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Understanding and Preventing Violence, Volume 3: Social Influences (1994)

Chapter: Alcohol, Drugs of Abuse, Aggression, and Violence

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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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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.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

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.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

(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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

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

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

are more likely to be violent than alcohol abusers with other personality subtypes. There is evidence that they may also form a specific genetic subtype (Cloninger, 1987).

ENVIRONMENTAL DETERMINANTS

The most significant environmental factors in determining the direction and magnitude of alcohol's effects on aggressive and violent behavior are the past and current social conditions (''set" and "setting"). Situational, social, and personal characteristics prior to alcohol consumption contribute significantly to the aggression-promoting effects of alcohol in barroom environments, in addition to the type and amount of alcoholic beverage (e.g., Boyatzis, 1975; Graham et al., 1980).

An important question in this filed is whether alcohol increases aggression and violence because of pharmacologic actions or because the drinker expects an increase in aggression as part of the effects of alcohol. In laboratory experiments, it has been demonstrated that subjects believe that a drunk will behave more aggressively (Gustafson, 1986b,c). Some researchers have reported that subjects will behave aggressively in the laboratory if they think they have consumed alcohol independent of their actual blood-alcohol content (BAC) (e.g., Lang et al., 1975; Rohsenow and Bachorowski, 1984), but others find that the pharmacologic effects of alcohol on aggression are stronger than any expectancy effects (e.g., George and Marlatt, 1986; Pihl and Zacchia, 1986).

The behavioral history of aggressive and violent behavior is a critical determinant in whether or not alcohol will increase these types of behavior, as demonstrated in studies with animals (e.g., Pettijohn, 1979; Miczek and Barry, 1977) and also with humans (e.g., Rydelius, 1988). In a longitudinal Finnish sample, 20-year-old violent male offenders were more likely to have been more aggressive at age 8; aggressiveness at age 8 also predicted heavy drinking by age 20 (Pulkkinen, 1983). Alcohol more than doubled the rate of attack and threat behavior by mice, rats, and monkeys that had previously exhibited these behaviors during social confrontations, whereas alcohol did not induce aggressive behavior in individuals who had displayed primarily submissive and defensive behavior during previous confrontations (Blanchard et al., 1987b; Winslow and Miczek, 1985; DeBold and Miczek, 1985). The interaction between the predisposition to antisocial personality and alcoholism on the one hand, and early life history with family

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

and peers on the other, needs to be investigated systematically to specify the respective contributions of these factors.

Research findings from the animal and human literature on alcohol, however, differ in that violent acts by alcohol-intoxicated humans preferentially target family members and friends, but animals direct their injurious aggressive acts toward unfamiliar opponents and less intensely toward their kin.

Alcohol in the victim or target of aggressive and violent behavior has been documented both in animals and in humans (Tables 2A and 3). Acutely or chronically alcohol-treated mice, rats, or monkeys provoke more frequent attacks and threats by an alcohol-free opponent (e.g., Miczek et al., 1984; Peterson and Pohorecky, 1989; Blanchard et al., 1987c). Correlational statistics in humans identify alcoholics as risking injury, often fatally, in violent interactions more often than nonalcoholics (Table 3; especially Wolfgang and Strohm, 1956; Virkkunen, 1974a; Abel et al., 1985). However, these statistics cannot assess the contribution by the alcoholics to the escalating interaction that eventually led to their being victims.

In a variety of countries, such as Australia, Finland, Sweden, South Africa, Canada, and the United States, an association between alcohol and violence has been noted. The major source of cultural differences in the prevalence of this association is usually attributed to nonbiologic factors. For example, the high rate of violent deaths and alcohol abuse in native Americans has been interpreted as part of a strategy to cope with acculturation (e.g., Westermeyer and Brantner, 1972; Seltzer, 1980). MacAndrew and Edgerton's (1969) accounts of alcohol effects in South and North American tribal societies emphasized social learning as the main source for the varied impact of imbibing alcoholic beverages on aggressive and violent behavior. Drinking parties transform the Abipone from nonargumentative and calm social intercourse into combative individuals, but cause the head-hunting Yurunas to withdraw socially. A simple disinhibition model is an inadequate explanation for these diametrically opposed effects of alcohol on social and aggressive behavior as reported in anthropological studies.

CONCLUDING STATEMENT

Alcohol stands out as the drug that is most consistently and seriously linked to many types of aggressive and violent behavior. Systematic experimental studies have identified (1) the early phase

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

after a low acute alcohol dose as a condition that increases the probability of many types of social interactions, including aggressive and competitive behaviors; and (2) the high alcohol dose intoxication as the condition most likely to be linked to many different kinds of violent activities. Individuals differ markedly in their propensity to become intoxicated with alcoholic beverages and to subsequently engage in violence, and group statistics describe the alcohol-violence link poorly. The sources of these individual differences may be sought in genetic, developmental, social, and environmental factors. Genetic linkage between antisocial personality, possibly diagnosed with the aid of certain electrophysiologic measures, and alcoholism remains to be firmly established. At present, the neurobiologic mechanisms of alcohol action remain to be identified for a range of physiologic and behavioral functions, although the actions on brain serotonin and the benzodiazepine-GABA-A receptor complex may become especially relevant to alcohol's effect on aggressive and violent behavior. Similarly, the actions of alcohol on neuroendocrine events that control testosterone and adrenal hormones are a promising lead for elucidating the mechanisms of alcohol's aggression-heightening effects. Among the environmental determinants of alcohol's effects on violence that are of paramount significance rank social expectations and cultural habits, as well as behavioral history in situations of social conflict. Impaired appraisal of consequences, inappropriate sending and receiving of socially significant signals, and disrupted patterns of social interactions are characteristic of alcohol intoxication that contribute to the violence-promoting effects. A particularly consistent observation is the high prevalence of alcohol in victims and targets of aggression and violence. In contrast to heroin or cocaine, alcohol's link to violence is not a characteristic of the economic distribution network for this substance.

OPIATES, AGGRESSION, AND VIOLENCE

In confirmation of experiences originating with the ancient opium culture, the earliest studies in experimental animal psychopharmacology began to show that acute administration of opiates reduces aggressive behavior. Morphine and similar drugs decrease different kinds and elements of aggressive behavior in fish, mice, rats, cats, and squirrel monkeys (see Table 4A). For example, drug-and brain stimulation-induced rage reactions, defensive biting in response to pain, and attack and threat behavior by

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

territorial males and by lactating females are suppressed by opiates. However, this antiaggressive effect is part of the opiate sedative, tranquilizing effects in both animals and humans.

Single opiate doses also decrease human hostility as, for example, reviewed by Sutker and Archer (1984; see Table 5). The reported feeling of well-being, and oftentimes euphoria, in humans under the influence of opiates is one of the key causes for the high abuse potential of this class of drugs.

Under conditions of chronic heroin use, the direct effects of drug administration on mood significantly change. The euphorigenic effects of opiates are often replaced with feelings of confusion, hostility, and suspicion (Mirin and Meyer, 1979). In animals, chronic methadone does not increase aggressive behavior, but continues to decrease social intercourse (see Table 4A).

A special focus of studies on opiates and animal aggression for the past 25 years has been the prolonged increase in irritability, defensive responses and aggressive acts during withdrawal from chronic exposure to opiates (e.g., Gianutsos and Lal, 1976, 1978; Miczek, 1987). Table 4B summarizes studies showing that under a range of pharmacologic parameters, withdrawal from chronic opiates leads to the display of aggressive and defensive acts and postures in pairs of mice, hamsters, and rats that extends in time beyond the physiologic withdrawal syndrome (Martin et al., 1963; Vivian and Miczek, 1991; Tidey and Miczek, 1992). The exact nature of the aggressive and defensive acts during opiate withdrawal varies as a function of the animal species, with attack bites being more common in pairs of mice and hamsters, and defensive postures and vocalizations being characteristic of rats (e.g., Lal, 1975a,b; Kantak and Miczek, 1986). Rhesus monkeys continuously shift from aggressive threat displays to exaggerated signs of submission when withdrawn from chronic morphine injections (Kreiskott, 1966).

Experimentally, opiate withdrawal may be precipitated if an opiate receptor antagonist such as naloxone is administered or if opiate administrations are suddenly discontinued. The effects of the opiate antagonists naloxone or naltrexone in opiate-naive animals are small and inconsistent. If given at high doses, opiate antagonists may increase certain types of defensive reactions (e.g., Fanselow et al., 1980; Rodgers, 1982; Tazi et al., 1983; Puglisi-Allegra and Olivierio, 1981), but may decrease offensive attack behavior in male mice, rats, and squirrel monkeys (e.g., Olivier and van Dalen, 1982; Benton, 1984; Winslow and Miczek, 1988).

The neurochemical mechanisms of aggression during opiate

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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withdrawal involve several neurotransmitters and neuromodulators. Disturbances in opioid receptors, as for example during narcotic addiction, may be responsible for altered affect and communication during social interactions. During the past decade, a critically significant role for endogenous opioid peptides and their receptors in social behavior became apparent, particularly in affective responses associated with conflict situations (e.g., Panksepp, 1981; Miczek et al., 1991b). For example, distress signals in infant rodents and juvenile primates, as well as feline defensive reactions, are potently attenuated by certain opioid peptides (e.g., Benton and Brain, 1988; Kalin and Shelton, 1989; Shaikh et al., 1990). By extrapolation, it may be expected that communicative signal systems during social conflict situations in several mammalian species, including humans, require intact endogenous opioid systems.

Many studies have focused on brain dopamine and norepinephrine and their receptors in mediating behavioral symptoms of opiate withdrawal (e.g., Lal, 1975b; Redmond and Krystal, 1984). Pharmacologic activation of brain dopamine receptors potentiates aggressive and defensive acts during opiate withdrawal, whereas blockade of dopamine synthesis or receptors reduces these behaviors (Gianutsos et al., 1974; Puri and Lal, 1973; Kantak and Miczek, 1988). Of particular clinical interest is the proposed application of clonidine, an a2-adrenergic receptor agonist, in the management of opiate withdrawal, possibly including the aggression-precipitating components (e.g., Fielding et al., 1978; Redmond and Krystal, 1984; Gold et al., 1981). At present, the neurobiologic mechanisms for the physiologic and behavioral phenomena during opiate withdrawal in humans can only be extrapolated from studies in rodents and primates.

Chronic methadone in the management of withdrawal from narcotic addiction given under controlled conditions in a hospital setting did not result in significant changes in hostility. Although withdrawal from methadone was associated with increased tension and anxiety, levels of hostility remained unchanged (Woody et al., 1983). Narcotic addicts self-administering heroin under controlled conditions reported increased feelings of hostility when they unknowingly received an opiate antagonist. However, hostility measures did not change when addicts were aware of the antagonist administration (Mirin and Meyer, 1979).

Opiate administration and withdrawal are accompanied by marked gonadal and adrenal hormone fluctuations. Plasma testosterone and cortisol are suppressed during acute and chronic opiate administration, while prolactin levels are elevated (Ellingboe et al.,

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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1979; Mirin and Meyer, 1979). During opiate withdrawal, cortisol levels exceed those of controls, while testosterone levels remain suppressed for up to three weeks (Woody et al., 1983). These data do not preclude or strongly support a hormonal role in the altered mood and behavior during phases of opiate administration and withdrawal.

Both men and women show a large increase in criminal activity during periods of narcotic addiction (Johnson et al., 1985; Anglin and Hser, 1987). The most important association between violence and narcotic addiction comes from the socioeconomic context of supporting a relatively expensive drug habit. Heroin addicts commit mainly property crimes and are less likely to be arrested for violent crimes compared to nonaddicted convicts (McGlothin, 1979). Violent crimes that are committed by heroin addicts usually occur in the course of property crimes and in interaction with drug dealers (Gossop and Roy, 1977; Simonds and Kashani, 1979b). In fact, drug sales and crime are more strongly related than drug use and crime (Chaiken and Chaiken, 1990). In the illicit drug business, violence or the threat of violence appears to be the primary means of maintaining order (Johnson et al., 1985).

Not all heroin addicts commit crime, in fact the majority do not. Only those individuals who already commit crimes at a high rate show a systematic increase in criminal activity with increasing drug use (Chaiken and Chaiken, 1990). It is difficult to break the circularity between sociopathy and narcotic addiction, since the latter often contributes to the definition of the former (see Table 5). High-frequency drug use often starts in adolescence, as does high-frequency criminal activity, but the onset of sociopathic behavior largely predates drug use (e.g., Hewett and Martin, 1980; Sutker and Archer, 1984). Although drug addiction enhanced certain types of criminal activity, the majority of both male and female heroin addicts had committed crime prior to their initiation to drugs (Anglin and Hser, 1987; Anglin and Speckart, 1988).

CONCLUDING STATEMENT

Neither animal nor human data suggest a direct, pharmacologic association between violence and acute or chronic opiate administration. Violence in the context of narcotic addiction is foremost instrumental in securing the resources to maintain the drug habit and in interacting with drug dealers. Although measures of hostility and anger are increased in addicts seeking methadone

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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treatment, these feelings usually do not lead to aggressive or violent acts. Rather, the tendency to commit violent crimes correlates with preaddiction rates of criminal activity. Experimental studies in animals point to the phase of withdrawal from chronic opiates as the most vulnerable period to be provoked to heightened levels of aggressive behavior. Although humans undergoing opiate withdrawal may experience increased feelings of anger, there is no evidence suggesting that they are more likely to become violent as a result.

AMPHETAMINES, AGGRESSION, AND VIOLENCE

Weckamine, originally synthesized in 1887, received their name for their arousing, antifatigue, endurance-enhancing effects, which may contribute to their effects on aggressive and violent behavior. The major types of amphetamines that relate to the topic of violence and aggression include dextro-and levo-amphetamine as well as d-methamphetamine. Recently, several ring-substituted methamphetamines have become of substantial health concern due to their potential neurotoxic effects; these "designer" drugs include MDA ("eve") and MDMA (''ecstasy"). However, there is as yet no evidence that these later two compounds are linked to any heightened aggressive or violent behavior. This fact is remarkable because MDMA and MDA exert severe and long-lasting cytotoxic actions on serotonin-containing neurons, particularly in primates (Ricaurte et al., 1985). "Ice" is methamphetamine in smokable form, first produced in 1893 in Japan, that leads to a "high" for 8-24 hours. The American Council for Drug Education reported late in 1989 that ice has become a widespread problem in Hawaii, causing aggressive behavior, hallucinations, paranoia, and fatal kidney failure.

PHARMACOLOGIC DETERMINANTS

The most significant pharmacologic determinants of the amphetamine-aggression/violence link are the dose, the route of administration, and the chronicity of exposure to the drug. It is useful to differentiate several important pharmacologic conditions and phases: (1) the aggression-enhancing effects of an acute low amphetamine dose, usually a single bolus dose; (2) the homicidal tendencies during dose escalations and bingeing, often as part of amphetamine-induced paranoid psychosis; and (3) the disruptive

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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and disorganizing effects of intermediate amphetamine doses on social, sexual, and agonistic interactions.

At acute low doses, amphetamines may increase various aggressive and defensive behaviors in several animal species, as well as competitive aggressive behavior in humans. Table 6 summarizes studies in fish, pigeons, mice, rats, cats, and monkeys that demonstrate how acutely given low amphetamine doses increase threat and attack behavior directed toward a territorial intruder or rival opponent, defensive-aggressive responses in reaction to pain, brain stimulation-evoked killing responses, and defensive reactions. Similarly, in experimental laboratory studies with human subjects, acute low doses of d-amphetamine increase aggressive and competitive behavior (Table 7; Cherek et al., 1986, 1989). Clear demonstrations of aggression-enhancing effects of low amphetamine doses come from studies in animals undergoing withdrawal from opiates (e.g., Lal et al., 1971; Kantak and Miczek, 1988) and from studies in animals that are habituated to aggression-provoking conditions (Winslow and Miczek, 1983).

Under many experimental conditions and in most animal species, amphetamines, however, do not increase offensive-aggressive behavior, but with increasing dose, defensive and flight reactions are enhanced and organized sequences of pursuit, threat, attack, and dominance displays are disrupted (see Table 6; e.g., Miczek et al., 1989). This disorganizing effect of high amphetamine doses extends to a range of social interactions from copulatory to maternal, play, and agonistic behavior. Correspondingly, human amphetamine users are rated to display less impulse control (Milkman and Frosch, 1980). Very high, near-toxic amphetamine doses induce in otherwise placid laboratory rodents, biting reactions and exaggerated defensive postures that deviate from the expected behavioral repertoire (e.g., Chance, 1946; Randrup and Munkvad, 1969).

Long-term amphetamine administration in animals, as well as long-term use in humans, result in dramatic changes in social behavior. Under experimental conditions, sensitization as well as tolerance develop to prominent behavioral effects of amphetamine, depending on the interval between consecutive amphetamine administrations (e.g., Segal et al., 1980). Discrete daily injections with methamphetamine or d-amphetamine decrease attack and threat behavior in mice, while continuous exposure to amphetamine initially results in social withdrawal and eventually in heightened threat and defensive reactions, as well as in violent fighting (e.g., Bovet-Nitti and Messeri, 1975; Richardson et al., 1972; O'Donnell

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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and Miczek, 1980; Ellison et al., 1978). These progressive amphetamine-induced changes in the quality and nature of social interactions in animals may be mimicked nonpharmacologically by restricting the environmental resources of the social group (Sorensen, 1987; Sorensen and Randrup, 1986). Continuously worsening social withdrawal also became evident in macaque monkeys or marmosets that were treated chronically with amphetamine (Garver et al., 1975; Schlemmer et al., 1976; Ridley et al., 1979). It is tempting to interpret the socially disruptive chronic amphetamine effects in rodents and monkeys as analogous to the suspicious and paranoid reactions of human amphetamine users (e.g., Schiørring, 1977).

In humans, numerous psychiatric evaluations of chronic amphetamine abusers and police records during the past three decades point repeatedly to individuals in whom chronic stimulant use engenders paranoid and psychotic behavior, which in turn is accompanied by violent behavior (see Table 7). Probably no other report is more frequently cited than Ellinwood's (1971) account of 13 male and female cases in whom chronic amphetamine use or high acute amphetamine doses induced paranoia that was directly linked to their homicidal activity. In fact, several clinical observations do find that aggressiveness and hostility, culminating in physical assaults and homicides, are secondary to the psychotic paranoid state produced by intravenous use of high amphetamine doses, often chronically (see Table 7; e.g., Rickman et al., 1961; Angrist and Gershon, 1969; Siomopoulos, 1981; Rawlin, 1968).

Although there is little disagreement as to the seriousness and intensity of violence during amphetamine psychosis, opinions differ substantially as to the actual frequency of these phenomena (see Table 7). The lowest reported proportions refer to 12 chronic amphetamine abusers out of 130 patients displaying episodic violent behavior (Bach-y-Rita et al., 1971), and 1 out of 50 juvenile delinquents committing an assault under the influence of amphetamine (Tinklenberg and Woodrow, 1974); a frequently mentioned proportion in the psychiatric literature is around 60 percent of each sample (see Table 7: 62%, Angrist and Gershon, 1969; 60%, Simonds and Kashani, 1979a,b). Recently, a substantially higher statistic was reported from San Diego county in 1987 where methamphetamine and cocaine were associated with one-third of all homicides for that year (Bailey and Shaw, 1989). To place these statistics into perspective, it is worth remembering that the many therapeutic applications of amphetamines in eating and sleep disorders do not mention increased aggressive, hostile, or violent

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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behavior as problems (e.g., Leventhal and Brodie, 1981; Allen et al., 1975). Moreover, amphetamines and similarly acting drugs actually reduce aggressive behavior in youngsters who had been diagnosed as hyperkinetic, autistic, explosive, unsocialized, or emotionally disturbed (Conners, 1972; Winsberg et al., 1972; Arnold et al., 1973; Maletzky, 1974).

BEHAVIORAL DETERMINANTS

The nature of the behavioral change that is brought about by amphetamine differs fundamentally according to the individual's prior history of amphetamine self-administration and aggressive behavior, as well as the environmental context, even under closely similar pharmacologic conditions. Clinical experiences, experimental evidence and drug abusers concur in highlighting the euphorigenic effects of amphetamines (e.g., Laties, 1961; Griffiths et al., 1977). Some amphetamine abusers also attribute anxiogenic effects to the drug (Smith and Davis, 1977). In terms of social behavior, withdrawal from social contact after chronic amphetamine exposure contrasts with the increased frequency of socializing after an acute amphetamine dose (e.g., Schiørring, 1977; Griffiths et al., 1977; Higgins and Stitzer, 1988). The assaultive and violent behavior represents yet a further facet in the behavioral profile of high-dose amphetamine action that appears limited to predisposed individuals. At present, neither prospective nor retrospective evidence from long-term studies in human amphetamine abusers or in experimental models in animals informs on the critical factors that predispose to violent behavior under the influence of amphetamine.

Amphetamine differentially alters offensive attack and threat behavior versus defensive and flight behavior in several animal species (see Table 6; Chance and Silverman, 1964; Hoffmeister and Wuttke, 1969; Miczek, 1974; Krsiak, 1975; Ellison et al., 1978; Sieber et al., 1982). At higher amphetamine doses, defensive and flight reactions are mainly enhanced, whereas attack sequences are disrupted. At present, it is not possible to specify an amphetamine dose-dependent behavioral profile for different types of human aggressive and violent behavior. When sufficient amphetamine has been administered to produce paranoia and psychosis, the probability of violent behavior appears to increase in 10-60 percent of the individuals (e.g., Allen et al., 1975; Sheard, 1977a). Lower amphetamine doses may increase a range of social behaviors

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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such as speaking or competing (Stitzer et al., 1978; Cherek et al., 1989) but do not specifically increase violent behavior.

The past and present success in social confrontations defines the social status or rank of an individual within a group that in turn determines how amphetamines influence individual levels of aggressive behavior. Experimental evidence from studies with laboratory rodents and primates shows that amphetamines may increase submissive displays and flight reactions in macaque monkeys that are very high or very low ranking in their groups, and may increase aggressive behavior in certain dominant animals (e.g., Schlemmer and Davis, 1981; Haber et al., 1981; Miczek and Gold, 1983; Smith and Byrd, 1984; Krsiak, 1975). The only possible parallel in humans may be found in retrospective psychiatric evaluations that find increased likelihood of violent episodes after amphetamine in individuals who had a history of unusual social behavior (Rubin, 1972; Black and Heald, 1975; Brook et al., 1976). It will be important to specify the constraints imposed on an individual by past and current social interactions as potential determinants of whether or not amphetamine will increase the likelihood of engendering violent outbursts.

NEUROBIOLOGIC MECHANISMS

The specific neurochemical mechanisms of action for amphetamine's effects on aggressive and violent behavior remain to be identified. Amphetamine acts as a sympathomimetic amine; one of its major actions in the brain is the release of dopamine from nerve endings in the striatum leading indirectly to dopamine receptor activation (e.g., Kuczenski, 1983). Many features of endogenous and amphetamine psychosis are successfully managed by antipsychotics that block the D2 subtype of dopamine receptors (e.g., Seeman, 1987). In laboratory rodents, the so-called amphetamine rage response and opiate-withdrawal aggression, as well as other stimulant-induced motor stereotypies, depend on an intact nigrostriatal dopamine system (Randrup and Munkvad, 1969; Lal et al., 1971; Hasselager et al., 1972; Rolinski, 1973, 1977; Kantak and Miczek, 1988). However, the socially disruptive effects of amphetamine have not been reversed by dopamine receptor blocking drugs (e.g., Schiørring, 1977; Miczek and Yoshimura, 1982; Poli and Palermo-Neto, 1986). The current evidence indicates that indirect dopamine receptor activation by amphetamine or, alternatively, the blockade of these receptors by certain antipsychotics

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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potently modulates aggressive or violent behavior, however, not in a selective fashion.

CONCLUDING STATEMENT

The most serious link of amphetamine to violence refers to those individuals who, after intravenous amphetamine, most often chronically, develop a paranoid psychotic state and commit violent acts. Most psychiatric reports and police records do not support Ellinwood's stern conclusion from 1971 that "even hippies have noted the dangerous aspects of amphetamine abuse in their slogan 'Speed Kills.' Reports of law enforcement personnel, psychiatrists, and drug abusers themselves indicate that amphetamines, more than any other group of drugs, may be related specifically to aggressive behavior." The prevalence of violence by individuals who experience amphetamine paranoid psychosis may be less than 10 percent in general population samples and as high as two-thirds among individuals who showed evidence of psychopathology prior to amphetamine use. Low acute amphetamine doses may increase various positive and negative social behaviors; higher doses often lead to disorganizing effects on social interactions and severe social withdrawal. At present, the neurobiologic mechanisms for the range of amphetamine effects on aggressive and social behavior remain unknown, rendering the development of a rationale pharmacologic treatment uncertain.

COCAINE, AGGRESSION, AND VIOLENCE

The crack-cocaine epidemic during the past decade in the United States has dramatically transformed the customs and traditions surrounding this drug in previous decades and centuries. Violence during the interactions between crack-cocaine dealers and users has attracted considerable media attention, and it is this aspect that has been the focus of several recent and ongoing epidemiologic research efforts.

Psychiatric examinations of chronic and recreational cocaine users during the 1970s emphasized the drug's potential to alter brain functions that are conducive to violent behavior (see Table 8; e.g., Post, 1975; Siegel, 1977; Fink and Hyatt, 1978; Egan and Robinson, 1979; Grinspoon and Bakalar, 1979). Similar to the sequence of events in chronic amphetamine users, violent or aggressive behavior is viewed as secondary to the occasional paranoia and psychosis that are triggered by chronic cocaine use. Notably,

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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one account found no difference in the frequency of violent acts committed by institutionalized cocaine users and those committed by inpatients who did not use this drug (Swett, 1985).

Pharmacologic studies in laboratory animals have attempted to characterize the dosage and environmental conditions under which cocaine may increase aggressive and defensive behavior (see Table 9). Acute but not chronic cocaine increases defensive bites and postures in mice, rats, and monkeys after isolated housing, crowding, or exposure to painful stimuli (e.g., Brunaud and Siou, 1959; Miczek and O'Donnell, 1978; Emley and Hutchinson, 1983). By contrast, aggressive behavior in confrontations with a rival or in territorial defense is disrupted by cocaine, similar to amphetamine's effects (e.g., Miczek, 1979b; Miczek and Yoshimura, 1982; Kantak, 1989). Significantly, chronic treatment with cocaine did not result in increased aggressive behavior in several animal species (e.g., Moore and Thompson, 1978; Kantak, 1989).

The recent increase in cocaine's association with violence appears to be dissociated from the direct neurobiologic and pharmacologic characteristics of this drug. Several recent studies support an association between cocaine use and violent crime in which this violence appears to result mainly from interactions with cocaine-crack dealers who practice their trade in a violent manner. For example, one account reports that the percentage of homicide victims with detectable cocaine rose from 1 to 18 percent in four years (Lowry et al., 1988); in San Diego county in 1987, cocaine was involved in one-fifth of homicides (Bailey and Shaw, 1989). Although 91 percent of a sample of adolescent drug-using criminals in inner city Miami reported frequently using cocaine or crack, the majority of offenses committed by this group was related to the drug business (59.9%) or represented property crimes (25.5%). However, the potential for violence among these individuals is ominous: 88.4 percent of this sample reported that they carry weapons most or all of the time (Inciardi, 1989). Furthermore, although crack users may not be extraordinarily violent among drug users, crack dealers are reported to engage in a wider range of violent acts than either heroin or marihuana dealers, and this violence is not limited to the drug-selling context (Fagan and Chin, 1989, 1991).

CONCLUDING STATEMENT

A small literature on pharmacologic and psychiatric evidence for cocaine's effects on aggression and violence points to psychopathologic

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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individuals who may develop the propensity to engage in violent acts. However, the far more significant problem is the violence associated with the supplying, dealing, and securing cocaine-crack as documented by ongoing epidemiologic studies.

HALLUCINOGENS, AGGRESSION, AND VIOLENCE

Hallucinogens comprise substances that are of disputed or limited medicinal value, but are mainly of ceremonial, recreational, and social significance. Their molecular diversity conveys varied effects and mechanisms of action, prompting separate discussions for each type of hallucinogen.

CANNABIS

Cannabis is one of the few psychoactive drugs acting on the CNS that does not contain a nitrogen in its molecule, with a poorly understood mechanism of action (Pertwee, 1985). It is used ubiquitously throughout the world, mostly in social settings, and in various forms (e.g., marihuana, hashish, bang). The violence-provoking image of cannabis was shaped by anecdotes such as Marco Polo's tale of the cannabis-intoxicated arabic assassins that gave rise to the name hashish, and by U.S. government-sponsored propaganda movies (e.g., Reefer Madness). However, all major reviews of the literature on cannabis and human aggression and violence during the past two decades conclude that cannabis has no effect on or actually decreases various indices of aggression (e.g., Casto, 1970; Abel, 1977; Tinklenberg, 1974; Cherek and Steinberg, 1987; Miczek, 1987).

As summarized in Table 10A, acute administration of cannabis extracts or the psychoactive ingredient Δ9-tetrahydrocannabinol (THC) decreases attack and threat behavior by isolated mice; by resident fish, rats, squirrel monkeys, and baboons; by pigeons or rats when provoked by omission of scheduled reinforcement, or by brain-stimulated cats (e.g., Dubinsky et al., 1973; Miczek, 1978; Frischknecht, 1984; Sieber, 1982). However, the antiaggressive effects of THC or cannabis extracts are often seen only at sedative doses (e.g., Olivier et al., 1984).

A further prominent effect of cannabis extracts or THC in social confrontations in animals entails the increase in submissive and flight reactions. Detailed ethological analyses document that acutely given THC promotes submissive and flight responses in those animals that are targets of social or aggressive behavior

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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(e.g., Siegel and Poole, 1969; Frischknecht et al., 1984; Cutler et al., 1975; Olivier et al., 1984; see also Table 10A).

Evidence on the effects of acutely given or self-administered cannabis on aggression in humans comes from crime and health statistics, personality evaluations, and experimental studies (see Table 11). For example, in laboratory studies, marihuana or THC decreased all measures of hostility in a staged social setting, and in punitive actions against a fictitious competitor (e.g., Taylor et al., 1976; Saltzman et al., 1976).

Of more significance are the findings on chronic cannabis, aggression, and violence. As reviewed previously (e.g., Krsiak, 1974; Abel, 1975; Frischknecht, 1984; Miczek, 1987), animal studies on pain-induced defensive reactions; isolation-induced, territorial, and dominance-related aggressive behavior; and frustration-provoked aggression show enduring decreases in aggression in most species over the course of chronic administration of cannabis extracts or THC (Table 10B, e.g., Cherek et al., 1980; Miczek, 1979a). Most studies on chronic THC in rats, mice, and hamsters find no evidence for tolerance to the drug's antiaggressive effects (see Table 10B).

Anecdotal reports and case studies of humans, ranging from GIs in Vietnam or naval criminal offenders to hemp abusers in India or Brazilian psychiatric patients, concur that there is no consistent relationship between long-term cannabis use and violent behavior (e.g., Chopra et al., 1942; Bromberg and Rodgers, 1946; Moraes Andrade, 1964; Colbach, 1971). In contrast to some questionnaire data and ratings of college students that suggest higher values for aggression, anger, and hostility, experimental indices of human aggression actually reveal decreases in hostility and aggression (see Table 11, especially Burdsal et al., 1973, versus Babor et al., 1978a,b; Saltzman et al., 1976). Psychopathologic illness and cannabis use interact in a complex way, each possibly aggravating the other (e.g., Halikas et al., 1972; Bernhardson and Gunne, 1972; Stefanis et al., 1976a,b; Weller and Halikas, 1985).

The most persuasive large-scale studies in incarcerated adolescent delinquents show that marihuana was the drug least likely to be implicated in serious sexual or assaultive crimes (Tinklenberg and Woodrow, 1974; Tinklenberg et al., 1974a,b, 1976). Correspondingly, experienced long-term cannabis users expect other users to be less violent than nonusers, which in fact is borne out by the low rate of commission of violent acts in cannabis users (e.g., Soueif, 1971; see Table 11).

Concurrent exposure to certain stresses and chronic cannabis

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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administration may be particularly significant in the emergence of certain unusual forms of aggressive behavior, as noted repeatedly in reviews of the animal as well as human literature (Carlini, 1972; Krsiak, 1974; Carlini et al., 1976; Abel, 1975, 1977; Cherek and Steinberg, 1987). When otherwise placid animals are exposed to such experimental stressors as REM (rapid eye movement) sleep deprivation, food deprivation, repeated and prolonged exposure to electric shock pulses, or neurotoxin treatment, chronic high-dose THC or cannabis extract injections and occasionally single administrations may induce self-mutilating responses, indiscriminate biting, intense bizarre defensive reactions, and killing behavior (e.g., Carlini and Masur, 1970; Carlini et al., 1972; Fujiwara et al., 1984; see Table 10B). So-called psychosocial stress due to crowding may also potentiate hyperirritability in rhesus monkeys treated chronically with THC (Sassenrath and Chapman, 1976), although similarly treated baboons do not show any alteration in social interactions (Levett et al., 1977). The significance of stress-cannabis interactions is mainly limited to experimental laboratory situations with rodents. At present, it remains unclear whether or not these reports are relevant to disturbed affect, impaired impulse control, and triggered psychopathologies including violent reactions in humans.

Concluding Statement

The majority of the evidence in experimental studies with animals and humans, as well as most data from chronic users, emphasizes that cannabis preparations (e.g., marihuana, hashish) or THC decrease aggressive and violent behavior. Due to its relatively widespread access, lower cost, and characteristic pattern of use, socioeconomic causes of violence in cannabis dealing and procuring are less significant than they are with cocaine or heroin.

LSD

With the discovery of selectively acting serotonin receptor drugs, it has become possible to link the hallucinogenic effects of LSD to the actions of this drug on brain 5-HT2 receptors (e.g., Cunningham and Appel, 1987; Green, 1985; Freedman, 1986). By contrast, LSD's psychotomimetic effects, as well as its specific effects on social, aggressive, defensive, and violent behavior, have not been identified in terms of their mechanisms of action.

Evidence of the effect of LSD on aggression in animals stems

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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primarily from the 1960s and 1970s. As summarized in Table 12 (section A), low acute doses of LSD (less than 100 micrograms (µg) per kilogram exaggerate defensive and timid reactions in mice and in rats, particularly when these responses are prompted by aversive, noxious stimuli (e.g., Brunaud and Siou, 1959; Krsiak, 1975; Sheard et al., 1977; Sbordone et al., 1979). Stumptail macaque monkeys display more frequent submissive gestures when given the hallucinogen 5-methoxy-N,N-methyltryptamine (Schlemmer and Davis, 1981). Aggressive displays may be enhanced when fish or rats are given a very low LSD dose (1-4 µg/kg), although most studies on attack and threats by isolated mice found systematic dose-dependent decreases after LSD administration (e.g., Abramson and Evans, 1954; Silverman, 1966; Krsiak, 1979; Rewerski et al., 1971; Siegel and Poole, 1969; see Table 12). It has been suggested that LSD treatment causes animals to become hypersensitive to social and environmental stimuli (Siegel, 1971). Similar to LSD, mescaline decreases or has no effect on aggressiveness in isolation-and drug-induced or dominance-related paradigms, but increases defensive reactions in procedures involving shock (see Table 12, section B). There have been very few reports of chronic LSD or mescaline administration and animal aggression.

Reviewers of the human literature agree that LSD use is infrequently associated with violence (e.g., Szara, 1967; Hollister, 1984; see Table 13). Anecdotal and case studies emphasize the rarity of LSD violence and associate violent reactions with individuals who are borderline personalities (e.g., Barter and Reite, 1969; Duncan, 1974). If psychopathology predates drug usage, LSD exacerbates these disturbances, including violent outbursts (e.g., Smart and Jones, 1970; Fink et al., 1966). At present, LSD use is not epidemic and no new information has become available to evaluate the significance of the LSD-violence link.

Concluding Statement

LSD is not of significance in the present violence discussion. The older literature suggests that certain psychopathological individuals who begin using LSD may engage in violent acts; however, this phenomenon is rare.

PHENCYCLIDINE (PCP)

PCP was introduced as synthetic surgical anesthetic in 1956, was withdrawn from human use because it induced psychotic reactions

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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in a significant number of patients, and then reappeared from illicit sources as a street drug (e.g., ''angel dust," "peace pill," "rocket fuel") in the mid-1960s. Repetitive, prolonged, and unusual acts of violence by individuals intoxicated with PCP have attracted considerable attention in the media (e.g., Siegel, 1980).

In the limited studies with animals, acutely administered PCP has been found to have unpredictable effects on aggressive behavior. Some studies find PCP to disrupt aggressive and defensive behavior engendered by painful stimuli, isolated housing, or territorial defense (see Table 12, section C). However, in other samples, PCP may increase some aspects of aggressive behavior in mice, rats, and squirrel monkeys (e.g., Burkhalter and Balster, 1979; Musty and Consroe, 1982; Emley and Hutson, 1983; Russell et al., 1984; Wilmot et al., 1987). In selected individuals, acute PCP has dose-dependent biphasic effects, with low doses increasing and high doses decreasing aggressive behavior (Miczek and Haney, in press). Notably, PCP-treated mice and stumptail macaque monkeys become the targets of more frequent aggressive behavior by drug-free opponents or group members, presumably due to inappropriate social signals, provocative actions, and hyperactivity (e.g., Tyler and Miczek, 1982; Schlemmer and Davis, 1983). In view of the use pattern in humans, it is surprising that no studies on chronic PCP and aggressive behavior in animals have been conducted.

In humans, PCP is usually part of polydrug use, including alcohol; therefore it is difficult to dissect the PCP-specific effects, especially those on aggressive and violent behavior (e.g., Hollister, 1984; Brecher et al., 1988). No experimental studies on PCP and human violence or aggression have been conducted. As summarized in Table 13, clinical reports from emergency rooms or psychiatric hospital settings indicate a prevalence of PCP psychosis and analgesia, and it is in this context that PCP-associated violence appears most often. Reports from different localities in the United States over the past two decades refer to cases of chronic PCP-induced psychosis that also include agitation, physical assaults, self-directed injuries, and homicidal activities due to poor judgment, panic reactions, and imagined frustrations (e.g., Fauman and Fauman, 1979; Yesavage and Zarcone, 1990; Convit et al., 1988; see Table 13). Overall these cases are relatively infrequent, but stand out by their bizarre and repulsive, stereotyped, repetitive nature.

Physical or pharmacologic restraint of PCP-agitated individuals is difficult to manage clinically. Since the neurobiologic action of PCP is only beginning to be identified with the characterization

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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of specific neural receptor sites, clinically useful agents interacting with PCP receptors will become available soon. Until that time, clinicians resort to antipsychotic drugs in order to manage PCP psychosis (see especially Smith and Wesson, 1980, and reviews in Table 13).

Concluding Statement

"Phencyclidine is not a magical drug. It does not magically produce violent, assaultive, or criminal behavior" (Siegel, 1978). Generally, personality predispositions and a history of violent behavior appear to determine whether or not PCP intoxication leads to violence. PCP violence is a relatively rare phenomenon, although it stands out by its highly unusual form and intensity, and it depends on the social and personal background of the individual.

SUMMARY

Drugs produce some of their effects on violent and aggressive behavior via action on the central nervous system. This action, however, can modify neural functions in a very intricate way and at multiple levels that ultimately target aggression-specific brain mechanisms. Alcohol and drugs of abuse do not engender violent behavior in every individual, and many imbibe alcoholic beverages or self-administer drugs without becoming violent. The impact of genetic predispositions to be susceptible to dependence-producing drugs such as alcohol, heroin, or cocaine and to act violently has, as of yet, not been delineated in terms of specific neural mechanisms. Similarly, the modulating influences of learning, social modeling, or parental physical abuse on the neural substrate for drug action and for aggressive behavior and impulse control have not been specified. Since these critical connections remain ill understood, it is not possible at present to propose specific modes of intervention at the neurobiologic level.

Alcohol is the drug that is most prevalent in individuals committing violence and those who are victims of violence. This association applies to various types of violent behavior and aggressive tendencies. Experimental studies have repeatedly demonstrated that alcohol causes an increase in aggressive behavior, in both animals and humans. Despite its apparent limitations, laboratory research represents the primary avenue to delineate the causative relationship among alcohol, aggression, and violence.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Alcohol's action on the brain mechanisms for aggressive behavior is modulated by genetic predispositions, learned expectations, social restraints, and cultural habits. Recent progress in understanding the actions of alcohol on brain serotonin and GABA systems may eventually offer diagnostic tools for individuals at risk and therapeutic options for intervention.

The violence associated with cocaine-crack is substantially different in nature and context from the aggression-enhancing effects of alcohol. Violent behavior under the influence of amphetamines, cocaine, LSD, and PCP is rare in the general population, but is considerably more likely in those individuals whose psychopathology predates the drug use. Significantly, most of the violence associated with cocaine and narcotic drugs results from the business of supplying, dealing, and acquiring these substances, not from the direct neurobiologic actions of these drugs.

We need to identify those individuals in whom either alcohol, opiates, cocaine, amphetamines, PCP, LSD, or other hallucinogens promote violent and aggressive behavior by attending to the precise pharmacologic conditions at the time of the violent act; the individual's physiologic conditions; the genetic, developmental, and social background; and the prevailing social conditions. Clearly, alcohol and other drugs of abuse differ markedly from each other in terms of pharmacology and neurobiologic mechanisms, dependence liability, legal and social restraints, expectations, and cultural traditions; no general and unifying principle applies to all of these substances. It should not be surprising that the conditions that promote violence in individuals under the influence of alcohol cannot be simply extrapolated to cocaine-crack or to narcotic drugs. Rational intervention strategies need to be based on an adequate understanding of the specific circumstances, individuals, and pharmacologic conditions that are implicated in any specific type of violent act.

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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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TABLE 1 Major Experimental Models of Aggression in Laboratory Animals

Model and Species

Procedure

Behavioral Topography

Biological Function

A. Aversive environmental manipulations

Isolation-induced aggression, mostly in mice

Isolated housing before confrontation with another isolate or group-housed animal

Complete agonistic behavior pattern: isolates attack, threaten, pursue opponent

Territorial defense or compulsive, abnormal, pathological behavior

Pain-elicited or shock-induced aggression, mostly in rats, also in monkeys

Pairs of animals are exposed to pulses of electric shock delivered through grid floor or to the tail

Defensive reactions, including upright postures, bites toward face of opponent, audible vocalizations; bites toward inanimate targets

Some similarity to reaction toward predator or toward large opponent

Aggression due to omission of reward, mostly in pigeons, also in monkeys

Conditioning history; schedule-controlled operant behavior; omitted or infrequent reinforcement

Attack bites or pecks, threat displays towards suitable object or conspecific

Competition for resources such as food, sex, protected niches (?)

B. Brain manipulations

Brain lesion-induced aggression, mostly in rats, also in cats

Destruction of neural tissue, and subsequent social or environmental challenges

Defensive reactions, biting

Neurological disease

Brain stimulation-induced aggression, mostly in cats, also in rats

Electrical excitation of tissue in diencephalon and mesencephalon, also in other limbic or cerebellar areas

(1) Defensive reactions accompanied by autonomic arousal; (2) Predatory attack and killing

Defense against attacker; Predation

C. Ethological situations

Aggression by resident toward intruder, in most species and in both sexes

Confrontation with an unfamiliar adult member of the species

Full repertoire of agonistic behavior (attack and threat vs. defense, submission, and flight)

Territorial or group defense (?); rivalry among males and among females

Female aggression, mostly in maternal rodents

Lactating female, in the presence of litter, confronting an intruder male

Species-specific repertoire of attack and threat behavior toward intruder

Defense of young, competition for resources and territory

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Dominance-related aggression, mostly in monkeys, mice, and rats

Formation or maintenance of a social group

Species-specific repertoire of signals (displays, sounds, odors) between group members of different social rank; low level and intensity of agonism

Social cohesion and dispersion

D. Killing

Muricide, mostly in rats, cats

Presence of prey, food deprivation

Stalking, seizing, killing, sometimes consuming prey

Food source; ''killer instinct"

 

Source: Adapted from Miczek and DeBold (1983).

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 2A: Effects of acute alcohol on aggression in animals

References

Methods and Procedures

Results and Conclusions

Isolation-induced aggression

Chamove and Harlow, 1970

Self-directed aggression in rhesus monkeys self administering ethanol

Biting and slapping increased proportional to the amount of ethanol consumed until sedation was observed; High doses reduced self mutilative behavior.

Chance et al. 1973

Krsiak, 1976

Yoshimura and Ogawa, 1983

Lister and Hilakivi, 1988

Single-housed male mice confront group-housed intruder in home cage

A low ETOH dose (0.4-0.5 g/kg, i.p.) increased compound measure of "aggression"; Higher ETOH doses produced sedation and reduced aggression.

Lagerspetz and Ekqvist 1978

Smoothy et al. 1982

Smoothy and Berry 1983

Single-housed male mice confronted group-housed intruder in home cage

ETOH (1-12 g/kg, i.p) decreased aggression and produced sedation.

Smoothy et al., 1983

Aggression in pairs of isolated male mice

ETOH (0.5-2.0 g/kg) dose dependently reduced time spent in agonistic behaviors and increased flight/defensive behaviors.

Benton and Smoothy, 1984

Aggression in pairs of ETOH-treated male mice

ETOH (0.5-2.0 g/kg) reduced aggressive behavior in resident-intruder confrontations.

Pain-induced Aggression and Defense

Irwin et al. 1971

Electric foot shock in pairs of male mice

ETOH (1-4.8 g/kg, i.p., p.o.) decreased defensive attacks.

Weitz 1974

Tramill et al. 1980, 1983

Bammer and Eichelman 1983

Electric foot shock in pairs of male rats

A low ETOH dose (0.6 g/kg, i.p.; 1.97 g/kg/day, i.p.) increased defensive aggression; Higher ETOH doses decreased it.

Al Hazmi and Brain, 1984

Smoothy and Berry 1984

Restraint-induced attack in single-housed mice

ETOH (0.125-2.0 g/kg) dose dependently reduced target biting; 1.0 g/kg increased latency to first bite.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Defensive Aggression Induced by Electrical Brain Stimulation

MacDonnell et al., 1971

Electrical brain stimulation in corticomedial or basomedial portion of the amygdala in female cats faced with an untreated stimulus cat

Low dose ETOH (0.37 g/kg) reduced the latency of "hissing" at the stimulus cat, whereas a higher dose (1.5 g/kg) prolonged hissing latencies.

Ruusunen et al., 1975

Electrical brain stimulation in cats

ETOH (1.5 g/kg) reduced defensive behaviors, where as lower doses (0.25-1.0 g/kg) did not alter behavior significantly.

Aggression by Resident toward Intruder

Ellman et al., 1972

Resident cichlid fish confronted intruder protected inside clear tube

0.18% ETOH in aquarium water increased aggressive displays and bites, whereas 0.34% ETOH reduced these behaviors.

Peeke et al., 1973

Peeke et al., 1975

Peeke and Figler, 1981

Resident cichlid fish confronted intruder protected inside clear tube

0.15-0.18% ETOH increased attacks and reduced the duration of threats, whereas 0.30-0.33% prolonged threats and reduced attacks.

Raynes et al., 1968

Raynes and Ryback, 1970

Galizio et al., 1985

Aggressive displays of Siamese fighting fish directed at mirror image

Low dose ETOH 0.25-29% increased aggressive displays; Higher doses (0.50%-0.75%) reduced displays.

Krsiak and Borgesova, 1973

Interactions between pairs of familiar male rats

ETOH (1.2-3.0 g/kg) reduced aggressive interactions.

Bertilson et al., 1977

Territorial aggression in pairs of male mice

ETOH (10-30%) dose dependently reduced aggression-prompted squeals, presumably by the targets of attack bites.

Miczek and O'Donnell, 1980

Resident male mice confront group-housed intruder in neutral and home cages

In the neutral environment, low doses of ETOH (0.1-0.5 g/kg, p.o.) increased attack and threat behaviors whereas higher doses reduced these behaviors.

DeBold and Miczek, 1985

Confrontations between castrated, testosterone treated residents vs. intact intruder mice

ETOH (3.0 g/kg) reduced aggression in intact males, whereas animals treated with a high dose of testosterone showed altered ETOH response; Specifically, 1.0-1.7 g/kg increased attacks and threats and a higher dose (5.6 g/kg) was required to suppress aggression.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Blanchard et al., 1987b

Resident male rats grouped according to baseline aggressive levels confront male intruder

ETOH (0.3-0.6 g/kg) increased frequency and duration of attack and threat postures in low to moderately aggressive animals, but not in highly aggressive animals; High dose (1.2 g/kg) ETOH reduced aggression in all animals.

Everill and Berry, 1987

Resident male mice of C57, DBA and BALB strains confronted group-housed intruders

ETOH (1.0 g/kg, i.p.) reduced aggression in isolated DBA mice, and increased defensive flight behavior in C57 and BALB mice; A low dose (0.5 g/kg) did not alter aggression in any strain.

Mos and Olivier, 1988

Group-housed (2 male, 2 female) resident rats confronted with naive male intruder

ETOH (2.0 mg/kg) reduced aggression in the dominant animal; Low doses (0.5-1.0 g/kg) did not enhance aggression.

Lisciotto et al., 1990

Confrontations between neonatally gonadectomized and androgenized residents and intact intruder mice

ETOH (1.0 g/kg) increased attacks in sham-gonadectomized males, with no suppression at 3.0 g/kg; Androgenized females and neonatally gonadectomized males only showed a suppression of aggression at 3.0 g/kg ETOH.

Miczek et al., in press

Confrontations between socially housed resident male rats vs. naive single-housed intruder male rats

ETOH (0.1-1.0 g/kg) increased aggressive threats and attack bites in a subgroup of animals while suppressing these behaviors in other animals; high doses (1.7-3.0 g/kg) supressed aggression in all animals. Sequential analysis indicated that once initiated, the attack sequence was preserved regardless of dose. In animals that showed enhanced aggression, low doses increased time spent in and number of elements within aggressive "bursts". Pro-aggressive effects of ETOH suggested to prevent termination of an aggressive sequence rather than alteration in initiation of these behaviors.

Female Aggression

Smoothy et al., 1986

Confrontations between singly-housed lactating female resident and group-housed male intruders

ETOH (0.5-2.0 g/kg) did not alter the duration of time spent in aggression except, at the highest dose, duration of aggression decreased.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Blanchard et al., 1987a

Resident female rats confronted male intruders of different sizes

ETOH (0.3 g/kg) increased attacks by female residents towards male intruders; Smaller intruders were attacked more often than larger opponents.

Dominance-related Aggression

Crowley et al., 1974

Aggression in group-housed pig-tailed macaques

ETOH (0.5-2.0 g/kg) did not alter aggressive behaviors, but 2.0 g/kg increased "playful" (non-injurious) fighting.

Miczek and Barry, 1977

Aggression by male rats during food competition

A low dose (0.5 g/kg) ETOH increased aggressive behavior in dominant rats but not in subordinate male rats.

Pettijohn, 1979

Aggressive displays in male and female Telomian dogs competing for food

ETOH (0.8 g/kg) increased the frequency of attacks in subordinate dogs but reduced attacks in higher ranking dogs; 1.6 g/kg ETOH reduced attacks in all dogs.

Miczek et al., 1984

Winslow and Miczek, 1985

Winslow and Miczek, 1988

Aggression in squirrel monkeys toward group members of both sexes

Low doses of ethanol (0.1-0.3 g/kg, p.o.) increased aggressive threats by dominant males, whereas higher doses (0.6-1.0 g/kg) reduced them; Subordinate males treated with higher doses of ETOH received more threats from untreated group members.

Walker and Gregory, 1985

Aggression in pairs of male hamsters

Dominant males treated with ETOH (2.0 g/kg) reduced incidence of fighting, whereas when subordinates were treated with the same dose, fighting remained at control levels.

Blanchard et al., 1987c

Aggression in male and female during group formation in rats

Female rats were attacked more frequently than males by males treated with ETOH (0.3-1.2 g/kg).

Winslow et al., 1988

Aggression in testosterone-treated male squirrel monkeys towards group members of both sexes

Low doses (0.1-0.3 g/kg) ETOH increased aggressive displays in testosterone-treated dominant males, but not in subordinate males.

Killing

MacDonnell and Ehmer, 1969

"Quiet biting" attack elicited by electrical brain stimulation of hypothalamus in cats

ETOH (0.37-1.5 g/kg) dose dependently increased latency to attack, but increased force of biting.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Ingle, 1973

Attacks in frogs presented with simulated prey or dummy "worm"

Frogs placed in ETOH (400 mg/100 ml for 2-2.5 hrs) consistently struck at moving dummy "worms" whereas control frogs habituated to the test.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 2B Effects of Chronic Alcohol on Aggression in Animals

References

Methods and Procedures

Results and Conclusions

Pain-induced Aggression and Defense

Tramill et al., 1980

ETOH (0.25-0.75 ml/100 g of 30%/15 days) in restrained, food deprived male rats exposed to electrical foot shock

Low to moderate dose ETOH (0.25-0.5 ml/100 g of 30%) increased target biting, whereas a higher dose (0.75 ml/100 g of 30% ETOH) reduced the biting response.

Tramill et al., 1983

Chronic (15 days) and acute ETOH-treated (0.25 ml/100 g of 30%, i.p.) restrained male rats exposed to electrical foot shock

Chronic ETOH treated rats had higher rates of target biting than acute ETOH treated or control rats.

Means et al., 1984

Male offspring of female rats treated with ETOH (14.08 g/kg/day) throughout pregnancy exposed to electrical foot shock as adults; Both animals treated

Prenatal exposure to ETOH did not alter aggressive behavior when tested as adults.

Aggression Induced by Omission of Reward

Nelson, 1967

Pairs of male rats trained to traverse runway on a 50% or 100% reinforcement schedule treated with ETOH (1.2 g/kg/day for 30 days) and confronted another subject at the goal box

ETOH-treated animals showed less aggression compared to dextrose-treated animals; when treatment groups were reversed, ETOH reduced aggression in highly aggressive dextrose-treated animals.

Drug-Induced Aggression

Pucilowski et al., 1987

20% ETOH administered for 3 weeks in pairs of male rats treated with apomorphine (10.0 mg/kg)

ETOH increased aggressive postures and vocalizations, but did not alter attacks.

Aggression by Resident Towards Intruder

Cutler et al., 1975

5% ETOH administered for 10 days in male mice housed in compartments of same cage of group-housed

ETOH given before establishment of territory resulted in the alcohol treated mouse expanding its territory to the entire area; No effect was seen if ETOH was given after the territories were established.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Cutler, 1976

Interactions in a neutral cage between ETOH-treated (8% for 3 weeks) and untreated group-housed mice

Defensive and flight behaviors were increased following cessation of alcohol administration.

Yanai and Ginsburg, 1976

Conspecific directed aggression in male offspring of C57 and DBA mice fed ETOH (10%) from 28 days of age through pregnancy and/or 14 days post parturition

DBA and C57 offspring had longer latencies to attack and a reduction in fighting; Time spent fighting was reduced by ETOH postnatal exposure and by both prenatal and postnatal exposure.

Ewart and Cutler, 1979

Conspecific directed aggression in offspring of CFW mice fed ETOH (5%) through pregnancy and 3 weeks post parturition

Frequency and duration of social interactions were reduced and defensive/flight behaviors were increased by prenatal and postnatal ETOH exposure.

Peterson et al., 1988;

Peterson and Pohorecky, 1989

24 hour observations of confrontations between untreated resident male rats with ETOH-treated intruders (1.0-2.0 g/kg 3 × day), and ETOH-treated residents (1.0-1.5 g/kg 3 × day) with untreated intruders; All animals were implanted with gastric and jugular catheters

ETOH-treated intruders received more threats and displayed an increase in defensive freezing in the first 20 minutes of testing. Blood corticosterone and epinephrine of ETOH-treated intruders were increased (338% and 129%, respectively) 20 minutes into the test and remained elevated (98% and 107%) 24 hours into the test; ETOH-treated residents wounded untreated intruders more severely and shifted point of attack from upper back to lower back and hind quarters. Blood norepinephrine levels were increased in residents (216%) and remained elevated 24 hours into testing.

Female Aggression

Tamimie, 1968

5-10 ml/kg of 33 % ETOH administered 2 × day and once nightly in White rock hens

More chicks were killed, stamped, and pecked by water treated hens than hens treated with ETOH.

Dominance-Related Aggression

Cressman and Cadell, 1971

Social interactions in juvenile rhesus monkeys during self administration of ETOH (2-7%) for 21 days

Mauling, biting and wrestling play behaviors increased in proportion to amount of ETHO consumed and time course of the drug.

Meinecke and Cherkin, 1972

Pairs of pit gamecocks treated with 10-30 ml/kg of 33% ETOH

ETOH did not alter attack latencies or fighting.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Ellison et al., 1979

Control and monoamine neurotoxin-treated (6-OHDA) group-housed and isolated male rats treated with ETOH (10% for 25 days)

Group-housed rats showed a delayed preference for ETOH concurrent with increased fighting and deterioration of the dominance hierarchy; Isolated rats did not show this effect.

Blanchard et al., 1987d

Group-housed male and female rats self administered 8% ETOH

ETOH reduced "composite" of aggression by dominant males; Subordinate males consumed more alcohol than dominants, and females consumed more than males.

Killing

Kovach, 1967

9 ml/kg of 33% ETOH administered for 5 days in domestic cocks

ETOH treated cocks sheltered and defended chicks, whereas control cocks attacked and actively killed chicks.

Yanai et al., 1976

Yanai and Ginsburg, 1977

Predatory aggression in offspring of C57 and DBA mice fed ETOH (10 %) from 28 days of age through pregnancy and/or parturition

DBA offspring with postnatal exposure to ETOH showed a 58% reduction in predation.

Molina et al., 1985

Isolated male rats treated with ETOH (11.5 g/kg/day for 1 mo.); tested with a mouse one day after ETOH withdrawal

One day of withdrawal from ETOH increased the percentage of rats displaying mouse killing behavior.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 3 Effects of Alcohol on Aggression and Violence in Humans

References

Methods and Procedures

Results and Conclusions

Criminal Violence

Shupe, 1954

Urine analysis for ethanol in 42 men arrested for rape in Ohio.

50% of rapists had ethanol in urine at time of arrest.

Wolfgang and Strohm, 1956

Review of Philadelphia police homicide records 1948-52.

Alcohol was involved in 64% of 588 homicides, 44% of the time in both victim and offender.

McCaldon, 1967

Psychiatric interviews and MMPI of 30 prisoners convicted of rape.

10% of rapists reported they were drunk, 53% were drinking at the time and for 6% the primary diagnosis was alcoholic.

Scott, 1968

Psychiatric interviews with 50 male murderers from British prisons.

10% of the murderers were alcoholics, 22% were intoxicated during crime.

Guze et al., 1968

Psychiatric interviews of 260 first degree relatives of convicted felons.

The authors found a high proportion of the male relatives of convicted felons were alcoholic (33%) and that 53% of these alcoholic relatives had histories of excessive fighting and 21% had a felony conviction of their own. This compared to 6% in nonalcoholic relatives.

Jenkins, 1968

Analysis of records of 1500 children examined at Institute for Juvenile Research, Chicago.

The fathers of children whose records showed stealing (215) were more likely to be classified as alcoholic than those of overanxious or hostile, disobedient children.

Selzer, 1971

Validation of Michigan Alcoholism Screening Test (MAST) with driving under the influence and drunk and disorderly arrestees.

Over 50% of DUI and D and D arrestees scored in the alcoholic range on the MAST.

Tuason, 1971

Interview of 30 mental patients selected for a history of assault of harmful acts of violence.

40% of the violent patients were chronic alcoholics and 20% were problem drinkers.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Gunn, 1972

Interviews and medical records of prisoners in the UK, comparing 155 epileptic and control prisoners.

Both groups were similar in the incidence of alcoholism (15-17%) and violence, although alcoholics more often had a history of arrests for violent crimes.

Szymusik, 1972

Psychiatric interviews with 50 male deliberate murderers from Polish prison.

60% had history of ''heavy" drinking, 12% were intoxicated during crime.

Waller and Whorton, 1973

Analysis of the DMV driving records of 62 people who "unintentionally" shot someone in Vermont in 1967 compared to the records of controls.

21% of the shooters had records of arrests involving alcohol compared to 5% of drivers not involved in shootings.

Hart-Hansen and Bjarnason, 1974

Review of records on all 21 homicides occurring in Iceland 1946-70.

In 77% of incidents the murderer was under the influence of alcohol, 7 of the victims were also.

Tinklenberg et al., 1974

Interviews with 50 physically assaultive and 80 nonassaultive adolescent offenders at California Youth Authority and review of medical and police records.

Alcohol or secobarbital were being used at the time of offense in 64% of the assaults, however the nonassaultive group used more drugs.

Virkkunen, 1974a

Autopsy and court records for 116 homicides in Helsinki 1963-68.

Alcohol was present in victim or murderer in 79% of cases, generally in both. Alcohol was particularly associated with homicides preceded by an altercation.

Virkkunen, 1974b

Analysis of case histories of 45 men examined at the Psychiatric Clinic of Helsinki University (1945-72) who had committed incest.

49% were alcoholic and of the alcoholics 77% had committed previous crimes and 88% were reported to have exhibited violence in the home.

Medhus, 1975

Follow-up of 71 female alcoholics who had undergone compulsory treatment by the Temperance Board in Malmo, Sweden, 1961-68.

38 probands committed 88 criminal offences through 1970. However, there was no higher rate of violent crime in these individuals than committed by Swedish women in general.

Rada, 1975

Analysis of autobiographies written by 77 convicted rapists as part of their treatment at Atascadero State Hospital in California.

35% of rapists were alcoholic and 50% were drinking at the time of commission (43% drunk).

Sobell and Sobell, 1975

Public opinion poll of 50 randomly selected Orange County, California respondents (29% refusal rate).

Respondents felt that the alcoholic who commits a violent crime while drunk should receive a more severe penalty than a non-alcoholic in the same circumstance.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Solursh, 1975

Analysis of 19 criminal cases seen in a private psychiatric practice.

Significant quantities of alcohol were reported in association with 6 of the 7 homicides in this sample.

Henn et al., 1976

Review of mental health records for 67 rapists.

In 4.3% the primary psychiatric diagnosis was drug or alcohol abuse, but it was the predominant secondary diagnosis.

Mayfield, 1976

Interviews with 307 new prisoners convicted of violent crime in North Carolina.

57% were drinking at the time and 36% were problem drinkers. Only 17% of the victims were strangers.

Petrich, 1976

Interviews of 96 felons given psychiatric referrals in Seattle jail.

26% of men and 30% of women prisoners were diagnosed as alcoholic.

Roslund and Larson, 1979

Psychiatric examination of 16 mentally disturbed men who had committed violent crimes in Sweden.

In 9 of the 16 alcoholism or habitual heavy drinking was part of the diagnosis and all but one was intoxicated during the crime. The authors suggest that alcohol weakened self-control and triggered violence.

Browning and Boatman, 1977

Analysis of case histories of 14 incest victims seen at the Child Psychiatry Clinic of University of Oregon.

50% of the fathers or uncles involved were alcoholics and many were described as prone to violence.

Hanks and Rosenbaum, 1977

Interviews with 22 repeatedly battered women and their alcohol-abusing male partners during counseling.

Identifies 3 clusters of family backgrounds differing in terms of parental style toward these women as children.

Grunberg et al., 1978

Analysis of court records of all convicted murderers (48) in Albany County, NY 1963-75.

Alcohol was involved in the crime 54% of the time.

Johnson et al., 1978

Review of Police files of 217 rapes in Winnipeg 1966-75.

Alcohol was involved in 72% of rapes (only the victim in 9%, only the offender in 24%).

Rada et al., 1978

Questionnaires given to 382 sex offenders, including 122 rapists.

57% of rapists were drinking at the time of rape and 48% were alcoholics. Similar data for child molesters, exhibitionists and incest offenders.

Sorrells, 1979

29 male juvenile offenders (murder) diagnosed as anxious or depressed with some being hostile and explosive.

1/4 of the homicides were committed when the assailant was intoxicated.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Barnard et al., 1979

Psychiatric interviews with 88 men arrested for rape.

65% had been drinking, 34% heavily, at the time of the rape. 27% were alcoholics and for the alcoholics the victim was usually an acquaintance or relative.

Martin et al., 1979

Interviews of 66 female felons from Missouri State Board of Probation 1969 and follow-up of 42, 5 years later.

47% diagnosed as alcoholic in 1969, 33% in 1974. Higher rates than the normal female population.

Bloom, 1980

Psychiatric interviews of 30 native and 27 non-native Alaskans on trial for murder.

83% of the native Alaskans and 56% of non-native subjects had been drinking just before the homicide.

Enos and Beyer, 1980

Case studies of rapes by alcoholics who were infertile due to the alcoholism.

Chronic alcohol abuse can cause aspermia.

Lester, 1980

Comparison of data on alcohol consumption and homicide and suicide rates in US 1940-73.

Suicide, but not murder, rates were highest in states with highest per capita alcohol consumption.

Tardiff and Sweillam, 1980

Psychiatric records of 5233 male and 4132 female patients in Long Island, NY mental hospitals.

21% of patients had histories of assaults or suicide attempts, but there was less alcohol abuse in these patients than in the non-violent patients.

Elliot-Harper and Harper, 1981

Gave a modified MAST to 16 criminal psychiatric patients, 16 psychiatry patients, 16 alcoholic patients and 16 surgical patients.

Both psychiatric groups showed more alcohol related problems than the medical patients but fewer than the alcoholics in for detoxification.

Heather, 1981

Questionnaire to 200 young (16-21) Scottish offenders.

63% had committed their crime under the influence of alcohol, however, the number of violent crimes was not different between drunk and sober offenders.

Rosenbaum and O'Leary, 1981

Level of physical abuse, marital adjustment and alcoholism of spouse assessed in 52 abused wives and 20 control women in NY.

Alcoholism was most common in husbands of physically abused wives, less common in nonviolent, maritally discordant couples and least common in control couples.

Tinklenberg and Ochberg, 1981

Police records of and interviews with 95 male adolescents convicted of homicide or assault with a deadly weapon.

Alcohol alone or in combination with other drugs was involved in 61% of the crimes.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Eberle, 1982

Interviews with 390 battered women in Denver and Discriminate Analysis of violence and alcohol abuse by the batterer in 4 episodes.

Alcohol abuse by the batterer predicted more severe injuries to woman and more likely abuse of children. In addition alcohol abuse by the batterer was frequently associated with the victim's use of alcohol.

Myers, 1982

Analysis of self report, police records, reports from wives or cohabitants, and victims for 50 violent Scottish prisoners and 50 control prisoners.

Violent offenders were more likely to have consumed alcohol at the time of the offence than non-violent offenders.

Bohman, 1983

Follow-up of all illegitimate births in Stockholm 1930-49 and later adopted. Correlational analysis of alcohol abuse, arrests, occupation and socioeconomic status with biological and adoptive parents.

Found genetic as well as environmental factors in alcohol abuse and criminality. When alcohol abuse and criminality co-occurred the crime was often repetitive and violent.

Corenblum, 1983

A.A. members, assigning responsibility to fictional abusing and abused spouses that were intoxicated or sober; Self report of histories.

Subjects who abused their spouses when intoxicated were not likely to do so when sober. Subjects assigned blame to fictional characters in relation to their situation (i.e. victims assigned blame to victims).

Holcomb and Anderson, 1983

Analysis of pretrial evaluations of 110 men charged with 1° murder (police reports, histories, medical records).

24% of the offenders were drinking at the time the offense occurred; correlations for history of alcohol abuse.

Rada et al., 1983

44 subjects were selected from a pool of 150 child molesters and rapists from a program for the treatment of mentally disordered offenders in California. Criteria for inclusion in the study were that the offender acted alone, that the offense was either brutally violent or non-violent, and that victims were over 18 for rapists or under 13 for child molesters.

55% of rapists (total n=18) and 46% of child molesters (total n=26) were intoxicated at the time the offense occurred. Violent rapists and child molesters were more likely to be intoxicated at the time of the offense than their non-violent counterparts

Bradford and McLean, 1984

Psychiatric interviews of 50 men charged with sex offenses, 20 of whom inflicted serious physical injury.

A high level of violence was correlated with a history of alcohol abuse and dependency. There was no relationship with testosterone level.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Hechtman et al., 1984

10 year psychiatric follow up of 75 hyperactive subjects (90% male) originally referred to Montreal Children's Hospital and 44 from local schools.

More hyperactives described as alcohol abusers and had a period of heavy drinking. Aggression was described as a problem in 55% of hyperactives vs 31% of controls and 47% vs 32% had been in court (types of offences not different and authors do not relate crime to alcohol use).

Heller and Ehrlich, 1984

Analysis of pre-sentence psychiatric reports randomly selected from 9600 done in 1966-83 in Philadelphia. Includes 431 non-violent offenders, 779 violent offenders and 315 violent recidivists.

Alcohol abuse and having alcohol-related prior convictions were more common among violent offenders and violent recidivists.

Roberts, 1987

Analysis of legal records on 234 men charged with battering wife (or cohabitant) in Indianapolis 1984-1985.

60% of the battered women reported that the abuser was under the influence of alcohol at the time and 21.8% used both alcohol and drugs.

Schuckit and Russell, 1984

Psychiatric interviews and background analysis of 275 male primary alcoholics in treatment at San Diego V.A.

29% of primary alcoholics had a violent history, including having used weapons in fights and inflicting injuries requiring medical attention.

Telch and Lindquist, 1984

Questionnaires to 19 violent couples (wife battering), 24 nonviolent but in counseling couples and 24 matched happy couples.

Significantly more drinking problems in couples with wife abuse.

Abel and Zeidenberg, 1985

Abel et al., 1985

Analysis of violent deaths and BAC from medical examiners files over a ten year period.

Alcohol (10-100 mg/dl or greater) was involved in all major categories of violent death ranging from homicides to traffic accidents.

Campion et al., 1985

15 case studies of men admitted to Bellevue who murdered their mothers.

4 of 15 had histories of alcohol abuse.

Kratcoski, 1985

Questionnaire on experience with violence (among other items) was given to 305 youths (75% male) in high school or a juvenile justice center.

Violence against parents was highest (43%) in families characterized as having a how integration level. The authors mention that the case records for these youths frequently include accounts of alcohol and drug abuse.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Kroll et al., 1985

Compared histories of 31 alcoholics severely physically abused as children with 21 age-matched nonabused alcoholics all from Ann Arbor V.A.

83% of the abuse was by alcoholic fathers and the abused alcoholic was about 10x more likely to have been involved in adult domestic violence (56% vs 6%), property destruction (48% vs 3%), legal difficulties (48% vs 0) and suicide attempts (23% vs 3%).

Leonard et al., 1985

Self report and family interview for 484 blue-collar men.

No direct correlation for alcohol consumption and fighting, but physical marital conflict was correlated with alcohol misuse or dependence (DSM III).

Van Hasselt et al., 1985

Questionnaires, including MAST, given to 26 couples referred because of wife abuse, 26 maritally discordant but non-violent couples and 15 happy couples.

Husbands that physically abused their wives had higher MAST scores (17.0 vs 3.5 & 4.6). No increase in problem drinking by the wives.

Haver, 1986

Follow-up interviews of 44 Norwegian women treated for alcoholism 3-10 years in past.

Current alcohol consumption correlated with history of sexual abuse by mother (r = 0.42).

Henderson, 1986

Interviews of 44 English inmates of a maximum security prison (about 50% murderers).

Found 8 different types of violent circumstances, alcohol most frequently involved in domestic violence at night and in fights outside of pubs.

Lindqvist, 1986

Sweden 1970-80 and corresponding court records of homicides.

30 of 64 murderers were intoxicated (BAC > 0.06%) and 56% were alcoholics. 47% of victims were intoxicated.

Lindquist, 1986

Counseling of battered women to deal with abusive, alcoholic partner, illustrative case study.

Intervention's focus is on support for the woman and getting the alcoholic's social network to encourage treatment for alcoholism.

Livingston, 1986

107 adults (90% male) receiving residential treatment for alcoholism and substance abuse given two psychological tests (MAST and CTS-Form N) to assess alcoholism and behavior in family conflicts.

83% of alcoholics had been violent in past relationships (55% in the past year) compared to 28% of nonalcoholics. Family violence by alcoholics was also more frequent and more intensely violent.

Myers, 1986

Interviews of 50 men in Scottish prison for violent crime and 50 men imprisoned for non-violent offences.

92% of the violent offenders reported consuming alcohol just prior to the offence as compared to 72% of controls.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Langevin et al., 1987

As a test for possible brain damage, 21 accused murderers, 21 men accused of assault and 16 controls were administered a battery neuropsychological tests and EEG.

Differences in measures of neurological impairment approached significance (p < .10) with killers and assaulters showing more pathology than controls. 22% of killers and 23% of assaulters also drank daily vs. 8% of controls, and violent subjects more often scored in alcoholic range on MAST. However, there was no correlation between alcohol abuse and impairment.

Muehlenhard and Linton, 1987

Questionnaires to 341 female and 294 male hetero-sexual undergraduates.

15% of women and 7% of men had been involved in date rape. Heavy alcohol use (in self and partner) was reported to be more common on dates with sexual aggression.

White et al., 1987

Longitudinal data from interviews of 441 male and 441 female adolescents tested when they were 12, 15, or 18 years old and again 3 years later when they were 15, 18, or 21 years old

52% of problem drinkers and 42% of the heavy drinkers of alcohol were also classified as delinquents or heavy delinquents (committed any offense > 3 times in last 3 years).

Collins and Schlenger, 1988

Analysis of court records of and interviews with 1149 male felons in NC prisons. Multiple regression of demographic and criminal history with drinking and offense.

Those who reported 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, but alcoholism was not predictive of offense type.

Fagan et al., 1988

Compared the quantity and frequency of drinking in maritally violent men (44) with married violent criminals (33) and control groups. Also administered a questionnaire on reasons for drinking.

Maritally violent men were most likely to drink at lunch, after work or alone. They also were the most likely to agree with the statement that they drank to forget. Drinking seen more as a consequence than a cause of marital violence.

Miller et al., 1989a, b

Interviews of 45 alcoholic women and 40 nonalcoholic women. Statistical analysis of conflict between the women and their spouse.

More of the alcoholic women had experienced verbal abuse and violence from their spouse (53% vs. 13%). Relationship to alcohol abuse in spouse was borderline (p < 0.06).

Rosenbaum and Hoge, 1989

Medical evaluation of 31 men referred for marital violence.

61% had histories of head trauma and most of these also abused alcohol, more frequently than those without trauma.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Pollock et al., 1990

Interviews and bio-medical evaluations of 131 sons of alcoholic fathers chosen from Danish registry and 70 controls. Both groups were 18-21 yrs old.

18% reported being violently abused by alcoholic fathers vs. 11% of controls, but sons of alcoholic fathers were not any more likely to engage in violent or antisocial acts. However, those that had been beaten as children were more likely to report that they had hit someone in a fight.

Dembo et al., 1991

Self-reported drug use, urinalysis test results and self-reported delinquency examined as possible predictors of delinquency in 201 incarcerated males and females; mean age 16 years

Self-reported use of alcohol consistently predicted drug sales offenses, index offenses, crimes against persons and total delinquency at follow-up.

Health Statistics

Wilentz and Brady, 1961

Review of New Jersey Medical Examiner records 1933-59.

In 31% of suicides, 36% of murders, and 49% of traffic deaths alcohol intoxication was a factor.

Le Roux and Smith, 1964

Review of autopsies and court records in 1739 deaths in South Africa.

22% had died violent deaths (traffic or homicide) and alcohol was associated with 64% of the victims.

Kellett, 1966

Interviews of 71 patient admitted for suicide attempts over a 3 month period in Durban, South Africa.

Alcohol abuse played a significant role in 33.8% of suicide attempts.

Derrick, 1967

Records and recollections of the pathologist to the coroner of Queensland.

In 1965 250 deaths in Australia due to alcoholism, 1541 traffic deaths probably related to alcohol, 547 deaths from cirrhosis of the liver and 27 deaths from alcoholic psychosis. Concludes that alcohol is probably the sixth most common cause of death in Australia.

King et al., 1969

Random sample interviews of 223 black men 31-35 born in St. Louis.

62% had some history of heavy drinking, including 17% who had medical or social problems directly attributable to alcohol since age 25. The heavy drinkers were more likely to have been arrested for crimes against property and violence than the "never heavy" drinkers.

Climent et al., 1972

Interviews of 80 emergency room patients, half of whom presented with a history of violence.

The violent patients were more often heavy drinkers and more frequently had alcoholic parents.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Westermeyer and Brantner, 1972

Review of Minneapolis autopsy data of deaths of Chippewa people 1965-67.

25.8% of Chippewa deaths were violent vs 5.3% among general population. In the majority of these violent deaths BAC was elevated.

Ripley, 1973

Interviews of 121 patients admitted to hospital in Seattle after suicide attempts 1957-1958 and 100 similar patients in Edinburgh, Scotland in 1970. Also analysis of Coroner's records of 114 suicide deaths in Seattle and 91 in Edinburgh for the same time periods.

43% of suicide attempters in Seattle and 28% in Edinburgh were problem drinkers and 36% and 25% respectively were drinking at the time of the attempt. 68% of suicide deaths in Seattle and 45% in Edinburgh had alcoholic problems.

Costello and Schneider, 1974

Follow-up of 400 admissions to an alcohol rehabilitation facility.

The alcoholics had a high death rate with violent deaths, particularly in the first few years after identification of problem, excessively over-represented.

James, 1974

Autopsy results on 107 suicides in Australia 1961-62.

48% of males and 18% of female suicides had BAC > 0.05 and 7% had been under psychiatric care for alcoholism.

Marek et al., 1974

Review of 1970 robbery reports in Krakow, Poland.

69% of the victims were intoxicated.

Choi, 1975

Follow-up of 863 patients seen in Alcoholism Clinic in St. Louis 7/69-6/72.

By 7/72 45 of these alcoholics had died: 24% by homicide and 4% suicides (all men) and average age of 42.

Weiss, 1976

Statistical analysis of violent death rates 1960-73 from National Center for Health Statistics.

Correlates increase in violent deaths with increase in per capita alcohol consumption.

Riddick and Luke, 1978

604 autopsies in Washington DC (8/74-2/75) of unnatural deaths and sudden death in those under 45.

176 had BAC > 0.03:48% of homicides, 27% of suicides, 46% of traffic accident deaths. In many of those with out BAC there was autopsy evidence of alcohol abuse (e.g. cirrhosis).

Robins et al., 1977

18-month follow-up interviews of 299 patients from a psychiatric emergency room.

A third were alcoholics, none had committed homicide or suicide.

Bohman, 1978

Review of Swedish records of 2324 adoptees and their biological parents.

Good evidence for a genetic predisposition for alcohol abuse but not criminality.

Robins, 1978

Interviews and records of three different samples of men to collect information on childhood and adult behaviors.

Childhood (before 15) alcohol abuse is correlated with later adult antisocial behaviors.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Schuckit et al., 1978

Interviews of 186 men admitted to Seattle V.A. 9/75-6/76 and 191 women admitted to Seattle Detox Center.

10% of male and 34% of female alcoholics attempted suicide and 18% of male and 6% of female alcoholics had been arrested for felonies at least once in their lives.

McCord, 1981

Follow-up interviews of 224 men who had been part of the Cambridge-Somerville Youth Project 1936-45.

40 were both criminals and alcoholics, 30 were alcoholic only and 34 were criminals but not alcoholic. The personal characteristics of alcoholic criminals were closer to non-alcoholic criminals than to non-criminal alcoholics.

Mendelson et al., 1982

Measured plasma LH at autopsy of 28 men killed while being violent or as victims.

LH levels were higher in the violent group than the nonviolent or controls. Suicides had higher LH if they also were positive for alcohol.

Combs-Orme et al., 1983

Follow-up of 1289 alcoholics 6-9 years after treatment.

22% had died and of these 3.5% were suicides, 3.2% were homicides.

Linnoila et al., 1983

Measured CSF levels of norepinephrine, catechol metabolites and 5-HIAA in 36 alcohol abusers arrested for murder or attempted murder.

The impulsive offenders (non-premeditated), those with explosive or antisocial personalities, had lower 5-HIAA levels than the other offenders.

Pulkkinen, 1983

Longitudinal interview study of 196 Finnish boys and 173 girls starting in second grade and 135 followed until age 20.

Aggressiveness in boys at age 8 significantly predicted heavy drinking at age 20, it also predicted more violent offences and criminality.

Berglund, 1984a, b

Follow-up of 1312 alcoholics admitted to University Hospital in Lund 1949-1969. Mean age = 42 and mean follow-up was 18 years.

537 had died -2.5 times the expected number. Suicide and violent death contributed 51% of the excess mortality.

Branchey et al., 1984

Interviews and blood chemistry of 43 alcoholic patients, 7 of whom had history of assault and 3 had attempted suicide.

Only alcoholic patients with a past history of violence had significantly higher levels of tyrosine and phenylalanine and lower tryptophan, suggesting altered serotonin turn-over.

Crompton, 1985

Analysis of autopsy data on 406 English suicides 1970-80.

61% of suicides had BAC > 0.1.

Jacobsson, 1985

Analysis of a physician's records on 316 assault victims seen in western Ethiopia 1962.

In 20% of cases the victim had been drinking and in 36% the assailant.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Williams et al., 1985

Statistical analysis of survey data collected by the National Opinion Research Center in urban areas of the US 1973-1980 (n = 6419).

29.9% responded that they had been threatened with a gun or shot at. Alcohol use was a weak discriminative predictor of being a victim of gun abuse.

Williams and Singh, 1986

Statistical analysis of survey data collected by the National Opinion Research Center in 1980 and 1984 of urban areas of the US (n = 2045).

Alcohol abusers were more likely to have been shot, beaten, arrested, or have aggressive attitudes than moderate drinkers or abstainers.

Virkkunen and Kallio, 1987

Glucose tolerance tests on 60 male prisoners who had killed or attempted to kill their wife or female companion.

The lowest glucose levels were seen in those with a history of violence under the influence of alcohol.

Branchey et al., 1988

Recorded EEG and event-related potentials in 51 alcoholic men during a tone discrimination task.

The alcoholics that had histories of violent crime had smallest P3 amplitude in their ERPs. No differences in P3 latencies.

Dermen and George, 1988

Questionnaires to 114 male undergraduates.

Relationship between drinking habits and frequency of fist fights was strongest amongst those who expected alcohol to increase aggression.

Helzer and Pryzbeck, 1988

Statistical analysis of alcoholism and psychological disorders from the Epidemiological Catchment Area study (1984, n = 20000, randomly selected urban dwellers).

13% had diagnosis of alcohol abuse/dependence and these people were 3 times more likely to also be diagnosed as antisocial personality.

Kratcoski, 1988

Review of Cuyahoga County, Ohio coroner's records on 1775 cases of homicide in which the assailant was known, 1970-83.

Only 21% were killed by a stranger. Of those killed by a family member 40.3% had alcohol in their blood and 23.6% were legally drunk. For those killed by an acquaintence the figures were 50.8% and 29% and by a stranger 34.9% and 16.5%.

Petersson, 1988

Investigation of 347 deaths of men approximately 50 years of age participating in a preventative medicine program and control men in Sweden.

151/347 deaths were alcohol related. 75% of the sudden unwitnessed deaths were of men registered with the Department of Alcohol Diseases.

Rydelius, 1988

Statistical analysis of violent death rates 1967-85 of cohort of 832 boys and 224 girls admitted to Swedish reform schools in 1967 (does not separate alcohol from ''drug" use).

47/110 male and 7/22 female deaths had an alcohol and/or drug abuse-related factor.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Lester, 1989

Statistical analysis of suicide and homicide rates, per capita alcohol consumption in US 1980, and social variables (e.g. income, population density, unemployment rate, etc.).

Suicide, but not murder, rates were highest in states with highest per capita alcohol consumption, however alcohol consumption was highest in states with less social integration (e.g., highest divorce rates).

Linnoila et al., 1989

Virkkunen et al., 1989b

Interviews and biochemical measurements in 54 alcohol abusers arrested for assault or arson.

The offenders with an alcoholic father had lower CSF 5-HIAA than those with a nonalcoholic father. Suicide attempters also had lower 5-HIAA. The authors liken these violent alcohol abusers to Cloninger's Type II alcoholics.

Personality Evaluations of Aggression

Selzer, 1967

An essay illustrated with two psychiatric case studies.

Describes the "alcoholic personality" as dependent, hostile, egocentric, and self-destructive.

Tomim and Glenn, 1968

Review of psychiatric admissions at Brooklyn State Hospital 4/67-9/67.

Of 446 patients diagnosed with psychopathic personalities 58 were alcoholics.

Whitelock et al., 1971

136 male psychiatric patients given MMPI and an alcohol abuse questionnaire.

Found subtypes of alcohol abusers based on MMPI scores. Moderate abusers' patterns were dominated by Pd (hostile psychopathic) while those with higher abuse scores had MMPI patterns dominated by D and Pt components (neurotic depressive).

Woodruff et al., 1971

Interviews with 35 sociopaths (a history of fighting was one criterion in the diagnosis).

60% of these patients were alcoholics.

Woodruff et al., 1973

Psychiatric interviews of 29 alcoholics, 139 depressives and 29 with alcoholism and unipolar depression.

Those men and women with both alcoholism and depression were the most antisocial and had more of a history of violence.

Cloninger and Guze, 1975

Psychiatric interviews of parents of 66 female felons.

55% of the fathers were alcoholic or sociopathic and in 76% of the families one parent had either alcoholism, sociopathy or hysteria. Sociopathy in fathers was predictive of hysteria in the daughter.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Deardorff et al., 1975

Power Orientation Semantic Differential and the Situations for Drinking questionnaires given to 253 problem drinkers, including 8 men with a history of violence.

Violent drinkers scored highest on the personal power scales, suggesting they drink in order to feel a sense of power.

Apfeldorf and Hunley, 1976

MMPI given to 233 residents at W. Va. V.A.

The F scale (considered to reflect overt hostility) distinguished problem drinkers (highest F) from alcoholics from controls.

Caster and Parsons, 1977

Personality inventories on 78 alcoholic veterans in a therapeutic program and 27 controls.

Alcoholics that failed to complete the program and recidivists scored highest on depression and sociopathy.

Van Valkenburg et al., 1977, 1983

Interviews of patients diagnosed as clinically depressed.

A subtype (Depression Spectrum Disorder) of depression includes patients more likely to be problem drinkers and show antisocial behavior. These patients were also more likely to have a parent that is/was alcoholic or have an antisocial personality.

Cloninger et al., 1978

Statistical analysis of alcoholism in male and female relatives of alcoholics.

Although alcoholism is more frequent in men than women, male and female alcoholics have equal numbers of alcoholic relatives. The correlation is stronger for men (r = .53 vs. 18) suggesting non-familial variables are more important in women.

Herzog and Wilson, 1978

Personal Reaction Inventory administered to female alcoholic inpatients and controls in Wisconsin.

Assertive antisocial behavior was higher in alcoholic women and predicted drinking behavior.

O'Leary et al., 1978

MMPI administered to male alcoholic inpatients in Seattle V.A.

48 out of 173 had sociopathic profiles.

Renson et al., 1978

26 male outpatients at a clinic for alcohol abuse and violent behavior were administered Buss-Durkee inventory self-rating true/false items to yield a total hostility score.

Violent alcohol abusers have higher hostility ratings than nonviolent abusers, scoring higher on scales measuring assault, irritability, verbal hostility and resentment.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Schuckit and Morrissey, 1979

Interview of 293 women admitted to Seattle detoxification center in 4/76-9/76.

53% of patients were primary alcoholics (the initial disorder), however primary antisocial personality patients (14%) were also secondary alcoholics. These patients actually drank the most, had the most legal problems and attempted suicide most often.

Virkkunen, 1979

Interviews of 50 adult male criminals referred for psychiatric exams in helsinki 1975-77 and 50 juvenile delinquent prisoners all of whom both were alcoholic and had antisocial personality. They were compared to 42 alcoholic prisoners without ASP.

The offenders with antisocial personality were more likely to have committed violent crimes under the influence of alcohol than those without antisocial personality (84% vs 40%).

Haramis and Wagner, 1980

60 alcoholic patients of Ashtabula County Council on Alcoholism and Drug Abuse, half with background of violent crime, given Rorschach and Hand Tests.

The alcoholics with the aggressive, criminal record scored higher on hostility, impulsivity, immaturity, lack of control, and had poor judgment. More than one "alcoholic personality".

Williams et al., 1980

166 undergraduates, in-and out-patients and staff of mental health center given Personality Research Form and Alcohol Use Inventory.

Aggression was the personality variable most highly correlated with the extent of alcohol use.

Conley, 1981

MMPI given to 337 male alcoholics at admission to Hazelden Foundation, to 265 of those at discharge and a 12-month follow-up interview to 228.

Half of the admissions could be classified into 4 groups: neurotic (high D), classic (high D, Pd and Pt), psychopathic (high Pd and Ma), and psychotic (high Sc, Pa, Pt and Ma). All but the psychopathic type showed foreshortening of the profile at discharge (they were also the youngest).

Williams et al., 1982

Questionnaires given to alcoholics in treatment and controls.

44% of alcoholics (8% controls) were using alcohol as their preferred way of coping with stress. 9% of alcoholics (1% controls) preferred starting a fight as a coping strategy.

Løberg, 1983

Interview, MMPI and neuropsychological assessments of 110 hospitalized alcoholics in Norway. Divided into passive (28), moderately belligerent (65), and highly belligerent (17 recent fighting while drinking).

The high belligerence group was earlier in onset of alcohol abuse and had more pronounced neuropsychological deficits and a more pathologically deviate personality.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Mosher and Sirkin, 1984

Administered "hypermasculinity" inventory and alcohol use survey to 135 male undergraduates.

Significant positive correlation (0.28) between alcohol abuse and the macho constellation, also with viewing violence as manly and danger as exciting.

Cadoret et al., 1985

Statistical analysis of 127 male and 87 female adoptees in Iowa selected by the researchers for antisocial or alcoholic family backgrounds. The adoptees were interviewed at an average age of 25.

Although antisocial personality and alcohol abuse were frequently associated the genetic determinants appear separate. However, the authors feel their sample is too small and young to look for the two different types of alcoholism as suggested by Cloninger.

Collins et al., 1988

Self report, medical and school records in black men rated by three psychiatrists.

Individuals with antisocial personality had a higher rate of alcoholism; drinking within the family, low education and increased irritability also were related.

Holcomb and Adams, 1985

Compared MMPIs from 41 men who committed murder while intoxicated, 48 sober murderers, 130 men admitted to a detox unit (no crime) and 40 acute psychiatric admissions with no alcoholic history.

Men who committed murder while intoxicated were less aware of psychological problems (high L scores). Sober murderers were more psychopathic (high PD) and less interpersonally sensitive (low MF).

Lewis et al., 1985a

Self report in unipolar depressive men rated by skilled observer using PHDD and SADS, and RDC by a family member.

Depressed men with antisocial personality have a higher incidence of alcoholism, more family disruption, and a lower socioeconomic status than depressive men without antisocial personality.

Lewis et al., 1985b

Reanalysis of King et al. 1969 interview data on urban black males.

About half were diagnosed as antisocial and those men had higher rates of alcohol abuse. Antisocial alcoholics had more alcohol related problems.

Downs et al., 1987

Miller et al., 1987

Retrospective interviews of 45 alcoholic women and 40 nonalcoholic women. Statistical analysis of conflict between the women as children and their parents, and incidence of sexual abuse.

More of the alcoholic women had experienced conflict with and violence from their fathers, but they were not different from the controls in conflict with mother. More of the alcoholic women had been sexually abused (rarely by a relative).

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Whitters et al., 1987

DIS/DSM-III interviews of 41 alcohol abusers with antisocial personality disorder.

Two clusters varying in concurrent level of depression, those with more depressive symptoms also had more symptoms of other psychopathologies as well.

Yates et al., 1987

Review of records of 274 patients treated at the Univ. of Iowa Chemical Dependency Center.

Twice as many alcoholics with antisocial personality had attempted suicide or were classified as violent as non-ASP alcoholics.

Collins et al., 1988

DIS/DSM-III interviews of 1149 convicted felons in North Carolina prison system.

28% of the felons met the criteria for antisocial personality disorder, of those 71% were alcoholic/abusers (compared to 40% of non-ASP). Those with alcohol problems also had more ASP symptoms.

Cooper, 1988

Analysis of records on 34 subjects involuntarily admitted to a psychiatric ward in Canada, 1984-85.

Assaultive behavior was one of the characteristics in 29%, and 35% were alcoholic along with other psychopathology; frequently antisocial personality disorder.

Jaffe et al., 1988

Behavior of 77 hospitalized, alcoholic patients, grouped by levels of childhood aggression and antisocial personality were rated while drinking and while sober.

Alcoholics report more anger and aggression when drinking than when sober without any relationship to presence of antisocial personality; Patients with high levels of childhood aggression showed a greater effect.

Palmstierna and Wistedt, 1988

Psychiatric analysis of 105 patients involuntarily admitted to a Swedish psychiatric clinic 10/85-4/86.

24 patients had history of alcohol abuse and 41 were physically violent (does not specify overlap or correlation between these two descriptors).

Schuerger and Reigle, 1988

Psychological assessment of 246 men (follow-up on 32) being treated for wife abuse in Ohio. Various personality and violence inventories used and alcoholism quantified with MAST.

69% of group considered alcoholic based on MAST score and report a positive correlation (.24-.33) between MAST and degree of violence.

Yates et al., 1988

DSM-III interviews of 260 male alcoholics at Iowa V.A.

24% met criteria for antisocial personality disorder. ASP alcoholics had begun drinking earlier in life, drank more and had more alcohol related problems, including violence while intoxicated, than non-ASP alcoholics.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Cloninger et al., 1989

Review of data on alcoholism in 1775 people born 1930-42 in Stockholm and their biological and adoptive parents and personality data from 286 hospitalized alcoholics in St. Louis.

Concludes there are two, partly over-lapping, subtypes of alcoholism. Type 1 is characterized by passive-dependent personality traits and has a larger environmental component. Type 2 is characterized by antisocial personality traits and has a larger genetic component.

Grove et al., 1990

32 monozygotic twins who had been separated shortly after birth and raised apart were interviewed separately as adults.

12 individuals met criteria for alcohol abuse but these were distributed among 10 pairs for a concordance rate of 33% and a minimal heritability for this characteristic. They report a somewhat higher heritability estimate for ASP. Cautions that this small, non-clinical sample may not be optimal for detecting genetic contribution.

Experimental Measures of Aggression

Bennett et al., 1969

16 male undergraduates given 0, 0.33, 0.67 and 1ml/kg ethanol in orange juice on separate days and given opportunity to select shock intensity administered to a confederate of the experimenter in a fake learning paradigm.

No statistically significant effect of alcohol on aggression under these test conditions.

Tamerin and Mendelson, 1969

4 male alcoholics from an inpatient hospital were observed and interviewed during a regime consisting of 2 weeks without alcohol. Then they were given alcohol (0.5 to 2.0 ml/kg of 86 proof bourbon) 4 times per day for 3 weeks, then 21 days of free access drinking and finally, 10 day withdrawal.

Euphoria was observed during the initial phase of intoxication. Depression and anxiety and feelings of guilt increased with intoxication. Increases in verbalization and aggressive interactions were also observed.

Butts and Shontz, 1970

20 alcoholic men were paired with either their wives or unfamiliar women. Subjects participated in a lab learning paradigm. Alcoholics received shocks chosen by the partner if his responses were too slow (passive invitation of shock) or if he admitted a mistake (invitation of punishment).

Alcoholic subjects received more shocks from partners than controls, and had less of a tendency to admit mistakes when it led to aversive stimuli.

Marinacci and Von Hagen, 1972

EEG testing of 800 patients accused of violent crime or antisocial acts, results illustrated with 13 case histories.

In 13% of total 2 oz alcohol induced abnormal EEG, suggests there is a small subpopulation with temporal lobe damage aggravated by alcohol.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Boyatzis, 1975

149 adult male volunteers attended staged parties. Each party had either distilled spirits, beer or soft drinks available. During the parties they were videotaped and filled out personality, mood checklists and TAT.

Measures of aggression were highest with distilled spirits. Heavy drinkers showed the most verbal aggression toward other "party" attendees. Those subjects also scored lowest on social integration.

Dotson et al., 1975

Administered Buss-Durkee Hostility Inventory and measured plasma testosterone before the beginning of a staged party. Alcoholic and soft drinks were freely available for 3 hrs. A second blood sample was taken at the end.

No correlation with pre-party testosterone or hydrocortisone levels or of pre-party levels and aggression. However, post-party BAC was correlated with aggression rating (r = .23) and change in testosterone (r = .26). Testosterone decreased with low to moderate BAC and increased with high BAC.

Lang et al., 1975

96 male undergraduates drank 1.3 ml/kg ethanol in tonic or placebo and were informed or misinformed about alcohol content. Then tested for "aggression" with modified Buss shock apparatus (willingness to administer high shock intensities to confederate).

If they thought they had received alcohol, independent of BAC, they delivered greater shock intensities (expectancy effect).

Taylor and Gammon, 1975

40 male undergraduates consumed 0.83 or 2.48 ml/kg of 100 proof bourbon or vodka in ginger ale. Tested in a reaction time competition with shock to the loser. The subject chose the level of shock to administer to the "opponent". Over trials the shock from the "opponent" was increased (provocation).

The mean shock intensity settings were higher with the higher dose of alcohol and increased with provocation. There was a trend for a greater effect with vodka. Although there was no control in this experiment, the authors state that the low dose of alcohol reduced aggression below normal.

Maletzky, 1976

22 patients with a history of violence under the influence were observed while receiving 25% ethanol i.v. 200 cc/hr.

41% showed inappropriate rage, 18% had a psychotic reaction and 9% showed a mixture of these responses. Response generally occurred at a high BAC.

Taylor et al., 1976

40 male undergraduates consumed 1.25 g/kg ethanol in ginger ale or control. Tested in a reaction time competition with shock to the loser. The subject chose the level of shock to administer to the "opponent". For half the subjects it was made clear that the opponent would only use the least intense shock ("no-threat").

In the "no-threat" condition alcohol had no effect on aggression (shock given to the opponent) but alcohol doubled the average shock setting when there was some degree of threat.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Taylor and Gammon, 1976

40 male undergraduates consumed 1.25 g/kg ethanol in ginger ale or control. Tested in a reaction time competition similar to Taylor et al. 1976 but no threat manipulation. An observer was present and for half of the subjects he provided verbal pressure re the subjects' performance.

Alcohol increased the intensity of shock the subject was willing to administer and the subject evaluated the opponent in less favorable terms. An observer that commented on performance moderated these effects.

Persky et al., 1977

40 alcoholic volunteers were admitted to Clinical Research Center PGH. Subjects abstained from alcohol and tobacco for 1 week, then were assigned to groups: 1, unlimited alcohol and cigarettes; 2, unlimited alcohol; 3, unlimited cigarettes; or 4, continued abstinence for a week. Psychological state assessed and testosterone measured.

Plasma testosterone decreased with unlimited alcohol access. Although these alcoholics had high levels of hostility and aggression as assessed by psychological tests, alcohol availability did not affect this. Cigarettes did not have any significant effects.

Taylor et al., 1977

40 male undergraduates consumed 1.25 g/kg ethanol in ginger ale or control and were tested in a reaction time competition with an artificial opponent. Frustration was produced in the subjects with an insoluble puzzle.

Alcohol increased the intensity of shock the subject was willing to administer but there was no effect of frustration on shock intensity or interaction with alcohol.

Mendelson et al., 1978

8 alcoholic men and 16 controls had hormone levels measured before, during and after bourbon (ad lib).

Testosterone levels were reduced during alcohol in both alcoholics and controls without an initial suppression of LH. Authors suggest LH may be important in alcohol's effects on aggression.

Graham et al., 1980

Direct observations (633 hr) of social interactions and aggressive behavior in 185 Vancouver bars.

The frequency of verbal and physical aggression varied across bars. The "aggressive bars" had a reputation for violence and were generally in poor areas.

Zeichner and Pihl, 1978

72 men drank 1.25 ml/kg ethanol in orange juice, placebo, or nothing and then were tested with a modified Buss shock machine. During the test subjects heard aversive tones, half thought there was malicious intent.

Subjects that received alcohol were most aggressive (highest and longest shocks) independent of intent manipulation.

Pihl et al., 1981

48 men trained on a modified Buss task (see Zeichner and Pihl, 1978) then drank 1.25 ml/kg ethanol or placebo and informed or misinformed about alcohol content.

Alcohol increased aggression independent of expectancy, but placebo subjects also were more aggressive if they thought they had received alcohol.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Baldwin and Randolph, 1982

Southern Mississippi undergraduates were divided on the basis of Alcohol Use Inventory into 308 light drinkers, 30 moderate drinkers and 30 abstainers. In the laboratory students received either a negative or a positive evaluation from a confederate and were then asked to rate the confederate with checklists.

Provocation (negative evaluation) produced higher hostility-aggression scores on the ratings. Moderate drinkers scored higher on these scales than light drinkers with abstainers intermediate.

Zeichner et al., 1982

72 men were trained on modified Buss task and drank 1.25 ml/kg ethanol or placebo. While in the task half recorded the level of pain they thought the confederate was receiving (forced attention).

Alcohol increased aggression but there was no effect of forcing the subject to attend to the consequences of his actions.

Bailey et al., 1983

Frustration-induced aggression measured with a modified version of Buss' aggression machine. 40 undergraduate males received either 0.83 or 2.48 ml/kg of 50% ethanol. Half of the subjects competed in the presence of a mirror and video camera (self aware).

Non-self-aware subjects administered higher shocks; alcohol increased the shock settings, but there was no interaction for awareness and dose.

Virkkunen, 1983

Psychiatric interviews of and fasting serum cholesterol measurements in 280 Finnish male murderers.

173 had a history of violence under the influence of alcohol and 73 of these had an antisocial personality. These 173 had lower mean cholesterol levels than those without this history.

Crawford, 1984

50 male and 50 female Scottish undergraduates asked to describe typical situations in which aggression is shown by (a) males and (b) females.

Alcohol was commonly seen as part of the cause of aggression in males by 60% of men and 36% of women but less commonly viewed as a source of female aggression (20% of men and 4% of women.

Gustafson, 1984

Frustration (failure to receive a monetary reward) induced aggression measured with Buss' aggression machine in 8 male undergraduates given brandy in orange juice (0, 0.33, 0.66 or 1.0 ml ethanol/kg). Subjects thought they were using shock to help shape learning in an unseen confederate.

No effect of either alcohol or frustration on shock administered in this paradigm perhaps because the subjects took the "teacher" role very seriously.

Kreutzer et al., 1984

54 male undergraduates given beer (0, 0.5 or 1.0 ml/kg alcohol) and tested verbal reaction to hypothetical situation and gave variety of psychological tests.

Hostility was increased by alcohol and profanity was increased with the high dose.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Leonard, 1984

30 pairs of male undergraduates given 0.96 g/kg ethanol or control and tested in intoxicated, sober or mixed dyads on Taylor competition paradigm.

Intoxicated dyads administered the highest shock level to each other and escalated the level over trials.

Rohsenow and Bachorowski, 1984

Male and female undergraduates drank tonic ± ethanol (informed or misinformed about the contents of the drink) and then received a negative evaluation of their personality by a confederate and were given a chance to retaliate.

Men told they were drinking alcohol had decreased verbal aggression. In women the lower dose of alcohol (0.75 ml/kg) increased aggression but at 1.1 ml/kg same result as with men. Authors emphasize expectancy effect.

Pihl et al., 1984a

60 male ''social drinkers" given MMPI, at a subsequent session given ethanol in orange juice, beer or control drinks and aggression measured with a Buss artificial shock paradigm.

Both ethanol and beer resulted in BAC = 0.7. The beer subjects that gave the highest shocks were also highest on family problems; the aggressive ethanol subjects scored high on social maladjustment.

Pihl et al., 1984b

Frustration-induced aggression measured with the Buss aggression machine in 64 male paid social drinkers.

Aggression was higher in subjects that drank or believed they had consumed distilled spirits than in subjects that drank beer or believed that they had drank beer (BAC = 0.7 in both); no differences between alcohol and placebo.

Wolf, 1984

15 Alaskan Native men that had committed murder while drunk were given the same amount of alcohol in the lab as they had when the crime was committed.

As BAC passed 150 mg % a "blackout" was recreated; EEG slowed to 3-7 Hz and each verbalized about one past salient event.

Gustafson, 1985a

Frustration-induced aggression measured with Buss' aggression machine in 30 male military recruits given brandy in orange juice (0, .33, or .6 ml/kg ethanol). Subjects thought they were using shock as feedback for incorrect performance in a vigilance task.

The 0.6 ml/kg dose of alcohol (BAC = 0.05%) increased mean shock intensity given during the frustration trials.

Gustafson, 1985b

The role of expectancy was tested in 48 male undergraduates and soldiers. Subjects consumed 0.8 ml/kg ethanol in tonic or control and were either informed or misinformed about alcoholic content. Expectancy was manipulated with film and readings on the link between alcohol and violence.

Shock intensity and duration were greatest in subjects that received alcohol independent of expectancy factors. The author does not rule out that expectancy can have important effects.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Jeavons and Taylor, 1985

Taylor et al., 1976

Frustration-induced aggression measured with a modified version of Buss' aggression machine in male undergraduates given vodka (45 ml of 100 proof/40 lbs bw) in ginger ale with peppermint oil or ginger ale and peppermint oil with 1/20 of an ounce of vodka as control.

Intoxicated subjects initiated higher levels of attack than sober subjects in "threatening situation"; intoxicated subjects that competed against a non-threatening opponent did not show similar effects.

Murdoch and Pihl, 1985

44 men drank 1.25 ml/kg ethanol or placebo and were informed or misinformed about alcohol level. They were then observed while interacting with either an obnoxious confederate or a friendly confederate.

There was little aggression in the social interactions, but the alcohol group showed the most.

Bond and Lader, 1986

45 adult paid male and female subjects drank 0, 0.25 or 0.75 g/kg alcohol in tonic. They completed a variety of scales and then "competed" in a Taylor reaction time task.

The subjects which received the highest dose of alcohol were consistently more aggressive (higher settings) on the competition task, however, they rated themselves as less aggressive.

George and Marlatt, 1986

Male undergraduates drank tonic ± ethanol (informed or misinformed about the alcoholic content) and then were allowed ad lib exposure to violent, erotic, violent-erotic and neutral slides. Later assessed aggression and sexual arousal with a questionnaire.

Alcohol expectancy more than BAC increased viewing of violent-erotic slides and sexual arousal but there was no effect of alcohol or expectancy on verbal aggression.

Gustafson, 1986a

Threat (being told the stooge was likely to use a high shock on them)-induced aggression measured with Buss' "shock-machine" in 40 male undergraduates and soldiers given vodka in orange juice (0 or 0.80 ml ethanol/kg). Subjects could vary the level of shock they thought they were using as a signal of incorrect performance in a vigilance task.

Alcohol (BAC = 0.065%) increased shock intensity and duration even in the absence of any instigation (e.g. frustration). Threat inhibited the increase.

Gustafson, 1986b, c

48 sober male and 48 sober female undergraduates had the Taylor version of the Buss "shock machine" explained to them. Half of each sex were told the opponent was drunk. Aggression assessed by asking the subjects what shock intensity they thought the opponent would give them and what shock they would administer to the opponent.

Males expected "drunk" opponents to be more aggressive and retaliated by giving higher shocks to drunks. Females also expected drunk opponents to be more aggressive but unlike men did not choose a more aggressive response.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Pihl and Zacchia, 1986

48 men were asked to imagine positive and negative moods then drank 1.25 ml/kg ethanol, placebo or nothing and were tested in a modified Buss shock machine paradigm.

Alcohol but not placebo (expectancy) increased aggression. This was not altered by mood. Authors argue for a direct drug effect.

Gustafson, 1987

Aggression indirectly assessed in 28 male undergraduates. They drank 0.8 ml ethanol/kg in orange juice (or control) and then watched a violent movie. Afterwards they wrote TAT stories and filled out semantic differential scales.

The alcohol group had a less negative reaction to the violent movie.

Lindman et al., 1987

Compared 25 male undergraduates selected to be aggressively or non-aggressively predisposed. They were tested in groups of 4 (2 aggressive and 2 not), allowed alcohol ad lib and measured mood, social interactions, BAC and salivary testosterone.

The aggressive subjects had higher testosterone but both groups had similar BACs. The aggressive subjects were more dominant in social interactions and showed more verbal aggression, but alcohol did not change these behaviors.

Gustafson, 1988b

Aggression assessed in 40 male undergraduates. They drank beer, non-alcoholic beer, wine or non-alcoholic wine and later completed a personality inventory and had blood alcohol determined.

Neither beer or wine (0.8 ml/kg, BAC = 0.05%) altered responses on aggression scale.

Gustafson, 1988a

Frustration induced aggression measured with Buss' aggression machine in beer drinking male undergraduates.

Beer (0.8 ml alcohol/kg bw) did not alter aggression.

Kelly et al., 1988, 1989

4 and 6 male volunteers tested in the Cherek free-operant procedure (money reward for button presses with option to subtract money from another subject instead) given 0, .125, .25, .5 and .75 g/kg 95% ethanol.

0.75 g/kg ethanol increased aggressive responding (money subtraction), lower doses (0.25 and 0.5 g/kg) had less effect. The effect of the higher doses was greatest when the work load was increased (FR 500 schedules).

Murdoch et al., 1988

39 female bar patrons drinking only beer or only distilled liquor while in all female groups filled out questionnaire. Verbal aggression was assessed according to the subjects answers to four questions. No control group.

Verbal aggression in subjects with high estimated BAC (> 0.05) was not significantly different from subjects with low estimated BAC. Both groups became more aggressive with repeated questioning; the high BAC group became aggressive sooner, but the low BAC group was most aggressive on the last question.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Taylor and Sears, 1988

18 male undergraduates drank ± 2.5 ml/kg ethanol in ginger ale and then were tested in a reaction time competition similar to Taylor et al., 1976. Assessed the effect of a pressure from a confederate to administer high shock intensities.

Alcohol resulted in the subjects being more compliant to pressure from the experimenter's confederate and these subjects were willing to give potentially injurious shocks to the "opponent.".

Wormith et al., 1988

23 male patients from Sexual Behaviors Clinic in Ottawa (all had been charged or convicted of sex offences) listened to 2 min. audiotapes depicting rape, consensual sex and nonsexual assault encounters and had penile circumference measured in response to tapes. Tested ± alcohol (BAC = 0.08%).

Alcohol reduced sexual arousal in nonrapist sex offenders but rapists were equally or more aroused with intoxication.

Gustafson, 1990

20 male undergraduates consumed either wine (0.8 ml alcohol/kg bw) or non-alcoholic wine and provocation induced aggression was measured with Buss' aggression machine.

Wine (BAC = .0455) did not increase shock intensity or duration, unlike ethanol but similar to the lack of effect of beer (Gustafson, 1988a) suggesting different expectancies about effects.

Literature Reviews

Goodwin, 1973

Literature review of alcohol in suicide and homicide (58 refs).

Homicide is associated more with drinking than with alcoholism but alcoholism is a common diagnosis of suicides.

Tinklenberg, 1973

Literature review on alcohol-violence relationships (77 refs).

Concludes that although other factors are important, excessive alcohol increases the probability of violence.

Fitzpatrick, 1974

Review of link between drugs and crime (29 references, primarily other reviews).

States that the most abundant evidence for a link between a drug and crime is with alcohol.

Pemanen, 1976

Critical literature review on the link between alcohol abuse and violent crime (218 refs).

Although alcohol may predispose an individual to violence, there are many other non-pharmacological factors which bias the statistical data on this relationship.

John, 1978

Literature review, 19 references.

Frequent association between alcohol in the offender and commission of rape, but the causal relationships are unclear.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Coid, 1979

Literature review of "pathological intoxication" in which consumption of alcohol is followed by senseless violence (52 refs).

This review argues that no explanation of the etiology of "pathological intoxication" has any clear experimental support. The author questions the psychological and legal usefulness of the term.

Gayford, 1979

Literature review on battered wives (44 refs).

40% of cases of violence only occurred when husband was drunk and 10-20% of the women went through a phase of heavy drinking, but many other factors to be considered.

Evans, 1980, 1986

Critical literature reviews on the methodological and statistical problems in the literature associating alcohol and violent crime.

Cautions that the published correlations may be misleading and that causal interpretations are premature.

Graham, 1980

Review of the major theories on the role of alcohol in aggression (94 refs).

Groups theories on alcohol-aggression interaction into 4 types: direct-causation; indirect; indirect conditional upon motive; and predisposition/situational. The conclusion is that the theories all have merit, as well as problems, and that they are not mutually exclusive.

Seltzer, 1980

Literature review on psychosocial strain in Eskimos (39 refs), illustrated with 2 case histories.

The author concludes that alcohol abuse and violence are both coping strategies to alleviate the stress of acculturation.

Anderson, 1982

Literature review (87 refs) on the environmental influence on aggression

Suggests alcohol increases aggressive feelings and behavior. Some studies showed that subjects that were provoked but were unable to express anger, consumed more alcohol than non-angered counterparts.

Shapiro, 1982

Literature review (41 refs) and a few case studies.

Reviews the alcohol and violence relationship focussing on violence against the family and the role of the family therapist in treatment.

Öjesjö, 1983

Critical literature review (76 refs) on the associations between alcohol and other drugs with crime.

Concludes that alcohol has an ill-defined role in violent crime but that it is one of many factors.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Taylor, 1983

Literature review (29 refs) on experimental studies on the associations between alcohol and human physical aggression

Concludes that neither pharmacological effects nor cues in the drinking situation can independently explain enhanced aggressive behavior following alcohol consumption. Suggests an interactive role of instigative cues and neuropharmacological mechanisms

Grande et al., 1984

Schubert et al., 1988

Literature reviews and meta-analysis of studies.

Approximately 80% of the reviewed studies find a positive association between alcoholism and antisocial personality.

Kaufman Kantor and Straus, 1987

Literature review (93 refs) and telephone interviews with couples in 5159 households.

Linear relationship between drinking index and wife battering (19% of binge drinkers were batterers), but best correlation was between approval of violence and actual battering.

Brain, 1986

Edited volume on alcohol and aggression which contains 8 chapters on the topic from many points of view.

The most relevant chapters are cited separately in this table.

Coid, 1986 a

Critical literature review (61 refs) on the association between alcohol and sexual assault.

Cautions against considering alcohol as a single important factor in rape.

Coid, 1986 b

Literature review (62 refs) on many of the sociocultural factors in alcohol-related aggression and some of the different responses to alcohol in different societies.

Discusses the role of cultural attitudes toward alcohol and drinking on shaping the likelihood of aggressive behavior following alcohol consumption. However, this does not rule out direct pharmacological effects as well.

Roy et al., 1986

Literature review of research on biochemical correlates of alcohol-violence relationship (67 refs).

Stresses the correlation of impulsive violence with low CSF 5-HIAA and with reactive hypoglycemia.

Kofoed and MacMillan, 1986

Literature review on the association of alcoholism and antisocial personality (28 refs).

The authors suggest that the association between alcoholism and antisocial personality can be explained by sociobiology.

Elliot, 1987

Review of 27 references on assessment and treatment of aggressive disorders

Concludes that in lower doses, alcohol interfers with inhibitory mechanisms to "disinhibit" aggressive behaviors. Individuals with poor impulse control are particularly susceptible.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Cloninger, 1987

Literature review on possible biological bases of clinical subgroups of alcoholism (93 refs).

Reviews the evidence for specific subtype of alcoholism (Type 2) with violence during drinking, a genetic background of alcohol abuse and perhaps different neurochemical responses to alcohol.

Hore, 1988

Critical review (44 refs) of the relationship between crime and alcohol.

Concludes the nature of the link between alcohol and crime is complex.

Norton and Morgan, 1989a, b

Literature reviews and meta-analysis on role of alcohol in violent crime in Great Britain (41 & 45 refs).

Alcohol was seen to greatly increase the risk of being involved in acts of violence, but there are also many acts of violence with no alcohol involvement. Also makes suggestions on how to improve the gathering of alcohol-violence information.

Van Thiel et al., 1988

Literature review on alcohol effects on testosterone and sexual behavior, including sex offenses (72 refs).

Separates alcohol's deleterious effects on testosterone and sexual functioning from its proaggressive effects.

Gorney, 1989

Review (54 refs) of the co-occurrence of domestic violence and abuse of alcohol and other drugs.

Concludes that effective therapy must reat both the violence and the substance abuse. Nature of the link between alcohol and crime is complex.

Bushman and Cooper, 1990

Literature review (81 refs) and meta-analysis of 30 experimental studies on alcohol induced aggression.

The meta-analysis indicates that alcohol can cause an increase in aggressive behavior in the laboratory, but that this is not a purely pharmacological effect.

Fagan, 1990a

Review (271 refs) of theories and research on the influence of alcohol and other drugs on aggression.

Makes the point that intoxication does not consistently lead to aggression and that other mediating internal and external factors are important. Concludes with a model of how these various factors may interact.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 4A Effects of Opiate Administration on Aggression in Animals

References

Methods and Procedures

Results and Conclusions

Isolation-induced Aggression

Janssen et al., 1960

Cook and Wiedley, 1960

DaVanzo et al., 1966

Poshivalov, 1974, 1982

Male mice confronted a group-housed male intruder.

Morphine, methadone, codeine and fentanyl decreased attack behavior, primarily at doses that also suppressed motor behavior.

Pain-induced Aggression and Defense

Irwin et al., 1971

Footshock in groups of female mice

Methadone (3, 6 ml/kg p.o.) decreased the duration of defensive and aggressive behavior at doses that also decreased motor activity.

Lal et al., 1975a

Footshock in pairs of male rats

Morphine (5.0, 10.0 mg/kg) decreased the frequency of fighting

Emley and Hutchinson, 1983

Tail shock-induced target biting in individually-housed male and female squirrel monkeys

A low dose of morphine (1.25 mg/kg s.c.) increased target biting, while higher doses (2.5-20 mg/kg s.c.) decreased target biting.

Brain lesion-induced aggression

Wikler, 1944

Sham rage in individually-housed cats following removal of cortical and subcortical tissue

Morphine (2-5 mg/kg i.v.) decreased the motor components of sham rage, at doses that decreased the righting reflex.

Defensive Aggression induced by brain stimulation

Kido et al., 1967

Sham rage induced by electrical stimulation of the posterior hypothalamus in cats

Morphine (5 mg/kg i.v.) increased the threshold to induce sham rage.

Drug-induced aggression

Yen et al., 1970

DOPA-induced target biting in male mice

Morphine decreased target biting (ED50=5.2 mg/kg i.p.).

Lal et al., 1975a

Apomorphine and d-amphetamine-induced fighting in groups of mice. Sex unspecified

Morphine (20.0 mg/kg) decreased the frequency of attack biting.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Krstic et al., 1982

Carbachol-induced fighting in groups of 4-6 male and female cats

Morphine (.2-1.0 mg i.c.v.) decreased the duration of aggressive responses at doses that altered locomotor activity. Methadone (.2-1.0 mg i.c.v.) did not affect aggression levels.

Aggression by Resident toward Intruder

Walaszek and Abood, 1956

Braud and Weibel, 1969

Male Siamese fighting fish confronting a male conspecific

Morphine (40 µg/ml) slightly increased attack and threat behavior.

Avis and Peeke, 1975

Male convict cichlids confronting a male conspecific

Morphine (5 mg/l, 10 mg/l) decreased aggressive gill display frequency.

Sieber et al., 1982

Benton et al., 1985

Male and female mice confronting a male conspecific

Morphine (1.0, 2.5, 20 mg/kg) did not significantly alter aggressive behavior.

Female Aggression

Panksepp et al., 1980

Lactating mice confronting a male conspecific

Morphine (1.0 mg/kg) decreased aggressive behavior.

Haney and Miczek, 1989

Lactating mice confronting a female conspecific

Morphine (6.0, 10.0 mg/kg i.p.) decreased aggressive behavior at doses that did not alter locomotor activity.

Plonsky and Freeman, 1982

Pairs of female rats were administered methadone daily and tested in a neutral arena for 6 consecutive days

Acute methadone (2.5, 4.0 mg/kg s.c.) decreased the duration of social behaviors, including aggressive grooming at doses that also suppressed locomotor activity. With chronic methadone, social behavior but not locomotion continued to be suppressed.

Kinsley and Bridges, 1986

Lactating rats confronting a male conspecific

Morphine (5 mg/kg s.c.) decreased the proportion of rats that attacked.

Dominance-related Aggression

Crowley et al., 1975

Established colony of 1 male and 4 female pigtail macaques: Each simultaneously administered morphine

Neither acute (.05-.20 mg/kg i.m.) or chronic (15-30 mg/kg p.o.) morphine significantly altered dominance or submission related aggressive behaviors.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Killing

Janssen et al., 1962

Muricide by isolated male rats

Morphine (10-80 mg/kg s.c.) decreased muricide at doses that also suppressed motor behavior.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 4B Effects of Withdrawal from Chronic Opiate Administration on Aggression in Animals

References

Methods and Procedures

Results and Conclusions

Kreiskott, 1966

Observation of singly-housed rhesus monkeys

Withdrawal from chronic morphine was associated with alternating threat and defensive behavior toward a human observer.

Pain-induced aggression

Crabtree and Moyer, 1972

Puri and Lal, 1974

Lal, 1975a

Stolerman et al., 1975

Footshock in pairs of male and female rats. Morphine was administered in incremental doses 2-3 times daily (i.p.) for a minimum of 6 days. Terminal doses ranged from 80-405 mg/kg.

Withdrawal from chronic morphine enhanced sensitivity to shock-induced fighting; d-amphetamine (2 mg/kg) potentiated aggressive responding in male-male pairings and defensive responding in male-female pairings; female-female pairings were not associated with high levels of aggressive or defensive behavior.

Aggression by a resident toward an intruder

Kantak and Miczek, 1986, 1988

Male mice confronting a group-housed male conspecific. Morphine pellets (75 mg s.c.) were implanted for 4-5 days. Behavioral testing occurred 48 hrs following pellet removal

Aggression in morphine-dependent residents and intruders is increased following withdrawal. Naloxone (1 mg/kg) did not increase agonistic behavior in morphine dependent mice. Sensitivity to the aggression-enhancing effect of dopaminergic agonists increases during morphine withdrawal, while sensitivity to the aggression-inhibiting effects of dopaminergic antagonists declines.

Female Aggression

Avis and Peeke, 1979

Female hamsters housed in groups of 4. Morphine pellets (75 or 150 mg s.c.) were implanted for 1, 2 or 3 days

Naloxone administration (.5-4.0 mg/kg) following chronic morphine increased aggressive and defensive behaviors; this effect was potentiated by d-amphetamine (2 mg/kg).

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Davis and Khalsa, 1971

Female rats housed in groups of 4 or 6. Morphine was administered in incremental doses (15-400 mg/kg/day i.p.) for 15 days. Behavior was observed over a 6 day period following the last morphine administration

Withdrawal from chronic morphine was not associated with heightened aggressive behavior.

Dominance-related Aggression

Thor et al., 1970

Thor, 1971

Singly-housed male rats were administered morphine in incremental doses (10-600 mg/kg/day) for 5 days. Following the last morphine injection, treated subjects were housed in groups of 6. Vocalizations were continuously recorded and used as indices of aggression

Withdrawal from chronic morphine was associated with increased vocalizations; this effect was potentiated by d-amphetamine (200 mg/ml p.o.). The number of vocalizations was positively associated with the amount of morphine received during chronic administration.

Avis and Peeke, 1979

Hamsters housed in groups of 4. Morphine pellets (75 or 150 mg s.c.) were implanted for 1, 2 or 3 days

Naloxone administration (.5-4.0 mg/kg) following chronic morphine increased aggressive and defensive behaviors; this effect was potentiated by d-amphetamine (2 mg/kg).

Boshka et al., 1966;

Thor and Teel, 1968

Borgen et al., 1970

Davis and Khalsa, 1971

Lal and Puri, 1971

Lal et al., 1971

Puri and Lal, 1973, 1974

Lal, 1975a

Gianutsos et al., 1975

Gianutsos et al., 1976

Rats housed in groups of 4-6. Morphine was administered in incremental doses (10-405 mg/kg/day i.p.) for 9-15 days. Administration of additional psychoactive drugs occurred 4-72 hours after the last morphine injection. Behavior was observed over a 6 day period

Withdrawal from chronic morphine increases the frequency of aggressive and defensive attack; this effect is potentiated by catecholaminergic agonists. Naloxone (4, 8 mg/kg did not precipitate aggression in morphine dependent rats, but nalorphine (2 mg/kg) did.

Carlini and Gonzales, 1972

Pair-housed rats. Morphine was administered in incremental doses (12-768 mg/kg/day i.p.) for 16 days. Behavioral observation occurred 24, 48 and 72 hours following the last morphine injection

THC (5 mg/kg) or d-amphetamine (2 mg/kg) 48 or 72 hours into withdrawal increased the duration of aggressive behavior.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Gellert and Sparber, 1979

Food-deprived rats competing for food reinforcement. Morphine was administered in incremental doses (25-100 mg/kg i.p.) 2 times/day for 9 days

Withdrawal from chronic morphine disrupted dominance-submissive hierarchies and increased the duration of aggressive behavior.

Crowley et al., 1975

Dominance-related aggression in group-housed male pigtail macaques. Methadone (15-30 mg/kg p.o.) was administered for 10 weeks

Frequency of aggressive acts did not change during withdrawal from chronic methadone.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 5 Effects of Opiates on Aggression in Humans

References

Methods and Procedures

Results and Conclusions

Experimental Studies of Aggression

Woody et al., 1983

Male opiate addicts were administered: Hopkins Symptom Checklist, Beck Depression Inventory and Profile of Mood States both during methadone treatment and following detoxification. Hospital staff served as controls

Measures of anger in hostile and non-hostile opiate addicts were not significantly different from controls during chronic methodone or following withdrawal.

Mirin and Meyer, 1979

Heroin was self-administered (i.v.) in a research ward setting, with and without the concurrent administration of opiate antagonists. Male opiate addicts were administered the Current and Past Psychopathology Scales, Brief Psychiatric Rating Scale and were evaluated by staff for levels of physical and verbal aggression prior to and during heroin self-administration, as well as during heroin-blockade

Acute heroin administration is associated with euphoria and tension release. Continuous self-administration increases feelings of suspicion, belligerence and hostility. Pharmacological blockade of heroin increased anger in double-blind but not in non-blind conditions.

Crime

Dole et al., 1969

1500 incarcerated heroin addicts were given the opportunity to volunteer for methadone treatment 10 days before release

Prisoners who sought methadone treatment were less likely to be re-incarcerated than prisoners that did not seek treatment.

Greene et al., 1973

Criminal records, urine analysis and interview data were measured in 2,133 arrestees

Arrestees with heroin or methadone present in the urine committed a higher proportion of non-violent: violent crime, compared to arrestees with negative urine results.

Gossop and Roy, 1977

25 male narcotic addicts and 15 non-narcotic drug users undergoing drug rehabilitation were interviewed and administered the Hostility and Direction of Hostility Questionnaire

Narcotic addicts were more likely to have been convicted of violent crime than non-narcotic addicts.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

McGlothin, 1979

Reviewed four studies comparing arrest records in narcotic addicts and non-drug users

Narcotic addicts had a higher proportion of property crime arrests and a lower proportion of violent crime arrests than non-addicted drug controls.

Simonds and Kashani, 1979b

Interview of incarcerated male juveniles

Delinquents reporting a history of heroin use were more likely to commit crimes against people (robbery, murder, rape) than crimes against property alone (vandalism, burglary, auto theft).

Tinklenberg et al., 1981

Compilation of police, laboratory, social worker and interview data compared in 293 incarcerated male juveniles

Relative incidence of narcotic abuse was comparable in juveniles classified as physically assaultive, sexually assaultive and non-assaultive. Heroin intoxication during the criminal act was infrequent.

Ball et al., 1983

243 male narcotic addicts randomly selected from a population of 4,069 addicts with police records were interviewed; validity of self-reports was compared to official records

12.4% of total arrests involved violent crimes.

Heller and Ehrlich, 1984

1,525 defendants undergoing court-ordered psychiatric evaluations were classified as non-violent, violent (1 violent conviction) or violent recidivists (more than 1 violent conviction); 245 demographic, socioeconomic and clinical variables were compared in the 3 groups

Non-violent offenders has a higher incidence of heroin abuse than violent offenders.

Nurco et al., 1986

Shaffer et al., 1987

Interview of 100 black, 100 white and 50 hispanic male heroin addicts undergoing outpatient methadone treatment

Self-report data indicate both violent and non-violent criminal activity increase during periods of active addiction. The rate of violent crime in heroin addicts is correlated with preaddiction rates of criminal activity and precocious drug experimentation.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Anglin and Hser, 1987

Anglin and Speckart, 1988

Examined criminal activity before, during and after narcotic addiction and methadone maintenance in 671 males and 238 women attending methadone treatment centers

Property crime and drug dealing are significantly higher during periods of elevated narcotic use (pre-and post-methadone treatment). Rate of violent crime was low and did not vary as a function of narcotic use. Deviant behavior pre-dated narcotics initiation in the majority of subjects.

Personality Assessments and Aggression

Sheppard et al., 1975

51 male, 6 female active heroin addicts seeking out-patient methadone treatment were interviewed and administered the Edwards Personal Preference Schedule and the Standard Progressive Matrices

Heroin addicts did not exceed a priori criteria of high aggressivity.

Berzins et al., 1974

1500 MMPI scores from male and female opiate addicts seeking drug rehabilitation

Multivariate clustering delineated 2 personality profiles: Type 1 (33%) had elevated levels of personal and social maladjustment. Type 2 (7%) scored above-average in personal and social competence. 60% of the addicts remained unclustered. Profile types did not differ as a function of sex or treatment motivation.

Khantzian, 1974

Wurmser, 1974

Psychoanalytic interpretation of opiate addiction based on personal observation of addicts undergoing methadone treatment

Theorize individuals with aggressive impulses become addicted to opiates to relieve dysphoria associated with rage and aggression. Methadone treatment decreases reported feelings of rage in heroin addicts undergoing psychotherapy.

Kurtines et al., 1975

59 male heroin addicts undergoing drug rehabilitation were administered the California Psychological Inventory. Scores were compared to male marijuana users, psychiatric patients, incarcerated delinquents and police officers

Heroin addicts scored significantly lower on levels of responsibility and socialization. Measures of interpersonal effectiveness and neurosis were comparable to other males, suggesting addicts have sociopathic as opposed to psychiatric difficulties.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Hewett and Martin, 1980

Incarcerated narcotic addicts, reformed alcoholics and controls with no drug or alcohol abuse history were administered the Personal History Questionnaire

Narcotic addict prisoners were more sociopathic than alcoholics and controls. The severity of adult sociopathy was inversely proportional to the age drug use was initiated. Both alcoholics and narcotic abusers were sociopathic pre-dating substance abuse.

Sutker and Archer, 1984

Reviewed literature on opiate abuse and psychopathology

MMPI indicators of sociopathy are consistently elevated in addicts across varied assessment conditions. Sociopathy appears to pre-date addiction.

Health Statistics

Monforte and Spitz, 1975

207 homicide victims were analyzed for the presence of narcotic and non-narcotic drugs.

11.3% of victims had morphine in their system at the time of death. 30.9% had needle tracks.

Concool et al., 1979

Reviewed deaths in 1,156 persons who had enrolled in a methadone program

37.8% of the 45 deaths occurring either during or after methadone treatment were due to violence.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 6 Effects of Amphetamines on Aggression in Animals

References

Methods and Procedures

Results and Conclusions

Isolation-induced aggression

Melander, 1960

Male mice, individually-housed, tested in pairs for latency to attack for up to 120 minutes after drug administration

10 mg/kg d-amphetamine increased activity and caused disorientation thereby decreasing aggressiveness.

DaVanzo et al., 1966

Male mice, individually-housed, tested in pairs

ED50 for inhibition of aggression was = 3 mg/kg i.p.

Valzelli et al., 1967

Male mice, individually-housed, tested in groups of three; rating scale

5 mg/kg amphetamine did not inhibit aggressive behavior.

Charpentier, 1969

Male mice, individually-housed, tested in pairs; rating scale

2 mg/kg i.p. amphetamine decreased latency to attack and increased fighting duration.

Le Douarec and Broussy, 1969

Male and female mice, individually-housed, tested in pairs in resident/intruder paradigm; rating scale

d-Amphetamine did not affect aggressiveness at low doses (0.5 and 2 mg/kg i.p.), inhibited aggressiveness at higher doses (4 mg/kg i.p.).

Welch and Welch, 1969

Male mice, individually-housed, tested in pairs in a clean cage; measured frequency of attack

Fighting was enhanced by a low amphetamine dose (2.0 mg/kg) and suppressed by a high dose (6.0 mg/kg).

Scott et al., 1971

Male mice, individually-housed, tested in pairs

10 mg/kg i.p. dl-amphetamine decreased fighting in C57BL/6 but not BALB/c, possibly due to hyperthermia

Hodge and Butcher, 1975

Male mice, individually-housed, tested in pairs; measured latency, frequency and duration of fighting

d-Amphetamine increased frequency of fighting at low doses (1.0-4.0 mg/kg i.p.) and decreased fighting at high (8.0 mg/kg) doses.

Krsiak, 1979

Male mice (n=404), individually-housed, confronted a group-housed male intruder, measured frequencies of motor, social, and aggressive acts

0.25-1.0 mg/kg amphetamine decreased threats and attacks without affecting locomotor behavior.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Poshivalov, 1981

Male mice, individually-housed, tested with a group-housed male mouse

0.5-3 mg/kg i.p. amphetamine decreased aggressive behavior in both normal mice and mice pre-treated with the dopamine-hydroxylase inhibitor FD-008 (100 mg/kg).

Poli and Palermo-Neto, 1986

Male mice, individually-housed, tested in groups of 15-20; measured latency, frequency, and duration of attack behavior

6 mg/kg i.p. d-amphetamine decreased attack frequency and duration, increased latency to attack; haloperidol (0.5, 1 mg/kg) further decreased aggressiveness; stereotypy may mask amphetamine effects on aggressiveness.

Aggression induced by crowded housing

Bovet-Nitti and Messeri, 1975

Measured population growth of densely housed mice (26 populations of 13-15 mice each); chronic administration

Amphetamine (0.25 g/kg in food, approximately 40 mg/kg/day) resulted in violent fighting (male-male and cannibalism of newborns) and a decrease in population.

Pain-induced aggression and defense

Stille et al., 1963

Kostowski, 1966

Hoffmeister and Wuttke, 1969

Irwin et al., 1971

Male mice, tested in pairs while exposed to electric foot shock

Amphetamine (0.1 mg/kg i.p.) increased aggressive behavior.; Methamphetamine (0.3, 0.5 mg/kg p.o.) increased defensive-aggressive behavior.

Emley and Hutchinson, 1972, 1983

Hutchinson et al., 1977

Male and female squirrel monkeys, individually-housed, electric tail shock, bit inanimate object

Amphetamine increased biting responses at doses of 0.125-1.0 mg/kg s.c. and decreased biting at 2.0 mg/kg.

Crowley, 1972

Male rats, individually-housed, tested in pairs while exposed to electric foot shock

Methamphetamine increased fighting time at low (0.25-1.0 mg/kg i.p.) doses and decreased fighting at higher (4.0 mg/kg) doses.

Powell et al., 1973

Male and female rats, pair-housed, exposed to electric shock through grid floor or subdermally

d-Amphetamine (0.2-5 mg/kg s.c.) had little or no effect on footshock-elicited aggression; when shock was administered subdermally, 1.0 mg/kg increased threat and attack and 3.0 mg/kg decreased aggression.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Crowley et al., 1974

Male rats, individually-housed, tested in pairs while exposed to electric foot shock; chronic administration

d-Methamphetamine (5 mg/kg-20 mg/kg/day in drinking water for 35 days) suppressed fighting; rats withdrawn from d-methamphetamine 24 hours prior to tests fought more than methamphetamine-treated but less than controls.

Sheard and Davis, 1976

Male rats, tested in pairs while exposed to electric foot shock

p-Chloroamphetamine (1.5, 2.5, and 5 mg/kg) initially depressed, and later enhanced aggression; the initial inhibition of aggression may be due to changes in pain threshold; 5-HT depletion is associated with increased aggression.

DeWeese, 1977

Male squirrel monkeys, individually-housed, aggression measured as bites to an inanimate object, intermittent shock and food reinforcement schedule

0.01-1 mg/kg d-amphetamine increased lever responding at low doses and decreased responding at higher doses while rate of biting only decreased.

Defensive aggression induced by brain stimulation

Panksepp, 1971

Male rats, electrical stimulation of hypothalamus, measured latency to attack mice

2 mg/kg methamphetamine increased affective attack and slightly decreased quiet-biting attack.

Sheard, 1967

Male and female cats, electrical stimulation of lateral hypothalamus and reticular formation, measured latency to attack rats

Amphetamine (5 and 10 mg/5 ml water, i.p.) facilitated attack behavior.

Baxter, 1968

Cats, electrical stimulation of hypothalamus, measured hissing behavior

1-4 mg/kg i.p. dl-amphetamine did not significantly inhibit hissing.

Marini et al., 1979

Male and female cats, electrical stimulation of medial and lateral hypothalamus, measured latency to attack an anethesized rat

Low doses of amphetamine (0.125-0.5 mg/kg i.p.) facilitated attack, higher doses (1.0-1.5 mg/kg) inhibited attack.

Maeda et al., 1985

Cats, electrical stimulation of left medial hypothalamic area, measured directed attack and hissing

0.5-3 mg/kg i.p. methamphetamine dose-dependently lowered the thresholds for defensive attack responses, these effects were almost identical to those of apomorphine (1 mg/kg i.p.) suggesting that this effect is dopamine-mediated.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Drug-induced aggression

Chance, 1946;

Randrup and Munkvad, 1969;

Hasselager et al., 1972;

Rolinski, 1973, 1977

Male mice, group-housed

High doses of amphetamine (>10 mg/kg) increased biting and defensive-aggressive postures; these effects were antagonized with neuroleptic drug treatment, implicating a dopaminergic mechanism.

Consolo et al., 1965a,b

Male mice, housed in groups or individually, tested in groups

Both individually-and group-housed aggressive mice were more sensitive to the toxic effects of amphetamine than normal controls.

Shintomi, 1975

Male mice, densely-confined; measured the effects of various drugs on methamphetamine-induced aggression; rating scale

5 mg/kg s.c. methamphetamine resulted in hyperactivity, fighting behavior, and increased vocalizations; fighting behavior was inhibited with dopamine antagonist or benzodiazepine administration.

Kantak and Miczek, 1988;

Tidey and Miczek, 1992

Male mice confronted a group-housed male intruder

d-Amphetamine (0.1-2.5 mg/kg i.p.) increased aggressive behavior in morphine-withdrawn mice and decreased aggressive behavior in normal mice.

Morphine-withdrawn mice exhibited higher levels of aggressive behavior after d-amphetamine (0.1-10 mg/kg) administration than normal controls.

Schrold and Squires, 1971

5 day-old chicks, pre-treated with p-Cl-phenylalanine (150 mg/kg i.p. 5 times per day for 3 days), tested in groups of 4

p-Cl-phenylalanine lowered brain 5-HT and 5-HIAA concentrations to approximately 30%; in these animals, d-amphetamine (6, 10 mg/kg i.p.) induced strong aggressive pecking to other chicks.

Hine et al., 1975

218 pairs of male and female chicks, group-housed observed in pairs (both treated); measured frequency of pecks for 4 hours

d-Amphetamine (3, 6 mg/kg i.p.) increased pecking, higher doses (9, 12 mg/kg) decreased pecking; imipramine administration did not affect amphetamine-induced pecking; haloperidol (10 mg/kg) selectively blocked amphetamine-induced pecking.

Fog et al., 1970

Individually-housed male rats with striatal lesions; tested in pairs

Striatal lesions suppress amphetamine (10 mg/kg)-induced stereotypy without affecting ''rage" reactions.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Lal et al., 1971

Puri and Lal, 1973

Male rats, group-housed during morphine withdrawal, measured attack biting and defensive rearing

d-Amphetamine (2, 4, and 8 mg/kg i.p.) increased attack bites, defensive rearing, and vocalizations 72 hours into morphine withdrawal; this is attributed to stimulation of "sensitized" dopamine receptors.

Thor, 1971

Male rats, group-housed during morphine withdrawal, measured attack frequency and vocalizations

Increased ingestion of d-amphetamine (approximately 5 and 20 mg/kg in drinking water) was correlated with increased intensity of fighting and vocalizations.

Eison et al., 1978

Ellison et al., 1978

Male rats, housed in social colonies for 75 days; implanted with amphetamine pellets or a refillable subcutaneous amphetamine delivery system; tested in groups; chronic administration

After 4-5 days of continuous amphetamine administration, rats which received amphetamine exhibited more aggressive behaviors than controls.

Aggression induced by REM sleep deprivation

Ferguson and Dement, 1969

125 male and female rats, housed on water-surrounded pedestals; tested in groups, measured duration of aggressive bouts

0.25-23 mg/kg i.p. d-amphetamine caused substantial stereotyped aggressive behavior in REM-deprived rats; neither REM deprivation nor amphetamine administration alone produced these effects.

Aggression by resident toward intruder

Miczek, 1977a,b, 1979b

Miczek and O'Donnell, 1978

O'Donnell and Miczek, 1980

Male mice and rats confronted a group-housed male intruder; resident drug treated

d-Amphetamine increased aggression at low doses in rats only and decreased aggression at higher doses in both mice and rats

Winslow and Miczek, 1983

Male mice confronted a group-housed male intruder in 10 consecutive tests; resident drug treated

d-Amphetamine (0.1-5.0 mg/kg) increased low levels of aggressive behavior induced by repeated confrontations.

Kantak and Miczek, 1988

Tidey and Miczek, 1992

Male mice confronted a group-housed male intruder; resident drug treated

d-Amphetamine (0.1-2.5 mg/kg i.p.) increased aggressive behavior in morphine-withdrawn mice and decreased aggressive behavior in normal mice.

Morphine-withdrawn mice exhibited higher levels of aggressive behavior after d-amphetamine (0.1-10 mg/kg) administration than normal controls.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Haney et al., 1990

Male mice, housed individually or pair-housed (with or without fighting experience) confronted group-housed intruders; resident drug treated

0.1, 1.0 mg/kg d-amphetamine (i.p.) enhanced aggression and 10 mg/kg d-amphetamine suppressed aggression in isolated and inexperienced pair-housed mice. All doses suppressed aggression in experienced pair-housed mice.

Silverman, 1966

Male rats, individually housed; resident drug treated

1-5 mg/kg dl-amphetamine (i.p.) reduced aggressive behavior.

Female and juvenile aggression

Karczmar and Scudder, 1967

Richardson et al., 1972

6 genera and several strains of mice living in a large colony were evaluated (checklist) for motor, social, and maternal aggressive behavior

Methamphetamine (7 mg/kg) decreased aggression in all strains; methamphetamine seems to increase stereotypic and motor activity while decreasing goal-directed behavior.

Beatty et al., 1984

Male juvenile rats, individually-housed, tested in pairs, both treated, repeated testing

d-Amphetamine (0.05, 0.1 mg/kg i.p.) decreased play-fighting; this was not antagonized by haloperidol, clonidine, chlorpromazine, phenoxybenzamine or a-methyltyrosine.

Dominance-related aggression

Keller and Poster, 1970

Male fish, individually-housed, paired with a like-treated male

d-Amphetamine (1.0, 2.0 mg % tank water) and d,l-amphetamine (1.0 mg % tank water) decreased both mobility and aggressive behavior.

Munro, 1986

Fish, individually-housed, measured aggressive activity toward mirrors and models of conspecifics

Immersion in d-amphetamine (20-200 mg/10 l tank water) did not affect aggressive responses; intracranial injection of d-amphetamine (10 and 20 µg/fish) significantly decreased aggressive displays and frequency of bites.

Gambill et al., 1976

Male rats, housed and tested in a social colony; rated for the presence or absence of aggressive and other behaviors; chronic administration

High doses of d-amphetamine inhibited the initiation of aggression in dominant rats; d-amphetamine induced hypervigilance and defensive behavior in subordinate rats.

Hoffmeister and Wuttke, 1969

Male cats confronted male conspecifics; rating scale

Methamphetamine (1-4 mg/kg p.o.) enhanced defensive-aggressive behavior but decreased attack behavior.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Miller et al., 1973

Male rhesus monkeys, conditioned to avoid electric shock by detecting and interpreting the facial signals of a paired monkey (cooperative conditioning); their dominance and social behaviors were later tested

Amphetamine (0.25 mg/kg i.m.) slightly facilitated cooperative conditioning and social behaviors while reducing aggression.

Crowley et al., 1974

Male macaque monkeys, living in a social group

d-Methamphetamine (.0625-.25 mg/kg i.m.) decreased dominance behaviors such as pursuits, bites, and attacks; administration of 2 mg/kg to one monkey engendered aggressive behavior toward that subject from others in the group.

Garver et al., 1975

Male stumptail macaques, living in social colonies, chronic administration

d-Amphetamine (2 mg/kg adminisitered via nasogastric tubing every 12 hours for 3-20 days) initially increased and later reduced the initiation of social activity and threats; haloperidol (0.57 mg/kg) "normalized" social behavior.

Haber et al., 1977, 1981

Rhesus monkeys, housed in social groups; chronic administration

Amphetamine (0.1-1.0 mg/kg i.m. for 3 weeks) significantly increased aggressive behavior by dominant monkeys and submissive behavior by subordinate monkeys.

Miczek et al., 1981

Miczek and Yoshimura, 1982

Male squirrel monkeys, housed in social groups

d-Amphetamine (0.5, 1 mg/kg p.o. three times over 24 hours) decreased social and aggressive behaviors and increased agonistic behavior by non-drugged animals to the amphetamine-treated monkey.

Schlemmer and Davis, 1981

Male and female stumptail macaques, housed in social groups; chronic administration

d-Amphetamine (3.2 mg/kg/day for 12 days) increased submissive gesturing in dominant-ranking females without increasing aggressive behaviors directed toward that monkey; the effects of amphetamine were very similar to those of apomorphine (1 mg/kg/day for 12 days).

Miczek and Gold, 1983

Male squirrel monkeys, housed in social groups, measured social behavior to others in group

d-Amphetamine (0.1, 0.3 mg/kg) decreased aggressive behavior initiated by dominant monkeys, higher doses (0.6, 1.0 mg/kg) caused dominant monkeys to receive aggression from others.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Winslow and Miczek, 1988

Male and female squirrel monkeys, housed in social groups; Male mice, tested with group-housed male intruders

d-Amphetamine (0.1-0.6 mg/kg i.m. in monkeys, 10 mg/kg i.p. in mice) decreased aggressive behavior; naltrexone enhanced the suppression of aggressive behavior by d-amphetamine.

Martin et al., 1990

2 adult male stumptail macaques, housed in social groups of males and females; social rank was disrupted to study within-subjects effects

d-Amphetamine (0.01-0.3 mg/kg, i.m.) increased aggressive behavior overall; a rise in dominance resulted in decreased sensitivity to the effects of amphetamine, and a decrease in dominance position resulted in increased sensitivity to amphetamine's effects.

Killing

McCarty and Whitesides, 1976

Male and female mice, pair-housed, tested for predatory behavior toward crickets

Both d-and l-amphetamine (1, 10 mg/kg i.p.) dose-dependently decreased predatory behavior.

Karli, 1958;

Horovitz et al., 1965, 1966

Salama and Goldberg, 1970

Malick, 1975, 1976

Gay et al., 1975

Barr et al., 1976

Male and female rats, individually housed, selected for muricidal behavior, acute administration

Amphetamine (0.125-15 mg/kg) dose-dependently inhibited muricidal behavior.

Panksepp, 1971

Male rats, electrical stimulation of hypothalamus, measured latency to attack mice

2 mg/kg methamphetamine increased affective attack and slightly decreased quiet-biting attack.

Fujiwara et al., 1980

Measured inhibition of THC-induced muricide in 8 singly-housed male rats

Methamphetamine (1-2 mg/kg) dose-dependently suppressed muricidal behavior while increasing motor activity.

Posner et al., 1976

Male rats, individually-housed, selected for muricidal behavior; one group food-deprived

d-Amphetamine (2 mg/kg s.c.) inhibited muricide in satiated rats but not in food-deprived rats.

Barr et al., 1977

36 male rats, individually-housed, selected for muricidal behavior; chronic administration

Inhibition of muricidal behavior was decreased by d-amphetamine (2.4 mg/kg twice daily for 8 days) but not by l-amphetamine (3.1 mg/kg twice daily for 8 days).

Russell et al., 1983

200 male rats, individually-housed, food-deprived

d-Amphetamine (0.5-3 mg/kg) dose-dependently inhibited muricide.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Yoshimura and Miczek, 1983

113 male rats, individually-housed, selected for muricidal behavior, feeding restricted and implanted with cannulae to 6 brain sites

d-Amphetamine (10-30 µg) injected to the lateral ventricles, lateral hypothalamus or central amygdala abolished muricidal behavior while injections to the substantia nigra, ventral caudate or nucleus accumbens were ineffective.

Sheard, 1967

Male and female cats, electrical stimulation of lateral hypothalamus and reticular formation, measured latency to attack rats

Amphetamine (5 and 10 mg/5 ml water, i.p.) facilitated attack behavior.

Marini et al., 1979

Male and female cats, electrical stimulation of medial and lateral hypothalamus, measured latency to attack an anethesized rat

Low doses of amphetamine (0.125-0.5 mg/kg i.p.) facilitated attack, higher doses (1.0-1.5 mg/kg) inhibited attack.

Zagrodzka and Jurkowski, 1988

Male cats, measured attack behavior toward mice

Amphetamine (1.5 mg/kg, i.m.) suppressed mouse-killing behavior and offensive behavior toward other cats.

Literature Reviews

Munkvad, 1975

Review of 34 articles spanning 1959-1975 concerning drug-elicited aggression

d-Amphetamine (15 mg/kg) induces aggressive behavior in mice tested in groups of 4; in monkeys, amphetamine administration reduces social activities; in humans, amphetamines can produce aggressive behavior and stereotypy; these effects of amphetamine administration can be antagonized by DA receptor antagonists.

Gianutsos and Lal, 1976

Review of 112 articles spanning 1948-1976 concerning drug-elicited aggression

d-or l-amphetamine alone, combined with l-DOPA, and during morphine-withdrawal increases defensive rearing, biting, and vocalizations; evidence is strong for the involvement of DA in aggression.

Kulkarni and Plotnikoff, 1978

Review of 101 articles spanning 1965-1975 concerning the effects of stimulants on muricidal, isolation-induced, shock-induced, lesion-induced, stimulant-induced and spontaneous aggression

While small doses of amphetamine may enhance aggression in certain models, the effects of amphetamines on aggressive behavior are predominantly inhibitory; amphetamine can potentiate aggression elicited by other drugs.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Looney and Cohen, 1982

Comparative review of aggression induced by the omission of reward in pigeons, rats, monkeys, and humans

While most drugs reduce aggression at doses which do not affect operant responding, d-amphetamine has been found to both increase and decrease aggression.

Miczek, 1987

Miczek and Winslow, 1987

Miczek and Tidey, 1989

Review of over 1500 articles concerning the psychopharmacology of aggression in humans and other animals

At intermediate and higher doses, amphetamine decreases isolation-and extinction-induced aggression while increasing motor activity; single low doses may increase isolation-induced aggression; amphetamine more consistently increases pain-induced aggression; the primary effect of amphetamines is to disorganize patterns of social and aggressive behavior.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 7 Effects of Amphetamines on Aggression in humans

References

Methods and Procedures

Results and Conclusions

Criminal Violence

Eisenberg et al., 1963

Ratings of 15 male institutionalized juvenile delinquents by peers, teachers, and supervisors

Symptoms of disturbed behavior improved with all doses of amphetamine (5-40 mg/day).

Cockett and Marks, 1969

Psychological evaluation of 82 juvenile delinquents (HDHQ and Form C of 16 PF personality tests) in London

Amphetamine users had significantly higher hostility scores, were more self-critical, introverted, and guilt-prone.

Hemmi, 1969

Interviews with male prisoners

28% were amphetamine users; these prisoners were more likely to have committed violent crimes.

Rubin, 1972

Literature review and anecdotal report of aggression in mentally ill criminals

While amphetamine abuse has been implicated in violent behavior, this relationship is probably not causal; a predisposing personality is likely necessary; drugs (including amphetamines) may act as "releasers" in predisposed persons.

Tinklenberg and Woodrow, 1974

Interviews of 152 male juvenile delinquents incarcerated in a moderate security facility in California

Amphetamines were involved in only 2% of offenses; subjects who had used amphetamines expressed opinions that these drugs do not affect aggressiveness.

Paul, 1975

Anecdotal account of acts of aggression perpetrated under the influence of amphetamines and other drugs

Suggested that amphetamines alone or combined with alcohol contribute considerably to aggressive behavior by releasing inhibitions.

Fink and Hyatt, 1978

Anecdotal overview of the association between crime and drug use

Suggested that although reports of ties between criminal behavior and amphetamine use are increasing, no definite association has been established.

Simonds and Kashani, 1979b

Interviews of 109 male juvenile delinquents institutionalized in Missouri, using DSM III criteria

60% of delinquents who committed crimes against persons were amphetamine users.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Siomopoulos, 1979

Psychiatric evaluation of 451 males referred to a psychiatric institute after being found unfit to stand trial in Cook county, Illinois; interviews were primarily concerned with drug use within 24 hours of a crime being committed

64% of the subjects had a history of drug abuse; 11% of the sample used drugs during the 24 hours preceding the criminal act; significantly more crimes were committed under the influence of amphetamines and amphetamine-like substances than with heroin, LSD, marihuana, or PCP; these crimes included murder, attempted murder, and unlawful use of a weapon.

Swett, 1985

214 male inpatients from a maximum security ward for the criminally insane

Many were poly-drug users; amphetamines were used by 23% of the sample; subjects who had used amphetamines were not more likely to commit violent acts than subjects who had not used amphetamines.

Mio et al., 1986

7 juvenile sex offenders completed questionnaires concerning their drug history, family history, and history of crime

4 of the 7 had used amphetamines among other drugs, all of these subjects reported that amphetamines and other drugs were used by family members; relationship between drug use and criminal behavior is correlative only.

Health Statistics

Scott, 1968

Anecdotal report of incidence of alcohol and drug abuse by 50 murderers in Great Britain

In 4 cases, amphetamine use may have played a part in the perpetration of the murder.

Carey and Mandel, 1969

Anecdotal reports from drug agents of 30 incidents of violence

Suggested that violent acts by amphetamine users are not usually premeditated; the violence is unpredictable and sparked by paranoia.

Greene et al., 1973

A survey of drug use in 2133 people incarcerated in the District of Columbia; a separate study reported on a sample of 144 incarcerated subjects surveyed for their history of amphetamine use; charges against the subjects were classified into violent and nonviolent categories

81.8% of the subjects who tested positive for amphetamine at the time of arrest (urine test) also tested positive for an opiate (heroin or methadone); in this population, the incidence of violent crime was lower in the drug abuse group than in the non-abuser group and amphetamine abusers were no more likely to have committed a violent crime than non-amphetamine abusers.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Bailey and Shaw, 1989

A retrospective report of methamphetamine-and cocaine-related deaths in San Diego county in 1987

Methamphetamine was involved in 23 homicides, 1/8 of homicides in San Diego county for that year. Methamphetamine combined with cocaine was involved in 4 homicides.

Personality Evaluations

Rickman et al., 1961

18 case studies of male and female chronic amphetamine users

Long-term amphetamine usage is accompanied by suspiciousness and aggressiveness.

Rawlin, 1968

Anecdotal account of the contemporary street use of amphetamines

Amphetamine use can lead to paranoid hallucinations resulting in attacks on bystanders, friends, or policemen.

Angrist and Gershon, 1969

Psychiatric reports of aggressive behavior in 60 male and female patients hospitalized for amphetamine use

62% of these patients had police records for offenses ranging from vandalism to attempted murder, however this relationship is more likely correlative than causal; paranoid behavior was present in 50% and was occasionally accompanied by violent behavior.

Smith and Crim, 1969

Anecdotal description of the lifestyle of the typical chronic amphetamine abuser in the Haight-Ashbury community

Paranoid amphetamine abusers are highly prone to erratic and violent behavior; most often this comes in the context of drug procurement.

Bach-y-Rita et al., 1971

Psychiatric evaluation of 130 patients displaying episodic violent behavior

12 of the 130 patients were chronic amphetamine users.

Ellinwood, 1971

13 case studies of male and female acute and chronic amphetamine users

Amphetamine-induced paranoia directly results in homicidal behavior.

Levine et al., 1972

Structured interview of 218 male and female young, middle class amphetamine users regarding health, drug history, family history

A high percentage of the subjects were depressed, with >80% showing psychiatric symptomatology; most engaged in multiple drug use; poor family and social histories appear to pre-date amphetamine use.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Black and Heald, 1975

MMPI evaluations of 40 male alcoholics and 50 male drug abusers from a military rehabilitation program; 72% of this group were amphetamine or other stimulant abusers

The drug-abuser sample showed a greater incidence of psychopathic, general personality maladjustment and significant emotional dysfunction than the alcoholic sample; a causal relationship between these illnesses and drug abuse could not be inferred.

Angrist and Gershon, 1976

Psychiatric evaluation of 9 chronic abusers after the administration of large doses of amphetamine

Violent behavior, associated with episodes of psychotic and/or paranoid behavior, was observed; however its incidence is infrequent.

Brook et al., 1976

Psychiatric evaluation (MMPI, WAIS, parent questionnaire, school records) of 117 residents of a drug treatment center in London, all chronic amphetamine abusers

Subjects scored consistently higher than controls on schizophrenic, psychopathic deviate, depression and other scales; drug use is probably a manifestation of underlying problems and not a cause.

Schiørring, 1977, 1981

Interviews with 50 Swedish and Danish stimulant abusers in drug treatment programs

Amphetamine use leads to stereotyped motor and social activity, social withdrawal, paranoia, and hallucinations.

Siomopoulos, 1981

8 case studies of male acute and chronic amphetamine users

Amphetamine-induced emotional lability and paranoia lead to criminal and homicidal behavior.

Atkinson, 1982

Anecdotal reports of violent behavior in hospitalized patients

Stimulants such as cocaine, amphetamines and methylphenidate can produce violence-prone paranoid or manic states.

Experimental Studies on Aggression

Laties, 1961

16 male subjects, sleep deprived and non-sleep deprived, completed questionnaires and were tested in groups for cooperative behavior

Sleep-deprivation slightly increased hostility and significantly decreased social initiation and task involvement; amphetamine (10 mg) and secobarbital (100 mg) increased friendliness, social initiation and task involvement.

Cameron et al., 1965

Questionnaires completed by 239 male and female college students before and 2 hours after amphetamine administration

d-Amphetamine (5 mg) and d,l-amphetamine (10 mg) increased positive mood and socialization and decreased negative mood.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Leichner et al., 1976

30 male and female psychiatric inpatients (diagnosed as schizophrenic, depressive, alcoholic or antisocial) were rated for sociability following methylphenidate administration

Methylphenidate (0.5 mg/kg i.v.) increased talkativeness in every group except antisocial subjects; methylphenidate also increased psychotic symptomatology in schizophrenics.

Griffiths et al., 1977

Higgins and Stitzer, 1988

3 male subjects with a history of amphetamine use were rated for social behavior, 11 normal volunteers were rated for behavior during dyadic verbal interactions; 4 male and female subjects, tested in same-sex pairs, were able to either socialize or perform a task for monetary reinforcement

d-Amphetamine (5-30 mg) increased socializing.

Smith and Davis, 1977

16 normal male and female subjects completed mood scales (POMS) after ingestion of amphetamine

Amphetamine (10 or 20 mg) increased both euphoria and anxiety.

Milkman and Frosch, 1980

10 male amphetamine users were administered 30 mg amphetamine, rated for sexual and aggressive drive states; with control group

Amphetamine users display less control over impulses and drives; aggressive behavior is more often verbal than physical.

Cherek et al. 1986, 1989

8 male subjects pushed buttons to earn points exchangeable for money; a second button allowed them to aggress toward (subtract points from) confederate ''opponents"

Amphetamine increased aggressive responding at low and moderate doses (5, 10 mg/70 kg) and decreased aggressive responding at the highest (20 mg/70 kg) dose.

Beezley et al., 1987

30 male subjects competed with confederate "opponents" in a reaction time task; subjects were able to vary the intensity of shock delivered to opponents

No relationship between d-amphetamine dose (2.5, 5 or 10 mg) and aggressive responding was found.

Literature Reviews

Kramer, 1969

Review of 28 articles spanning 1939-1968 which address problems of amphetamine abuse

Amphetamines predispose users to violent behavior by producing suspiciousness, hyperactivity and mood lability.

Allen et al., 1975

Review of 54 articles spanning 1937-1974 concerning the relation between psychostimulant drugs and aggression

Amphetamine use does not lead to aggressive behavior except when the dose and pattern of usage induce a state of paranoid psychosis.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Fitzpatrick, 1974

Discussion of the relationship of drug use or abuse to violent or nonviolent crime

Amphetamine users are no more likely to commit crimes of violence than non-drug users.

Greenberg, 1976

Review of 75 articles spanning 1952-1975 on the relationship between amphetamine abuse and crime

A causal connection between amphetamine use and criminal behavior cannot be inferred from present studies; amphetamine use is not particularly tied to violence, this connection involves more variables.

Sheard, 1977a, 1983

Two reviews (1977:14 references spanning 1939-1975, 1983:60 references spanning 1956-1981) of literature linking drug use and aggression

While amphetamine use does not lead to aggression except when psychosis is induced, amphetamine use indirectly increases the potential for violence by causing reckless hyperactive and impulsive behavior.

Ellinwood, 1979

Review of 113 articles from 1967 to 1979 on the behavioral effects of amphetamines

Chronic amphetamine psychosis is marked by paranoia and hallucinations.

Cherek and Steinberg, 1987

Review of 191 articles spanning 1937-1986 on the effects of drugs on aggressive behavior

Amphetamine use could predispose individuals toward violence due to its stimulant and paranoia-inducing effects; d-amphetamine treatment often reduces aggression in hyperactive children and may be effective in treating aggressive adult patients.

Miczek, 1987

A review of over 1500 articles concerning the psychopharmacology of aggressive behavior in humans and other species

Evidence that amphetamine use leads to aggressive behavior is split; when aggression occurs it is most likely secondary to the psychotic paranoia induced by high doses administered intravenously.

Miczek and Tidey, 1989

A literature review of over 150 articles investigating the link between amphetamines and aggressive and social behavior

While amphetamines may induce dose-dependent biphasic effects on aggression in experimental studies, the main overall effect of amphetamines is to disrupt social and aggressive behavior patterns.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 8 Effects of Cocaine on Aggression in Animals

References

Methods and Procedures

Results and Conclusions

Isolation-induced aggression

Hadfield, 1982

Hadfield et al., 1982

Male mice, individually housed, tested in groups of 4 identically treated animals under high-density crowding

Cocaine (10, 35 mg/kg i.p.) dose dependently increased fight duration; this increase peaks at 30 minutes after injection and may be due to general stimulatory effects.

Miczek and O'Donnell, 1978

Male mice, housed individually or pair-housed with a female, tested with a group-housed "intruder"

Cocaine (0.125-8 mg/kg i.p.) selectively decreased aggressive behavior, isolated mice were less sensitive to the aggression-reducing effects of cocaine than non-isolated mice.

Pain-induced aggression and defense

Brunaud and Siou, 1959

15 male rats, tested in pairs while receiving electric foot shock

Cocaine (5-50 mg/kg) increased the display of aggressive postures.

Emley and Hutchinson, 1983

23 male and female squirrel monkeys bit a rubber hose in response to electric tail shock

Cocaine (0.3-10 mg/kg s.c.) dose-dependently increased biting and lever pressing responses; higher doses (20, 30 mg/kg) decreased both response types.

Aggression due to the omission of reward

Hutchinson et al., 1976

Acute and chronic effects of cocaine measured using shock-induced aggression and extinction-induced aggression paradigms in squirrel monkeys, mice and pigeons

Acute and chronic cocaine generally decreases aggressive behavior relative to nonaggressive activity.

Moore and Thompson, 1978

2 male pigeons pecked on a response key for food reinforcement; aggression elicited during extinction was measured by pecks to a mirror; acute and chronic administration

Acute cocaine (.01-17 mg/kg i.m.) decreased aggressive behavior at doses which did not affect key responding. Chronic cocaine (1-13.3 mg/kg/day for 150-160 days total) resulted in partial tolerance to food-reinforced but not aggressive responding.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Drug-induced aggression

Kantak and Miczek, 1988

Male mice, pair-housed with a female, confronted a group-housed male intruder

0.05-10 mg/kg cocaine increased attack bites and threats in morphine-withdrawn but not control mice.

Aggression by resident toward intruder

Miczek, 1977b

Miczek and O'Donnell, 1978

Male mice, singly housed or pair-housed with a female, confronted a group-housed male intruder

Cocaine (0.125-8 mg/kg i.p.) selectively decreased aggressive behavior; isolated mice were less sensitive to the aggression-reducing effects of cocaine than non-isolated mice.

Miczek, 1979b

10 male rats, pair-housed with a female, confronted a male intruder in the home cage

Low doses of cocaine (0.5, 2 mg/kg) did not affect aggressive behavior; higher doses (8, 32 mg/kg) significantly and selectively decreased attack and threat behavior.

O'Donnell and Miczek, 1980

30 male mice, pair-housed with a female, confronted an intruder in the home cage; tested with cocaine while being treated chronically with amphetamine or saline

Cocaine (2-16 mg/kg) dose-dependently decreased attack frequency in both amphetamine-and saline-maintained animals.

Kantak, 1989

123 male mice, pair-housed with females and tested with a male intruder in the home cage; acute and chronic

Acute cocaine (.125-20 mg/kg i.p.) increased attacks and threats at low doses and decreased aggressive behavior at high doses. Chronic cocaine (.5 mg/kg i.p. daily for 15 days) significantly decreased aggressive behavior. Dietary magnesium altered the effects of cocaine.

Dominance-related aggression

Miczek and Yoshimura, 1982

Male squirrel monkeys, housed in social groups

Cocaine (10 mg/kg p.o., 3 times over 24 hours) decreased all social and aggressive behavior; these effects were unchanged by administration of antipsychotic drugs.

Filibeck et al., 1988

40 group-housed male mice were treated chronically with cocaine (20 mg/kg, twice per day for 10 days), were administered a challenge dose and tested with an untreated intruder

Cocaine (20 mg/kg) caused an increase in defensive upright and escape in chronically-treated animals.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Literature Reviews

Woods, 1977

Review of the behavioral effects of cocaine (116 articles, 1932-1977)

Cocaine can both increase and decrease aggression elicited by environmental events in pigeons, rodents, and squirrel monkeys.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 9: Effects of Cocaine on Aggression in Humans

References

Methods and Procedures

Results and Conclusions

Criminal Violence

Fink and Hyatt, 1978

Anecdotal report of the association between criminal behavior and drug use

Suggested that while relationship between cocaine use and criminal behavior is unknown, the pharmacologic effects of cocaine suggest a potential for drug-induced violence.

Inciardi, 1989

Interviews of 611 males and females adolescent drug using criminals in inner city Miami

91% used some form of cocaine or crack 3 or more times per week; 14.9% reported having committed assault and 59.1% reported having participated in robbery during the 12 months preceding the interview.

Moore, 1990

Interviews of males and females who have been gang members in East Los Angeles

No significant relationship was found between gang member involvement in cocaine sales and violence; crack dealing may involve violence but firm evidence is lacking.

Roberts, 1990

Discussion of the evolutionary and social roots of violence

Gang-related violence throughout the United States is increasing, as is the involvement of gangs in the drug trade. Author cites reports that 83% of arrested men in New York City in 1986 had traces of cocaine in their urine.

Dembo et al., 1991

201 incarcerated males and females in a Florida prison, mean age 16 years; self report of drug use, delinquency, urinalysis; interviews and urine samples took place within 48 hours of admission; longitudinal study

Self-reported cocaine use did not significantly predict delinquency; self-reported drug use, positive urinalysis test and delinquency predicted cocaine use at follow-up.

Health Statistics

Swett, 1985

214 male inpatients from a maximum security ward for the criminally insane; drug use history related to violent behavior

Many were poly-drug users and cocaine was used by 22% of the sample. Subjects who had used cocaine were not more likely to commit violent acts than subjects who had not used cocaine.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Honer et al., 1987

Evaluation of 52 male and 28 female cocaine and crack users admitted to an emergency room in 1985 and 1986

Crack users exhibited significantly more psychotic symptoms and threats or acts of violence than freebase, intravenous, or intranasal cocaine users; this may be due to route of administration (hence rate of absorption), dose or frequency of use, or differences in socioeconomic background or personality.

Brower et al., 1988

Reports of 100 admissions to a psychiatric emergency room

Method of ingestion (intranasal, intravenous, smoking) did not significantly affect violent behavior. Violent cocaine users ingested more cocaine in the month before interview than nonviolent cocaine users.

Lowry et al., 1988

Reports of 694 criminal homicide victims killed in New Orleans during 4 years

Cocaine was among the 3 most commonly abused drugs by black victims; percentage of victims with detectable cocaine increased from 1 to 18% in the years tested.

Bailey and Shaw, 1989

Report of methamphetamine-and cocaine-related deaths in San Diego county in 1987

Cocaine was involved in 39 homicides, this constituted 1/5 of homicides in San Diego county for that year. Cocaine combined with methamphetamine was involved in 4 homicides.

Fagan and Chin, 1989

Analysis of 3,403 crack arrests and 3,424 cocaine arrests from New York City

Violence was not a factor in arrests for either cocaine or crack; felony violence was charged in fewer than 4% of either crack or cocaine arrests.

Personality Evaluations

Siegel, 1977

Physical and psychological examination, including MMPI, administered to 85 male recreational cocaine users; no control group

Along with stimulant and euphoric effects, subjects reported occasional negative effects such as hyperexcitability, irritability, anxiety, restlessness and paranoia.

Atkinson, 1982

Anecdotal reports of violent behavior in hospitalized patients

Stimulants such as cocaine, amphetamines and methylphenidate can produce violence-prone paranoid or manic states.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Fagan and Chin, 1990, 1991

Interviews of 559 male and female drug users in northern Manhattan

While crack users more often reported feelings of depression and paranoia, crack users did not differ from other drug users in violent behavior. Crack sellers are more violent than marihuana or heroin sellers, and their violence is not confined to the drug selling context.

Literature Reviews

Post, 1975

Egan and Robinson, 1979

Review of articles concerning the physiological and psychological safety of cocaine

Cocaine can induce a psychotic state, characterized by hallucinations, delusions of persecution, and the potential for violent behavior.

Grinspoon and Bakalar, 1979

Review of the acute and chronic physical and behavioral effects of cocaine use

Cocaine can produce irritability and paranoia, may cause physical aggression and crime but there is no evidence of any consistent association.

Busch and Schnoll, 1985

Review of criminal violence, health statistics, and psychiatric evaluations

In some cases, either acute or chronic cocaine use may be associated with violent behavior resulting from paranoia or loss of impulse control, however, the literature is too premature to draw conclusions.

Nadelman, 1989

Discussion of the costs and consequences of drug prohibition in the United States

Evidence does not yet support the depiction of crack cocaine as a drug which unleashes aggressive tendencies.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 10A Effects of Acute Cannabis on Aggression in Animals

References

Methods and Procedures

Results and Conclusions

Isolation-induced Aggression

Garattini, 1965

Santos et al., 1966

Dubinsky et al., 1973

ten Ham and de Jong, 1975

Dorr and Steinberg, 1976

Miczek, 1978

Male Swiss and T.O. mice; resident or intruder drug treated

0.125-1.0 mg/kg i.p. THC had no effect on attack frequency. 2.5-400 mg/kg THC dose dependently decreased attacks and sideways threat, increased crouch and upright behaviors; maximal effects 1-2 hr after administration, not due to behavioral depression. Higher doses had a general depressant effect.

Kilbey et al., 1972

Learning of maze rewarded with an opportunity to attack a conspecific in male Balb/cJ mice

0.6-2.5 mg/kg i.v. THC dose dependently decreased attacks and attack latency.

Matte, 1975

Male wild mice; both subjects drug treated; aggression score comprised of motor activity, attack latency and fight duration

Prefight: 20 mg/kg i.p. hashish increased tail rattling and irritability. Dyadic interactions: hashish had no effect on total fighting time, decreased the latency to attack and increased aggression scores.

Frischknecht et al., 1984

Learning of submissive behaviors in male C3H mice

1-10 mg/kg p.o. THC dose dependently decreased submissive behaviors (defensive upright, sideways and immobility).

Pain-induced aggression and defense

Carder and Olson, 1972

Footshock to pairs of male Sprague-Dawley rats; both subjects drug treated

0.5 mg/kg i.p. THC increased the number of attacks in one or both animals and induced more fighting at higher shock intensities.

Manning and Elsmore, 1972

Footshock to pairs of male Walter Reed albino rats; both subjects drug treated

0.064-6.400 mg/kg i.p. THC had no effect on percentage of fights elicited, regardless of vehicle or time after administration.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Dubinsky et al., 1973

(1) Footshock to male albino mice or Long-Evans rats (2) Reactions to prodding with an inanimate object in restrained bilaterally septal lesioned male Long-Evans rats rated with 0-3 scoring system

(1) THC dose dependently decreased fighting duration 1-3 hr after administration; ED50 (mice): 22 mg/kg i.p., ED50 (rats): 14.9 mg/kg. Antiaggressive effects might be due to sedation. (2) 10-40 mg/kg i.p. THC dose dependently increased excitable and aggressive behavior 1 hr after administration.

Loev et al., 1973

Razdan et al., 1976a,b,c

Winn et al., 1976

Footshock to pairs of male albino BALB/cJ mice; responsiveness to prodding with an inanimate object in rhesus monkeys

Various carbocyclic and sulfur analogues (with and without alkyl substitution), esters of nitrogen of cannabinoids predominantly increased aggression. Heterocyclic analogues containing aromatic side chains predominantly decreased aggression.

Fujiwara and Ueki, 1979

Female Wistar rats 22 hr food deprived for 30 days followed by 70 days ad lib; responsiveness to prodding with inanimate object

Prior to 6 mg/kg i.p. THC, rats did not attack the inanimate object. 1 hr after administration, attack behavior approached 100% and showed no signs of decrease. Attack behavior was abolished when animals were group housed.

Pradhan et al., 1980

Footshock to male Wistar rats; 3 point aggression scale

5-25 mg/kg i.p. THC dose dependently decreased attack scores at 40 min and increased attack scores at 120 min after administration.

Sethi et al., 1986

Footshock to male and female albino mice; both subjects drug treated

100 mg/kg p.o. cannabis had no effect on the frequency of fighting.

Aggression due to omission of reward

Masur et al., 1971

Masur et al., 1972

Food competition between pairs of male and female Wistar rats; dominant or subordinate drug treated

2.5-10 mg/kg i.p. cannabis extract dose dependently increased "winning" behavior.

Cherek et al., 1972

Aggression toward restrained conspecific due to intermittent reinforcement schedule in pigeons

0.125-1.0 mg/kg i.m. THC decreased attack responses.

Jones et al., 1974

Water competition between pairs of male squirrel monkeys; dominant and/or subordinate drug treated

0.25 mg/kg p.o. THC increased competition and 1 mg/kg decreased competition without changing the frequency of fighting.

Uyeno, 1976

Competition for female in estrus between pairs of male Wistar rats; one subject drug treated

0.25-1.0 mg/kg i.p. THC dose dependently decreased dominance; maximal effects after 2 hr

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Giono-Barber et al., 1974

Food competition between pairs of Cynocephalus monkeys; dominant drug treated

30-100 mg/kg (in food supply) cannabis dose dependently decreased dominance.

Miczek and Barry, 1974

Food competition in male albino Sprague-Dawley rats; dominant or subordinate drug treated

1-4 mg/kg i.p. THC decreased defensive-submissive behaviors of subordinate animals, attacks and threats of dominant animals.

Defensive aggression induced by brain stimulation

Dubinsky et al., 1973

Hissing response of male mongrel cats elicited with hypothalamic stimulation

5-20 mg/kg i.p. THC elevated the hiss threshold due to sedation.

Drug-induced aggression

Carlini and Gonzalez, 1972

Pairs of male Wistar rats undergoing morphine withdrawal

48 and 72 hr after morphine abstinence, 5 mg/kg i.p. THC and 10 mg/kg marihuana extract produced aggressive behavior appearing 30 min after administration.

Fujiwara et al., 1984

Social behavior among groups of bilaterally 6OHDA lesioned (i.c.v.) male Wistar rats

6 mg/kg i.p. THC produced fighting and marked hyperirritability from 10-100 days after lesioning.

Aggression induced by REM sleep deprivation

Alves et al., 1973

Karniol and Carlini, 1973

Carlini and Lindsey, 1975

Takahashi and Karniol, 1975

Musty et al., 1976

Carlini, 1977

Carlini et al., 1977

DeSouza and Palermo Neto, 1978

Pairs of male and female Wistar 96 hr REM sleep-deprived rats; various DA and NE pre-and post-treatments

1.25-20.0 mg/kg i.p. Δ9-THC (and various cannabis extracts) dose dependently increased elements of fighting, decreased submissive behavior. This was potentiated with 250 µg pretreatment of 6OHDA. THC or REM sleep deprivation alone did not produce aggressive behavior. THC induced aggression by altering the DA/NE balance.

Aggression by resident toward intruder

Siegel and Poole, 1969

Novel mice (''strangers") introduced to group housed male CF1 mice

2-10 mg/kg i.p. THC and 50-100 mg/kg i.p. Cannabis sativa extract reduced aggression and group aggregation. Stranger males treated with THC or cannabis were hypersensitive to auditory and tactile stimuli and aggregated in small groups apart from the rest of the mice.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Miczek, 1977a;

Miczek, 1978;

Sieber et al., 1982

Male Swiss or C3H/HeJ mice, Sprague-Dawley rats or male squirrel monkeys; resident or intruder drug treated

THC dose dependently decreased resident and intruder elements of aggressive behavior (mice: 20 mg/kg p.o., rats: 0.125-1.0 mg/kg i.p., monkeys: 0.25-2.0 mg/kg p.o.). THC treated intruder mice displayed increased submissive behaviors and THC had no effect on rat or monkey submissive behaviors.

Sieber et al., 1980a,b

Dominant-subordinate interactions with and without an intruder between male C3H/HeJ mice; dominant and/or subordinate drug treated

20 mg/kg p.o. THC produced sedation, decreased aggression and had inconsistent effects on submissive behaviors. THC had no effect on the dominant-subordinate relationship.

Olivier et al., 1984

Resident-intruder interactions between male Wistar or Wezob rats; resident drug treated

At doses below 1.0 mg/kg i.p., THC produced minimal effects on aggression; at 1.0 mg/kg i.p. THC decreased aggression moderately (40%) while markedly increasing inactivity (175%).

Dominance-related aggression

Siegel and Poole, 1969

Social behavior in groups of male CF1 mice; novel mice ("strangers") introduced to group housed mice

2-10 mg/kg i.p. THC and 50-100 mg/kg i.p. Cannabis sativa extract reduced aggression and group aggregation.

Cutler et al., 1975

Pairs of male CFW mice; one subject drug treated

4-50 mg/kg i.p. cannabis dose dependently increased flight behavior without altering aggression.

Ely et al., 1975

Social behavior among groups of male and female CBA mice; dominant or subordinate drug treated

0.5 mg/kg i.v. THC decreased aggressive behavior by dominant without altering hierarchy while 2, 20 mg/kg decreased aggressive behavior and dominance permanently when a rival was present. 20 mg/kg had no effect on aggressive behavior of the subordinate.

Sassenrath and Chapman, 1976

Social settings in groups of monkeys

0.6-2.4 mg/kg (in food supply) THC generally reduced aggressive interactions.

Sieber, 1982

Dyadic observation of male baboons (Papio c. anubis)

40 mg/kg (in food supply) THC decreased threats and attacks.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Killing

McDonough et al., 1972

Turtle (Pseudomys ornata) killing behavior in male albino Walter Reed rats

6.4 mg/kg i.p. THC decreased attacks by approximately 50% relative to control for the first 2 hr after administration. Control attack behavior returned by 4 hr.

Alves and Carlini, 1973

Muricidal behavior in male Wistar rats

20 mg/kg i.p. cannabis extract decreased muricidal behavior.

Dubinsky et al., 1973

Muricidal behavior in male Long-Evans rats; rat killing behavior elicited by hypothalamic stimulation in male mongrel cats

Rats: 2.5-10 mg/kg i.p. THC dose dependently decreased muricidal behavior; ED50:4.9 mg/kg. Cats: 5-20 mg/kg i.p. THC increased attack latency. Antiaggressive effect was not due to behavioral depression.

Kilbey et al., 1973a,b

Kilbey et al., 1977

Frog killing behavior in female Holtzman and male Long-Evans rats with and without 23 hr food deprivation

0.25-2.5 mg/kg i.v. THC dose dependently decreased attack latency and kills in females and food deprived males with maximal effect 30 min after administration; increased whole brain 5HT levels were associated with inhibition of aggression.

Yoshimura et al., 1974

Fujiwara and Ueki, 1978

Fujiwara and Ueki, 1979

Fujiwara et al., 1980

Muricidal behavior in male and female Wistar King-A rats 24 hr food deprived up to 30 days followed by 70 days ad lib

Prior to THC, rats did not display muricidal behavior; 2-16 mg/kg i.p. THC dose dependently induced muricide 1 hr after administration in 60-70% of the rats and stabilized at 50% over the following 100 days. No differences in ACh, AChE levels between muricidal and non-muricidal rats. Group housing decreased muricide.

Literature Reviews

Siegel, 1971

Siegel, 1973

Review of over 65 articles between 1943 and 1973 on hallucinogens and behavior

Cannabis induces hypersensitivity and decreases social interactions.

Carlini, 1972

Carlini et al., 1972

Carlini, 1974

Paton, 1975

Review of over 265 animal and human articles between 1942 and 1975 on the acute and chronic administration of cannabis

Cannabis decreases spontaneous and isolation-induced aggression in Betta splendens and mice and does not decrease fighting in the electric shock paradigm.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Mills and Brawley, 1972

Review of 92 animal and human articles between 1944 and 1972 on the psychophamacology of cannabis

Reduced aggression accompanies hypoactivity, increased aggression accompanies food deprived and food competitive animals. This aggression is more pronounced in the female.

Krsiak, 1974

Review of 193 articles between 1948 and 1974 on the acute and chronic administration of drugs and aggression

Low doses of cannabis increase electric shock-elicited aggression and muricide.

Abel, 1975

Review of 90 articles between 1934 and 1975 on the acute and chronic administration of cannabis and animal aggression

Cannabis decreases aggression due to suppression of locomotor activity and motivation. Cannabis increases aggression in stressed (cold environment, REM sleep deprivation, foot shock) animals.

Carlini et al., 1976

Review of 80 articles between 1964 and 1976 on the environmental effects on acute and chronic administration of marihuana

High doses of marihuana induce hyperexcitability and aggressiveness in rats stressed by cold environment, food-and REM sleep-deprivation and morphine withdrawal through sensitized dopaminergic systems.

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

Cannabis reduces aggression in isolation, pain, schedule controlled, brain stimulation and predatory paradigms; attack and threat behavior is decreased at low doses (0.25-4.0 mg/kg) in mice, rats, squirrel monkeys and rhesus monkeys. Higher doses (>10 mg/kg) reduce defensive and submissive behaviors. Cannabis increases aggression in REM sleep deprived rats.

Frischknecht, 1984

Review of 139 articles between 1963 and 1984 on the acute and chronic administration of cannabis and social behavior in rodents

Cannabis reduces aggression in isolated males and territorial residents, higher doses cause sedation.

Dewey, 1986

Review of 300 human and animal articles between 1929 and 1986 on cannabis pharmacology

Generally, cannabinoids induce aggressiveness in laboratory animals and potentiate aggressiveness in laboratory animals induced by other modalities such as foot-shock, hunger, sleep deprivation.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

TABLE 10B Effects of Chronic Cannabis on Aggression in Animals

References

Methods and Procedures

Results and Conclusions

Isolation-induced Aggression

Carlini, 1968

28 day administration to male mice; resident drug treated

20 mg/kg i.p. cannabis extract decreased fighting duration until day 4; subsequently, there were no differences between treated and untreated rats.

ten Ham and van Noordwijk, 1973

30 day administration to male Swiss-Webster mice; both animals drug treated

50 mg/kg i.p. ∆8-THC, 5 mg/kg i.p. ∆9-THC decreased fighting which showed no signs of tolerance.

Pain-induced aggression and defense

Carder and Olson, 1972

Footshocks to pairs of male Sprague-Dawley rats; 14 day administration; both subjects drug treated

0.12-0.5 mg/kg THC increased and 1.0-2.0 mg/kg THC reduced defensive aggression on test day 1. On day 7 and 14, 0.12-2.0 mg/kg THC decreased aggression.

Pradhan et al., 1980

Footshocks to pairs of male Wistar rats; 19 day administration; 3 point aggression scale

20 mg/kg THC decreased aggression 40 min after administration and produced minimal to moderate increases 120 min after administration.

Sethi et al., 1986

Footshocks to pairs of male and female albino mice; 28 day administration; both subjects drug treated

100 mg/kg p.o. cannabis increased the frequency of fighting.

Aggression due to omission of reward

Cherek et al., 1980

40 day administration and aggression toward restrained conspecific due to intermittent reinforcement schedule in pigeons

0.5, 1.0 mg/kg i.m. THC markedly decreased aggressive behavior and showed no signs of tolerance.

Giono-Barber et al., 1974

35 day administration and food competition between pairs of Cynocephalus monkeys; dominant drug treated

Initially, 100 mg/kg (in food supply) cannabis was depressive with a loss of dominance; after 7 days, increased aggressiveness was present and showed no signs of tolerance.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Drug-induced aggression

Carlini and Masur, 1969

Carlini and Masur, 1970

Carlini et al., 1972

Palermo Neto and Carlini, 1972

18-30 day administration to pairs of male and female Wistar rats with and without footshock; PCPA and DOPA pretreatment

Doses up to 10 mg/kg i.p. THC produced no effect on "spontaneous" aggressive behavior in male and female rats. 10-20 mg/kg increased irritability and spontaneous and shock-induced aggression in both sexes appearing within 2-18 days in 22 hr food deprived rats. This was potentiated with a cold environment (14° C), 40 mg/kg i.p. DOPA and/or 300 mg/kg i.p. PCPA.

Palermo Neto and Carvalho, 1973

30 day administration to pair-housed male Wistar rats separated into two "emotional" groups (HIGH, LOW)

Highly emotional animals were more susceptible to cannabis-induced (0.39 mg/kg i.p./day) aggression than less emotional animals. Whole brain 5HT levels decreased to 50% of control in aggressive highly emotional animals, mainly in cerebral hemispheres, midbrain and hypothalamus.

Palermo Neto et al., 1975

25 day administration to ovariectomized female Wistar rats; both subjects drug treated

After 6-7 days, 20 mg/kg i.p. cannabis produced irritability and hyperactivity. Aggressive behavior appeared after 8 days in estrogen-treated rats and after 14 days in subjects without estrogen. Estrus reduced aggression due to chronic cannabis administration.

Aggression by resident toward intruder

Sieber et al., 1980a,b

Dominant-subordinate interactions with and without an intruder between male C3H/HeJ mice; 4 administrations; dominant and/or subordinate drug treated

Tolerance developed to the sedating and antiaggressive effects of 20 mg/kg p.o. THC after 4 administrations. Effects on submissive behaviors were inconsistent.

Dominance-related aggression

Gonzalez et al., 1971

9 administrations to pairs of male adult Siamese fighting fish (Betta splendens)

0.5 µg/mL THC and 1.0 µg/mL (in aquarium water) cannabis extract decreased fighting episodes, produced mild signs of depression and no escape response. After 9 exposures, THC treated fish regained control levels of aggression.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

ten Ham and van Noordwijk, 1973

30 day administration to male Chinese hamsters; both animals drug treated

50 mg/kg i.p. Δ8-THC abolished and 5 mg/kg i.p. Δ9-THC decreased fighting which showed no signs of tolerance.

Rosenkrantz and Braude, 1974

26 day administration to male and female fischer rats

Inhalation of 0.7-4.2 mg/kg marihuana dose dependently increased aggression after 15-19 days. Fighting occured 1-2 hr after administration and lasted for 2-10 min; aggression was more pronounced in high dosed females.

Culter et al., 1975

14 day administration followed by 7 day abstinence to pairs of male CFW mice; dominant or subordinate drug treated

23 mg/kg (in food supply) cannabis increased flight behaviors and had no effect on aggressive behaviors of dominants; abstinence increased aggression. Cannabis administration and abstinence had no effect on aggressive or timid behaviors of subordinates.

Luthra et al., 1975

Thompson et al., 1973

4-6 month administration to male and female Fischer rats

Initially, cannabinoids produced sedation; fighting developed within 2-3 weeks, was greater in males than in females and more marked at 10 mg/kg p.o. Δ9-THC than at 50 mg/kg. Tolerance might develop to proaggressive effects. Proaggressive potencies were: Δ9-THC > Δ8-THC > marihuana extract.

Sassenrath and Chapman, 1976

15 month administration to groups of monkeys

Initially, 2.4 mg/kg (in food supply) THC reduced aggression, after 2 months, hyperirritability, increased aggressiveness was evidenced which was potentiated by psychosocial stress (e.g., crowding).

Levett et al., 1977

14 day administration to pairs of female Chachma baboons (Papio ursinus )

Daily administration of 33 g (in food supply) cannabis did not effect aggressive interactions.

Miczek, 1977a

Miczek, 1979a

60 day administration to pairs of male Sprague-Dawley, Long-Evans, Wistar and Fischer rats

10-50 mg/kg THC did not produce aggressive behavior regardless of route of administration (i.p. or p.o.), rat strain or vehicle.

Sieber et al., 1981

3 day administration to groups of male C3H/HeJ mice; dominant and subordinate animals drug treated

20 mg/kg p.o. THC weakened dominant position in social, food and sexual interactions which recovered after 2-3 days except with drug treated dominants in the food interaction test.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
×

Killing

Ueki et al., 1972

Muricidal behavior in female King A Wistar rats; 30 day administration; 22 hr food deprived

6 mg/kg i.p. THC induced muricide on the 17th day of administration and showed no signs of tolerance even after the drug was withdrawn; muricide was potentiated in individually housed and food deprived rats.

Alves and Carlini, 1973

Muricidal behavior in "killer" and "non-killer" male Wistar rats; 4 day administration to killer rats, 50 day administration to non-killer rats with or without 22 hr food deprivation

20 mg/kg i.p. cannabis extract decreased muricidal behavior and showed no sign of tolerance in killer rats; after 10 days of administration of 20 mg/kg, non-killer rats displayed muricide which was potentiated with food deprivation.

Miczek, 1976

Miczek, 1977a

Miczek, 1979a

Muricidal behavior in single and pair housed male Sprague-Dawley, Long-Evans and Fischer rats over a 60 day period

THC (2-50 mg/kg i.p.) dose dependently increased the proportion of rats displaying muricide; maximal effects with 10, 20 mg/kg and after 5-6 weeks of treatment. Increased motor behavior and housing conditions had no effect on muricide induced by THC.

Literature Reviews

Carlini, 1972

Carlini et al., 1972

Carlini, 1974

Krsiak, 1974

Paton, 1975

Carlini et al., 1976

Frischknecht, 1984

Review of over 300 animal and human articles between 1942 and 1984 on the acute and chronic administration of cannabis

Cannabis induces aggressive behavior on "stressed" (food-and REM sleep-deprived, cold environment, morphine withdrawn) animals, mainly due to changes to catecholamine systems.

Abel, 1975

Review of 90 articles between 1934 and 1975 on the acute and chronic administration of cannabis and animal aggression

Cannabis increases "irritability" while decreasing inter-male aggression.

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

Cannabis reduces attack and threat behavior in mice, hamsters, rats and monkeys.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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TABLE 11 Effects of Cannabis on Aggression in Humans

References

Methods and Procedures

Results and Conclusions

Criminal violence

Fossier, 1931

Anecdotal account of cannabis violence

Acute and chronic cannabis increased criminality and violence.

Bromberg and Rodgers, 1946

Criminality and psychiatric classification of 8280 male Naval criminal offenders from 1943 to 1945

No relationship between marihuana use and aggressive crime. 8240 nonusers of marihuana more likely to commit aggressive crimes than 40 (0.0048%) users. Users more likely to have asocial personality or schizophrenia.

Gardikas, 1950

Criminality of 379 Greek cannabis users from 1919 to 1950; no control

Acute and chronic cannabis increased violent crimes (possession of firearms, threats and assaults).

Moraes Andrade, 1964

120 cannabis users committed to a Brazilian psychiatric hospital from 1951 to 1960

No relationship between cannabis use and criminality.

Malmquist, 1971

Psychiatric evaluation of 17 male and 3 female juveniles (age: 13 to 18 years) charged with murder in Minnesota

Events prior to homicide included drug use, behavioral and emotional changes. Drug use occurred in two ways: sporadic use of amphetamines and psychotomimetics with or without marihuana, barbiturates and tranquilizers to "contain" impulses and affects.

Soueif, 1971

Criminality of 553 hashish users and 458 hashish nonusers from 1967 to 1968 in Egyptian prisons; questionnaire to 850 hashish users and 839 hashish nonusers

Except for hashish related offenses, 5.7% of the users versus 13.5% of the nonusers had criminal records. 6% of users thought criminal action more likely in users than nonusers whereas 56% of the nonusers thought criminal action more likely in users than nonusers.

Tinklenberg et al., 1974

Tinklenberg et al., 1976

Tinklenberg et al., 1981

Structured interview, police and clincial records of over 350 male adolescents imprisoned between 1971 and 1977 in northern California

Only 6% of the drug-related assaults involved cannabis. Cannabis is the single drug most likely to decrease the possibility of violence. Cannabis use was not a positive predictor of assaultive crime.

Suggested Citation:"Alcohol, Drugs of Abuse, Aggression, and Violence." National Research Council. 1994. Understanding and Preventing Violence, Volume 3: Social Influences. Washington, DC: The National Academies Press. doi: 10.17226/4421.
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