AGGRESSION AND DRUGS: RESEARCH ISSUES

Alcohol, narcotics, Hallucinogens, and Psychomotor Stimulants differ markedly one from the other in terms of pharmacology and neurobiological mechanisms, dependence liability, legal and social restraints, expectations and cultural traditions. No general and unifying principle applies to all these substances, and it would be misleading to extrapolate from the conditions that promote violence in individuals under the influence of alcohol to those with other drugs. Different types of drugs interact with aggressive and violent behavior in several direct and indirect ways from (1) direct activation of brain mechanisms that control aggression, mainly in individuals who have already been aggressive in the past; (2) drug states, such as alcohol or hallucinogen intoxication, serving as license for violent and aggressive behavior; (3) drugs such as heroin or cocaine serving as commodities in an illegal distribution system, drug trafficking, that relies on violent enforcement tactics; to (4) violent behavior representing one of the means by which an expensive cocaine or heroin habit is financed. Systematic experimental studies in animals represent the primary means to investigate the proximal and distal causes of aggressive behavior, whereas studies in humans most often attempt to infer causative relationships mainly from correlating the incidence of violent and aggressive behavior with past alcohol intake or abuse of other drugs. The ethical dilemma of research on aggression in animals and humans is the demand for reducing harm and risk to the research subject, on the one hand, and on the other, to validly capture the essential features of human violence that is by definition injurious and harmful.

Methodologically, aggression research stems from several scientific roots, the experimental-psychological, ethological, and neurological traditions being the most important. The use of aversive environmental manipulations in order to produce defensive and aggressive behavior has been the focus of the experimental-psychological approach. During the 1960s, "models" of aggression were developed that rely upon prolonged isolated housing or crowding; exposure to noxious, painful electrical shock pulses; omission of scheduled rewards; or restricted access to limited food supplies as the major aversive environmental manipulations. The behavioral endpoints in these models are defensive postures and bites in otherwise placid, domesticated laboratory animals. The validity of such experimental preparations in terms of the ethology of the animal, i.e. how animals normally react outside of the laboratory, and in their relation to human aggressive and violent behavior remains to be determined. Aggression research using human subjects studied under controlled laboratory conditions has employed aversive environmental manipulations, such as the administration of electric shocks, noxious noise, or loss of prize money to a fictitious opponent. This type of experimental aggression research highlights the dilemma of attempting to model essential features of valid violence under controlled laboratory conditions without risking the harm and injury that are characteristic of such phenomena. While it is unethical to demand experimental studies that involve "realistic" violent behavior, the relation between competitive behavior in laboratory situations to violence outside the laboratory remains to be validated.

In addition to environmental manipulations, histopathological findings of brain tumors in violent patients prompted the development of experimental procedures that ablate and destroy tissue in areas of the brain such as the septal forebrain, medial hypothalamus, or certain midbrain regions of laboratory rats and other animals. Such experimental manipulations most often result in ragelike defensive postures and biting, often called rage, hyperreactivity, hyperdefensiveness. Alternatively, electrical stimulation of specific brain regions can evoke predatory attack, aggressive and defensive responses in certain animal species. When animals are given very high, near-toxic amphetamine doses and similar drugs, bizarre, rage-like responses may emerge. Similarly, aggressive and defensive behavioral elements are induced by exposure to very high doses of hallucinogens and during withdrawal from opiates. The inappropriate context, the unusually fragmented behavioral response patterns, and the limitation to domesticated laboratory rodents make aggressive and defensive reactions that are induced by lesions, electrical brain stimulation, drugs and toxins difficult to interpret or generalize to the human situation.

In contrast to the emphasis on aversive environmental determinants or on neuropathologies, the ethological approach to the study of animal aggression has focused on adaptive forms of aggressive behavior. 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 anti-predator defense are examples of these types of aggressive, defensive, and submissive behavior patterns, often referred to as agonistic behavior. Sociobiological analysis portrays these behavior patterns as having evolved as part of reproductive strategies ultimately serving the transmission of genetic information to the next generation. The focus on aggressive behavior as it serves an adaptive function in the reproductive strategies, however, complicates the extrapolation to violent behavior as it is defined at the human level. How the range of human violent acts relate to the various types of animal aggression and how they may share common biological roots remains to be specified.

How have these ethological, neurological, and experimental-psychological research traditions contributed to our understanding of the link between drugs of abuse and alcohol to human aggression and violence? Epidemiological and criminal statistics link alcohol to aggressive and violent behavior in a human pattern large in magnitude, consistent over the years, widespread in types of aggressive and violent acts, massive in cost to individual, family, and society, and serious in suffering and harm. Systematic experimental studies have identified the early phase after a low acute (short-term) alcohol dose as a condition that increases the probability of many types of social interactions, including aggressive and competitive behaviors, and high-dose alcohol intoxication as the condition most likely to be linked to many different kinds of violent activities. Yet, most alcohol drinking is associated with acceptable social behavior. This is because individuals differ markedly in their propensity to become intoxicated with alcoholic beverages and to subsequently engage in violent and aggressive behavior, rendering population averages poor representations of how alcohol causes individuals to behave violently. The sources for the individual differences may be genetic, developmental, social, and environmental. Genetic association between antisocial personality, possibly diagnosed with the aid of certain electrophysiological measures, and alcoholism remains to be firmly established. In the early 1990s, the neurobiological mechanisms of alcohol action for a range of physiological and behavioral functions began to be identified; it appears that the actions of alcohol on brain serotonin and the benzodiazepine/GABA_A receptor complex are particularly relevant to alcohol's effects on aggressive and violent behavior. For example, studies in rodents and primates indicate that benzodiazepine-receptor antagonists prevent the aggression-heightening effects of alcohol. Similarly, the actions of alcohol on neuroendocrine events that control testosterone and adrenal hormones appear important in the mechanisms of alcohol's aggression-heightening effects. Among the environmental determinants of alcohol's effects on violence that are of paramount significance are social expectations and cultural habits as well as the early history of the individual in situations of social conflict. Impaired appraisal of the consequences, inappropriate sending and receiving of socially significant signals, 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 and cocaine, since alcohol is not an illicit drug, its link to violence is not a characteristic of the economic distribution network for this substance.

Violence in the context of drug addiction is due largely to securing the resources to maintain the drug habit as well as to establishing and conducting the business of drug dealing. Neither animal nor human data suggest a direct, pharmacological association between violence and acute or chronic administration of opiates. Although measures of hostility and anger are increased in addicts seeking methadone treatment, these feelings usually do not lead to aggressive or violent acts. Rather, the tendency to commit violent crimes correlates with pre-addiction rates of criminal activity. However, 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. Nevertheless, 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.

The most serious link of amphetamine to violence is in individuals who, after taking intravenous amphetamine—most often chronically—develop a paranoid psychotic state during which they commit violent acts. Most psychiatric reports and police records do not support a psychiatric opinion of the early 1970s 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 67 percent among individuals who showed evidence of psycho-pathology prior to amphetamine use. Low acute amphetamine doses can increase various positive and negative social behaviors; higher doses often lead to disorganizing effects on social interactions and to severe social withdrawal. At present, the neurobiological mechanisms for the range of amphetamine effects on aggressive and social behavior remain unknown.

There are surprisingly few pharmacological and psychiatric studies on cocaine's effects on aggression and violence; the available evidence points to psychopathological 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 of crack-cocaine, as documented in epidemiological studies.

Most experimental studies with animals and humans, as well as most data from chronic users, emphasize that Cannabis preparations (e.g., marijuana, hashish) or the active agent tetrahydrocannabinol (THC) decrease aggressive and violent behavior. Owing to the 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 was not of significance in the early 1990s, but older data suggest that certain psycho-pathological individuals who begin using LSD may engage in violent acts; however, this phenomenon is rare.

Phencyclidine (PCP) cannot be causally linked to violent or assaultive behavior in the population as a whole. Generally, personality traits 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 when it occurs, it stands out by its highly unusual form and intensity. It depends on the individual's social and personal background.

The impact of genetic predispositions to be susceptible to becoming involved with 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 have not been specified. Since these critical connections remain poorly understood, it is not possible at present to support specific modes of intervention on the basis of neurobiological data.

(See also: Alcohol: Psychological Consequences of Chronic Abuse ; Crime and Alcohol ; Crime and Drugs )

BIBLIOGRAPHY

Evans, C. M. (1986). Alcohol and violence: Problems relating to methodology, statistics and causation. In P. F. Brain (Ed.), Alcohol and aggression. London: Croom Helm.

Miczek, K. A. (1987). The psychopharmacology of aggression. In L. L. Iversen, S. D. Iversen, & S. H. Snyder (Eds.), New directions in behavioral pharmacology (Handbook of psychopharmacology, vol. 19). New York: Plenum.

Miczek, K. A., et al. (1994). Alcohol, drugs of abuse, aggression and violence. In A. Reis & J. Roth (Eds.), Understanding and preventing violence, vol. 3. Washington, DC: National Academy of Sciences Press.

Klaus A. Miczek