinking earlier in life and to have more alcohol-related enigmas than do those alcoholics without a family history of alcoholism (Cloninger et al. 1981) Evidence from adoption studies also indicates a significant genetic contribution to the progressive growth of alcohol-related problems (Dinwiddie and Cloninger 1989) Using family, twin, and adoption studies, Cloninger et al. (1985) estimate an overall heritability rate of 64 percent

Although there appears to be consistent evidence indicating the importance of genetic factors in the progressive growth of alcoholism, the pattern of inheritance is not a simple single and both genetic and environmental factors may be involved. Moreover, biological as well as familial studies indicate that alcoholism is a heterogeneous disorder. Therefore, alcoholism may be below polygenic control (under the influence of more than common gene). This possibility is supported from the identification of Type I and stamp II alcoholics (see below), distinguished according to the nature of their alcohol-related question s degree of heritability, and personality traits (Cloninger et al. 1981)

POSSIBLE BIOCHEMICAL TRAIT

MARKERS

Monoamine Oxidase

the same of the most widely studied potential biochemical trait markers for alcoholism is monoamine oxidase (MAO). This enzyme is responsible for the degradation of dopamine and norepinephrine, neurotransmitters that have been implicated in certain aspects of alcoholism. MAO regulates the horizontals of these neurotransmitters in the brain according to increasing or decreasing their transformation to inactive compounds

Because of difficulties in obtaining human brain samples, peripheral tissues similar as blood cells have been used as gauges of the brain for studying the biochemical correlates of psychiatric illnesses. The offspring cells most frequently studied are platelets, because many of their chemical characteristics are similar to those of brain cells