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Discuss the contribution of biological and psychological
factors to the development of aggressive and violent behaviour ←
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Violence and aggression has puzzled psychologists for centuries;
there is a huge cost to individuals in society when a minority seems to be inflicted by and inflict upon others, extreme forms of physical violence that is intended to cause harm and may result is severe trauma or death. It is generally accepted that all humans are capable of aggressing and there is a strong base of biological evidence that supports this notion along with early evolutionary and ethological psychological investigations that demonstrate the ubiquity of aggression across species. How aggressive behaviour develops and escalates into violent offending is a question that requires an integrative approach combining genetics and evolutionary psychology, which establish a biological basis for human aggression as a common behaviour, with personality and social psychology, to account for much of the individual differences seen in the expression of violence and aggression. It is not within the scope of this essay to thoroughly deal with all potential ontogenetic processes of aggression and violence, but several key areas of focus provide a coherent account of some of the major influences on the development of antisocial behaviours (ASB). Blackburn (1993) states that violence denotes the forceful infliction of physical injury whereas aggression equals the intention of harm, including psychological discomfort and injury. However what is perceived as harmful is entirely dependent on the salient value
structure within the social context. From a biological viewpoint aggressive behaviour depends on organic structural properties of the brain and musculature, which are assumed to be under the control of innate and specialized systems (Baron & Richardson, 1994). Biological factors contributing to the development of ASB (specifically, violence and aggression), will be discussed before considering a range of psychological contributors that have received interest from researchers; concluding that only through combining these approaches, do we get any closer to understanding this complex and multifaceted problem that presents a serious arena of concern for citizens and academics alike. �
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Olweus (1979) likened the stability of aggressive reaction
patterns over time to the stability of intelligence after reviewing 16 longitudinal studies into aggression. Indicating that whether these behaviours are acquired congenitally, postnatally, or across the lifespan: once acquired, these characteristics take on the form of a trait and as such, remain consistent across time. This provides a rationale for the investigation into the development of such behaviours, in that, if we understand how violence and aggression is promoted by biological and environmental agents, the chances of intervening and interrupting such a developmental course are greatly improved and provide a rare opportunity for reducing levels of violent crime, domestic violence, aggressive responses and other ASB in excessively and increasingly violent societies. If aggressive tendencies are as stable across time as the evidence suggests, the chances of reversing the detrimental sequelae of perpetrating and being a victim of such behaviours seems far more unlikely than the chances of preventing such behaviours from manifesting in the first place.
The question
remains however, from where does this aggressive tendency or trait originate? �
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In a fairly recent meta-analytic review of 24 genetically informed
studies using personality measures of aggression, Miles & Carey, (1997) found that 50% of the variance found in these measures of aggression was accounted for by genetic effects which were not attributable to methodological inadequacies of the twin/adoption paradigms used in the studies. Rende et al., (1985) reported correlations of ASB as high as .85 in their Colorado Adoption Project, whereas in Texas, Loehlin et al., (1985) found correlations of nearly zero in their adopted relationships. Gottesman, (1963) reported correlations of .57 for monozygotic and .18 for dizygotic twins and a further distinction was found by Poegue-Geile & Rose, (1985) with significant genetic effects being present at age 20, but not at age 25. Although striking variability is common, the overall consensus is that there is some genetic influence on the expression of aggression and Miles & Carey (1997) believe that the genetic architecture of aggression may change over time.
Jarvik et al., (1973), found that
prison inmates were 15 times more likely to carry a genetic abnormality resulting in XYY syndrome, characterised by excessive and predictable outbursts of violence, than the normal population, providing tentative support to Meyer-Balhburg’s, (1981b) ‘Ychromosome/extra-X hypothesis’, that the more X material in the genotype, the less aggression will develop and the more Y material,
the more aggression. Witkin, (1976) found that 30% more XYY subjects than XY subjects had been convicted, attributing this to the intellectual dysfunction associated with the genetic abnormality. In bears noting that XY individuals commit most violent crimes, so possessing an extra Y chromosome is not a necessary condition for the development of violence. �
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Other biological factors worth noting are the effects of ethanol
and androgens on aggressive behaviour. Goldstein, (1989) distinguishes three ways in which substance use and abuse may be causally involved in violence: Psychopharmacological violence – where the effects of the drug itself facilitate violent acts; Economically compulsive violence – where the need to support a drug habit motivates instrumental crimes and; Systemic violence – where the system of drug distribution and dealing create conflicts which are resolved through violence. Testosterone is related to sensation seeking, dominance/assertiveness and aggression. It would seem that this effect is bidirectional and ultimately hormonal processes cannot be isolated from the social context. Bushman & Cooper, (1990) confirm a special relationship between alcohol and aggressive crimes and the facilitative effect of alcohol on aggression with consistently more than half of offenders evidencing intoxication after arrest. These biological effects do not exist independently of the social context. The case of alcohol and aggression, presents a problem for pure biological explanations, which cannot account for why people choose to drink in the first place, nor the variables of interest in the environment that influence behavioural norms and potential social causes of frustration, anger and aggression when people drink. For the doorman of a nightclub, on a weekend, all aggression may seem to be totally linked
with the consumption of alcohol, and yet this effect seems to represent variably not more than half of all case of violence and aggression. �
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Eysenck & Gudjonsson, (1989) argue that the inheritance of a
stimulus-insensitive nervous system predisposes individuals to participate in high-risk activities, associated with ASB (crime, substance abuse, sexual promiscuity) in order to increase arousal, in their General Arousal Theory of Criminality. Dispositional arousability or reactivity accounts provide more biological evidence in the ontogenesis of aggression. Hinton et al., (1980) demonstrated that violent psychopaths showed less anticipatory anxiety than nonpsychopathic controls and this could be due to adrenaline levels being lower in these excessively violent individuals. The implication here is that these physiological mechanisms subserving hormonearousal networks are largely inherited and therefore provide a strong biological basis for contributing to the development of ASB. It seems that biological heritage potentiates aggression and violence (amongst other behaviours) and various instinct theories of aggression encompass similar implications. Dollard, (1939) influenced by Freudian psychodynamic-hydraulic models, suggested that frustration always leads to some form of aggression, providing an early but far too broad, scope for theoretical understanding of the mechanisms underlying human aggression. Zillmann, (1988) focussed on motivational aspects of aggression, implicating arousal and excitation as prerequisites for ASB, where aggression is determined by the level
of physiological arousal and that too-high or too-low a level of excitation minimises cognitive mediation of ASB. Zillmann, (1988) adds a psychological component to his theory when he places attributional failures as central to facilitating aggression, meaning that the aggression-arousal connection is only salient in specific circumstances, when the prepotent response to provocation is a learned, aggressive one. (Highly reactive individuals being more prone to aggression than their less reactive peers). Clearly biology plays a role in the expression of aggression but the environment influences neural connections, just as biological processes influence our responses to the environment. It seems that aggression alone, is influenced by both. �
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It is unscientific to discuss the development of violent and
aggressive behaviour without considering a variety of psychological factors, which overlap with biology in personality and cognitive domains, and branch away from biology in psychosocial domains. It is intuitive to assume that factors from a person’s background (their family of origin/childhood circumstances) may predispose to or protect against aggressive interactions later in life. The family is a primary source of reinforcement and exposure to violence, as are interactions with peers and watching violent movies and television programmes. It is possible that youth murderers tend to come from disorganised, noncommunicative homes where a disregard for feelings accompanied with physical brutality and lack of support and involvement are the norm. Although this relationship may not be causal or unitary, it does emphasise the importance of relationships and supports the ‘violence breeds violence’ hypothesis: a popular psychological theory of the development of violent and aggressive behaviour. Severe punishment has been found to relate to high levels of aggression in children (Olweus, 1980), this could be accounted for by socialisation processes that endorse modelling of aggressive behaviour, thus encouraging later aggressiveness (Bandura, 1986). Frequent peer interaction, as seen in day-care settings also relates to subsequent aggressiveness, due to the increase in opportunities to practice and relative ease of
generalising aggressive responses to novel situations (Haskins, 1985). It comes as no surprise that children learn aggressive responses from being exposed to and modelling such behaviours from the individuals in their frame of reference (the environment/significant others) ← ←
Huesman’s model (1986) provides a comprehensive account of
how watching violent TV and films may contribute to the development of aggressive behaviours. Huesman et al., (1984) found that viewing habits at age 8 correlated with seriousness of criminal acts and convictions at age 30, supporting a stable conception of aggressiveness and indicating media influences as portent. ←
The model does not explicitly refer to selection processes, such as, children from a lower SES or with a lower IQ choosing to watch more aggressive TV because of their impoverished backgrounds. Freedman, (1984) found such a synchronous correlation in children who preferred to watch violent TV tending to be more aggressive. Lefkowitz et al., (1972) found the amount of TV watched at age 9 to be the best single predictor of juvenile delinquency offences related to aggression at age 19. Exposure to high levels of aggression on TV may increase levels of aggression in the viewer through long-term emotional desensitization. This, essentially social learning account provides provisional support for another major theory in the psychology of aggression and violence: the ‘Cycle of violence hypothesis’, and highlights the need for attention to the degree of tolerance and acceptance of violence in our culture and the fact that cartoons aimed at young audiences, often contain the most violence on television and what impact these things have on levels of interpersonal aggression in normal family settings. �
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Widom (1989) critically examined the ‘violence begets violence’
literature and refers to several keys studies in the field. Kaufman & Zigler (1987), for instance, estimate the rate of intergenerational transmission (IGT) of abuse to be approximately 30%; meaning 2/3rds of abuse cannot be explained by this hypothesis. Gelles (1980) underline the issue by reporting that individuals who have experienced violent and abusive childhoods are statistically more likely to become violent and abusive themselves. Owens & Strauss (1975), explicate that the amount of violence experienced in childhood is one of the factors contributing to the development and maintenance of cultural norms supporting the use of violence. ←
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Could SES play a stronger role than IGT? Attar et al., (1994)
found that children living in the most disadvantaged neighbourhoods experienced more stressful life events than children in other neighbourhoods, and stressful life events predicted teacher-rated aggression. Richters & Cicchetti, (1993) see ASB, not as a form of pathology, but as a necessary and inevitable response in children surviving in settings where threats to their well-being are common (schools where fighting is common/high-crime neighbourhoods), claiming that children from these backgrounds are forced to victimise less they become victims themselves. Blackburn, (1993) summarises that the histories of aggressive children and delinquents are characterised by higher rates of parental deviance, marital conflict, parental indifference and lack of supervision, and that violent adults often report a history of witnessing violence and experiencing physical abuse in childhood. It seems that social class and adversity influences the development of ASB, and cannot be ignored. �
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Despite, the wealth of known socio-psychological and biological
risk factors for ASB, little is known about how these two sets of factors interact. Raine, (2002) reviewed 39 empirical examples of biosocial effects for ASB, highlighting the key influences of genetic and environmental processes in giving rise to socio-biological risk to individual and interactive predispositions to ASB. What constitutes a biological or social variable is open to debate and whether social factors constitute psychological factors is another area of confusion, but what is clear, and what the biosocial perspective assumes, is that genetic processes need an environment in which to become expressed. Plomin & Rutter, (1998) also believe that environmental changes can turn genetic influences on and off across the life-span. Evidence for gene x environment interactions suggest that when both genetic and environmental risk factors are present, they account for a greater number of ASBs than either of them on their own (Cadoret, Cain & Crowe, 1983). Cadoret et al (1995), studied nearly 200 male and female adoptees whose parents had either Antisocial Personality Disorder (APD) and/or alcoholism, and showed that parental APD predicted increased aggression in offspring and that adverse adoptive home environments interacted with adult APD in predicting increased aggression (gene x environment interaction). �
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Psychophysiology is a prime candidate for possible interaction
effects with psychosocial variables as it taps into the dynamic between psychological and physiological processes. Heritability accounts for a route through which genetic influences on ASB find expression, but there are stronger effects for those from benign social backgrounds, lacking classical psychosocial risk factors for crime. The bestreplicated biosocial effects consist of birth complications interacting with negative home environments to predispose to adult violence, particularly life-course persistent ASB (Raine, 2002). What processes trigger these deleterious effects are unknown, as are the fundamental mechanisms underlying these interactions. In combining biological and psychological factors, Raine et al., (1997), refer to another case of birth complications, interacting, this time with early maternal rejection to predispose to adult violent crime, finding highly significant interactions for subjects in a Danish study, who suffered both risk factors. Biosocially, disruption to the early mother-infant bonding process results in more callous, affectionless, unempathic, psychopathic-like interpersonal behaviour, increasing the likelihood of violent interpersonal behaviour and birth complications result in neuropsychological and cognitive deficits and lack of self-control and may result in explosive, impulsive aggression (Mungas, 1983)) �
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Loeber & Hay, (1997) review the different manifestations of and
developmental pathways to aggressive behaviour across childhood, contrasting short- and long-term escalation over time (as social processes) and consider temperamental, emotional and cognitive aspects to aggression as precursors or co-morbid conditions to aggression. Loeber et al., (1997) showed that the age of onset of aggression gradually increases for fighting and violence and that there is a developmental ordering of the seriousness of aggression with age. Minor aggression emerged first from the ages of 3 to 16, followed by physical fighting accelerating from the age of 10 onward. Fighting is followed by onset of violence from the age of 11, again accelerating from there. This work illustrates that the onset of aggression in boys, is concentrated in the pre-adolescent period. Moffitt (1993) delineated a life-course persistent (LCP), who experience early-onset ASB, and an adolescent-limited (AL) group whose deviance appears later and does not persist. Loeber, (1982) states that the highest prevalence of aggression is early in life, decreasing from the ages of 14 to 16, whereas more serious crime tends to increase with age. All this suggests that interactive hypotheses, of a biosocial nature are required to be tested and validated, in their attempts to combine psychological and biological factors (some of which have been discussed in this essay) in understanding the mechanisms through which children are
exposed to the antecedents to violence and aggression (poor family integrity, violent media, alcohol etc) which interact with known genetic predispositions to escalate levels of violent offending. � �
On a final note, one example of aggression and violence that is
currently, sweeping across our major cities, is the phenomenon of gang violence. This disturbing trend, is clearly placed in a social context and cannot be understood using pure biology, nor does the psychological research on territorial violence, intergroup conflict or social adversity, fully account for the sudden rapid increase in the numbers of youth (predominantly non-white males) and the shocking figures of teenage murders flooding our headlines. Only through combining biological and psychological factors to the development of violence and aggression; using a biosocial approach to analyse all the influences coming in on the young person, do we have any hope of curtailing an epidemic that is succeeding in making the lives of large majorities of disadvantaged young people, not only dangerous and fearful, but profoundly and deeply damaging to their physical and psychological well-being.