AQA A2 Psychology PSYA3/PSYA4 Revision Thread 2016

Are you sure? On my timetable it says 2pm so that's okay isn't it? Its not wrong if thats what it says?

How many pages are people planning on writing per essay?

My school starts at 2 PM always for afternoon exams. But at my friends college their exams are at 1:15 PM so seemingly it depends on your school/college.

No, it's not, some will start at 13:30 some at 14:00, as long as it's around the same time it's fine I believe


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If I got mid-high A last year on AS psychology, how much do I have to get this year to get an A at least?

Don't give a **** about UMS just the overall grade.


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How many pages are people planning on writing per essay?

Yeah my timetable says 1pm so I guess it varies

Does anyone have an essay for biological explanations of anorexia I could possibly look at?

They're acting pretty much the same thing. The structure I do is:

1 side or so of AO1 theory
4 Research studies supporting/criticising the theory including a methodological issue of 2 of them
2 IDAs

Also don't be put off if it asks about research as they consider theories to be under the umbrella of research.

Ahh cause I'm at 1.30, so do you wanna run out the exam and message me whats on there at like 1:45 XD

What do you mean 2 IDAs?
Like referring to two of gender bias, reductionist, ethical etc?

I can only remember about 2 sides of paper per essay, but seen that some people do 4 sides which scares me however i'm not going for a top grade

Here, you could add more studies and develop in some areas

Despite biological explanations being heavily criticised for their reductionist nature, it is now generally agreed that there is a significant genetic component to eating disorders such as AN. A better approach than looking at family occurrences of AN is looking at adoption studies and comparing twin studies, as it is an opportunity to see whether the development of AN is truly genetic. Perhaps the most notable research is Holland et al’s who researched the significant genetic link by comparing MZ and DZ twins where one twin was suffering from AN. They hypothesised as MZ twins are genetically identical, if AN was truly entirely genetic then AN would be a shared trait. Holland et al found concordance rates of 55% of MZ twins and 7%in DZ twins. There is a significant difference between these concordance rates and as the only difference between MZ and DZ is the greater genetic similarity of MZ twins, the findings point to a significant involvement of genes in AN.

There is substantial research which directly supports Holland et al’s findings. Reviews from Kendler et al (1991), Klump et al (2001) and Bulik et al all conclude that genetic contribution to AN is around 50%-80%, which is considerably high.From this statistic and supporting research, it would make only make sense to assume that genes have a significant role in AN and can ultimately explain the cause of AN, the increasing reliability of the findings consequently strengthens the validity of genes as a biological explanation.

Although there is considerable supporting research, the genetic explanation is not without its limitations.The main problem with Holland et al’s study, and indeed many of twin studies,is the small sample size involved in the research. To be an MZ is uncommon, and to be an MZ with AN even more so, hence why most studies are accused of lacking reliability which not only implicates much of supporting research but also the ability of genes as an explanation of AN.

Furthermore much of the studies assume that environmental influences are the same for both types of twins and the only difference is in their genes. However it is possible that MZ twins are treated more similarly than DZ twins while growing up (always dressed the same etc). This similarity in environments may have contributed in the higher concordance rates in MZ twins, ultimately revealing a major flaw in supporting research leading us to questions whether the environment is a stronger or equally contributing factor. This has further implications for genes as an explanation as it presents it as an insufficient explanation. From this perspective the genetic explanation seems slightly reductionist in the way it explains the development of AN. Not acknowledging the importance of nurture portrays genes as a simplistic explanation especially when AN is most likely an interplay of nature and nurture e.g. genetic predisposition with environmental trigger. Ultimately, not adhering to the principle of parsimony will inevitably affect its acceptability as well as the image of psychology as a science, even though it redeems it credibility by using objective scientific measures in contrast to the evolutionary approach.

Due to its unfalsifiable nature,the evolutionary explanations has inevitably attracted much controversy and criticism despite research finding a role for evolution in AN. Guisinger (2003) proposed the AFFH considering the idea that AN is a reflection of behaviours that were adaptive in the EEA. Key AN traits include denial of hunger and restlessness which were present in hunter-gatherers millions of years ago. Due to food restrictions hunter-gatherers needed to migrate to escape famine in the local area in order to survive, which ultimately posed as an evolutionary advantage. The underlying assumption of this approach is that AN and its characteristics has been passed down from early societies as it posed as an evolutionary advantage.

As previously mentioned the unfalsifiable nature of the evolutionary approach has certainly hindered its wider credibility and even threatens its validity. However, it does seem to maintain face validity and is able to explain some characteristics of AN such as denial of hunger and restlessness which is correct and certainly valid.However, for it to be true or sufficiently valid there needs to be supporting evidence for AFFH. There is no evidence as it is virtually impossible to test which totally undermines its existence and questions whether it will ever be able to explain it all. In Guisinger’s defence the hypothesis is actually post-hoc but this only presents more problems as it could be based on weak or insufficient evidence, thus the theory is also likely to be inadequate which emphasises its insufficiency as a whole.

The criticisms for Guisinger’s explanations do not end there. Its inability to explain the prevalence of AN in women, once again heavily jeopardises its validity. Neither free will nor determinism can explain why some and not the majority of people do not develop these disorders. It would make sense from an evolutionary perspective that AN would be equally prevalent in men and woman as they both would have needed the AN characteristics to survive. Perhaps other factors which can explain why women are more prone to AN, such as media/the behaviorist approach, may be more credible and in fact more logical thus a more inclusive integrated (nature and nurture)approach would be able to universally explain the development to of AN.

who's f*cked?