Issues in mental health-The Medical model?

The Medical Model, assumptions?
Disorders have an organic or physical cause. The focus of this approach is on genetics, neurotransmitters, neurophysiology, and neuroanatomy. The approach argues that mental disorders are related to the physical structure and functioning of the brain
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The Medical Model, assumptions? 2
Behaviors such as hallucinations are 'symptoms' of mental illness, as are suicidal ideas or extreme fears such as phobias about snakes and so on. Different illnesses can be identified as 'syndromes'
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assumptions 2 extra?
clusters of symptoms that go together and are caused by the illness (these form the criteria in the diagnostic manuals used by clinicians to diagnose disorders).
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assumptions 3?
Once a correct diagnosis is made, the physiological cause can be identified, as all symptoms in the cluster should be related to the same cause. Therefore, physiological treatments are prescribed.
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assumptions 3 extra?
The approach assumes that all people with the same syndrome have the same physiological causes.
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Biochemical explanations: Neurotransmission?
Signals travel through your brain, as electrical impulses, via neurons (cells which are the wires of the brain). When the signal reaches the end of one neuron, and needs to travel to the next, it has to bridge the gap, which is called the synapse
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Biochemical explanations: Neurotransmission? 2
a chemical to be released into the synapse, which will activate receptors on the dendrites (the beginning) of the next neuron, in order to transmit the impulse.
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Biochemical explanations: Neurotransmission? 3
These chemicals are called neurotransmitters. There are many different types which transmit different signals, telling us how we feel and controlling biological processes such as arousal and sleep.
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Biochemical explanations: Neurotransmission? 4
One such neurotransmitter is Serotonin, which is involved in the regulation of sleep and mood
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Biochemical explanations: Neurotransmission? 5
. LOW levels of serotonin have been correlated with an increase in symptoms of depression (i.e. fatigue (tiredness), negative affect (mood)). For the neurotransmitter to activate the next neuron
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Biochemical explanations: Neurotransmission? 6
the chemical must bind with a receptor in the dendrite; an analogy for this is a spaceship docking, where the docking site must be the same size/ shape to dock properly for its cargo to pass
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Low Serotonin hypothesis, what did Freis (1954) find?
a number of hypertensive (high blood pressure) patients he treated with reserpine suffered from severe side effects – namely major depressive episodes. He reported that a number of these patients had gone on to commit suicide.
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what did freis lead to?
This led to researchers testing the drug, reserpine, on animals. It was found that this drug lowered levels of dopamine (DA), Noradrenaline (NA) and Serotonin (5-HT).
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how are post- mortem used?
Further research into post-mortem studies of suicide victims found lowered levels of serotonin, suggesting that lowered levels of serotonin may be related to suicidal feelings ( a symptom of Depression).
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what does this claim?
Support for the hypothesis stems largely from the effectiveness of SSRIs.
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how do they work?
They inhibit (prevent) the re-uptake of serotonin from the synapse, meaning it can continue to bind with receptors at the dendrite and activate serotonin pathways, which are thought to be responsible for mood, sleep and social behaviours.
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evaulation 1?
It is difficult to test because it is not possible to measure levels of serotonin in the brain very precisely. We can do so by looking at indirect markers, like urine or spinal fluid. can look at the number of serotonin neurons in a brain after death
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evaulation 2?
Animal studies supporting this theory are ungeneralizable to humans because animal brains have less complex structures, and animals experience emotion differently to humans.
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evauation 3?
Although post-mortem studies allow us to research humans and the findings are therefore more applicable to explain human disorders such as Depression, they can be confounded by the rapid deterioration of the brain following death + chemical changes
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evauation 4, reductionist?
it ignores the roles of other neurotransmitters in depression, such as Dopamine (sleep) and Noradrenaline (alertness and arousal) treatments such as DRI (Dopamine reuptake inhibitors) and NRIs Noradrenaline reuptake inhibitors) also elevate depressio
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evaulation, 5?
Using drug trials as evidence means researchers are making assumptions about the causes based on the effects of drugs. Drugs may indirectly affect other processes, such as neurogenesis. It may be these indirect effects
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evaulation 5 extra?
rather than the increase in levels of serotonin in the synapses, which improves symptoms of Depression.
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Mintun et al. (2003), background?
Mintun studied neurons in the hippocampal region of the brain, which can interpret whether an experience is good or bad, or whether a person is angry, happy or sad at you from their facial expression.
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Mintun et al. (2003), background? 2
It is also part of the limbic system; the limbic system controls arousal, emotion, and motivation, by influencing the nervous system and the release of hormones.
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aim?
To investigate whether people with the symptoms of major depressive disorder (MDD) show decreased binding of serotonin to receptors, in the Hippocampal region of the brain.
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sample?
46 patients with Major Depressive Disorder, not on anti-depressants, and 29 healthy control participants.
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method?
Controlled quasi-experiment with an independent measures design
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procedure?
A PET (Positron Emission Tomography) scan was conducted, to measure the levels of serotonin binding to the receptors of neurons in the hippocampal region of the brain.
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results?
Depressed patients showed a 29% reduction in levels of serotonin binding with receptors, compared to controls (p=0.004). Depressed patients had fewer serotonin receptors in the Hippocampus.
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Conclusions?
It is likely decreased serotonin receptor binding is responsible for inability to regulate moods in depressed patients, as this would result in less activation of serotonin pathways
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conclusions 2?
Sheline, researching alongside Mintun, found that the volume of the hippocampus in depressed patients was smaller; this suggests that the volume loss causes receptors to become damaged meaning the serotonin cannot bind with them
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conclusions 3?
Therefore, serotonin levels in depressed patients may not be abnormal; depression may be caused by hippocampal damage.
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Evaluation, BRAIN SCANS?
Brain scans only demonstrate neurological correlates of behaviour; this means this study only shows a relationship between a dysfunctional neurological process and depression.
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evaluation, brain scans? 2
This does not demonstrate cause and effect; the relationship could be explained by damage to the Hippocampus CAUSING depression, or it could be explained by depression CAUSING damage to the Hippocampus.
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evaulation brain scans ethics?
What are the ethical issues raised by the use of PET scans (refer to terms from DC COWPAD)? Remember that we should consider cost/ benefit when we discuss ethics- why is the use of this brain scan technique justifiable?
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Injections of radioactive material?
medical procedure with potential side effects. Patients may be distressed by needles. The scanner can be a distressing environment particularly with patients with Claustrophobia, or a fear of loud noises. Issues with protection from harm.
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how is ethics justified?
Justified by the usefulness of the data collected for the Ps and others with depression. If an abnormality in the brain is found to be the cause of depression, treatments which trigger neurogenesis can be used.
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evaluations data collected?
Brain scans gather quantitative data which is translated by a computer programme into precise imaging of structures or activity in areas of the brain. Considering this statement, what is the benefit of using brain scans?
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data collected reliable?
data can be analysed in a consistent way. It is more objective and scientific than trying to interpret qualitative data as people use language differently to express themselves.
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data collected reliable 2?
The quantitative data gathered is precise because of the specialised equipment used to measure it. More objective and scientific. It allows researchers to compare brain activity in the Hippocampi of people with and without depression.
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evaulation, POPULATION VALIDITY?
What is a weakness of the sample used regarding its generalisability to the target population? (Make sure you identify the target population in your answer)
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example small pop validty?
Small (46 patients with Depression) Individual differences in structure of brain and processes of neurogenesis may effect applicability of results to all individuals with MDD.
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Why did the researchers use a sample limited in size?
Cost/ time required to conduct PET scans
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Genetic explanations?
The 5-HTT gene is responsible for the production of a serotonin re-uptake transporter. This transporter is responsible for the reuptake of serotonin into the presynaptic neuron
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genetic explanations 1 extra?
after it has been released into the synapse to bind with receptors on the post-synaptic neuron
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genetic explanations, 2?
In the 5-HTT gene, the two alleles which were studied by Caspi were known as the 'long' and 'short' alleles. The 'long' allele was thought to lead to the production of a greater number of serotonin transporters, giving greater control
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genetic explanations 2 example?
i.e. having an optimum balance over the levels of serotonin in the synapse.
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Method?
Caspi et al. determined the 5HTT alleles (variation) for each of their 847 participants (s/s, s/l, l/l). Then, when the participants were 26 years old, the researchers evaluated
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method 2?
1. Whether or not the participants had experienced one or multiple stressful events since their 21st birthday. 2. Whether or not they had depression in the past year.
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what did the results suggest?
individuals having two short forms (s/s) of the gene were most likely to be depressed after stressful events
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what did the results suggest 2?
Individuals with one long and one short (s/l) form were moderately likely to be depressed after stressful events. * Those with two long alleles (l/l) typically responded as if no stressful events had occurred.
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What % of participants with at least one short allele developed depression following 3 stressful life events, compared to the % of participants with two long alleles?
27% compared to 11%
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What % of participants with at least one short allele developed depression following 4 stressful life events, compared to the % of participants with two long alleles?
33% compared to 17%
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What % of participants with at least one short allele developed depression following 0 stressful life events, compared to the % of participants with two long alleles?
10% compared to 10%
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Conclusion?
Short alleles predispose an individual to Depression, but an interaction is required with the environment (stressors) in order to express the gene
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conclusion 2?
People with short versions of the gene, which produce less reuptake transporter, are more vulnerable to depression, because the long version of the gene produces more of the reuptake transporter
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conclusion 3?
This allows serotonin to be taken back into the pre-synaptic cell faster, i.e. like reloading your gun faster to fire again.
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conclusion 4?
This opposes the serotonin hypothesis as SSRIs are presumed to work by inhibiting re-uptake to leave more serotonin in the synapse to continue to active the serotonergic pathways
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conclusions 5?
This opposes the serotonin hypothesis as SSRIs are presumed to work by inhibiting re-uptake to leave more serotonin in the synapse to continue to active the serotonergic pathway
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In what way could the conclusions presented be considered holistic?
It concluded that short alleles predispose an individual to Depression, but an interaction is required with the environment (stressors) in order to express the gene.
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What evidence shows that short versions of the 5HTT gene cannot be the only explanation for Depression?
People with two long versions of the 5HTT gene still developed Depression
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Key Research: Gottesman et al. (2010), aim?
To investigate the probability (chance) of a child with TWO parents with psychiatric illness being diagnosed with the same disorder as their parents.
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sample?
Using the Civil Registration System of Denmark, those aged 10+ before Jan 2007, born during or after 1968, who had clear records of biological parents, were sampled from. * There were 2,685,301 studied: some with more than one child.
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METHOD?
This was a quasi experiment: individuals who had been admitted to a psychiatric hospital and diagnosed with either depression, bipolar, or schizophrenia were identified from the Psychiatric Central Register.
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method 2?
The children of each couple were checked on the Register as well for records of admittance to a Psychiatric hospital and their diagnosis upon discharge. This diagnosis was made using the ICD-8 or ICD-10.
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Conditions?
BOTH parents with same diagnosis: either Schizophrenia (270 children), Bipolar (146 children), or Depression * ONE parent with a diagnosis: either Schizophrenia (473 children), Bipolar (23,152 children), or Depression
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conditions 2?
NEITHER parent admitted with diagnosis * General public: people who were not registered as having a diagnosis or not
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findings?
When BOTH parents have Bipolar, there’s a 24.9% probability of the child having Bipolar, and when ONE parent has the disorder, there’s a 4.4% probability of the child having Bipolar, whereas when NEITHER parent has Bipolar,0.48% probaby for child
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finding 2?
When BOTH parents have the disorder, there’s a 27.3% probability of the child having Schizophrenia, and when ONE parent has the disorder, there’s a 7% probability of the child having Schizophrenia, whereas when NEITHER parent has a disorder
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finding 2 extra?
there is a 0.86% probability of the child having Schizophrenia
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findings 3?
Children did not always have the same diagnosis as their parents.
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conclusions?
The risk of developing Bipolar is approximately 50x as great when both parents have Bipolar compared to when neither do, and 4x as great when one parent has Bipolar compared to when neither do,
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what does conclusion 1 indicate?
ndicating this is due to the possibility of inheriting a gene predisposing you to Bipolar.
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conclusion 2?
The risk of developing Schizophrenia is approximately 30x as great when both parents have Schizophrenia compared to when neither do, and 8x as great when one parent has Schizophrenia compared to when neither do,
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what does conclusion 2 indicate?
indicating this is due to the possibility of inheriting a gene predisposing you to Schizophrenia.
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conclusion 3?
This could be explained by the fact that there must be an interaction between a genetic vulnerability and an environmental trigger for Schizophrenia or Bipolar to develop.
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evaluation, reductionisum?
Explaining mental illness through genes is too simplistic, as it ignores other explanations for inter-generational transmission, such as the fact that the children are likely being raised by their parents +may have learnt abnormal behaviour from them
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reductionsium 2?
or the environment in which their living may be disrupted because of their parent’s illness.
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evaluation, Reliability (Psychology as a Science)?
As this study gathered secondary data, it cannot be certain whether records are being input in a consistent way by all hospitals, whether the quality of diagnosis is consistent for all patients in the population
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evaluation, Reliability (Psychology as a Science)? 2
and whether all people with a mental illness are consistently seeking a diagnosis (particularly considering zeitgeist as the stigma surrounding mental illness may be worse in older populations).
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Determinism?
Explaining that mental illness is controlled by genes means that it is outside of the individual’s control. This can be beneficial because it results in less self-blame, or blame from society, for the condition.
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determinisum 2?
This has led to improvements in medical treatments, such as the development of SSRIs to improve symptoms of depression.
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Ethics (Confidentiality and Consent)?
The study gathered data from the Civil Registration System and Psychiatric Central Register. This is accessible by the public and therefore the participants’ agreement was not required.
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Ethics (Confidentiality and Consent)? 2
The data is anonymised, as each individual is assigned a unique identifying number which is used on both systems. There are safeguards in place to ensure the anonymity of this data is inviolable
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Social Sensitivity (ethics/ usefulness)?
Eugenics: research suggesting a genetic, and therefore hereditary, explanation for mental illness can be used to discriminate against individuals considered to have maladaptive genes; this has resulted in eugenics programmes during the Holocaust
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Social Sensitivity (ethics/ usefulness)? 2
which aimed to exterminate anyone with a mental or physical disability. This also occurred during the early 1900s in the USA; women considered to be mentally retarded or disabled were forcibly sterilised - prevent them passing trait to their kids
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Population validity (usefulness)?
It is representative of the target population of Denmark, as it recruits all individuals with children registered in Denmark born during or after 1968. Researchers could not select only participants who showed hereditability.
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Population validity (usefulness)? 2
However, there’s an issue with ethnocentrism, as The Medical Model assumes universality (that one disorder can be explained in the same way for all cultures)
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Population validity (usefulness)? 3
and Gottesman has only demonstrated that genes may be an influential factor in Bipolar and Schizophrenia in a Danish sample.
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Application: Biological treatment, Karp & Frank (1995)? aim
to compare drug treatment and non-drug treatments for depression.
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Methodology?
A review article of previous research into the effectiveness of single treatments and combined drug and psychotherapeutic treatments of depression.
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Participants?
The research which was reviewed was concentrated on women diagnosed with depression. There were nine pieces of research, from 1974 to 1992. In total, 529 women took part in the selected studies.
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Design?
Much of the research used an independent design, with patients either having: single drug treatments, single psychological treatments, combined treatments and some placebo groups.
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Procedure?
Depression was analysed using a variety of depression inventories, and patients were generally tested prior to treatment, after treatment and in some cases after a period of time as a follow up.
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procedure 2?
Some health practitioner assessments of symptoms were also used in some of the research
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Findings?
Many studies found that adding psychological treatments to drug therapy did not increase the effectiveness of the drug therapy. Occasionally studies did show less attrition when combined therapies were used.
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findings 2?
This means that individuals were more likely to continue with their treatment when cognitive therapy was given in addition to drug therapy.
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Conclusions?
Although it seems logical that two therapies are better than one, the evidence does not show any better outcomes for patients offered combined therapy as opposed to only drug therapy, showing the effectiveness of drug therapy on depression.
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Evaluation?
Kirsch et al. (2002) conducted a meta-analysis of published and unpublished studies, and found that 57% of drug trials for anti-depressants, funded by pharmaceutical companies, showed that they had no significant effect.
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evaulation 2?
Side-effects can include vomiting, nausea, insomnia, sexual dysfunction or headaches, which may be a barrier to patients taking the drug. Seroxat, a type of anti-depressant
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evaluation 2 ?
was also banned for under 18s followed an exposé showing it increased risk of suicide in children.
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evaluation 3?
The medical treatment for depression is deterministic because it assumes that dysfunctional behaviour is caused by biological factors like issues with neurotransmission, brain function, or genes, which cannot be controlled by the patient.
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evaluation 3 extra?
For example, Karp and Frank concluded that biological drug treatments were the most effective at treating depression in women. This treatment has negative consequences because it takes control from the patient
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evaluation 4 extra?
resulting in them becoming dependant on the drugs to maintain a healthy state of mind. However, it can be beneficial for patients because they are not blamed for their disorder if a biological cause is assumed
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evaluation 5 extra?
and therefore it becomes the responsibility of society to intervene to improve their condition, i.e. through providing access to pharmaceutical treatments.
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The Medical Model, assumptions? 2

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Behaviors such as hallucinations are 'symptoms' of mental illness, as are suicidal ideas or extreme fears such as phobias about snakes and so on. Different illnesses can be identified as 'syndromes'

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assumptions 2 extra?

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assumptions 3?

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assumptions 3 extra?

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