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psychosocial dwarfism. Thus, these speculations suggest that endorphin mechanisms may assume a much greater role and significance in somatosensory affectional deprivation phenomena than has heretofore been realized.
The findings of Behling (1979) highlight the relationship between alcohol abuse, child abuse, and failure of nurturance, showing that in 69 percent of 51 instances of child abuse, at least one parent had a history of alcohol abuse.
In the context of the SAD theory, it is not surprising to find the compensatory behaviors of violence in the primitive culture study cited above or the finding of Barry (1976) that the single greatest predictor of drunkenness in 13 primitive cultures was the large amount of crying during infancy (r=0.77). Drunkenness was also significantly correlated with low general indulgence during infancy (r=0.40; N=26) and low duration of bodily contact with caretaker during later stages of infancy (r=0.42; N=23). Significant relationships between deprivation of parental physical affection and use of drugs and alcohol have been reported for college students (Prescott 1975), for prisoners (Prescott and Wallace 1978), for institutionalized alcoholics, and for participants in a drug treatment program (Prescott and Wallace 1976). Significant relationships between high drug and alcohol usage with attitudes rejecting premarital and extramarital sex have also been reported for college students (Prescott 1975).
An interpretive statement of these relationships with respect to somatosensory pleasure seeking, isolation rearing (somatosensory affectional deprivation), altered neuronal communication, and altered states of "consciousness" appears necessary. Briefly, the SAD theory postulates that somatosensory deprivation from isolation rearing leads to impaired brain neuronal systems that mediate pleasure which now lack the neuronal structural bases to interact with and influence higher brain (cognitive) centers (neocortex). This impairment prevents an integration of somatosensory pleasure with higher brain centers and precludes the normal development of altered states of consciousness or states of "transcendent being." (See Teilhard de Chardin's 1933 essay "The Evolution of Chastity" on the role of pleasure in achieving states of "transcendent being.") Consequently, most of the somatosensory pleasure-stimulus-seeking behaviors of contemporary Western civilization (not just America) appear to be "nonintegrative" in nature, i.e., primarily "reflexive." This means the "pleasure experience" is a momentary and transitory phenomenon that produces a temporary reduction of physiological tension and discomfort but does not represent a true positive state of "integrative pleasure" that is essential for experiencing an "altered state of consciousness." Thus, anomie remains, a high need for another "pleasure fix" remains, and the complex of perseverative behaviors remains. Drugs and alcohol "bypass" the somatosensory process and provide a direct route to higher brain centers that alter "states of consciousness" which simulate states of "transcendent being." It should be noted that somatosensory affectional deprivation from social isolation results in an aversion to touch and thus constitutes a barrier to the "touch therapy" that is essential for rehabilitation, namely, the establishment of emotional/affective-social relationships.
Within the context of SAD theory, three basic groups of substance abusers are proposed to exist and need to be evaluated and treated differently. These are (a) pleasure seekers (marijuana, heroin, etc.),
(b) pleasure avoiders (alcohol, depressants, tranquilizers), and (c) "altered states of consciousness" seekers (hallucinogens).
A factor-analytic study involving items of drug and alcohol usage produced orthogonal (independent) factors for alcohol and marijuana usage (Prescott and Wallace 1976). Unfortunately, time and space do not permit review of these data or an elaboration of SAD theory of drug typologies and their implications for research and therapy. It is suggested, however, that a sensory process orientation would be highly heuristic. Special attention should be given to evaluating vestibular-cerebellar processes in alcoholics, somesthetic-cerebellar processes in pleasure-seeking drug users, and visual/auditory neocortical processes in hallucinogen users. It should be recognized that these suggestions are highly speculative and have many limitations, but they may, nevertheless, have some merit in attempting to identify specific neurobiological brain processes with specific choices of substance use and abuse.
Evidence that social isolation rearing alters neurochemistry of brain function has been partially reviewed elsewhere (Prescott 1971a, 1976a; Lal et al. 1972; Essman 1971, 1974, 1979; Essman and Casper 1978; Welch and Welch 1969; Valzelli 1967; De Feudis and Marks 1973; Rosenzweig 1979; Rosenzweig et al. 1968). Certain studies, however, deserve special commentary, and recent developments with respect to the endorphins are especially relevant to somatosensory affectional deprivation theory and data, as is the basic alteration of the CNS's response to drugs that is induced by SAD of isolation rearing.
In this specific social-neurobiological context, Lal et al. (1972) have demonstrated that social isolation rearing of mice (somatosensory affectional deprivation) significantly altered the pharmacological effects of hexobarbital, pentobarbital, chloral hydrate, barbital, and chlorpromazine. Specifically, social isolation enhances stimulant drug effects and reduces CNS depressant effects.
Bonnet et al. (1976) reported that mice reared in social isolation (somatosensory affectional deprivation) for 20 weeks showed a significant reduction in narcotic agonist and antagonist binding. No differences could be found in stereospecific binding between the rearing groups with 15 weeks of differential rearing, but were found at 17 and 21 weeks. These authors also reported a significant reduction of the number of opiate binding sites in the brains of isolation-reared mice compared to aggregation-reared mice. This loss of opiate receptor sites in isolation-reared mice may be analogous to the loss of dendrites consequent to social isolation rearing.
Panksepp et al. (1978) and Herman and Panksepp (1978) reported a significant decrease in distress vocalizations of puppies which were briefly separated from their mothers (15 minutes) with an injection of 0.125 mg/kg of oxymorphone, and they found that naloxone increased group vocalization of two- to five-day-old white Leghorn chicks briefly separated from their mother. These authors discuss the parallels between the biological nature of narcotic addiction and the formation of social bonds, and their theoretical position is similar to SAD theory and my belief that the brain endorphin systems may be one of the most important neurobiological systems mediating the development of affectional bonds, including sexual affectional bonds.
The role of endorphins in sexual behavior has been studied by Gesa et al. (1979), and they have reported the following findings from their rat study:
a) DALA (D-Ala?-Met-enkephalinamide) given intracerebroventricularly
at a dose of six micrograms completely inhibited copulatory behavior and the ability to ejaculate in sexually active rats. Naloxone (four mg/kg) given intraperitoneally completely reversed this effect.
b) Naloxone does not enhance sexual behavior in sexually active rats.
c) Naloxone (four mg/kg) given intramuscularly significantly enhances
mounting, intromission, and ejaculation in sexually inactive rats.
These authors suggest that endorphins may mediate sexual disorders and that opioid antagonists "might become potentially useful therapeutic agents for sexual disturbances in man" (p. 204). A similar statement might be made for the treatment of alcoholics whose somatosensory pleasure system is dysfunctional and often inoperable. Whether pleasureinducing drugs, such as marijuana and the opioids, may prove to be a useful first step in a program of somatosensory rehabilitation for alcoholics and other somatosensory impaired individuals remains to be demonstrated. Different therapeutic strategies appear indicated, however, for differing classes of substance abusers.
Veith et al. (1978) have also reported the effects of endorphin compounds upon emotional and sexual behaviors in rats. They examined the consequences of a single intraperitoneal injection of 100mg of a-endorphin (B-LPH 61-76), y-endorphin (ß-LPH 61-77), and B-endorphin (B-LPH 61-91), and a (D-Ala?] analog of Met-enkephalin upon several measures of open field behavior compared to saline controls.
In brief, these authors found that B-endorphin enhanced grooming behavior; y-endorphin and its analog (D-Ala?] increased emotional responses (ran to the wall faster and greater defecation); and aendorphin (D-Ala?) increased sexual arousal (penile erection and seminal discharge). The selective behavior effects of these various peptides were emphasized, and it was suggested that each peptide may be coded to act upon receptor rates in a differential manner to mediate the differing behavioral effects.
From this writer's perspective it is sufficient to emphasize the social, emotional, and pleasure (sexual) behaviors that are induced by endorphin compounds. In this context, it is heuristic to note the findings of Houck et al. (1980) who reported two B-endorphinlike materials in human placenta from three patients undergoing natural childbirth. These authors speculate upon the possible role of placental endorphins "as a natural antidote to the pain and stress of parturition." This writer cannot help but speculate further that the positive emotional state toward pregnancy of women electing natural childbirth may be reflected in a "positive intrauterine state that is characterized by the presence of placental endorphin. This raises additional questions whether "stressful" pregnancies or "unwanted" pregnancies are characterized by a significant decrease or lack of placental endorphins.
Finally, does the presence or absence of placental endorphins reflect, in any way, the integrity of fetal endorphin mechanisms or the future developmental integrity of neonatal/infant/child endorphin mechanisms? Does obstetric medication have any adverse effect on fetal endorphin
mechanisms? Do such events have any long-term developmental implications for how pain and pleasure are experienced, the quality of development of emotional-social relationships, and whether and what coping/ compensatory behaviors may be adopted as a consequence of dysfunctional psychobiological affectional mechanisms?
These studies are cited because of the increasing evidence that has linked affectional variables and early social isolation to (a) violence, drug and alcohol abuse, and sexual dysfunctioning; (b) altered neurochemistry, electrophysiology, and dendritic structures (neuronal communication) in somatosensory and motor cortex and cerebellar cortex; (c) altered narcotic agonist and antagonist binding; and (d) altered CNS response to stimulant and depressant drugs. The role of sexual functioning and sexual pleasure in the developmental continuum of affectional bonding and its relationship to endorphins, drug and alcohol use, and violence, particularly alcohol-induced violence, brings a convergence of theories and experimental evidence that were heretofore considered disparate entities and phenomena. The report of Pradelles et al. (1979) that visual deprivation decreases Met-enkephalin in various amygdaloid and striatal structures provides further support for linking sensory deprivation phenomena to enkephalin neurotransmitter or neuroregulatory processes.
The findings of Gesa et al. (1979) and of Panksepp (1978), however, appear contradictory and inconsistent with this proposed convergence. In the former study, stimulation of opiate receptors induced pleasuredeficit behaviors (failure to copulate and ejaculate), whereas in the latter study, stimulation of opiate receptors induced pleasureenhancement behaviors (decrease in distress vocalizations). Similarly, in the Gesa study naloxone enhanced pleasure behaviors (increased copulation and ejaculation), whereas naloxone decreased pleasure behaviors (enhanced distress vocalization) in the Panksepp study. These apparent fundamental contradictions are, it is proposed, resolvable within SAD theory and Cannon's Law of Denervation Supersensitivity (Cannon 1939; Cannon and Rosenbleuth 1949; Collier 1968; Sharpless 1975), which is an integral and essential neurophysiological mechanism of SAD theory (Prescott 1971a, 1972b).
Briefly, fundamental distinctions must be made between CNSs that are characterized by or not characterized by denervation supersensitivity, which is induced by deafferentation, i.e., a loss of afferent input. Sexual inactivity, like social isolation rearing, involves somatosensory deprivation that constitutes a special case of functional deafferentation. As reported by Struble and Riesen (1978), primate isolation rearing results in loss of dendrites in somatosensory cortex. The loss of opiate receptor sites, reduced narcotic agonist and antagonist binding, enhancement of stimulant drug effects, and inhibition of depressant drug effects are also all consequent to social isolation and thus share, in my view, a common explanatory mechanism, namely, Cannon's Law of Denervation Supersensitivity. It is within this context that it is relevant to emphasize that opioid substances act on their receptors to depress the activity of cells bearing these receptors and, consequently, are classed as inhibitory neurotransmitters (Frederickson and Norris 1976). The enhancement of these inhibitory neurotransmitters through the mechanism of denervation supersensitivity might account for the inhibition of copulatory and ejaculatory behavior as reported by Gesa et al. (1979). Similarly, the absence of denervation supersensitivity in Panksepp's experimental subjects could account for his endorphin stress-reducing (pleasure-enhancing?) effects.
The findings of Gispen et al. (1976) that low doses of B-endorphin (0.01-0.3 micrograms) induced excessive grooming behavior in rats, and of Meyerson and Terenius (1977) that "higher" doses of B-endorphin (one and three micrograms) significantly reduced mounting and copulatory behavior in Wistar rats exposed to estrous females support the "bidirectionality" (prosocial versus asocial behaviors) of endorphin mechanisms. Naltrexone given subcutaneously 30 minutes before the peptide blocked the effect of one microgram B-endorphin, thus confirming that impaired sexual functioning was mediated via opiate receptors. It should be noted that one microgram B-endorphin did not interfere with sexual exploratory behavior that included active pursuit and investigation of the anogenital area of the female.
These reports of bidirectionality of endorphin activity as a function of dosage level, the endorphin antagonistic effects, and the naloxone agonistic effects concerning sexual behaviors are not unrelated to the naloxone agonistic effects concerning pain perception.
Levine et al. (1978), in a study of human clinical pain (tooth extraction), found that naloxone produces analgesia at low doses (0.4 and 2 mg) and hyperalgesia at high doses (7.5-10 mg) for a placebo-respondent group. Interestingly, naloxone had little effect on placebo nonresponders. Questions must be raised whether placebo responders and those experimental preparations that manifest naloxone agonistic effects (bidirectionality) could be characterized by SAD or other forms of induced denervation supersensitivity. These questions are relevant to the findings of Buchsbaum et al. (1977), who divided their subjects into pain-sensitive and pain-insensitive groups as determined by their ratings of an electric shock. They found that only the pain-sensitive subjects reported a naloxone (2 mg) analgesic effect and that paininsensitive subjects showed naloxone hyperalgesia.
Although the studies of Levine et al. (1978) and Buchsbaum et al. (1977) are not directly comparable since Levine employed multiple doses of naloxone and Buchsbaum employed a single naloxone dose, it is of interest to contrast the two naloxone hyperalgesia groups with respect to the issue of placebo responding. Levine et al. reported a naloxone bidirectional effect for placebo responders, whereas Buchsbaum's pain-insensitive bidirectional responders (naloxone hyperalgesia) were characterized as placebo "nonresponders" since their placebo response was less than half that of the pain-sensitive group. These "inconsistencies" require further experimental study.
These observations only complicate an already very complicated set of issues and phenomena of endorphin-related behaviors. However, the bidirectionality phenomena of naloxone and the naloxone agonist effects and endorphin antagonist effects involving not only pain phenomena but also sexual-social and motor behaviors (Gesa et al. 1979; Meyerson and Terenius 1977; Gispen et al. 1976; Bloom et al. 1976; Jacquet and Marks 1976) suggest an extremely complex role of modulation, regulation, and integration of sensory, social, emotional, and motor behaviors by the endorphin system.
A theory of cerebellar regulation and integration of sensory, social, emotional, and motor behaviors within the context of SAD theory has been previously elaborated (Prescott 1971a, 1976a, 1978). Heath and his coworkers (Heath 1972, 1975a,b, 1976, 1977; Heath et al. 1978, 1979) have established a wealth of data describing cerebellar-limbic