Cassel and Bernstein, (2001) report the futile attempts to prove the existence of a ‘criminal gene’, but some studies have demonstrated a genetic link between anti-social personality disorders (ASPD’s) and criminality (Rhee &Waldman, 2002; Rutter et al., 1998). However, environmental influences on why individuals with ASPD may display greater levels of criminality have not been taken into account. For example, if a child suffers from ASPD, they may be treated differently from other ‘normal’ children, or placed in a separate class, and the subsequent proneness to criminality may be down to these environmental influences. Holmes et al. (2001) state that a child’s family experience is one of the most influential environmental factors contributing to APD.
Individual personality traits have also been shown to be predictors of crime, and Farrington, (1992) found extreme scores on a number of personality traits which have been reported to correlate with juvenile delinquency. For example, traits such as extraversion, low self-image and sensation seeking have been linked to criminality (Eysenck, 1996). Eysenck (1996) believed that characteristics related to low arousal levels in the brain, which have been linked to criminality, were similar to personality traits displayed by extraverts. He attempted to explain the link to criminality by stating that extraverts, due to the low levels of arousal in their brain, seek out stimulation through high risk activities. Miles and Carey (1997) defined high risk activities as including anti-social behaviours and crime.
Eysenck’s (1996) extensive research into the notion that personality is a heritable trait concludes that if certain personality traits are found to be prevalent in individuals who commit crime, then crime must have a genetic basis. He (1996) devised a psychoticism, extraversion and neuroticism model (PEN model) which attempted to predict criminal behaviour based on personality traits. He found that these three factors could be used as a predictor for criminal behaviour, and found that it was especially true of psychoticism. It has been argued, however, that it is the interaction of a number of personality traits, rather single traits that may predispose to criminality (Oliver, et al., 1993).
However, the notion that personality is hereditary is assumed when using this research to attempt to prove that predisposition to crime is genetic. Bouchard (1994) states that the assumption that personality is genetic may stem from early twin studies which seem to overestimate the genetic influence on personality variation.
Twin studies are conducted to compare concordance rates of monozygotic (MZ) or identical twins to dizygotic (DZ) or non-identical twins and attempt to make assumptions about how much of criminal behaviour has a genetic basis. Many studies have produced significant results, with MZ twins providing higher concordance rates than DZ twins, therefore attempting to imply that criminal behaviour has a genetic basis (Joseph, 2001). However, the methodology employed in most twin studies has come under heavy criticism, despite yielding apparently supporting evidence (Joseph, 2001). Rhee and Waldman (2002) observed that twin studies comparing MZ and DZ twins assume that the environment influences are equal for both sets of twins, even though they suggest that MZ twins may be treated more similarly because they look more alike than DZ twins. In twin studies, the past criminal behaviours are often self-reported, and this therefore compromises the reliability of the information being provided as individuals may tend to refrain from presenting the truth about their past behaviours (Joseph, 2001). To achieve more relevant information regarding MZ and DZ twins, Grove et al. (1990) and Bouchard et al. (1990), among others, studied reared apart twins to try and prove a higher genetic concordance of MZ twins than DZ twins, even if they do not share the same environment. They report ‘significant heritability’ for anti-social and criminal behaviour, but again displayed methodological errors by not controlling for common environmental influences shared by reared apart twins, such as strong twin bond-ship (Joseph, 2001).
In an attempt to control the errors and criticism that twin studies received due to the impression that not all environmental influences could be controlled for, studies using children who had been separated at birth from their biological parents and raised by adoptive parents were initiated. These studies theoretically provided a natural experiment to examine further the existence of biological predispositions by separating nature and nurture. Tehrani and Mednick (2000)’s examination of major adoption studies from three different countries concluded that adopted-away children had an increased risk of criminality if their biological parents were convicted criminals.
Despite this research supposedly leaning towards the idea that the aetiology of criminal behaviour is due to genetic predisposition, many reviews of twin and adoption studies (e.g., Carey, 1994; Gottesman & Goldsmith, 1994; Joseph, 2001; Plomin et al., 1990) conclude that both genetic and environmental factors play significant roles in the individual differences associated with criminal and antisocial behaviour, and they cannot be separated from each other.
Biological and genetic explanations of why people commit criminal acts have generally been criticised for being unable to separate the nature and nurture aspects of predisposition to criminality. If all biological research is examined together (brain chemistry, obstetric problems and genetics), evidence for predisposition to criminality is always stronger when these explanations are shown to interact with environmental influences (Rhee & Waldman, 2002). Rhee and Waldman (2002)’s review of many of the twin and adoption studies relating to criminal behaviour established that although genetic background may have a substantial influence on whether an individual will engage in criminal behaviour, the influence of environmental factors is even stronger. For example, Cadoret et al. (1995), studied children adopted at birth, and found that adoptees that had ‘genetic risk’ of committing crime were more likely to do so when exposed to chronic stress in their adoptive family.
Schmitz, (2003) highlighted the importance of a stable family environment on minimising predisposition to crime. Risk factors within the family environment were identified as poverty, education, parenting practices, and family structure. Further, a positive and caring parent-child relationship, a stimulating home environment, and consistent disciplinary techniques were found to be correlated with a child’s well-being. Garnefski and Okma (1996) found that development of criminal behaviour was correlated with poor family communication and weak family bonds.
Abuse in childhood may also be an environmental risk factor which contributes to criminality. Widom (1994) suggested that childhood victimization may lead to the development of behavioural problems including impulsive behavioural styles which may lead to inadequate school and occupational performances. Adaptations to maltreatment, such as desensitization, may lead to personality disorders later in life. Such adaptations in a child may prompt a parent to react negatively towards this behaviour, leading to poor parenting practices and a negative parent-child relationship. Physical abuse may lead to bodily changes which allow a child to become desensitised to pain, and emotion, and this may continue into later life, becoming insensitive towards others and not feeling guilt or remorse. Widom (1994) found that that children who experienced abuse or neglect had a 50% increased risk of later engaging in criminal acts.
In conclusion, there is not enough evidence to state that both biological and genetic factors are completely responsible for whether a person commits crime, or whether it is completely determined by environmental cues. It is therefore likely to be a combination of many factors whether an individual commits crime. Even if individuals have an elevated natural genetic predisposition, they may never engage in any criminal or anti-social behaviour unless they are exposed to the necessary nurture and environmental factors.
Word Count: 1847
References
Bouchard, T (1994). Genes environment and personality. Science, 264, 1700-1701.
Bouchard, T.J., Lykken, D.T., McGue, M., Segal, N.L., & Tellegen, A. (1990). Sources of
human psychological differences: the Minnesota study of twins reared apart. Science, 250,
223-228.
Brennan, P., Grekin, E. R., & Mednick, S. A. (1999). Maternal smoking during pregnancy
and adult male criminal outcomes. Archives of General Psychiatry, 56, 215-219.
Brunner, H. G., Nelen, M., Breakefield, X. O., Ropers, H. H., & van Oost, B. A. (1993).
Abnormal behavior associated with a point mutation in the structural gene for monoamine
oxidase A. Science, 262, 578-580.
Cadoret, R. J., Yates, W. R., Troughton, E., Woodworth, G., & Stewart, M. A. (1995).
Genetic-environmental interaction in the genesis of aggressivity and conduct disorders.
Archive General Psychiatry, 52, 916-924.
Carey, G. (1994). Genetics and violence. In A. J. Reiss, Jr., K. A. Miezek, & J.A. Roth (Eds.)
Understanding and preventing violence (pp. 21-58). Washington, DC: National Academy
Press.
Cassel, E. & Bernstein, D. (2001). Criminal behaviour. Massachusetts: Allyn & Bacon.
Eysenck, H. J. (1996). Personality and crime: Where do we stand? Psychology, Crime, &
Law, 2, 143-152.
Farrington. D. P. (1992). Explaining the beginning, progress and ending of antisocial
behaviour from birth to adulthood. In J. McCord (Ed.) Facts, Frumeworks and Forecasts.
Advances in Criminological Theory (pp. 253-286). London: Transaction Publishers.
Garnefski, N., & Okma, S. (1996). Addiction-risk and aggressive/criminal behavior in
adolescence: Influence of family, school, and peers. Journal of Adolescence, 19, 503-512.
Gibson, C. L., & Tibbetts, S. G. (2000). A biosocial interaction in predicting early onset of
offending. Psychological Reports, 86, 509-518.
Gottesman, I. I., & Goldsmith, H. H. (1994). Developmental psychopathology of antisocial
behavior: Inserting genes into its ontogenesis and epigenesis. In C. A. Nelson (Ed.) Threats
to optimal development: Integrating biological, psychological, and social risk factors (pp.
69–104). Hillsdale, NJ: Erlbaum.
Grove, W., Elke, D., Ecker, L., Heston, L., Bouchard, T.J., Segal, D., et al. (1990).
Heritability of substance abuse and antisocial behavior: a study of monozygotic twins
reared apart. Biological Psychiatry, 27, 1293-1304.
Holmes, S. E., Slaughter, J. R., & Kashani, J. (2001). Risk factors in childhood that lead to
the development of conduct disorder and antisocial personality disorder. Child Psychiatry
and Human Development, 31, 183-193.
Joseph, J. (2001). Is crime in the genes? A critical review of twin and adoption studies of
criminality and antisocial behavior. The Journal of Mind and Behavior, 22, 179-218.
Miles, D. R., & Carey, G. (1997). Genetic and environmental architecture of human
aggression. Journal of Personality and Social Psychology, 72, 207-217.
Oliver, L., Nagayama, L., Hall, G. C., & Neuhaus. S. M. (1993). A comparison of the
personality and background characteristics of adolescent sex offenders and other
adolescent offenders. Criminal Justice and Behavior. 20, 359-370.
Plomin, R., Chipuer, H. M., & Loehlin, J. C. (1990). Behavior genetics and personality. In L.
-
Pervin (Ed.). Handbook of personality theory and research (pp. 119–133). New York:
Guilford Press.
Raine, A. (2002). Annotation: The role of prefrontal deficits, low autonomic arousal, and
early health factors in the development of antisocial and aggressive behavior in children.
Journal of Child Psychology and Psychiatry, 43, 417–434.
Raine, A., Brennan, P., & Mednick, S. A. (1994). Birth complications combined with early
maternal rejection at age 1 year predispose to violent crime at age 18 years. Archives of
General Psychiatry, 51, 984-988.
Raine, A., Brennan, P., & Mednick, S. A. (1997). Interaction between birth complications
and early maternal rejections in predisposing individuals to adult violence: Specificity to
serious, early-onset violence. American Journal of Psychiatry, 154, 1265-1271.
Raine, A., Park, S., Lencz, T., Bihrle, S., LaCasse, L., Widom, C.S., et al. (2001). Reduced
right hemisphere activation in severely abused violent offenders during a working memory
task: An fMRI study. Aggressive Behavior, 27 111-129.
Rhee, S.H. & Waldman, I. (2002). Genetic and environmental influences on antisocial
behavior: a meta-analysis of twin and adoption studies. Psychological Bulletin, 128, 490–
529.
Rutter, M., Giller, H. & Hagell, A. (1998). Antisocial Behavior by Young People. Cambridge
University Press: Cambridge.
Schmitz, M. F. (2003). Influences of race and family environment on child hyperactivity and
antisocial behavior. Journal of Marriage & the Family, 65, 835-849.
Tehrani, J., & Mednick, S. (2000). Genetic factors and criminal behavior. Federal
Probation, 64, 24-28.
Volkow, N. D., Tancredi, L. R., Grant, C., Gillespie, H., Valentine, A., Mullani, N ., et al.
(1995). Brain glucose metabolism in violent psychiatric patients: A preliminary study.
Psychiatry Research: Neuroimaging, 61, 243-253.
Widom, C.S (1994) childhood victimization and risk for adolescent problem behaviours. In
M.E Lamb and R . Ketterlinus (Eds.) Adolescent Problem Behaviors (pp. 127-164).
Hillsdale, NJ : Erblaum
