to their ability to release dopamine. The narcotic analgesics are thought to mimic the enkephalins and endorphins. The LSD-like hallucinogens act both as serotoninergic and tryptaminergic agonists. Benzodiazepines, which also produce feelings of well-being, are thought to interact with a brain receptor; however, a natural agonist has not been identified. Thus there is reason to believe that there is a neurochemistry and neurophysiology of euphoria and that a variety of neurotransmitters, including catecholamines; the endorphins; the enkephalins; and the indoleamines, serotonin and tryptamine, may all play a role in maintaining mood. Further deficiencies of these neurotransmitters may give rise to feelings of hypophoria.

CONCLUSIONS

It is now apparent that the brain has a variety of receptors and several neurotransmitters that are involved in feelings of well-being. Further many addicts and alcoholics have an affective disorder, hypophoria, that appears to be the polar opposite of feelings of well-being produced by drugs of abuse. The pathophysiology of hypophoria is not known. A deficiency of neurotransmitters that are involved in feelings of well-being is a reasonable hypothesis that should be testable. It is known that the protracted abstinence syndrome, associated with morphine physical dependence, is characterized by an exacerbation of feelings of hypophoria. Genetic and heredity factors may also be of importance. Further, hypophoria may have a reactive component, possibly related to exaggerated needs and drives particularly during adolescence and young adulthood, a time when social coping skills are not fully developed.

Thus work on problems of addiction over some 20 years has led to some interesting speculations about the psychopathology and pathophysiology of drug abuse and to some innovations in the area of treatment. It was at first blush disappointing that the narcotic antagonists had such a poor patient acceptance. In retrospect this should have been anticipated, for the narcotic antagonists do not in any way relieve the hypophoric feelings of patients. This in no way detracts from the validity of the concepts of Wikler concerning the role of conditioning in relapse, for hypophoria and conditioned abstinence and drug-seeking behavior are probably coexisting pathologies. If treatment is to be optimized, in all probability both will have to be dealt with. It is my conviction at this time that extinction of conditioned abstinence and drug-seeking behavior using antagonist therapy will be better accepted by patients whose hypophoria has been decreased. One of the fundamental questions is how we can develop antihypophoric drugs which will not induce tolerance and/or dependence and not exacerbate existing hypophoria. Perhaps in this regard we have attended too much to the early abstinence syndrome and not enough to the pathophysiology of the protracted abstinence syndrome.

There seems little question now that a variety of neurotransmitters and receptors are involved in affective disorders. It thus should be possible to identify agonists which when administered under appropriate circumstances should be able to relieve feelings of hypophoria and thus rectify this pathologic situation.

This may represent a radical departure from current strategies in drug development for it is aimed at developing drugs that will be highly

Somatosensory Affectional Deprivation (SAD) Theory of Drug and Alcohol Use

James W. Prescott, Ph.D.

The somatosensory affectional deprivation (SAD) theory of drug and alcohol use is a developmental psychobiological theory that is proposed to account for the common ground of the many and diverse theories of substance abuse. The first basic proposition of this theory is that the neurobiology of our behavior is not only inseparable from, but is in fact largely shaped by, culture. The shaping process of culture upon the developing brain (the organ of behavior) is accomplished through our various sensory modalities and through the sensory processes of deprivation and stimulation.

With few exceptions, the developing mammalian brain, particularly the primate brain, is highly immature at birth and is dependent upon sensory stimulation for its normal growth, development, and functional and structural organization. The richness or paucity of dendritic structures of the neurone (brain cell), for example, is largely influenced by the sensory processes of stimulation and deprivation during the formative periods of brain development. The complexities and possibilities of neuronal communication (and thus behavior) are dependent upon the complexity of dendritic structures of brain cells (Greenough 1975; Greenough and Juraska 1979; Rosenzweig 1979; Floeter and Greenough 1979; Riesen 1975; Globus et al. 1973; Coss and Globus 1979; Coleman and Riesen 1968; Horn et al. 1979; Spinelli and Jensen 1979; Blakemore and Cooper 1970; Hirsch and Spinelli 1970; and Hubel and Wiesel 1970). Dendritic structures are analogous to telephone cables that interconnect various telephone centers (brain cells) with one another. These dendritic structures of brain cells form the structural basis of interneuronal communication. Another major element in the story of interneuronal communication is neurochemical transmitter substances which are present at synaptic junctions between dendrites and which make possible the transfer of "information" from one brain cell to another. These events are accompanied by electrophysiological activity, which is another manifestation of interneuronal communication. The point of this synoptic overview of interneuronal communication is to emphasize that the morphological (structural) and the neurochemical and electrophysiological (functional) processes of interneuronal

communication are all strongly influenced by the sensory processes of stimulation and deprivation. Thus, the effects of the social, physical, and cultural environment are ultimately transformed into perceptual experiences through the encoding and decoding of sensory processes. Further, whether certain perceptual experiences can ever be realized will be dependent upon the quality and quantity of our sensory experiences, as structured by our social, physical, and cultural environment during the formative periods of brain development (Prescott 1967, 1971a,b, 1972a,b, 1973, 1975, 1976a,b, 1977, 1978, 1979b).

The second basic proposition of SAD theory is that certain sensory modalities and processes are more important than others in accounting for emotional/social disturbances and substance abuse. Specifically, it is the emotional senses of somesthesis (touch), vestibulation (movement), and olfaction (smell), that are the primary mediators of our emotional/ affective behaviors. Substance abuse that alters primarily our emotional/affective state must be understood within the context of our emotional senses. It is the deprivation of our emotional senses and not our cognitive (visual-auditory) senses during the formative periods of brain development that can account for and predict our emotional/affective social behaviors, which include not only substance abuse but abusive social behaviors in general. Thus, the question of destructive and exploitive behaviors toward ourselves and others becomes a question of whether affectional bonds are formed or not formed during the formative periods of brain development. Within an evolutionary context, it should be noted that olfaction assumes a greater role in lower mammals, and vestibular functions assume a greater role in higher mammalian forms, specifically the primate, in the formation of affectional bonds (Prescott 1976a, 1977). Similarly, substance abuse that alters primarily our cognitive state (e.g., hallucinogens) must be understood within the context of our cognitive (visual/auditory) senses. It should be noted that movement (vestibulation) is often involved in altered cognitive states and it has been proposed that the vestibular-cerebellar neuraxis may be a master integrating/regulating system of sensoryemotional and motor processes. Thus, the vestibular-cerebellar system may serve as a "bridge" between our "emotional" and "cognitive" senses (Prescott 1976a, 1977; Erway 1975).

In previous studies, the SAD theory has been successful in predicting physical violence (high and low) in 100 percent of 49 primitive cultures distributed throughout the world. This was made possible by evaluating the degree of physical affection (touching, holding, carrying) of the infant by its mother or caretakers and by the degree of physical affection that was permitted to be expressed through the acceptance or rejection of premarital sexuality (Prescott 1975, 1977, 1979b).

The issue of violence, i.e., the failure of nurturance and the failure to form affectional bonds, is strongly related to the issue of substance abuse in several aspects. First, in a very general sense, the body needs and "searches" for a state of harmony, contentment, and in higher life forms (homo sapiens), an altered and transcendent state of conscious "being." A necessary condition for the attainment of this "state of being" is the experiencing of physical (somatosensory) pleasure that is essential for the formation of affectional bonds. When somatosensory pleasure and affectional bonds are denied, then compensatory behaviors to reduce tension, discomfort, and "anomie" become imperative. The common compensatory behaviors are physical violence (toward others and oneself), alcoholism and drug abuse, and perseverative stimulus-seeking behaviors that attempt to provide the sensory

stimulation that was deprived early in life. The stereotypical rocking behaviors of isolation-reared Harlow monkeys and of institutionalized children is a case in point. The "quieting" effect of stimulant drugs upon some hyperactive children is another illustration of a "need for neural activation" that is met by pharmacological stimulation rather than by sensory stimulation. The chronic stimulus-seeking behaviors, particularly of a sexual and violent nature, in the American culture (evidenced, for example, by massage parlors, pornography, violent films, rape) are also illustrative of this basic principle of stimulusseeking behaviors consequent to early somatosensory deprivation (Prescott 1972a, 1973, 1975, 1976a,b). Additional studies that relate early sensory experiences to later behaviors, particularly aberrant sensory behaviors, can be usefully consulted (Ainsworth 1972; Cairns 1966, 1972; Bowlby 1969; Harlow 1971; Harlow et al. 1963; Dokecki 1973; Lichstein and Sackett 1971; Lynch 1970; Mason 1968, 1971; Mason and Kenney 1974; Mason and Berkson 1975; Fuller 1967; Freedman 1968; Friedman et al. 1968; Melzack and Burns 1965; Melzack and Thompson 1956; Melzack and Scott 1957; Mitchell 1968, 1970, 1975; Mitchell and Clark 1968; Sackett 1970; Riesen 1960, 1961a,b, 1965; Schaffer and Emerson 1964a,b; Spitz 1945, 1965; Suomi and Harlow 1972; Zubek 1969).

The self-mutilation and pain agnosia of children characterized by psychosocial dwarfism consequent to somatosensory affectional deprivation and child abuse reported by Money et al. (1972), is a classic verification at the human level of the same behaviors (self-mutilation and pain agnosia) found in animals reared under conditions of somatosensory affectional deprivation (social isolation) (Lichstein and Sackett 1971; Melzack and Burns 1965; Melzack and Scott 1957; and Mitchell 1968, 1970, 1975). The pain agnosia of children subjected to physical restraint and immobilization reported by Friedman et al. (1968) is another demonstration of these relationships at the human level. Another important dimension to these early experiences and behaviors is the neurochemical and neuroendocrine mediators of pain hypersensitivity and pain hyposensitivity (pain agnosia) consequent to somatosensory deprivation. Harvey and Yunger (1973) have shown that decreases in brain serotonin (5-HT) result in an increased sensitivity to pain, and Coleman (1971) has shown that isolation-reared monkeys who are characterized by both tactile hypersensitivity and hyposensitivity (Lichstein and Sackett 1971) have significantly decreased levels of platelet serotonin.

A number of investigators have also shown that there is significant reduction in growth hormone (GH) and adrenocorticotropin (ACTH) in psychosocial dwarfism (reversible hyposomatotropism) (Patton and Gardner 1975; Powell et al. 1967a,b; Wolff and Money 1973; Money and Wolff 1974; Brown 1976). Significant to these findings is the report that endogenous opioids are involved in the regulation of serum growth hormone (GH) and prolactin (PRL). Specifically, naloxone depresses basal serum concentration of GH and PRL. Related to the above are the well-known phenomena that stress elicits an increase of endogenous opioids in the brain; and of ACTH and B-endorphin in the systemic circulation; and that serotonin increases prolactin, growth hormone, and adrenocorticotropin (Meites et al. 1979).

These observations are made to suggest that psychosocial dwarfism may well be characterized by abnormal endorphin mechanisms which may be responsible for the observed abnormalities of GH and ACTH in