AQA A2 Psychology PSYA3/PSYA4 Revision Thread 2016

Is it likely they'll ask same questions as last year? any reason to learn them in full detail?

I have a full essay if you would like it!

Has anyone revised the maintenance of relationship?


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Yes please that would be great

SOMEONE PLEASE HELP!

I'm evaluating sexual selection theory (relationships) and i've come across the Penton-voak et al study but I can't work out how it is evaluating the theory?

Is it supporting, going against or what?

Brief outline of their study:

- Found female mate choice varies across menstrual cycle
- Women choose feminised face for long-term relationships as it represents kindness and cooperation
- Choose a masculine face for short-term sex during high-risk conception phase of menstrual cycle
- Masculinity represents high testosterone linked to suppression of immune system
- Such males must have highly efficient immune system -> valuable characteristic for offspring

SOMEONE PLEASE HELP!

I'm evaluating sexual selection theory (relationships) and i've come across the Penton-voak et al study but I can't work out how it is evaluating the theory?

Is it supporting, going against or what?

Brief outline of their study:

- Found female mate choice varies across menstrual cycle
- Women choose feminised face for long-term relationships as it represents kindness and cooperation
- Choose a masculine face for short-term sex during high-risk conception phase of menstrual cycle
- Masculinity represents high testosterone linked to suppression of immune system
- Such males must have highly efficient immune system -> valuable characteristic for offspring

Do we know the predictions for aggression? I know nothing for group display (or even what to put in it for 24 marks), is it likely that one will come up?

Has anyone revised the maintenance of relationship?

Do we know the predictions for aggression? I know nothing for group display (or even what to put in it for 24 marks), is it likely that one will come up?

Is anyone bothering with sex differences in investment or influence of childhood on adult relationships?

I've learnt some A01 incase and like 2 A02 studies for influence of childhood...

Does anyone know what the key arguments are for influence of childhood experiences on adult relationships? For example, Formation is Reward/need satisfaction and/or similarity theory. I dont have a clue what they are for childhood influences

Discuss the role of genetics in human aggression (8 + 16 marks)

:
There is much debate among psychologists surrounding the degree of influence of nature and nurture in causing human aggression. Biological explanations propose that aggression is the result of differences in the biological makeup of individuals, with one explanation proposing that aggression may have a genetic basis. Twin studies have been used in this area of research to assess the role of genetic and environmental influences on aggression. Support for a genetic basis was provided by McGuffin and Gottesman (1985) who found concordance rates for aggressive behaviours were higher between monozygotic twins (0.87) than dizygotic twins (0.72). This indicates that genes have a greater influence on aggression behaviour than the environment on, therefore supporting a genetic contribution.

However research has yet to show 100% concordance rates for MZ twins, which strongly suggests that environmental influences are contributing factors in aggression. Moreover, some psychologists argue that the high concordance rates found in MZ twins could be caused by being brought up with an aggressive family member and learning through imitation, rather than by genetics. Thus it is therefore difficult to validate findings and draw conclusions from such studies. There is also much concern over the validity of twin studies, due to the fact it is difficult to disentangle nature from nurture. For example, Coccaro (1997) compared MZ and DZ twins for aggressive behaviour and found genes to be accountable for 40% of the differences between individuals in aggression, but that the environment accounts for 50% of individual differences in physical aggression and 70% in verbal aggression. Although this supports a genetic basis to aggression, it suggests that the type of aggression to be carried out by individuals is heavily influenced by environmental factors. This therefore implies strong nature-nurture interaction and questions the reliability of previous research findings.

On the other hand, adoption studies into aggression have been carried out which provide a more clear separation of genetics from the environment. Support for a genetic component was provided by Hutchings and Mednick (1973) who studied the criminal records of 14,000 adopted children. They noted a significant correlation between the criminal convictions of biological fathers and the number of criminal convictions of their sons who had been adopted into other families, implying a strong genetic factor in such behaviour. But findings also showed that the risk of criminality was highest among the children who had both a criminal biological father and criminal adoptive father, which therefore implies that environmental factors must also play a causal role alongside genetics. However such research focused more on criminality, which does not always involve violence. This limits the applicability of findings to aggression, and means conclusions surrounding the role of genetics in aggression cannot be drawn from such studies.

On the other hand, further research has identified a positive correlation between a variation of the MAOA-L (low activity form) gene and aggression. The MAOA gene produces the enzyme MAO which degrades neurotransmitters. However the MAOA-L mutation causes less MAO to be produced. This results in the brain becoming flooded with excessive amounts of serotonin and dopamine, which are also thought to be implemented in aggression due to their mood regulating roles. This eventually leads to the brain becoming desensitised to these neurotransmitters, with a build up of these chemicals then causing individuals to respond to stressful situations aggressively.

Support was provided by 

Cases et al, who disabled the MAOA gene in mice and found that this led to increases in the mice’s serotonin and dopamine levels, and heightened aggression. This would imply a direct link between aggression and MAOA deficiency as the genetic explanation proposes. However due to differing physiologies, generalisations of findings to humans should be treated with caution. But nonetheless, studies into aggression involving non-human animals have helped significantly in increasing understanding of human aggression, as genes can be manipulated and their precise role identified.

There is also much research on humans providing strong evidence for the MAOA gene and aggression. Brunner et al (1993) discovered a defective MAOA gene in a Dutch family of whom had a history of male violence. This supports a genetic basis, as it suggests the MAOA-L gene is inherited and can influence aggression in males. However the external validity of Brunner's research is weakened by its focus on only a small sample of males. Consequently findings may not be reflective of female aggression, meaning generalisations should be treated with caution. Additionally it is again difficult to separate out the effects of genes from that of the environment, as families aggression may have also been influenced by shared environmental factors and not the sole the product of a deficient MAOA gene. Therefore such research only points to a correlation, and thus a causal role for the MAOA-L gene cannot be established.

Though, Moffat et al (2002) provided further supportive evidence for a genetic contribution after noting that males who had suffered abuse as children and possessed the MAOA-L gene were more likely to engage in aggressive behaviours, than those who were maltreated but had the MAOA-H (high activity) gene. These findings suggest that different variations of the MAOA gene have differing effects on behaviour and may partly explain why not all victims of maltreatment grow up to victimise others, due to the possession of a particular gene variation. However Moffat’s findings only partially support a genetic basis, as they highlight aggression as being sensitive to social experiences in early development.

This implies that aggression is likely the result of a diathesis stress relationship, whereby an ‘aggression’ gene only exerts its effect when triggered by particular environmental conditions. This could have important real-world applications, including the use of genetic engineering as a way to manipulate or change aggression inciting genes to reduce such behaviour, and implications for the legal system when dealing with acts of aggression; If certain individuals are biologically determined to be aggressive than they arguably cannot be held responsible for their actions.

The biological approach can be criticised as highly deterministic, due to its assumption that the possession of an inherited gene will lead to aggression in some individuals. It therefore ignores the role of free will humans have to override this and consciously choose not to engage in such behaviour. However by reducing aggression to a single gene the biological approach has allowed for the causes of human aggression to be more easily understood, highlighting genetic research as being highly valuable in this area of study. But research surrounding the MAOA-L gene as being the cause of aggression is inconclusive, and it is reductionist to assume that one isolated gene is the cause of aggression. A more holistic approach to explaining human aggression would consider nature nurture interaction, whereby genes increase the risk of aggression in individuals from environments where certain risk factors including abuse and neglect, are apparent.
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