Survey data from the United States indicate that tobacco use is associated with the initiation of use of other addicting substances, and that increasing levels of tobacco use are associated with increasing levels of use of other psychoactive substances. Furthermore, factors affecting initiation, abstinence, and relapse to the use of tobacco, alcohol, and opioids are similar in nature. In addition, there are similarities in the addictive process underlying the use of these substances. Taken together, these data suggest that tobacco use is involved, possibly more than by simple association, in the use of other substances containing psychoactive chemicals. In the present paper we discuss the involvement of tobacco in the use of alcohol, opioids, cocaine, and other substances, as well as some of the implications of these observations for researchers and clinicians. One such implication is that it may be possible to use tobacco and nicotine as models for phenomena of interest to other substance use researchers. For example, drug abuse treatment and prevention strategies could be explored using tobacco use as a target behavior, and biological phenomena such as the development of tolerance and physical dependence may be more readily studied with nicotine than with many other drugs. Certain pharmacologic differences across substances are also discussed in light of their implications for development of treatment and drug control policies.

Large oral doses of individual amino acids were given three or four times daily for periods of 1 week to schizophrenic patients, some of whom were maintained on iproniazid. Marked alterations in behavior in some patients were associated with the administration of l-methionine and of l-tryptophan.

Monoamine oxidase activity in blood platelets was measured, with [(14)C]tryptamine as substrate, in 13 monozygotic twin pairs discordant for schizophrenia and in 23 normal volunteers. The monoamine oxidase activity of both schizophrenic and nonschizophrenic co-twins was significantly lower than it was for the normals, and it was highly correlated between twins. In addition, there was a significant inverse correlation between a measure of the degree of the schizophrenic disorder and the monoamine oxidase activity. These data suggest, but do not prove, that reduced platelet monoamine oxidase activity may provide a genetic marker for vulnerability to schizophrenia.

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