Aggression Flashcards
How is the Limbic System involved in aggression?
It has been identified as including the cingulate gyrus, hypothalamus, fornix and amygdala. The speed and sensitivity of the limbic system to stimuli are important predictors of aggressive behaviour in humans
How is the Amygdala associated with aggression?
It plays a key role in how we assess and respond to environmental threats.
Gospic et al (2011) carried out fMRI’s on participants in a lab-based game that provoked aggression.
Scans showed that aggressive reactions were associated with a fast and heightened response from the amygdala. Benzodiazepine (reduces arousal of the autonomic nervous system) taken before the game halved the number of aggressive reactions and also decreased amygdala activity.
How is serotonin involved in aggression?
Normal levels of serotonin in the orbitofrontal cortex are inhibitory and linked with reduced firing of neurons and associated with greater behavioural self-control.
Decreased serotonin disturbs this mechanism, reduces self-control and increases impulsive behaviours, including aggression.
Virkkunen et al (1994) compared levels of a serotonin metabolite (breakdown byproduct, 5-HIAA) in cerebrospinal fluid of violent impulsive and violent non-impulsive offenders.
Levels significantly lower in impulsive offenders - disturbance of this pattern implies disruption of serotonin functioning.
How is testosterone linked to aggression?
Testosterone is a hormone responsible for the development of masculine features. It helps regulate social behaviour via influence on areas of the brain involved in aggression.
Dolan found a positive correlation between testosterone levels and aggressive behaviours in male offenders in UK maximum security hospials. Most suffered from personality disorders (e.g psychopathy) and had histories of impulsively violent behaviour.
Animal studies show experimental increases in testosterone are related to aggressive behaviour. Converse is also true testosterone decrease leads to reduction in aggression castration studies.
What are two limitations of neural and hormonal explanations of aggression?
The limbic system explanation excludes other possibilities. Studies show that the amygdala works with the orbitofrontal cortex (OFC) to maintain self-control and inhibit aggression. One study showed that in psychiatric patients that have aggressive disorders OFC activity is reduced. This reduces the internal validity of the theory - as it shows aggression cannot be explained purely by the limbic system.
Role of testosterone is limited. Research suggests that hormones other than aggression are involved in aggression. One hypothesis claims that high testosterone only leads to aggression when cortisol is low, as high cortisol blocks testosterone’s influence. Therefore the combined activity of of testosterone and cortisol may be a better predictor
What are two strengths of neural and hormonal explanations for aggression?
Supporting evidence for serotonin. Research shows drugs that increase serotonin activity also reduce levels of aggressive behaviour. One study found that participants who took a serotonin enhancing drug gave fewer and less intense electric shocks to a confederate group, compared to those in a placebo. This was only true for participants who had a history of aggressive behaviour, but it suggests that the link between serotonin function and aggression goes beyond correlationonal findings, which increases the internal validity of the theory.
There is research to support the theory. One model of biosocial model of status (BMoS) suggests changes in testosterone levels following a loss of status in a competition should effect aggressive behaviour. One study (that took place in a lab) found that 73% of loser (whose testosterone levels rose afterwards) decided to rechallenge their opponent. But only 22% of losers (whose testosterone levels fell) decided to do the same. These findings confirm the prediction that BMoS effects aggression and so increases the external validity of the theory as it has research to support.
What are the genetic factors in aggression?
Monoamine oxidase A (MAOA) is an enzyme that breaks down and recycles excess neurotransmitters into their constituent chemicals after a nerve impulse has been transmitted between neurons. Production of this enzyme is controlled by the MAOA gene that leads to abnormal MAOA activity and leads to low levels of serotonin.
An example of this is the ‘warrior gene’, which is a variant of the MAOA gene and leads to low serotonin levels (affecting aggression). One study looked at 28 male members of a dutch family repeatedly involved in impulsively violent behaviour (rape, murder, assault,etc.). It found that the men had abnormally low levels of MAOA in their brains and the low-activity version of the MAOA activity.
How are twins studies used in the genetic account for aggression?
One study looked at MZ and DZ twins. For direct physical aggression researchers found concordance rates of 50% for MZ twins and 19% for DZ twins. For verbal aggression MZ twins were 28% and 7% for DZ twins. This shows genetic factors account for about 50% of variance in aggressive behaviours.
How are adoption studies used in studying aggression?
Similarities between a child and its biological factors suggest that genetic influences are at play - but if there are similarities with the adopted parents then this suggests environmental factors.
A meta-analysis of adoption studies found that genetic influences accounted for 41% of the variance in aggression.
How are violent abusers and MAOA linked?
A study of 97 men (all from a treatment programme for domestic abusers) who had inflicted IPV.
Men with low MAOA activity were found to be the most violent perpetrators of IPV and engaged in the greatest psychological and physical aggression and inflicted the worst injuries on partners.
How is MAOA linked to early trauma?
Another study found a link between anti-social aggression and low MAOA activity in adult males who had experienced significant trauma (sexual or physical abuse) during the first 15 years of life. Those who had not experienced trauma were not particularly aggressive as adults even if they possessed the gene. This is strong evidence for the diathesis stress model (that the environment and genes interact).
What are two limitations of the genetic explanation for aggression?
It is difficult to separate genetic and environmental factors. Someone with an aggression associated gene may only behave agressivley if the environmental conditions are suitable. One study showed that participants with a low-activity MAOA gene behaved agressivley in a lab based task - but only when they were provoked. This means it is hard to establish how influential the genes are in aggression.
Moreover their are multiple genetic influences. The sizes of genetic effects are significant, but small. One study found that with IPV in men was associated with the serotonin transporter gene (5-HTT), this combined with MAOA was the gene most closely linked with IPV. Many genes interact in complex ways, which reduces the internal validity over explanations using just one gene.
What are two strengths of the genetic explanation?
Support from the prosocial research. The low activity variant of the MAOA gene is associated with greater aggression so presumably those with the high activity variant should be more pro-social. One study found that males with the high activity variant were more co-operative in a lab based task and made fewer aggressive moves than participants with the low-activity variant. This confirms the importance of the MAOA gene in aggressive behaviour. The predictions of the MAOA explanation (i.e antisocial and prosocial behaviour) are opposite sides of the same coin.
Support from animal studies. Genetic deletion techniques allow researchers to ‘knockout’ single genes in mice - letting them observe the effects on aggression. One study show MAOA ‘knockout’ mice have increased brain serotonin and are hyper-aggressive. When the serotonin is blocked by fluoxentine the mice revert to non-aggression. These findings show MAOA must normally have some function in keeping serotonin at ‘normal’ levels by removing it from synapses.
