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Understanding and Preventing Violence - Volume 3: Social Influences Alcohol, Drugs of Abuse, Aggression, and Violence Klaus A. Miczek, Joseph F. DeBold, Margaret Haney, Jennifer Tidey, Jeffrey Vivian, Elise M. Weerts The alcohol-drug abuse-violence nexus presents itself in several distinctly different facets: alcohol and other drugs of abuse may act on brain mechanisms that cause a high-risk individual to engage in aggressive and violent behavior. Individuals with costly heroin or cocaine habits may commit violent crimes in order to secure the resources for further drug purchases. Narcotic drug dealers, but not alcohol vendors, practice their trade in a violent manner. Alcohol, narcotics, hallucinogens, and psychomotor stimulants differ substantially from each other and in the way that they are related to different kinds of violent and aggressive behavior. Generalizations about the linkage of alcohol, drugs of abuse, and violence are complicated by the many direct and indirect levels of interaction (e.g., Goldstein 1985); these range from (1) drugs activating aggression-specific brain mechanisms, through (2) drugs acting as licensure for violent and aggressive behavior, as well as (3) drugs as commodities in an illegal distribution system that relies upon violent enforcement tactics, to (4) violent behavior representing one of the means by which a drug habit is maintained. The persistently overwhelming alcohol-violence link as well as Klaus Miczek, Joseph DeBold, Margaret Haney, Jennifer Tidey, Jeffrey Vivian, and Elise Weerts are at the Department of Psychology, Tufts University.
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Understanding and Preventing Violence - Volume 3: Social Influences the recent outbreaks of ''crack" cocaine and "ice" methamphetamine epidemics in the United States provide dramatic examples of serious and complex public health problems that need to be dissected in a careful and comprehensive manner. Systematic evidence for alcohol and other drugs of abuse acting on aggression-specific brain mechanisms stems mainly from studies in animals, although a few neuroendocrine and other neurochemical and neurophysiologic measures have been obtained in humans. Data from studies in animals represent the primary means to investigate experimentally the proximal and distal causes of aggressive behavior, whereas studies in humans most often attempt to infer causative relationships mainly by correlating the incidence of violent and aggressive behavior with past alcohol intake or abuse of other drugs. It is the objective of the present discussion to consider, integrate, and highlight accounts of empirical data that relate alcohol, opiates, amphetamines, cocaine, cannabis, and other hallucinogens to aggressive and violent behavior, with a particular emphasis on the pharmacologic determinants and potential biologic mechanisms. The major methodological features and the key results of the empirical studies are detailed in tables that appear at the end of this paper. The information is organized so that (1) for each drug class, tables for the data on aggression and violence in animals and in humans are separated; (2) the data on human violence are organized according to how they were collected by separating those that stem from criminal statistics, public health records, psychological evaluations, and experimental manipulations; and (3) drug effects on different types of aggressive and violent behavior in animals are grouped according to the aggression-and violence-provoking conditions. ANIMAL MODELS OF AGGRESSION AND VIOLENCE During the past two decades the focus of research on animal aggression has been ethological investigations of adaptive forms of aggressive behavior (e.g., Archer, 1988; Huntingford and Turner, 1987; see also Table 1). Defense of a territory, rival fighting among mature males during the formation and maintenance of a group, defense of the young by a female, and antipredator defense are examples of these types of aggressive, defensive, and submissive behavior patterns, oftentimes referred to as agonistic behavior (Scott, 1966). Sociobiologic analysis portrays these behavior patterns as having evolved as part of reproductive strategies ultimately serving
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Understanding and Preventing Violence - Volume 3: Social Influences the transmission of genetic information to the next generation (Wilson, 1975). The damaging and injurious consequences of adaptive agonistic behavior exclude-at least transiently-competing individuals from access to important resources. Strikingly, even in the absence of physical injury, among the most severe consequences of being exposed to aggression or the threat of aggression is the prevention of reproductive behavior. One such example is the so-called psychological castrate monkey who maintains group membership but resides at the periphery, with subordinate access to protected sleeping places, nutritious and palatable foods, grooming interactions, and rest periods. However, the focus on aggressive behavior as it serves an adaptive function in reproductive strategies complicates the extrapolation to violent behavior as it is defined at the human level. How human violence and animal aggression are related in their biologic roots remains to be specified; excessively aggressive behavior may represent an extreme on a continuum with adaptive aggressive behavior patterns. Alternatively, however, adaptive and maladaptive aggressive behavior patterns may differ fundamentally in their functions and causes. Particularly during the 1960s, in a different research tradition, experimental preparations were developed that focused on aversive environmental manipulations to engender certain elements of defensive and aggressive behavior in otherwise placid, domesticated laboratory animals. These so-called animal models of aggression relied on prolonged isolated housing or crowding; exposure to noxious, painful electric shock pulses; omission of scheduled rewards; or restricted access to limited food supplies, as the major environmental manipulations (Malick, 1979; Valzelli et al., 1967; Sheard, 1981; Blanchard and Blanchard, 1984; Kelly, 1974; Looney and Cohen, 1982). The behavioral end point resulting from such experimental setups rarely extended beyond defensive postures and bites that were difficult to interpret in terms of the ethology of the animal. Such preparations have been questioned in terms of their validity for modeling human aggressive and violent behavior. Similarly, human aggression research under controlled laboratory conditions has employed aversive environmental manipulations that entail the administration of electric shocks, noxious noise, or loss of prize money to a fictitious opponent (e.g., Taylor, 1967; Cherek and Steinberg, 1987). Again, this type of experimental aggression research highlights the dilemma of attempting to model the essential features of "real-world" violence under
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Understanding and Preventing Violence - Volume 3: Social Influences controlled laboratory conditions without risking the potential harm and injury that are characteristic of violence. A third approach used to investigate aggressive behavior in animals under laboratory conditions relies on physiologic and pharmacologic manipulations. Histopathological findings of brain tumors in violent patients (e.g., Mark and Ervin, 1970) prompted the development of experimental procedures that ablate and destroy tissue in the septal forebrain, medial hypothalamus, or certain mesencephalic regions of laboratory rats and other animals. Such experimental manipulations may result in rage-like defensive postures and biting, often called rage, hyperreactivity, or hyperdefensiveness (e.g., Brady and Nauta, 1953; Albert and Walsh, 1982, 1984). Alternatively, electrical stimulation of discrete subcortical regions can evoke predatory attack, as well as aggressive and defensive responses in certain animal species (see Delgado, 1963; Flynn et al., 1979; Kruk et al., 1979; Mirsky and Siegel, in Volume 2). Treatment with near-toxic amphetamine doses and other catecholaminergic agonist drugs may result in bizarre, rage-like responses in otherwise placid laboratory animals (Chance, 1946; Randrup and Munkvad, 1969; Maj et al., 1980). Similarly, aggressive and defensive behavioral elements are induced by exposure to very high doses of hallucinogens and during withdrawal from opiates (e.g., Sbordone et al., 1981; Gianutsos and Lal, 1978). It is noteworthy that mescaline-, amphetamine- and morphine-withdrawal-induced aggressive responses in rats, in conjunction with exposure to electric foot shock, are proposed as "pathological" aggression. The inappropriate context, the unusually fragmented behavioral response patterns, and the limitation to domesticated laboratory rodents render aggressive and defensive reactions that are induced by lesions, electrical brain stimulation, drugs, and toxins problematic in their interpretation. Often these laboratory phenomena are termed bizarre and ambiguous. This brief introduction to and critique of the methodological and conceptual frameworks for studies of animal aggression will guide the subsequent discussion of research findings. It also highlights how a consideration of different kinds of human violence and animal aggression spans a range of environmental determinants, social contexts, functions, causative mechanisms, and consequences in general physiology and, particularly, in the central nervous system (CNS). Even a rudimentary understanding of the evolutionary origins of violent behavior in humans and its underlying brain mechanisms needs to begin with an appreciation of the range of agonistic behavior patterns subserving important survival
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Understanding and Preventing Violence - Volume 3: Social Influences functions in various animal species. There is no direct evidence, however, that demonstrates homology between the neural circuitry and physiologic activity that mediate aggressive behaviors in animals and those responsible for human violence. As a matter of fact, as reviewed repeatedly (see also Brain, and Mirsky and Siegel, in Volume 2), one major conclusion from work with cats and rats is that discrete neural circuits underlie each type of aggressive, defensive, and submissive behavior, and that the concept of a single neural center or command unit for aggressive behavior, as it has been studied in invertebrates, may not be simply extrapolated to complex mammalian nervous functions. CONCLUDING STATEMENT The evolutionary origins of aggressive and violent behavior need to be investigated by systematic comparisons of animals belonging to different species in order to delineate functional and neurobiologic common developments. The current animal models of aggression focus mostly on adaptive forms of agonistic behavior during social conflict. In order to relate experimental preparations in animals to issues of human violence, harmful and injurious forms of aggressive behavior must be considered. Similarly, there is a need to define how experimental laboratory measures of irritable, hostile, and aggressive human behavior relate to violence outside the laboratory context. However, such considerations prompt ethical demands about reducing harm and risk to animal and human research subjects. ALCOHOL, AGGRESSION, AND VIOLENCE The strong statistical association between alcohol and engaging in a violent or aggressive act or being the target of violent behavior prompts the identification of possible causal relationships. Conventional wisdom attributes disinhibiting effects to alcohol that release aggressive impulses from their cortical inhibition. Yet, the experimental evidence from studies in animals as well as in humans provides a complex pattern of results at the level of the cellular site of action, physiological system, whole organism, social setting, and culture that requires detailed examination. In fact, alcohol's effects on a given individual's aggressive and violent behavior do not follow simply a monotonic pharmacologic dose-effect relationship; this is evident from three decades of research
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Understanding and Preventing Violence - Volume 3: Social Influences with various animal species and humans under many conditions. Whether or not alcohol, in a range of doses ingested orally, causes a certain individual to act aggressively more frequently or even to engage in "out-of-character" violent behavior depends on a host of interacting pharmacologic, endocrinologic, neurobiologic, genetic, situational, environmental, social, and cultural determinants. PHARMACOLOGIC DETERMINANTS Experimental studies in animals and humans demonstrate that the effects of acutely given alcohol engender a biphasic dose-effect curve on a range of aggressive and competitive behaviors. Low acute alcohol doses increase, and high doses decrease, threat and attack behavior in fish, mice, rats, cats, dogs, primates, college students, and other paid experimental subjects (see Tables 2A and 3). This dose-dependent increase and decrease in aggressive behavior are seen in virtually all experimental models of animal aggression. The biphasic pattern of alcohol dose dependence characterizes many behavioral, endocrinologic, and other physiologic actions of this drug (Pohorecky, 1977). However, Tables 2A and 3 also summarize reports that do not detect a reliable aggression-enhancing effect of low alcohol doses under a range of experimental conditions. During more than two decades of laboratory research in humans, the aggression-heightening effects with acutely consumed drinks containing 0.6, 0.8, 0.9, or 2.5 ml/kg of 50 percent alcohol (vodka) or 0.8-1.25 ml/kg of ethanol have been repeatedly confirmed. For example, Cherek et al. (1984, 1985) documented extensive alcohol dose-effect determinations on human aggressive behavior in an experimental competition task, showing large aggression-heightening effects in a dose range from 0.5 to 1.25 ml/kg of 50 percent alcohol. Outside of the controlled laboratory situation, no comparable alcohol dose determinations for violence-heightening effects are available. One critical issue in the analysis of alcohol dose-effect relationships pertains to the use of group statistics. Population samples in virtually all animal species are composed of individuals that show clear-cut aggression-enhancing effects and those that show a reduction in aggressive behavior in the same range of alcohol doses. Individual differences in the aggression-enhancing effects of alcohol are not adequately detected by the use of pooled data and statistical averages. The source of the individual differences in sensitivity to the proaggressive effects of alcohol may eventually
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Understanding and Preventing Violence - Volume 3: Social Influences be traced to genetic and neurobiologic determinants, current and past social experiences, and other situational variables. Alcohol is a short-acting drug whose early phases of action are associated most often with motor-activating, arousing, euphoric effects that contrast with the dysphoric and depressive effects during the later phases of its action (e.g., Babor et al., 1983). Experimental studies on acute alcohol doses and aggressive behavior have focused on the early activating phase of drug action (i.e., 15-30 minutes after administration), limiting their relevance to the problem of increased violent and aggressive behavior in later phases of alcohol action. Detailed ethological analyses of a range of behavioral elements and signals during social confrontations begin to identify how the effects of alcohol qualitatively change as a function of increasing dose in mice, rats, and monkeys (Krsiak, 1975, 1976; Miczek and Barry, 1977; Miczek and O'Donnell, 1980; Yoshimura and Ogawa, 1983; Miczek, 1985; Winslow and Miczek, 1985, 1988; Blanchard et al., 1987c). Whereas very low alcohol doses (0.1-0.6 grams (g) per kilogram) increase elements of threat and attack under appropriate conditions, a two-to threefold increment in alcohol dose (1.2-1.6 g/kg) decreases the initiation of aggressive acts and postures, and a further twofold increase in alcohol dose leads to sedation. Chronic alcohol administration, at intoxicating levels, and aggressive behavior have been investigated in a few methodologically diverse studies in mice, rats, and rhesus monkeys (Table 2B). There are several demonstrations of unusual and intense forms of aggressive behavior in stressed animals when given alcohol chronically (e.g., Tramill et al., 1980, 1983; Pucilowski et al., 1987). For example, recently Peterson and Pohorecky (1989) reported that three daily alcohol administrations caused resident rats to attack and wound intruders more severely by targeting their bites at unusual sites of the opponent. This shift in aggressive behavior appears to indicate a disruption of species-specific ritualized patterns of fighting and an exaggeration to more intense and injurious forms of attack. The evidence on chronic alcohol effects in primates is limited to a few studies that show increased play fighting in juveniles, self-biting in isolation-reared rhesus monkeys, and aggressive displays in pigtail macaques (Chamove and Harlow, 1970; Cressman and Cadell, 1971; Kamback, 1973). Although most relevant to the human situation, the evidence from chronic alcohol studies under controlled laboratory conditions is still preliminary.
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Understanding and Preventing Violence - Volume 3: Social Influences The effects of alcohol abuse on human aggression and violence have to be inferred from statistics involving individuals who were at various stages of intoxication at the time of the aggressive or violent activity (see Table 3). Violent crimes such as murder, rape, and assaults are prevalent in alcohol-abusing individuals that are diagnosed as alcoholic, as well as those that do not fulfill psychiatric criteria of alcoholism. Alcohol abuse was found to be consistently and highly represented among convicted rapists (50%, Shupe, 1954; 53%, McCaldon, 1967; 35%/57%, Rada 1975, and Rada et al., 1978; 72%, Johnson et al., 1978; 65%, Barnard et al., 1979); incestuous offenders (49%, Virkkunen, 1974b; 50%, Browning and Boatman, 1977); wife abusers and individuals committing other types of family violence (40%, Gayford, 1979; 15-20%, Eberle, 1982; 83%, Livingston, 1986); individuals with a history of injurious violent acts (29%, Schuckit and Russell, 1984), particularly at home (48-56%, Kroll et al., 1985); imprisoned murderers (36%, Wilentz and Brady, 1961; 10%, Scott, 1968; 57%, Grunberg et al., 1978; 56%/83%, Bloom, 1980; 56%, Lindqvist, 1986); adolescents convicted of homicides (61%, Tinklenberg and Ochberg, 1981), and convicted felons (33%, Guze et al., 1968; 57%, Mayfield, 1976), although there are also occasional reports indicating no overrepresentations of alcoholics, as for example, among Swedish female criminal offenders (e.g., Medhus, 1975). These overwhelming statistics stem mainly from studies in Scandinavia, the United Kingdom, Australia, Canada, and various localities in the United States, indicating wide generality. The marked correlations between alcoholism and various types of violent acts do not permit, however, any clear insight into the pharmacologic conditions of alcohol exposure that are necessary or sufficient for these violence-promoting effects. Based on verbal recall by convicted felons, Collins and Schlenger (1988) indicated that those who were drinking just before the offense were 1.74 times more likely to be in prison for a violent crime than those who said that they were not drinking. Of course, these and similar types of data based on verbal report are tainted by the amnesic effects of alcohol intoxication. Blood alcohol levels in excess of 0.06 percent were found in nearly half of the convicted murderers at the time of the arrest (Lindqvist, 1986). Unfortunately, blood alcohol levels, if determined at all, frequently refer to values only after considerable time has elapsed since the violent act was performed. A critically limiting issue in studies on alcohol with animals is the way in which the drug is administered. Whereas oral self-administration is the rule in humans, animal studies most often
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Understanding and Preventing Violence - Volume 3: Social Influences rely on alcohol administration by the experimenter or on forced drinking. Voluntary intake of alcohol at intoxicating doses has been achieved only in selected experimental preparations in animals (e.g., Samson et al., 1989; Crowley and Andrews, 1987), but these methodologies have not been applied to the issue of alcohol's effects on aggressive behavior. There is also some indication that distilled beverages are more effective than beer in enhancing aggressive tendencies in laboratory competitive task in humans (Pihl et al., 1984a,b). ENDOCRINOLOGIC INFLUENCES The frequent statistical association between sexual violence and alcohol in humans (see Table 2) may suggest an alcohol effect that targets endocrine processes. Alcohol's action on androgens and its trophic hormones was postulated to mediate its effects on aggression (e.g., Mendelson and Mello, 1974; Mendelson et al., 1978). As a matter of fact, acute alcohol doses generally decrease testosterone in blood and higher doses also impair the gonadotropic hormones from the pituitary, such as luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in animals and in humans (Van Thiel et al., 1988). The decrease in testosterone in blood is primarily due to alcohol's action on the testes and the liver, rather than on the neuroendocrine events governing testosterone synthesis. That the action of alcohol outside the brain is relevant to the aggression-and violence-increasing effects of this substance is unlikely. Direct experimental investigations of alcohol-androgen interactive effects on aggression were conducted in mice, rats, and squirrel monkeys (DeBold and Miczek, 1985; Winslow and Miczek, 1988; Winslow et al., 1988; Lisciotto et al., 1990; see Table 2A). In individuals with experimentally or naturally elevated blood testosterone levels, acute low alcohol doses increase aggressive behavior toward a drug-free opponent. This alcohol-testosterone interaction appears to depend on the actions of testosterone on targets in brain rather than on peripheral sites of action. Males and females differ as to whether or not they engage in violent and aggressive behavior after alcohol (see Table 3). However, this difference is chiefly a statistical phenomenon due to social or environmental factors, rather than to endocrine differences. Men and women students differ in their expectations about the aggression-heightening effects of alcohol and about male versus female targets of aggression under the influence of alcohol
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Understanding and Preventing Violence - Volume 3: Social Influences (Crawford, 1984; Gustafson, 1986b,c). Epidemiologic data find male and female victims of homicides and suicides associated with alcohol abuse in comparable proportions, although males are much more frequently represented than females (Rydelius, 1988; Schuckit et al., 1978). No experimental data exist on human violent behavior that directly compare males and females while under the influence of alcohol. NEUROBIOLOGIC MECHANISMS At least a dozen mechanisms have been proposed and continue to be investigated for alcohol's action on the central nervous system (Anggard, 1988; Koob and Bloom, 1988; Myers, 1989), ranging from fluidization of neuronal membranes to relatively specific actions on receptors that are associated with gamma-aminobutyric acid (GABA), serotonin (5-HT), catecholamines, peptides, and steroids. Alcohol's violence-or aggression-heightening effects have not been linked firmly to a specific mechanism, although several proposals deserve attention. The relationship between high incidences of violent and aggressive behavior in alcoholics and some aspects of brain serotonin metabolism or serotonin receptor regulation has been investigated (Table 3; e.g., Linnoila et al., 1983; Virkkunen et al., 1989a,b). This correlational research finds some evidence for a link between low cerebrospinal fluid (CSF) levels of 5-HIAA (5-hydroxyindoleacetic acid) and poor impulse control found in some violent alcohol abusers (see also discussion of 5-HT in Miczek, Haney, et al., in Volume 2). Recently, some of alcohol's behavioral and neurochemical effects were linked with the action on the GABA-A receptor complex in brain (e.g., Suzdak et al., 1986; Lister and Nutt, 1988). Pharmacologic blockade of the benzodiazepine sites on the GABA-A receptor complex has already proven to be effective in antagonizing some of alcohol's neurochemical (e.g., Harris et al., 1988; Mehta and Ticku, 1988) and behavioral effects in animals (e.g., Lister, 1988a,b; Koob et al., 1989). Preliminary data demonstrate that antagonists at the benzodiazepine-GABA-A receptor complex block the aggression-heightening effects of alcohol in rats and monkeys (e.g., Weerts et al., 1993). At present, these experimental substances have not been explored in humans for their effects on alcohol-enhanced violence or aggression. In a small subgroup of individuals having committed a violent crime or antisocial act, a challenge dose of alcohol produces an
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Understanding and Preventing Violence - Volume 3: Social Influences abnormal electroencephalogram (EEG), suggesting temporal lobe damage that is aggravated by the drug (Marinacci and von Hagen, 1972). Individuals with underlying neurologic disturbances may represent a small proportion of the total number of alcohol-related violent acts. More recently, a study of EEG and event-related potentials (ERPs) in alcoholics found that the P300 component of ERPs was reduced in amplitude in alcoholics with a history of violence but not in alcoholics in general (Branchey et al., 1988). These studies suggest that there may be some physiologic differences between those few alcohol abusers that become violent and those that never experience any proaggressive effects of alcohol. GENETICS AND PERSONALITY FACTORS There are consistent demonstrations of a genetic component of alcohol abuse based on several series of studies in Scandinavia and in the United States (e.g., Goodwin, 1973). In parallel, antisocial personality has also been found to have a strong genetic component, and these two disorders frequently co-occur (see Table 3; also Schubert et al., 1988). The question as to whether or not there is a common genetic basis for antisocial personality disorder and alcoholism remains a source of controversy, with some claiming independence (e.g., Cadoret et al., 1985) and others linkage, at least in some alcoholics (e.g., Cloninger et al., 1989). In a recent sample of 32 identical twins from the United States, the heritability of alcohol abuse was very small and somewhat higher for antisocial personality (Grove et al., 1990). However, due to the small nonclinical sample size, no firm conclusions on the "permissive" role of the genetic influence on the gene-environment interaction are possible as yet. It is most astounding that no systematic investigations into the genetic influence on the alcohol-aggression link have been performed in animal preparations; promising starting points for such studies are animals that are selectively bred for high-preference for alcohol or for high levels of aggressive behavior. The evidence on personality factors of alcoholics differentiates several "alcoholic personalities" (see Table 3). Most significantly, a subpopulation of alcoholics may be identified as sociopathic via several personality testing instruments (e.g., O'Leary et al., 1978; Yates et al., 1987), and conversely, individuals that are diagnosed with antisocial personality disorder frequently abuse alcohol as well as other drugs. It is these latter individuals that
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Understanding and Preventing Violence - Volume 3: Social Influences C. Phencyclidine (PCP) Isolation-induced Aggression Rewerski et al., 1971 Rewerski et al., 1973 Male albino Swiss mice; aggression test with 2 conspecifics; 5 point aggression scale 1 mg/kg i.p. PCP abolished aggression in mice isolated for 14 days and was less effective in 28 day isolates. 5 mg/kg increased aggression in 14 and 28 day isolates. Wilmot et al., 1987 Male CF1 mice; resident drug treated 1.25-5.0 mg/kg i.p. PCP dose dependently decreased the number of animals fighting after 21 days isolation. In animals that fought (55-82%), 1.25, 2.5 mg/kg increased fight duration. Burkhalter and Balster, 1979 Male albino ICR mice; resident drug treated 1.0 mg/kg i.p. PCP increased attack bites and the number of animals that fought, 3.0 mg/kg produced no effect on aggression. Fico and Vanderwende, 1988 Male CF1 mice offspring of dam administered 20 mg/kg s.c. PCP prenatally PCP produced no effect on the percentage of mice fighting, ontogeny or intensity of aggressive behavior. Miczek and Haney, (in press) Male albino Swiss-Webster mice; resident drug treated 0.1, 0.3 mg/kg i.p. PCP produced increased and 6, 10 mg/kg decreased aggressive behavior. Pain-induced aggression and defense Cleary et al., 1981 Exp. 1: Footshocks to pairs of male Sprague-Dawley rats; both subjects drug treated. Exp. 2: Footshocks and reaction to inanimate bite target in 3 restrained male Wistar rats 0.5-2.0 mg/kg i.p. PCP dose dependently decreased mutual upright and bites in dyads and biting toward inanimate object. Emley and Hutchinson, 1983 Exp. 1: Footshocks and reaction to inanimate bite target in restrained male squirrel monkeys. Exp. 2: Same procedure without shock delivery Exp. 1:0.01-0.4 mg/kg s.c. PCP increased biting in first administration and decreased biting in second. Exp. 2:0.01-0.4 mg/kg had no effect on biting. Jarvis et al., 1985 Footshocks and reaction to inanimate bite target in restrained male Swiss mice 1-8 mg/kg i.p. PCP dose dependently decreased biting.
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Understanding and Preventing Violence - Volume 3: Social Influences Aggression induced by REM sleep deprivation Musty and Consroe, 1982 Male Sprague-Dawley 72 hr REM sleep-deprived and nonsleep-deprived rats; both subjects drug treated 0.025-0.2 mg/kg i.p. PCP modestly increased aggressive postures and attacks in rats not deprived of sleep. 0.025-0.2 mg/kg increased aggression in sleep-deprived rats with maximal effects at 0.05 mg/kg. Aggression by resident toward intruder Tyler and Miczek, 1982 Male albino Swiss-Webster mice; resident or intruder drug treated 3-10 mg/kg i.p. PCP dose dependently decreased aggressive behavior in resident mice while increasing motor behavior. 3-10 mg/kg increased attacks toward PCP treated intruders. Dominance-related aggression Miller et al., 1973 Groups of male rhesus monkeys 0.25 mg/kg i.m. PCP increased aggressive displays by untreated toward drug treated animals. Russell et al., 1984 Pairs of male Wistar rats; one subject drug treated 0.25 mg/kg s.c. PCP increased attack behavior by drug treated animals; 1.0 mg/kg decreased attack behavior by drug treated animal and increased attack behavior of saline treated animal. PCP alters responses to social signals which prevent attack behavior. Killing Rewerski et al., 1971 Muricidal behavior in male Wistar rats 5 mg/kg i.p. PCP non-significantly decreased muricidal behavior and increased the number of non-reacting animals. Musty and Consroe, 1982 Muricidal behavior in male 72 hr REM sleep-deprived and nonsleep-deprived Sprague-Dawley rats 0.025-0.2 mg/kg i.p. PCP produced no effect on muricide in rats not deprived of sleep. 0.025-0.2 mg/kg increased muricide in sleep-deprived rats with maximal effects at 0.05 mg/kg. Literature Reviews Krsiak, 1974 Review of 193 articles between 1948 and 1974 on drugs and aggression 5 mg/kg i.p. PCP increases aggression in isolated mice but only with animals which have a low baseline level of aggression.
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Understanding and Preventing Violence - Volume 3: Social Influences Miczek and Barry, 1976 Miczek and Krsiak, 1979 Miczek and Thompson, 1983 Miczek, 1987 Review of over 1500 animal and human articles between 1920 and 1987 on the pharmacology of aggression Increases in aggression due to PCP are inconsistent; increases in aggression toward PCP treated subjects is a robust finding. PCP alters sending and receiving of communicative signals important in social and aggressive interactions. Uyeno, 1978 Review of 32 articles between 1956 and 1978 on hallucinogens and aggressive behavior PCP decreases or has no effect on isolation-induced, predatory and spontaneous aggression. D. Other Hallucinogens Isolation-induced Aggression Uyeno, 1966b Psilocybin or BOL-148 administered to male Swiss-Webster mice; resident drug treated 1-8 mg/kg i.p. psilocybin dose dependently decreased the number of animals attacking; maximal effects 30 min after administration. 0.5-2.0 mg/kg i.p. BOL-148 dose dependently decreased the number of animals attacking; maximal effects 30 min after administration Valzelli et al., 1967 Valzelli and Bernasconi, 1971 Hybogaine or yohimbine administered to male Swiss albino mice; resident drug treated; 5 point aggression scale 20 mg/kg i.p. ibogaine decreased aggressive behavior; 10 mg/kg i.p. yohimbine abolished aggression for 6 hr. Kostowski et al., 1972 Psilocybin, JB-336, ibogaine or bufotenine administered to male Swiss albino mice; resident drug treated 10 mg/kg i.p. psilocybin, 5 mg/kg i.p. JB-336, 10 mg/kg i.p. ibogaine and 10 mg/kg i.p. bufotenine decreased aggressiveness. Rewerski et al., 1973 JB-336 administered to male Swiss albino mice; aggression test with 2 conspecifics; 5 point aggression scale 5 mg/kg i.p. JB-336 strongly inhibited aggressiveness in mice isolated for 14 days and had no effect in 28 day isolates. Pain-induced aggression and defense Walters et al., 1978 Footshocks to pairs of male albino Sprague-Dawley rats; both subjects treated with DMT or 5MeODMT 4-8 mg/kg DMT and 2.0 mg/kg 5MeODMT dose dependently decreased the percentage of animals fighting. Sbordone et al., 1979 Footshocks to pairs of male Sprague-Dawley rats; both subjects treated with psilocin, DMT, DMPEA 0.4-10 mg/kg i.p. psilocin, 0.4-10 mg/kg i.p. DMT and 8-200 mg/kg i.p. DMPEA decreased the number of fights and duration of fighting.
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Understanding and Preventing Violence - Volume 3: Social Influences Aggression due to omission of reward Uyeno, 1966a Food competition between pairs of male Wistar rats; one subject drug treated with BOL-148 0.4-1.0 mg/kg i.p. BOL-148 dose dependently decreased attack behavior; maximal effects after 45 min Uyeno, 1972 Food competition between pairs of male Wistar rats; one subject drug treated with DOM 0.4-1.2 mg/kg i.p. DOM dose dependently decreased attack behavior and ''dominance"; maximal effects after 30-45 min Uyeno, 1976 Competition for female in estrus between pairs of male Wistar rats; one subject drug treated with DOM 0.25-1.0 mg/kg i.p. DOM dose dependently decreased "dominance"; maximal effects after 45 min Drug-induced aggression Siegel et al., 1974 Siegel et al., 1976 Solitary rhesus monkeys treated with DMT or BOL-148 0.5-4.0 mg/kg i.m. DMT, 100 µg/kg i.m. BOL-148 modestly decreased threat behavior. Aggression by resident toward intruder Siegel and Poole, 1969 Introduction of novel mice ("strangers") to groups of male CF1 mice; bufotenine administered to both group housed and intruder subjects 5-30 mg/kg (in water supply) bufotenine decreased aggression and group aggregation. Bufotenine treated strangers were hypersensitive to auditory and tactile stimulation and aggregated in small groups. Dominance-related aggression Thor et al., 1967 Male Siamese fighting fish (Betta splendens) treated with diethylamine 1, 2 mg/cc (in aquarium water) diethylamine abolished fighting in pairs of fish for 40 and 48 hr, respectively. Siegel and Poole, 1969 Social interaction within groups of male CF1 mice treated with bufotenine 5-30 mg/kg (in water supply) bufotenine decreased aggression and group aggregation.
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Understanding and Preventing Violence - Volume 3: Social Influences Schlemmer et al., 1977 Schlemmer and Davis, 1981 Colonies of female Stumptail macaques treated with acute and chronic (12 day) 5MeODMT Acute: 5-250 µg/kg i.m. 5MeODMT dose dependently decreased normal affiliative and increased submissive behaviors. Chronic: Daily administration of 250 µg/kg 5MeODMT increased submissive gestures displayed by the treated animal without increasing aggressive gestures by untreated animals; there were no signs of tolerance. Tyler et al., 1978 Pairs of female Stumptail macaques treated with acute and chronic (5 day) DOM; one subject drug treated 0.17 mg/kg i.m. DOM decreased social and submissive behaviors with modest signs of tolerance after 5 days. Killing Valzelli and Bernasconi, 1971 Muricidal behavior by male Wistar rats treated with yohimbine; 3 point aggression scale 10 mg/kg i.p. yohimbine abolished muricide for 1.5 hr and decreased "friendly" in favor of "indifferent" behavior for 4 hr. Kostowski et al., 1972 Muricidal behavior by male Wistar rats treated with psilocybin, JB-336, ibogaine or bufotenine 10 mg/kg i.p. psilocybin, 5, 10 mg/kg i.p. JB-336, 10 mg/kg i.p bufotenine decreased the number of kills. 10 mg/kg i.p. ibogaine had no effect on muricidal behavior. Molina et al., 1986 Muricidal behavior by olfactory bulbectomized or nonlesioned male Wistar rats treated with 5MeODMT 1, 1.5 mg/kg i.p. 5MeODMT dose dependently decreased muricidal behavior in lesioned and nonlesioned animals; maximal effects 15 min after administration Literature Reviews Siegel, 1971 Siegel, 1973 Review of over 65 articles between 1943 and 1973 on hallucinogens and behavior Bufotenine induces hypersensitivity and decreases social interactions. Miczek and Barry, 1976 Review of over 500 articles between 1932 to 1976 on the pharmacology of sex and aggression Aggressive behavior is decreased with psilocybin in isolation-induced, competitive, social behavior and predatory paradigms.
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Understanding and Preventing Violence - Volume 3: Social Influences Sheard, 1977b Review of 119 articles between 1928 and 1977 on animal models of aggressive behavior DMT has a weak and inconsistent excitatory effect on electric shock-elicited fighting between 0.125-1 mg/kg; 4 and 8 mg/kg DMT decrease aggression. 5MeODMT has no effect on electric shock-elicited fighting at low doses, and depressant effects at high doses (range: 0.12-8.0 mg/kg). Uyeno, 1978 Review of 32 articles between 1956 and 1978 on hallucinogens and aggressive behavior Bufotenine, DOM, ibogaine, JB-336 and psilocybin have no effect or decrease aggression in isolation-induced, predatory and competition paradigms. Sbordone et al., 1981 Review of 73 human and animal articles between 1939 and 1981 on drug-induced aggression; electric shock-elicited paradigm highlighted with animals When both animals are drug treated, low doses of psilocin, DMT and DMPEA have no effect on aggression; at high doses these hallucinogens decrease aggression.
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Understanding and Preventing Violence - Volume 3: Social Influences TABLE 13 Effects of Hallucinogenic Drugs on Aggression in Humans References Methods and Procedures Results and Conclusions A.LSD Criminal violence Knudsen, 1967 Case study of a 25 year old female who committed homicide after 5 LSD treatments (50 ng LSD/treatment for depression, anxiety) in Norway LSD diminished some behavioral control, including aggressive impulses. Barter and Reite, 1969 Case studies of 3 LSD induced homicide Homicide associated with LSD use was rare, perhaps due to a disorganization of purposeful conduct. Williams, 1969 Case study of a 37 year old male who committed homicide in the U.K. Subject experienced "bad trip" and had amnesia for the homicide. Baker, 1970 Case studies of 67 LSD related hospital admissions in the U.K. between 1966 and 1967 5 categories of LSD effects: acute psychotic reaction (39%) including assaultiveness, suicidal (3%), aggressive (4%), LSD specific effects uncertain due to multidrug use (39%) and other (13%). Reich and Hepps, 1972 Case study of a 22 year old male, long term LSD user who committed homicide in Massachusetts 200 µg (normal dose) LSD produced persecutory delusions ("bad trip") Klepfisz and Racy, 1973 Case study of a 22 year old male, long term LSD user who committed homicide in New York Physical assault occurred within 12 hours of LSD ingestion, homicide within 48 hours. Subject was psychotic during homicide and for the 6 previous months. Not known if LSD exaggerated the psychosis or caused it. Duncan, 1974 Case studies of 4 male incarcerated adolescent schizophrenics All 4 patients had ingested LSD and were assaultive. LSD induced psychoses in 2 patients and exaggerated existing psychoses in others.
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Understanding and Preventing Violence - Volume 3: Social Influences Health statistics Allen and West, 1968 Interpretation of the "Green Rebellion" of 1967-68 in Haight-Ashbury LSD was crucial in the "hippie" rebellion; these individuals showed decreased aggressiveness and competitiveness. Brickman, 1968 Interpretation of psychedelic experiences due to LSD and mescaline in terms of Freudian death instinct Psychedelic experience caused "the symbolic rebirth and development of a new self which, affirming death, no longer needs to extemalize destructiveness." Personality evaluations Edwards et al., 1969 Psychiatric evaluation of 60 male and female heavy psychedelic users (LSD, DMT, STP) and nonusers Polydrug use common; drug experienced subjects were more hostile than controls (Comrey test); hostility was not related to drug usage. Smart and Jones, 1970 Psychiatric evaluation of 100 male and female LSD users and 46 non user controls (age: 15-37 years) in Canada LSD users showed more psychological disturbances and scored higher on MMPI scales Hy, Ma, Pd, Sc, Mf (males only) than nonusers; psychopathology predated drug use. Experimental studies of aggression Fink et al., 1966 Repeated administration of LSD (0.5-10.0 µg/kg) to 65 long-term psychotic patients Adverse reactions including hostility and irritability occurred in only 2% of the patients and were not dose related. Cheek and Holstein, 1971 Social behavior measured among 16 male reformatory inmates after LSD administration 25, 50 µg p.o. LSD increased and 200 µg decreased social interaction. Hostility increased among behaviorally aggressive reformatory patients; positive and negative behaviors were increased in schizophrenics. Literature Reviews Szara, 1967 Brill, 1969 Sbordone et al., 1981 Sheard, 1983 Hollister, 1984 Miczek, 1987 Review of over 1500 human and animal articles between 1920 and 1987 on the pharmacology of drugs and aggression LSD use is rarely associated with violence. Effects are dependent on the psychopathology and expectations of the subject and the environmental surroundings. Exaggeration of psychoses will result if given to psychotic, borderline psychotic and not informed normally functioning subjects.
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Understanding and Preventing Violence - Volume 3: Social Influences B. Phencyclidine (PCP) Criminal violence Fauman et al., 1976 Fauman and Fauman, 1977 Fauman and Fauman, 1979 Fauman and Fauman, 1980a,b Fauman and Fauman, 1982 Psychiatric classification of PCP violence via interview; case studies Acute administration of PCP produced psychosis in a small fraction of users and was related to pathologic personality; polydrug use was common. Chronic PCP use was associated with violence. Noguchi and Nakamura, 1978 Study of 16 PCP related deaths in Los Angeles County in 1976 PCP use might be related to psychosis, homicide and accidental death. Simonds and Kashani, 1979a Structured interview and review of juvenile files of 109 delinquent males (mean age: 16 years) in Missouri 8% of the subjects used PCP and were polydrug users. Of these, 22% reported fighting or hostile feelings while using PCP. Siegel, 1980 Study of 51 PCP related violent crimes in males and females in California between 1977 and 1979 PCP might produce abrupt spontaneous changes in personality functioning resulting in violent acts. PCP users had polydrug history, were assaultive and combative. Verbal or physical fighting reported during PCP intoxication in 50% of Supreme Court cases. Foster and Narasimhachari, 1986 30 year old female with no history of substance abuse who attempted homicide Flu-like illness followed by confusion and delusion preceded attempted homicide. Patient recovered with 2 mg/day haloperidol and urine acidification. Brecher et al., 1988 Review of 350 published reports on PCP use in humans from 1966 to 1986 Polydrug use common in PCP users; reports of violence due to PCP exaggerated (only 0.8% of the reports demonstrated PCP use and violence). Clinical and forensic assumptions about PCP and violence were not warranted. Health statistics Luisada, 1978 11 male exclusive PCP users admitted to a Washington DC hospital from 1973 to 1974 PCP psychosis was nearly indistinguishable from schizophrenia and might last for weeks. Violent behavior was more likely to occur in the first 5 days.
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Understanding and Preventing Violence - Volume 3: Social Influences Bailey, 1979 Relationship between plasma and urine PCP concentrations and physical symptoms of PCP intoxication in 22 California patients Combativeness-agitation present in 64% of the patients; there was no correlation between plasma PCP levels and behavior. Smith and Wesson, 1980 Diagnosis and treatment of PCP intoxication in San Francisco PCP and violent reactions were exaggerated. Acute PCP toxicity included combativeness (usually low doses), catatonia, convulsions, and coma; treatable with diazepam, chlorpromazine. PCP toxic psychosis included agitation and usually occurred with chronic users; treatable with haloperidol. PCP-precipitated psychotic episode included agitation and was treated with haloperidol, chlorpromazine. McCarron et al., 1981 1000 case studies of acute PCP intoxication in males and females in Los Angeles High doses of PCP produced "acute brain syndrome" (24.8%), toxic psychosis (16.6%), catatonic syndrome (11.7%) and coma (10.6%). Low doses produced lethargy and bizarre behavior including violence and agitation which lasted for a few hours. Heilig et al., 1982 Psychiatric assessment of 44 1977-78 male and female Los Angeles County PCP related deaths PCP users had a history of physical fighting and polydrug use. There was considerable psychosocial maladjustment evidenced. Personality evaluations Wright, 1980 Interview of 10 schizophrenics and frequency of PCP use Violent behavior and PCP use was indicated in 6/10 schizophrenic patients (3 chronic and 3 first time users). Chronic users best described by Fauman and Fauman Type 2 classification. Khajawall et al., 1982 Comparison of PCP or heroin rehabilitation in California hospital setting with 325 chronic users No difference between PCP and heroin patients on measures of aggression; PCP users demonstrated low levels of overt aggression. There was no correlation between urine PCP levels and aggression. Rawson et al., 1982 68 male and female (age: 14-38 years) chronic PCP users seeking detoxification in Los Angeles County hospital between 1979 and 1980 More than 30% of the patients report increased anger and violent behavior while using PCP.
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Understanding and Preventing Violence - Volume 3: Social Influences Convit et al., 1988 Yesavage and Zarcone, 1990 Psychiatric evaluation of 85 male schizophrenics in California hospital; 79 male schizophrenics in New York hospital; follow up 6 months after release Polydrug use common, PCP use strongly related to assaults during hospital stay and 6 month follow up. Literature Reviews Siegel, 1978 Petersen, 1980 Sbordone et al., 1981 Hollister, 1984 Pradhan, 1984 Cherek and Steinberg, 1987 Miczek, 1987 Review of over 1500 human and animal articles between 1920 and 1987 on the pharmacology of aggression Incidence of violent behavior with PCP intoxication is very rare. Polydrug use common; personality predispositions and history of violent behavior is important in determining PCP effects. Acute: Low doses can induce aggression during psychotic episodes. Chronic PCP use may lead to aggressive outbursts due to real or imagined frustrations, poor judgment and panic reactions.
Representative terms from entire chapter: