Youth Violence: Causes and Prevention

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Youth Violence: Causes and Prevention
Frederick P. Rivara, MD, MPH Disclosures

Crime and violence have traditionally been considered to be the bailiwick of the criminal justice system, backed primarily by the research expertise of the disciplines of criminology and sociology. However, the sheer magnitude of the rise in violent injuries and deaths in the 1980s caused violence to be viewed as a public health problem as well. Of particular concern has been the degree to which violence affects the lives of youth. In the mid-1980s, homicide became the leading cause of death among minority youth.[1-3]

Because pediatricians and child healthcare providers focus on and advocate for the health and welfare of children and adolescents, they are naturally concerned about the problem of youth violence. This session of the PAS/AAP year 2000 joint meeting brought together 3 outstanding criminologists to discuss the state-of-the-art research into causes and prevention of youth violence.[4] These individuals are key members of the National Consortium on Violence Research, a multi-institutional consortium of individuals from various disciplinary fields including sociology, biology, medicine, law, and political science. It is a true consortium, comprised of 57 scholars in the field of violence research affiliated with 32 institutions across 19 states and 3 countries.


Early Childhood Interventions
Researchers have examined the issue of prevention of youth violence at different stages of life. Richard Tremblay, PhD,[4] of the University of Montreal, in Quebec, Canada, discussed the rationale behind early childhood interventions to prevent later youth violence. After having worked first in prisons with adults, and then later with juvenile delinquents in detention, he found that interventions after the fact were not overly successful. In 1985, Dr. Tremblay turned his attention to young school-aged children and began a longitudinal study of 1037 6-year-old boys from low-income neighborhoods in Montreal.[5] Those boys identified by their kindergarten teachers as being most disruptive were entered into a randomized controlled trial of an intervention aimed at preventing future behavior problems and ultimately delinquency and violence. The 2-year intervention consisted of 3 components: a home-based parent training program based on the model developed by Patterson and colleagues[6] at the Oregon Social Learning Center, a child intervention consisting of social skills training in which the disruptive boys received training within a larger group of prosocial children, and a teacher training component in which the teachers were taught how to best promote prosocial behavior and how to deal with disruptive behavior.
A follow-up study found no difference during the first 2 years after the program. However, by the end of elementary school, significant differences began to emerge.[7] Compared with the control group, the boys in the intervention group were more likely to be well adjusted and half as likely to have serious behavior problems. They were less likely to be friends with boys with problem behaviors, while the boys in the control group primarily associated with other disruptive kids. The intervention group also had a lower rate of delinquency, a lower rate of gang involvement, and a decreased likelihood of school failure.

The study found, however, that the intervention did not reduce the level of aggressive behavior in these boys. This led Dr. Tremblay and his research team to move even further back in the life cycle and study children beginning at 5 months of age.[7] He found that aggressive behavior was not exhibited much before age 5 months and that it peaked at around 24 months and slowly declined thereafter. Children who had siblings were more likely to be aggressive than those without siblings at home; this was especially true for girls.

Dr. Tremblay concludes that physical aggression is an innate characteristic of children rather than a learned behavior. As Donald Hebb said in 1972, "Neither a human baby nor a chimpanzee needs to learn how to have a temper tantrum." However, what is learned is prosocial behavior and control of aggression. St. Augustine came to the same conclusion during the 4th century.


Continuity of Antisocial and Violent Behavior
Most children learn to control aggression successfully and grow up to be well-functioning members of society. However, 4% to 5% of boys do not learn it and constitute the group of children who later become involved with delinquency and violence and lead lives of crime. Daniel Nagin, PhD,[4] from the H. John Heinz III School of Public Policy and Management at Carnegie Mellon University, in Pittsburgh, Pennsylvania, discussed the risk factors that have been shown to be important predictors for, if not causally related to, the likelihood of continued aggressive behavior. Using the same group of 1037 boys described above, Dr. Nagin and Dr. Tremblay found that by age 17, 4% of the boys continued to have high levels of physical aggression while 28% of the boys who had high aggression in kindergarten showed substantial declines in their aggression.[8] This subgroup of boys, comprising 32% of the initial group, exhibited a variety of behavior problems in middle and high school. In this subgroup, 33% were arrested by age 17, 90% were academically behind by 1 or more grades by age 14, and more than 40% were sexually active by age 13.[8]
The risk factors that are most important in predicting high aggression are shown in the Table below. The accompanying odds ratio reflects the risk for high aggression in the group having the risk factor compared with the group not having the risk factor.

Table. Risk Factors in Predicting High Aggression[8]

Risk Factor
Odds Ratio

Low maternal education when child was age 6
1.8

Teenage mother at birth of the child
1.5

Nonintact family at age 6
1.4

Low IQ at age 10
2.0

Hyperactive at age 6
3.1

High opposition at age 6
3.0




Low maternal education and having a teenage mother were the risk factors that distinguished those who were chronically aggressive at age 17 from those who had high aggression initially with substantial declines over time. Together, these 2 risk factors increased the likelihood of high levels of physical aggression by more than 9-fold. Dr. Nagin noted that more than one fifth of boys with these 2 risk factors will be highly aggressive at age 17.

Reasons for the Recent Rise and Decline in Violence
The question remains as to why there was a violence epidemic in the late 1980s and early 1990s.[1-3] Alfred Blumstein, PhD,[4] from the H. John Heinz III School of Public Policy and Management at Carnegie Mellon University, discussed the rise and decline in violence over the past 15 years, and offered some explanations for the trends.[1] The homicide rate reached a peak in 1991 and has since been in a steady decline.[2] To understand what is really going on, Dr. Blumstein emphasized that the data must be disaggregated -- the rates for different age and racial groups and for different mechanisms must be examined separately.
The increase in the homicide rates that began in the mid-1980s resulted from large upswings in the victimization rates of those younger than 25 years of age.[3] Homicide rates for adults 25 and older have been flat or have shown modest declines for nearly 20 years. Victimization rates for 12- to 17-year-olds doubled, and those for 18- to 24-year-olds increased by two thirds between 1985 and their peak in 1991-93. This increase was most dramatic for African-American youth for whom the homicide rate in 1995 at 32 per 100,000 was more than 6-fold greater than the rate for whites.

These same trends are also observed when examining homicide offender trends.[2] The peak age for homicide offenders is age 18; the rate for this age group more than doubled between 1985 and 1991. By contrast, homicide offending by those over age 25 remained flat during this time period. Thus, the "violence epidemic" of the late 1980s and early 1990s was really a problem of youth, both as offenders and as victims. However, the decrease since 1993 is a product of both the recent sharp drop in offending among young people and the continuing decline in offending among older persons.

The change in homicide rates over the past 15 years is solely the result of a change in the number of gun-related homicides, nearly all of which involve the use of handguns.[1,2,9] Compared to 1985, handgun homicide among young adults increased by 100% by 1994, and use of handguns by those younger than 18 years increased by 300%. Homicides by other means have changed very little.

Dr. Blumstein has hypothesized that this increase in violence was due to the development and spread of crack cocaine.[10] Between 1985 and 1993, the arrest rates of nonwhite juveniles on drug charges more than doubled, and most of these were attributable to cocaine. In the United States as a whole, the incarceration rate has quadrupled since 1975 after a 50-year period of stability in the rates, resulting in the United States having the highest rate of incarceration of any industrialized country.[1] This increase in the rate of incarceration is almost entirely due to drug arrests.

Crack cocaine was different from prior illicit drugs in that it was both very addictive and cheap. This resulted in an enormously expanded drug market, requiring many new sellers. Juveniles in inner cities were a natural source of labor, since there were large numbers of unemployed youth and the criminal penalties for juveniles are lower than for adults. These juveniles carried guns for self-protection, because they dealt with a considerable amount of a valuable commodity and were likely to be subject to robbery as well as involved in turf wars. Other young people in the community resorted to arming themselves as a result of this widespread ownership -- and use -- of guns.[1] Given this wide diffusion of guns and the recklessness of youth, gun use and homicides began to rise, resulting in the "youth homicide epidemic" of the late 1980s and early 1990s. The change took place first among minority youth in large cities and then spread to smaller cities and other population groups.

As mentioned above, the homicide rate appeared to peak in the 1991-1993 period, and has shown a decline every year since. Current rates of less than 6 per 100,000 are lower than rates have been for more than 30 years. Dr. Blumstein stated that the reasons for the decline are much more complicated than the reasons for the rise in homicides and are almost certainly due to a combination of a variety of factors. There have been restrictions on gun ownership, such as that imposed by the Brady Bill, which has prevented more than 400,000 individuals with criminal records from purchasing handguns.[1] The number of federally licensed gun dealers has also decreased dramatically from 284,000 in 1993 to 100,000 in 1998,[11] and some states have restricted the number of guns that can be purchased at one time. Police in many cities have vigorously pursued illegal gun carrying, especially by youth.[12] Drug markets have matured and sales of crack appear to have declined. The robust economy has increased opportunities for legitimate employment, including opportunities for inner-city youth. Finally, the high rate of incarceration has certainly taken a large number of criminals off the street.

The duration of this downturn in crime and violence is unclear. New drugs such as methamphetamine have appeared and may represent a new drug market. There are a large number of children and young adolescents coming into the peak age for delinquency over the next few years. The economy is still strong, but all predict that the bubble will burst at some point.

In summary, current research emphasizes the need for early childhood interventions to teach prosocial behavior and aggressive behavior control, especially in those youths at high risk for continued antisocial/violent behavior. The recent youth homicide epidemic has emphasized the need for societal preventive measures to deter drug use in our youth and to prevent gun access.


References
Blumstein A, Rivara FP, Rosenfeld R. The rise and decline of homicide - and why. Annu Rev Public Health. 2000;21:505-541.
Federal Bureau of Investigation. Crime in the United States. Washington, DC: US Government Printing Office, 1999.
Fox JA, Zawitz MW. Homicide trends in the United States. Crime Data Brief. US Department of Justice, Bureau of Justice Statistics. Washington, DC, 1999.
Rivara FP, Tremblay R, Nagin D, Blumstein A. Youth violence: causes and prevention. Program and abstracts of the Pediatric Academic Societies and the American Academy of Pediatrics Year 2000 Joint Meeting; May 12-16, 2000; Boston, Massachusetts. Topic Symposium.
Tremblay RE, Vitaro F, Bertrand L, et al. Parent and child training to prevent early onset of delinquency: the Montreal longitudinal-experimental study. In: McCord J, Tremblay RE, eds. Preventing Antisocial Behavior: Interventions From Birth Through Adolescence. New York, Guilford Press; 1992:117-138.
Patterson GR, Reid JB, Jones RR, Conger RR. A Social Learning Approach to Family Intervention: Families With Aggressive Children. Eugene, Ore: Castalia Publishing Company; 1975.
Tremblay RE, LeMarquand D, Vitaro F. The prevention of oppositional defiant disorder and conduct disorder. In: Quay HC, Hogan AE, eds. Handbook of Disruptive Behavior Disorders. New York: Plenum Publishers, 1999:525-555.
Nagin D, Tremblay RE. Trajectories of boys' physical aggression, opposition, and hyperactivity on the path to physically violent and non-violent juvenile delinquency. Child Dev. 1999;70:1181-1196.
Blumstein A, Cork D. Linking gun availability to youth gun violence. Law and Contemporary Problems. 1996;59:5-24.
Blumstein A. Youth violence, guns and the illicit-drug industry. Journal of Criminal Law and Criminology. 1995;86:10-36.
Cook P. The epidemic of youth gun violence. Perspectives on Crime and Justice. Washington DC: National Institute of Justice, NCJ 170597, 1999.
Kennedy DM, Peihl AM, Braga AA. Youth violence in Boston: Gun markets, serious youth offenders, and a use-reduction strategy. Law and Contemporary Problems. 1996;59:147-196.
 
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