Abnormalities Flashcards

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1
Q

Ao1: What is the genetic explanation for Schizophrenia?

A

That schizophrenia is caused by genes so it should be passed down to children from parents. This should mean the disease runs in families.

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2
Q

Ao1: What studies do we use to test if schizophrenia is due to genes and why?

A

We use twin, family and adoption studies as this tells us whether the disease does commonly run in families and how commonly it does and also rules out the environment as a cause.

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3
Q

Ao1: What would you expect the concordance rate of schizophrenia for twins would be?

A

You would expect it to be 100% for monozygotic twins as they share 100% of their genes and around 50% for dizygotic twins because they share about around 50% of their genes on average.

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4
Q

Ao1: What is a concordance rate?

A

This is the likelihood of a person developing a disease someone else already has it.

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5
Q

Ao1: What is the concordance rate for the general population?

A

1%.

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6
Q

Ao2: What did Joseph find?

A

They found that the concordance rate for MZ twins was 40.4% and was 7.4% for DZ twins.

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7
Q

Ao2: What does Joseph’s findings tell us about schizophrenia?

A

That it most likely is genetic as this is a very large concordance rate and different between MZ and DZ as MZ share considerably more genes, therefore we expected this.

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8
Q

Ao2: How does Gottesman support Joseph’s findings about schizophrenia?

A

They found that the less genes shared the less likely you are to develop schizophrenia which supports the idea that it is genetic also as this means the more genes shared the more likely you are to both have the gene/genes for schizophrenia.

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9
Q

Ao2: What is a problem with Joseph and Gottesman?

A

You would expect MZ twins to have a concordance rate of 100% as they share 100% of their genes meaning if it is genetic they would both have the gene/genes for schizophrenia. Because it isn’t 100%, the environment must have a play in the development of schizophrenia. Maybe there needs to be something in the environment to set it off? Also, Gottesman’s study is quite inconclusive as it could just be that you are less likely because you share less of your environment, we cannot draw a clear link between genes and schizophrenia.

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10
Q

Ao2: What did Rosenthal Study?

A

They studied identical quadruplets that all had schizophrenia. They all differed in age of onset and their symptoms. They also had a very bad upbringing as their parents were very unstable.

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11
Q

Ao2: What does Rosenthal suggest about Schizophrenia?

A

That it is genetic because they all had the schizophrenia which is very unlikely if it is not genetic as no one person can have exactly the same environment. The fact their parents seemed very unstable also supports a genetic cause as they could have had the disease themselves.

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12
Q

Ao2: What are 2 problems with Rosenthal’s study?

A

It could quite easily be an environmental cause as it could be that the unstable home and upbringing was bad enough to cause the schizophrenia. This would explain why they differed in age of onset and symptoms as maybe parts of the environment triggered the disease at different times. Seems likely that maybe genes and environment interact. This is also a case study meaning we cannot generalise to all families and quadruplets as we do not know the same thing would happen.

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13
Q

Ao1: What did Freud say about people with Schizophrenia?

A

He said that the id (the instinct driven part of the mind) took over when the person regressed back to primary narcissism (self-importance). This means they cannot make a distinction between what is real and what is fantasy and they cannot delay gratification much like a child cannot either. Their ego struggles to regain consciousness.

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14
Q

Ao1: What did Freud think causes schizophrenia?

A

He believed that schizophrenia developed due to the upbringing of the mother and family relationships.

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15
Q

Ao2: What did Fromm-Reichmann do to develop on Freud?

A

They said that schizophrenia was caused by schizophrenogenic mothers. These are mothers who are at one minute rejecting the child and then the next minute overprotective. They are dominant and moralistic and constantly talking about what is right and wrong. They said this confused the child and ended up causing the schizophrenia.

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16
Q

Ao2: What does schizophrenogenic mothers suggest about schizophrenia?

A

That it has an environmental cause rather than a genetic one, it seems genetic because the parents seem quite erratic themselves but it isn’t, it is caused by how they have been brought up.

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17
Q

Ao2: What is a problem with the theory about Schizophrenogenic mothers?

A

That the schizophrenogenic mothers could have actually had schizophrenia themselves which means that it could quite possibly be a genetic cause. This theory does not make a direct link between the environment and schizophrenia. It could also be a case of genes and the environment interacting.

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18
Q

Ao2: What is a problem with Freud’s theory?

A

It is unfalsifiable as it is all to do with he unconscious mind which we cannot see for ourselves. This means we cannot test the theory empirically, so we have no evidence to say whether it is true or not. Freud provided no physical evidence himself which just emphasises on this point.

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19
Q

Ao2: Is schizophrenia caused by the genes or the environment, or do the two of them interact?

A

It is difficult to say whether schizophrenia is just caused be genes or the environment as it is virtually impossible to actually test this in way of ruling out the other. The environment could even play a part in the mothers womb so it is impossible to control this. However, it seems very likely that maybe they both interact. This can be named as the diathesis stress model. This states that you have a genetic predisposition to something(diathesis) and then something in the environment(stress), like the shcizophrenogenic mothers sets this off.

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20
Q

Ao1: What is ECT?

A

This is when a electric shock is passed through someones brain to induce an epileptic like seizure.

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21
Q

Ao1: Why did people start using ECT to cure schizophrenia?

A

Because schizophrenia is very uncommon in people with epilepsy.

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22
Q

Ao1: What happens in modern ECT?

A

The person is given a general anaesthetic and electrodes are placed unilaterally (one of the temple of non-dominant side of brain and one in middle of forehead). Then 0.6 amps are passed through the electrodes for half a second. This induces a seizure which lasts for 30 to 60 seconds.

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23
Q

Ao1: How many treatments of ECT does one person have?

A

Around 3-15.

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24
Q

Ao1: What problem arises from the use ECT?

A

Memory loss and severe confusion.

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25
Q

Ao2: What are the 3 explanations of Brenton?

A

1) That the pain acts as a punishment, therefore it is like operant conditioning, as the person will think that they will not have an episode again because it will result in the ECT again.
2) That the memory loss caused allows for the patient to reconstruct their life.
3) The biochemical changes produced help to reduct the symptoms.

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26
Q

Ao2: What is a problem with each explanation?

A

1) When patients given an electric shock which would cause pain but not enough for a seizure it did not work. General anaesthetic and used now also meaning the patients will not feel pain therefore it cannot be a punishment.
2) Unilateral ECT is used now which causes minimal memory loss, definitely not enough for someone to be able to reconstruct their life.
3) Biochemical changes are only temporary but some have found the affects to be permanent.

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27
Q

Ao2: What is Breggin’s explanation for why ECT works?

A

That it causes severe brain damage which makes the person delusional, like being drunk. This means that the ECT does not actually work, people just think it has.

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28
Q

Ao2: What did Thayran and Adam’s do and find?

A

They did a review of 26 studies which compared the effects of real ECT with simulated ECT. They found that the real ECT produced much larger affects in the reduction of symptoms.

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29
Q

Ao2: What does Thayran and Adam’s research suggest about ECT?

A

That it is the real thing that works and not a placebo, therefore it is a successful treatment for schizophrenia.

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30
Q

Ao2: What did Sarita et al do and find which contradicts Thayran and Adam?

A

Sarita et al tested 36 patients and compared real ECT with simulated ECT and found that there was no significant difference between the affects of the two. This heavily contradicts Thayran and Adams as it suggests that ECT isn’t effective after all as you could just as easily use a placebo.

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31
Q

Ao2: What is a problem with Sarita et al?

A

It is a very very small sample size compared to Tharyan and Adams which makes it very hard to generalise because of the fact that we do not know everyone else would react in the same way.

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32
Q

Ao1: How does CBT help treat Schizophrenia?

A

It challenges and replaces maladaptive thoughts with constructive thinking. This eventually leads to healthy behaviour. Schizophrenics are generally unaware they are thinking in this maladaptive way so therapists try and bring this into consciousness so that they can challenge it and see there is no basis for this way of thinking. The cognitive aspect looks at altering the way the person thinks about the world and the behavioural aspect looks at changing their behaviour through learning.

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33
Q

Ao2: What did Drury find about CBT and what does this suggest about CBT?

A

They found a reduction of symptoms and of recovery time of about 25-30% when combines with antipsychotic drugs. This shows CBT to be affect and suggests the drugs help people to access the benefits of CBT.

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34
Q

Ao2: What is a problem with Drury’s research?

A

Surely for CBT to be completely successful it should work on its own.

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35
Q

Ao2: What did Kulper’s suggest about Drury’s research?

A

That it was all down to the drugs, and that CBT had no effect. It is true we cannot infer a cause and effect relationship here because we have the drug as a confounding variable with could be affecting the person more than the CBT is.

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36
Q

Ao2: What did Kingdon and Kirchell suggest about CBT?

A

That it is not suitable for some people because they are unwilling to participate in the CBT, probably because they think it isn’t going to work. They said this is most common for older people because of the fact they have had more episodes and are therefore probably more delusional.

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37
Q

Ao2: What is a problem with Kingdon and Kirchell’s suggestion?

A

This generalisation to older people means that doctors are probably more likely to just prescribe them drugs, even though it may be possible that CBT could work for them better. Also surely some older people will be more likely to comply as they have had so many episodes and are so fed up with it all now.

38
Q

Ao2: What is a general problem with schizophrenia?

A

That people are generally too out of touch with reality to be able to change their thought pattern and to be able to think rationally about things.

39
Q

Ao2: Can one treatment be successful in treating schizophrenia on its own or do we need to combine treatments to completely satisfy the diathesis-stress cause?

A

It is inconclusive as to whether schizophrenia is successful or not as there is lots of conflicting evidence. If Briggins in right about the brain damage then it cannot be successful. However, we still do not know the full effects of ECT therefore meaning we cannot draw a conclusion yet. CBT on the other hand does seem successful but only with drugs which suggests drugs help the diathesis and CBT helps the stress. However we should combine this also with family and social support to satisfy the diathesis-stress model completely.

40
Q

Ao1: What is the genetic explanation for depression?

A

This that depression is a genetic disease which is passed down to children from parents. This means it should run in families.

41
Q

Ao1: What studies do we use to test if depression is due to genes and why?

A

We use twin, family and adaption studies as this shows us how common it is for the disease to run in families and rules out the environment as a cause.

42
Q

Ao1: What is the concordance rate for the whole population for depression?

A

5%

43
Q

Ao2: What did McGuffin et al find?

A

The concordance rate for depression is MZ twins is 46% and for DZ twins it is 20%.

44
Q

Ao2: What are 2 problems with McGuffin’s findings?

A

This information is only correlational therefore we do not know that genes are causing this concordance rate, it could quite easily be due to the fact that they live in the same environment. Also, we would expect MZ twins to have a 100% concordance rate if the cause was purely genetic as they share all their genes but it is not. This makes you think there must be something in the environment causing that 54% which shows how their must be an interaction between the two.

45
Q

Ao2: What is comorbidity and how does it support a genetic cause?

A

This is when a gene can be the cause of more than one mental disorder, for example one twin may develop depression and the other general anxiety disorder. This could mean that the other 45% of twins get a different disorder but it is still caused by the same gene. However, there must be something in the environment which triggers each disorder otherwise they surely they would just get the same.

46
Q

Ao2: What did Wender find?

A

They found that biological relatives of adopted children had 7 times more chance of developing depression if the child has it compared to adoptive relatives. Biological parents had 8 times more chance.

47
Q

Ao2: What are 3 problems with Wender’s findings?

A

Firstly it involves case studies (as it is such a rare occurrence) therefore we cannot generalise the findings to every adopted family with a child with depression because we do not know that it would be the same.
Secondly, Adopted children are usually treated quite similarly to how they would in their real families homes, meaning we cannot rule out the cause of the environment completely.
Lastly, adoption can be very upsetting for both the child and the family therefore, isn’t it likely that they got depression because of the adoption.

48
Q

Ao1: What did Seligman theorise about the cause of depression?

A

They said that it was caused by the fact that the person had learned helplessness. This means that so many bad things have happened to them in their lives which eventually makes them think bad things will always happen and it will always be their fault because they are always involved. This is like a downward spiral of negative thinking which leads to depression.

49
Q

Ao2: What did Seligman do and find?

A

Electrocuted dogs inside a fence which they could not escape and eventually learned helplessness as when they were able to jump over the fence after being electrocuted they weren’t.

50
Q

Ao2: What is a problem with Seligman’s research?

A

It was conducted on animals which means we cannot generalise the results to humans as we do not know we would act in a similar way.

51
Q

Ao2: How did Hiroto solve Seligman’s problem?

A

He conducted a similar study on humans using loud noises and found similar results.

52
Q

Ao2: What is a problem with the theory of learned helplessness?

A

It is very reductionist as it is reducing many complex symptoms down to one way of thinking which many would find unappealing.

53
Q

Ao1: How did Abramson develop the learned helplessness theory?

A

He called his theory Attribution theory and stated that the depression was a result of attributing failures to an internal cause (e.g personality) a stable cause (e.g it will happen again in the future) and a global cause (e.g it will happen in every situation).

54
Q

Ao1: What did Beck theorise about depression?

A

They theorised that it is due to a negative self-schema (this being a packet of information about ourselves). He said this was due to having negative things said about themselves when they were growing and learning. This then results in them interpreting any information about themselves in a negative way. For example, if a child drew a picture and their mum threw it away they may end up thinking every piece of art they ever do is worth throwing away, even if it is amazing. He also created the cognitive triad and this when a person will have a negative view of themselves, which causes them to have a negative view of the world which then causes them to have negative view of the future and this carries on in circles.

55
Q

Ao2: What is a problem with saying negative thinking is the cause of depression?

A

We don’t actually know if the negative thinking is the cause or if the depression caused the negative thinking.

56
Q

Ao2: What did Lewinsohn find?

A

That there is no relationship between negative thinking and later depression.

57
Q

Ao2: What is a problem with Lewinsohn’s research?

A

It could be that the control group did think negatively but they succumbed to social desirability bias as they thought it would look better on them if they made it look like they don’t think negatively.

58
Q

Ao2: What did Nolen and Hoeksma find?

A

That there is a link between negative thinking in older children and later depression but only when they had experienced negative life events.

59
Q

Ao2: What does Nolen and Hoeksma’s research suggest about depression?

A

That the cause is very complex and not just down to one thing but down to many, showing that there is most likely an interaction between the genes and environment.

60
Q

Ao2: Is the cause of depression due to genes or the environment or is there an interaction between the two?

A

It is too difficult to be able to completely rule out genes or the environment as a cause therefore it is most likely due to an interaction. This is generally called the diathesis-stress model which theories a person will have a genetic predisposition to something and a stress in the environment will set it off. In this case the diathesis could possibly be the short-short version of the serotonin transporter gene which causes a vulnerability to negative thinking and which is triggered by negative life events (stress).

61
Q

Ao2: What did Sackheim do and find?

A

Reviewed controlled comparisons of real ECT and simulated ECT and found that the Real ECT had a much larger effect on depression. Also found ECT had a larger effect than drugs did (however these help prevent relapse).

62
Q

Ao2: What is a problem with Sackheim’s research?

A

It was conducted in 1989 which means that if they compared it to more modern drugs like SSRI’s we may find they have a larger impact than drugs used to. It is also possible to say that therapies have probably greatly increased in effectiveness and qualities since then has mental health has greatly improved.

63
Q

Ao2: What did Scott do and find?

A

They conducted 18 studies which used 1144 patients and found that real ECT was more effective than simulated ECT in the short term.

64
Q

Ao2: What is a problem with Scott’s research?

A

If it only works in the short term this will mean the patient will have to keep getting treatments when it wears off which could cause catastrophic memory loss which will be damaging to all involved. Maybe if we combined the ECT with antidepressants and family and social support then this would prevent relapse.

65
Q

Ao2: What is good about Scott’s study?

A

It has a very large sample size which means we can be fairly sure that the ECT is actually effective and it isn’t just effective on those involved.

66
Q

Ao1: How does CBT help people with depression?

A

It gets people to challenge their negative way of thinking and helps them to think more objectively and see things in proportion. They use a dysfunctional though diary also. They challenge their thinking by asking questions about it and they also question the evidence they have for it. Examples of questions include ‘would it be so bad if that happened?’.

67
Q

Ao1: What is a dysfunctional though diary?

A

This is where the therapist gets the patient to write down any negative thoughts they have and then rate these out of 100. They then try and get them to come up with a rational thought to counter it and rate the belief in the rational thought and they then rerate their belief in the original negative thought.

68
Q

What did Butler et al do and find?

A

They looked at 16 meta analyses and found that CBT was more effective than drugs and other therapies.

69
Q

What did Holmes find that countered Butler et al?

A

Holmes conducted the single most largest study into the effectiveness of treatments for depression and found that CBT was much less effective than drugs and other therapies. However it was effective for people who only had depression.

70
Q

How can we make CBT work for those with depression and other mental disorders.

A

We could combine them with other treatments. For example a common disorder that comes with depression is psychosis. Obviously CBT would not work on its own because they would be too delusional. However if you gave the patient antipsychotics also this would allow them to access the benefits of CBT.

71
Q

What sort of things can jeopardise the effectiveness of CBT?

A

Kuyken and Tsivikos found that 15% of variance in outcome was due to the competence of the therapist. Byrant et al found that outcome of the patient depended upon how successful the therapist was in engaging the patient to do their ‘homework’. Elkin said that some people are just too resistant to change. Attrition bias can also affect.

72
Q

What is attrition bias?

A

This is when some people may believe that the therapy is working for them so they drop out because they think they don’t need it anymore. The people left go right to the end and it wasn’t successful for them. This makes it look like it was 0% effective when it actual fact it was effective, just not on everyone. This can effect in the opposite way with it looking 100% effective when in actual fact the people who thought it wasn’t dropped out.

73
Q

Ao2: Is one treatment successful in treating depression on its own or do we need to combine treatments to fully satisfy the diathesis-stress cause?

A

ECT has been shown to be effective but only in the short term which means it should only ever be a last resort because of memory loss problems. However CBT is not effective on its own but could be effective if we combined it with drugs which should satisfy the genetic cause and also with family and social suppport which could help to prevent any negative life events.

74
Q

Ao1: What does diagnosis bias mean?

A

This is when certain people or groups of people are more likely to be diagnosed with a mental disorder than other people.

75
Q

Ao1: What classification system does psychology use to diagnose mental disorders?

A

The DSM V.

76
Q

Ao1: What did Cochrane and Sashidharan find?

A

They found that black afro-carribean immigrants in the UK are 7 times more likely to be diagnosed with schizophrenia than white people.

77
Q

Ao1: Why might diagnosis bias in culture be due to a genuine difference?

A

Because many people feel that the stress of being an immigrant could cause someone to become schizophrenic. There is a large stigma around black immigrants in the UK and racism occurs regularly so it would make sense. Many people feel that they may have a genetic predisposition to the disease and the racism acts as a stress which sets of the disease.

78
Q

Ao2: What did McGrath find?

A

They found that South African pregnant women living in high altitudes had a vitamin D deficiency. This is because of a dark pigment called melanin found in the skin which blocks UV rays which are needed to produce Vitamin D. This then ends up causing a deficiency in their child, causing them not to develop properly in the womb. This makes the child much more likely to get schizophrenia.

79
Q

Ao2: What does McGraths findings suggests about schizophrenia?

A

That it has a genetic cause in people of dark skin which could be triggered by the stress of being a minority.

80
Q

Ao2: What are 2 problems with McGrath’s findings?

A

They are only correlational meaning we do not know that vitamin D deficiency causes schizophrenia, we cannot draw a cause and effect relationship. It has also been found that high levels of vitamin D can make you more likely to get schizophrenia also showing us this relationship can be ver complex.

81
Q

Ao2: What did Lewis (1990) do and find?

A

They gave 139 psychiatrists written case histories of someone and asked them to prescribe a treatment for them and say if they have committed any criminal offences. They were told that the person was either afro-carribean or white, but the the symptoms were identical. They found that the afro Caribbean were more likely to be prescribed drugs and seen as more violent showing how they diagnosed based on social stereotypes.

82
Q

Ao2: What are two problems with Lewis’ (1990) study?

A

It was done just over 25 years ago meaning that peoples views have probably changed considerably since then as times have changed massively, therefore it is hard to generalise today. It also uses an artificial measure as people usually diagnose face to face meaning this could have affected their diagnosis. This means it lacks mundane realism.

83
Q

Ao1: Where was the DSM created?

A

Mainly the USA and Europe

84
Q

Ao1: Why might this cultural bias be due to over diagnosis?

A

Because the DSM V could be missing out important symptoms found in other cultures that we don’t find in the USA and europe. For example Nigeria has very different symptoms for depression, like a burning and crawling sensation.

85
Q

Ao1: Why is diagnosis biased when it comes to gender?

A

Because in the USA men are much more likely to be diagnosed with alcoholism and females are much more likely to be diagnosed with depression. Men are completely outnumbered when it comes to depression with females being 2-6 times more likely to be diagnosed with it.

86
Q

Ao1: Why might this gender bias be due to genuine differences?

A

We know that men and women are different biologically so it would make sense for us to have different rates of mental illnesses, if they are caused by biology. We know hormones fluctuate at different times, like around a woman’s period. We also have to deal with different stressors than men do, e.g childbirth and childcare.

87
Q

Ao2: What did Weismann (1977) find?

A

That there was some contribution of hormones to depression however it doesn’t completely account for the high rates of diagnosis compared to men as it is not that big a difference. This suggests that it must be due to an over diagnosis rather than a real difference.

88
Q

Ao2: What are 2 problems with Weismann’s study?

A

It was conducted around 40 years ago which means that modern technology is probably far more advanced than what was used back then to determine how much hormones attribute to depression. This means we may find they have a much larger impact now. Also, there is no difference in diagnosis rates for bipolar and schizophrenia so surely if it was due to over diagnosis then we would expect these to have different rates too?

89
Q

Ao1: Why might this gender bias be due to an over diagnosis?

A

They may ignore the fact that women have different circumstances to men and think they have depression when in actual fact they are just dealing with a lot more e.g childbirth, post natal depression and childcare. Or they may look at traditional sex role stereotyping and see women as more vulnerable.

90
Q

Ao2: What did Boverman et al (1981) do and find?

A

They asked healthcare professionals to describe what a healthy adult, male and female would be. They found that the description of the male was very similar to the adult which included words like ‘independent, decisive and assertive’ whereas the female description included words like ‘submissive, dependent and emotional’.

91
Q

Ao2: What are two problems with Boverman et al’s research?

A

It was conducted a long time a go which means it is no longer valid. This is because stereotypes like this have considerably reduced meaning that this research almost looks racist. Also, if emotional is seen as healthy for a female, surely they would not being over diagnosing them with depression because depression is a very emotional disease. This means it mustn’t be due to an over diagnosis from stereotyping.

92
Q

Ao2: What is a problem with concluding wether the bias is due to genuine differences or an over diagnosis?

A

The majority of the research is very outdated meaning we cannot generalise the findings to today as times have changed quite a lot since then.