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relationships, which were postulated by SAD theory. They have further dramatized how cerebellar stimulation can modulate extreme states of emotional expression (positive and negative) in human subjects. According to SAD theory, the cerebellum is not itself the site of these behaviors, but it exerts a regulatory influence on limbic, reticular, and frontal cortical structures to modulate these behaviors. Cerebellar modulation of limbic-endorphin activity would be a natural extension of SAD theory and could be tested in both animal and human studies. It would be expected, for example, that endorphin/naloxone behaviors would be altered with chronic cerebellar electrical stimulation that resulted in profound changes in emotional behavior, as described by Heath et al. In particular, since Heath (1972, 1975a,b) has documented abnormal electrical spike discharges in the limbic and cerebellar structures of isolationreared primates, and Saltzberg and colleagues (Saltzberg et al. 1971; Saltzberg and Lustick 1975; Saltzberg 1976) have developed signal analysis methods to detect these deep brain spike discharges from scalp EEG recordings, it is now possible to undertake studies that could link a known history of somatosensory affectional deprivation to abnormal deep brain spike activity and to specific patterns of endorphin/naloxoneinduced behaviors associated with dysfunctional behaviors, e.g., alcoholinduced violence and impaired sexual functioning. Effective therapies should be reflected in elimination of spike discharges, altered endorphin/ naloxone behaviors, development of affectional emotional behaviors, and elimination of drug and alcohol dependence.
The role of the cerebellum in somatosensory affectional deprivation has been given support by Berman et al. (1974); and Floeter and Greenough (1979), who reported significant increases in spiney branchlets of Purkinje cells in the para flocculus and the nodulus of the cerebellum in monkeys reared in colony conditions compared to isolate-reared and socially experienced animals (environmental variation of SAD). The finding of opiate receptors in the cerebellum should be noted in this respect (Meunier and Zajah 1979). Although denervation supersensitivity mechanisms inherent in somatosensory affectional deprivation are offered as a major explanatory process in accounting for the variety of diverse and often apparently inconsistent and contradictory findings from the endorphin/naloxone behavioral literature, it is recognized that other factors, e.g., neonatal anoxia, can induce denervation supersensitivity (Berman and Berman 1975; Burch et al. 1975) and that the "family" of endorphins and their antagonists are additional factors that can contribute to the complexity of findings reported in the literature and their interpretation.
The major theoretical orientation of this paper is to emphasize that any study of endorphin/naloxone behaviors or drug/alcohol behaviors must take into account the developmental history of the organism to determine whether the CNS of that organism is characterized by denervation supersensitivity, whether induced by somatosensory affectional deprivation or other etiological developmental factors.
The phenomenon of "hyperendorphinism" of affective disorders (Buchsbaum et al., in press), which may well be an expression of "neurotransmitter density" due to denervation supersensitivity, is an example of a construct that might be benefited by a developmental perspective. (Neurotransmitter density in neurochemistry is analogous to current density in electrophysiology and expresses the relationship of the amount of released neurotransmitter substance available to the number of available receptors.)
Since isolation rearing results in a reduction of the number of opioid receptors, a state of "hyperendorphinism" may not reflect a change in absolute volume of released endorphin but rather a change in the number of opioid receptors (endorphin density). The converse could also occur (increased volume of endorphin with receptor number remaining constant for different etiological reasons. This is mentioned for the purpose of suggesting that "hyperendorphinism" may not be a unitary phenomenon since different mechanisms and etiologies could mediate this effect.
It would be a serious omission not to mention the classic theoretical system developed by Petrie (1976), which has unusual relevance to the issues of substance abuse and to somatosensory affectional deprivation theory. Briefly, Petrie has proposed a theoretical system that postulates CNS processes of reduction and augmentation of the sensory environment to describe an individual's "reactance" to pain and sensory deprivation. The "CNS augmenters" are characterized by an intolerance for pain and a tolerance for sensory deprivation. This pattern of reactance occurs because the CNS of these individuals acts to augment or enhance the impact of a sensory event upon the CNS. Conversely, the "CNS reducers" are characterized by a tolerance for pain and an intolerance for sensory deprivation. This pattern of reactance occurs because the CNS of these individuals acts to reduce or inhibit the impact of a given sensory event upon the CNS. Thus, the "CNS reducers" are characterized by a chronic state of insufficient afferent stimulation (stress of sensory insufficiency or sensory deprivation) and engage in behaviors that are designed to maximize afferent stimulation of the CNS. Consequently, these "CNS reducers" are those who engage in a variety of stimulus-seeking behaviors, e.g., when punished with solitary confinement, delinquents who are CNS reducers will frequently engage in self-mutilativę behaviors, such as cutting themselves with razors or burning themselves with cigarettes (note selfmutilation of isolation-reared animals).
Petrie (1976) described the response of reducers, moderates, and augmenters to alcohol and found that augmenters were most affected by dramatically changing from an augmenting reactance mode to a reducing reactance mode. Similar but less strong reducing effects were obtained with reducers. Comparable results were obtained with other drugs, such as aspirin and chlorpromazine. Thus, augmenters as a group were shifted away from pain intolerance to pain tolerance. Buchsbaum (1978) has provided a review of a number of neurophysiological studies from his laboratory and others on reducers and augmenters. Without reviewing all of his findings, suffice it to point out that he reported that reduction of the amplitude of sensory-evoked potentials to increased stimulus intensity was associated with pain tolerance and analgesia, and that augmentation was linked to substance abuse. The studies of Buchsbaum and Ludwig (in press) and von Knorring and Oreland (1978) are also relevant to these issues.
It has been previously suggested that somatosensory affectional deprivation of isolation rearing is a major contributing factor in the developmental neuropsychobiological substrate of Petrie's typology of reducers and augmenters (Prescott 1967). Chronic or perseverative stimulusseeking behaviors and impaired pain perception, for example, are predominant characteristics of somatosensory affectional deprivation (denervation supersensitivity) and the "CNS reducer." There are, however, significant differences in the communality of the two theoretical systems in which SAD is characterized by "paradoxical" behaviors,
e.g., simultaneous supersensitivity to touch and impaired pain perception that are not accounted for by Petrie's typology. Zuckerman's (1979) theory of sensation seeking is also intrinsically related to the theories of Petrie (1976) and Prescott (1967, 1971a,b, 1972a, b, 1973, 1975, 1976a, b, 1977).
This writer has attempted to link these basic developmental neurobiological processes of SAD to cross-cultural characteristics of childrearing practices; to social and religious mores and customs that regulate sexual behaviors; and to personality characteristics of authoritarianism, exploitation, and narcissism in contrast to egalitarianism, nurturance, and altruism. Further, it is postulated that these contrasts in personality characteristics, considered at the microsocial level, constitute the bases for the political structure of a culture, namely, egalitarian-democratic Societies versus authoritarian-fascist societies (Prescott 1975, 1976, 1977). It is of some significance that Petrie (1976) draws exactly the same parallels from her theory to the characteristics of both personality and culture with her typologies of "compassion" (augmenter) versus "callousness" (reducer) (pp. xii-xiv).
In concluding this theoretical essay it hardly needs to be emphasized that the social-emotional dysfunctioning of the individual in society, in whatever form it may be expressed, is not only an intrinsic aspect of neurobiological functioning of the individual but also of the socialpsychological forces of culture that shape the individuality of neurobiological functioning through the formative developmental processes of sensory stimulation and deprivation, and through a culture of chemical and physical environments that influence fetal, neonatal, and postnatal development. Maternal habits of chemical ingestion, e.g., alcohol, drugs, food/ spice preferences, or exposure to certain chemical environments during gestation, may well "imprint" upon the developing fetus certain "sensitivities" and "predispositions" for use or avoidance of those chemical agents during postnatal life with all the implications that this has for behavior.
It necessarily follows that preventive and therapeutic programs cannot be restricted to molecular biological strategies that are directed at the individual organism. The reconstruction of the individual requires also the reconstruction of society and culture.
The elements of societal and cultural reconstruction involve not only shaping a safe, beneficent physical environment but also a nurturant, caring, and affectionate environment of human relationships. The latter touches deeply upon philosophical and religious ideologies that regulate the morality of pain and pleasure in human relationships and the role of women in society.
The matrilineal/patrilineal structure of human cultures and their relationship to nurturance in human relationships, as well as the construction of the supernatural in human cultures, are a logical extension of SAD theory. However, it is beyond the scope of this essay to develop these topics and relate them to what has been reviewed herein.
A Theory of Alcohol and
Marc A. Schuckit, M.D.
A GENERAL OVERVIEW
Genetically influenced biological factors explain only one part of the variance in the development of alcoholism and drug abuse. Even for those persons genetically predisposed, the final clinical picture involves a combination of genetic factors (leading both toward and away from substance abuse) and environmental events (with similar positive and negative aspects).
Before proceeding with the theory on the importance of genetics in substance abuse, it is necessary to present briefly some of the data supporting the conclusion that genetics plays any role at all. The picture is not irrefutable, as it is difficult to carry out human studies while controlling enough factors to make definite conclusions. The most important aspect of this research is the manner in which the different methods carried out in different settings generate such consistent data (Robins 1978).
DATA SUPPORTING GENETICS IN
The most impressive amount of information is available on alcohol, with much less data on other substances. Thus, the two topics will be discussed separately.
The first indication of a possible genetic influence comes from the studies of families of alcoholics, where it has been repeatedly shown that the chances of a child developing alcoholism as an adult increase with the number of alcoholic relatives, the severity of the alcohol problems in those relatives, and the degree of genetic closeness to the ill relative (Schuckit et al. 1972; Goodwin 1976). The hypothesis is further strengthened by genetic marker studies demonstrating a possible link between the number of factors known to be genetically influenced
(e.g., blood type) and alcoholism within certain populations or families, although these results are difficult to replicate. Data from animal studies are consistent with the theory of the importance of genetics in that they show that it is possible to breed strains of animals with relatively higher and lower tendencies toward drinking alcohol, a factor which may shed light on the onset of drinking but not necessarily on alcoholism itself.
The most persuasive alcoholism-related genetic information in humans comes from twin studies and adoption investigations. In twin research the level of similarity for alcoholism (i.e., concordance) in fraternal twins, who share only 50 percent of their genes, is compared to the level of concordance in identical twins, who share 100 percent of their genes. These studies have shown a level of heritability for drinking and drinking problems (Partanen et al. 1966), as well as a higher concordance rate for alcoholism in identical twins (around 60 percent) than in fraternal twins (around 30 percent) (Kaij 1960). The adoption studies, comparing the outcome for alcoholism in children of alcoholics separated from their parents near birth to that of a suitable control population, have used diverse methodologies ranging from half-siblings to actual adoption records in three different countries and yet have shown similar results (Schuckit et al. 1972; Goodwin 1976; Bohman 1977). The children of alcoholics demonstrate elevated risks for alcoholism even if separated from their parents near birth and raised without knowledge of their biological parents, while the children of nonalcoholics do not have elevated risks for alcoholism even if reared by alcoholic adoptive parents (Schuckit et al. 1972; Goodwin et al. 1974).
The data supporting the importance of genetic factors for abuse of
A number of investigations have looked for possible ties between genetic factors which might underlie drug abuse and those which might be responsible for alcoholism. The results are tentative, demonstrating, for instance, that alcohol and drug problems may run in the same families (Tennant 1976), but such studies rarely define what is meant by alcoholism or drug abuse and almost never control for related diagnoses such as the antisocial personality (Schuckit 1973). This latter diagnosis might be responsible for the demonstration of secondary alcohol and drug problems within the same family group. Animal studies do demonstrate some degree of crossover between alcohol- and morphine-seeking behavior in strains of animals (Eriksson and Kiianmaa 1971; Sinclair et al. 1973; Nichols 1972). In another approach, a number of theorists have attempted to establish a tie between alcohol and drug abuse and a vulnerability to stress factors such as overcrowding, but the data are inconclusive (Bihari 1976; Westermeyer 1971; Jonas and Jonas 1977). Finally, we must consider the possibility that abuse of one drug (e.g., alcohol) might induce biochemical changes similar to those noted with other drugs (e.g., opiates) (Davis and Walsh 1970; Doust 1974). However, in the absence of more conclusive data, I feel that while alcoholism may be a genetically influenced disorder