Clinical Flashcards
What are the criterion (symptoms) of Anorexia nervosa?
Criterion A: restriction of energy intake and low body weight- BMI of less than 17kg/m^2 or using DSM-5 tend to accept the ICD-10 definition.
Criterion B: intense fear of gaining weight even if the current body weight is low. This is done by excessive exercise, restriction, binge purging, and the use of laxatives or diuretics. DSM-5 gives no examples but the ICD-10 does
Criterion C: Distortion of body image where the weight is hugely overestimated and emphasis on body weight in the patient’s view of themselves- poor self-image, overuse of body weight in self-evaluation.
DSM-5 uses the three symptoms
What are the subtypes of Anorexia nervosa?
1) Restricting- weight loss through diet, excessive exercise, and fasting within the past three months.
2) Binge type/purging- alternate with purging, with the misuse of laxatives, self-induced vomiting, diuretics or enemas in the past three months.
What are the ratio, onset, and stressor of Anorexia nervosa?
Ratio: females to males (10:1)
Onset: 13-18 years old
Stressors: leaving home or university are examples
What is the prognosis of Anorexia nervosa?
6x as many deaths were expected for females with Anorexia nervosa. The highest mortality rate of all mental disorders. Amenorrhoea (lack of menstruation). High prevalence of the disorder in high-income countries. Dahlgren et al. (2017), the lifetime prevalence rate for females ranged from 1.7%-3.6% and was 0.1% for males.
What are some examples of secondary symptoms of Anorexia nervosa?
Brittle nails, amenorrhoea (lack of menstruation), hair thinning, dry flaky skin, osteoporosis (weaken bones)
What is co-mobility and what is co-mobility for Anorexia nervosa?
Co-mobility is the presence of another/more mental disorder in someone. Anorexia nervosa usually also shows anxiety, depression, and OCD
What is the strength of the diagnosis of Anorexia nervosa?
DSM-5 is reliable. Sysko et al. (2012) measured the test-retest reliability of Anorexia nervosa diagnosis, participants were given a telephone interview, and between three and seven days later, a different assessor telephoned each participant and repeated the assessment. The extent of agreement across the two occasions was described as ‘excellent’. Trained assessors can reliability diagnose AN using the DSM-5 criteria.
What is the competing argument for the strength of the diagnosis of Anorexia nervosa?
Doesn’t support that the view DSM-5 criteria are reliable. Thomas et al (2015) most studies go beyond the official DSM-5 criteria in operationally defining AN. Researcher- defined cut-off point for ‘significantly low weight’ because none is specialised in the DSM-5. Research studies are higher than what they would be in real life (easier to achieve agreement between raters when criteria are defined in detail)
What is a weakness of the diagnosis of Anorexia Nervosa?
The lack of validity. Smith et al (2017) looked at the validity of four severity specifiers. 109 adults diagnosed with AN, higher BMI was linked with greater eating disorders psychopathology. Opposite of what was expected outcomes. Failed to distinguish accurately between people.
What is EPHX2?
It is a gene that codes for an enzyme called epoxide hydrolase that breaks down (metabolises) cholesterol and if there is a fault, the enzyme will misshape and disrupt the metabolism of cholesterol as the cholesterol can’t bind to the enzyme, causing higher chronic cholesterol. This can cause people not to be reminded to eat. Found by Scott-Van Zeeland
What is ITPR3 and how does this affect Anorexia nervosa?
It is a gene that encodes for a protein which is the receptor for inositol triphosphate (detecting sweet and bitter tastes). Dysfunction of the taste pathway so people with AN are indifferent to tastes that others enjoy and that partly motivates eating. A dysfunction causes a misshape of the receptor, so serotonin can’t bind. Found by Scott-Van Zeeland with 1205 AN participants and 1948 control participants
What are the 4Ds of diagnosis?
Deviance
Dysfunction
Distress
Danger
What is deviance?
Behaviours that are unusual. Understand the statistical and social norms of particular social groups and cultures. Failure to conform to social norms can lead to negative attention
What is dysfunction?
Inability to do everyday activities. Looks at what is going on around them and their deterioration.
What is distress?
Emotional pain or anxiety and this may manifest in physical symptoms. Gather quantitative data using scales like Kessler Psychological Distress Scale (K10), which is a 10-item self-report questionnaire taken over 4 weeks.
What is danger?
Careless, hostile, or hazardous behaviour which could jeopardise the safety of the individual and/or others. People could be detained under the Mental Health Act which requires the agreement of 3 professionals and people are taken to a mental health hospital for treatment.
What is the supporting evidence for the 4D model?
It is valid as it is not over or under inclusive like the deviance from social and statistical norms are used with another 4D. However, subjective like cultures in Fiji praise curvy shapes over slimmer ones like in the west.
How does the 4D model lack reliability?
Distress is objective and people may show distress in different ways. However, quantitative data can be gathered with the Kessler Psychological Distress Scale (K10).
How does the 4D model affect labelling?
By labelling someone as dangerous then people are less likely to get diagnosed. It could also have an effect on a ‘self-fulfilling prophecy’ as their behaviour may become dangerous from being labelled dangerous. But labelling doesn’t cause danger.
What is the DSM?
It is made by the American Psychiatric. There are 3 sections. Section 1 is about the guidance of the system. Section 2 gives details of the disorders. Section 3 is a section on new disorders. It is a ruling of best fit and rules out other disorders. It is done by observation and unstructured interviews with Beck Depression Inventory with 21 questions.
What is the kappa score (overall)?
The test is then retested later on or by another clinician. 0.7 felt like a good score.
What are the different types of validity?
Descriptive (symptoms), aetiological (causal factors), concurrent (method), and predictive.
What is the reliability of DSM?
Good. Field trials of DSM-5- kappa score of 0.46 (Regier) and Sartorius= 0.86 of schizophrenia (consistent)
What happens to the agreement (increase/decrease) of the DSM?
The agreement falls (Cooper). Least reliable in the major depressive disorder of the DSM.
Why was the DSM-III better than the DSM-5?
Kupfer and Kraemer (2012) found that the DSM-5 field clinicians say they would ‘work as they usually would’. DSM-III used careful testing and retesting.
What is the validity of the DSM?
Kim-Cohen concurrent validity of conduct disorder as they got interviews from mothers and children, observing children’s anti-social behaviour and questionnaires from teachers. The predictive validity to give accurate treatment.
Why is there low validity in the DSM?
Co-mobility and illness share similar symptoms. There are also cultural variations. Rastafarians- neologism (new words) clinicians may not be aware of this.
What is the ICD?
It involves mental and physical disorders created by the WHO. It is multilingual and is mostly used in the UK. Used by policymakers and organisations. Chapter 5 focuses on mental disorders and is coded as F with F20-F29 representing schizophrenia, schizotypal and delusion disorders. Each section has leftover code allowing new disorders to be added. Comprehensive and inclusive enough without overlap. Clinicians select keywords from interviews like hallucinations a go by alphabetical index or straight to the section.
What is the dopamine hypothesis?
Excitatory neurotransmitters as it increases the likelihood of the next neurotransmitter firing. This is known as the ‘feel-good’ hormone.
What is hyperdopaminergic and how does this impact schizophrenia?
The excess of dopamine. Schizophrenia patients have too much dopamine as it is firing to easily and too often.
What are amphetamines and their effect on non-schizophrenia people?
Increase dopamine energy (drug)- mode of action on dopamine. If a ‘normal’ (non-schizophrenia) person took amphetamines they would experience similar symptoms to a schizophrenia patient like hallucinations. We infer that schizophrenia is the result of excess dopamine.
What do antipsychotics do to dopamine and people with schizophrenia?
It decreases dopamine levels by binding to the postsynaptic receptors neurone which then dopamine can’t bind to the receptors and is then taken up by the reuptake channel. This means the action potential can’t be triggered. The dopamine is displaced and left in the synaptic cleft. This reduces schizophrenia symptoms by acting on dopamine the cause of dopamine is excess dopamine.
What does reduced beta hydroxylase?
The enzyme that breaks down dopamine, if there is less of this then dopamine is more likely to bind to the postsynaptic receptors and then trigger more action potential.
What does the proliferation of D2 receptors do?
If there are more receptors then it is more likely to fire.
What did Davis et al. find with hyperdopaminergic?
It causes positive symptoms, which is adding to someone’s normal function like delusions, disordered thinking, hallucinations, and thought insertion. This is in the mesolimbic pathway (reward pathway)
What did Davis et al. find out about hypodopaminergic?
It causes negative symptoms, which are taking away someone’s normal function like the flat effect, which reduces the range of emotions, and alogia, which is a poverty of speech in catatonic schizophrenia. In the mesolimbic pathway (wakefulness)
What is serotonin?
An inhibitory neurotransmitter
What did Carlsson et al. (2000) find out about serotonin?
Carlsson et al. did a meta-review which analyses the findings of other research on neurotransmitters (secondary data). He found that Clozapine binds to the D1 and D4 receptors but only weakly to the D2 receptors to reduce positive symptoms. Based on existing knowledge D2 is important for schizophrenia. The study suggests this is reductionist as D2 doesn’t work with Clozapine. It also binds with serotonin reducing positive and negative symptoms. Focusing on the interaction between neurotransmitters as serotonin regulates dopamine in the mesolimbic pathway- reward pathway.
What are the 4 key symptoms for schizophrenia?
Thought insertion, hallucinations, delusions, disorganised thinking.
What are the features of schizophrenia?
It has a lifetime prevalence which is 0.3-0.7%. This varies with the ethnicity, nationality and geographic origin of immigrants. Onset is slightly earlier in males than females (early to mid-20s vs late 20s). Males tend to have a poorer prognosis than females. Females are overrepresented in late-onset cases (40+). The prognosis is variable and hard to predict. A minority recover completely, but most experience chronic, episodic impairment and some show progressive deterioration, with increasingly brief periods of remission and severe cognitive deficits. Positive symptoms reduce over time but debilitating negative symptoms often remain.
What is the strength of the diagnosis of schizophrenia?
Made to a high degree of certainty with both the DSM-5 and ICD-10. Field trials of the DSM-5 reported a kappa of 0.46 (good)- Regier et al. 2013- Sartorius et al. 1995- 0.86 kappa score (very good). Only 3.8% of clinicians said they lacked confidence in their diagnosis of schizophrenia using the ICD-10. Schizophrenia is sufficiently detailed and distinguishes other disorders with the same symptoms and features.
What is a weakness of the diagnosis of schizophrenia?
The diagnosis of schizophrenia is not easy as it shares symptoms with various disorders. For example, hallucinations can be experienced by people with depression and post-traumatic stress disorder and can be caused by drug withdrawal, metabolic disorders and sleep deprivation while catatonic behaviour can be symptomatic of major depression or bipolar disorder.
How does culture affect the diagnosis of schizophrenia?
If the client is from a different background than the psychiatrist. Rastafarians often use neologism (new words) which is a play on words like ‘overstand’ for ‘understand’, and a clinician who is unaware of this may see this as a sign of disordered thinking. This means that the diagnosis of schizophrenia requires awareness and sensitivity to culture and linguistic differences.
What did Luhrmann et al. (2015) find out regarding culture?
Interviewed 60 Americans, Indian and Ghanaian people with schizophrenia. They found that 70% of the American people said their voices told them to hurt people while 50% of Ghanaians said their voices were mainly positive.
Classic study: Rosenhan (1973)- Aims
Show the flaws in the process of psychiatric diagnosis. Demonstrated the psychiatrists were unable to distinguish the ‘sane from the insane’ and aimed to provide evidence to support the idea that mental disorders lie not with individuals but with the person making the diagnosis. He gained access to psychiatric wards as a patient and obtain information about how clients/patients were treated by staff and each other.
Classic study: Rosenhan (1973)- Sample
A psychology student, paediatrician, psychiatrist, painter, housewife and three psychologists (3 females and 5 males including Rosenhan)
Classic study: Rosenhan (1973)- Procedure
Each person took on the role of a pseudo-patient (fake). Each person presented themselves at a psychiatric hospital complaining of the same symptoms; hearing same-sex, an unfamiliar voice that was unclear but said ‘empty’, ‘hollow’ and ‘thud’, terms not normally linked to schizophrenia. They gave false information. They approached 12 hospitals in 5 different states and once they were admitted they would behave normally following a period of unsurprising nervousness. In order to be released they had to convince the staff that they were sane by cooperating and following orders. They observed.
What was the follow-up study of the classic study Rosenhan?
The hospitals were told to expect pseudo-patients (fake patients) but none were sent. The staff at the hospitals were to rate every patient from 1-10 (with 1 being that the patient was fake.
What was the mini study of Rosenhan?
Pseudo-patients approached a staff member on the hospital grounds and asked a polite question about their release. Responses were compared with a similar encounter of that between people on the Stanford University Campus.
What were the findings of the initial study?
All pseudo-patients were admitted (seven with schizophrenia and one with bipolar disorder), most released with ‘schizophrenia in remission’. The length of stay was between 7 to 52 days, with 19 being the average. 30% of real patients were suspicious of the pseudo-patients
What were the findings of the follow-up study?
41/193 patients were wrongly reported as fake by at least one member of staff, 23 by at least one psychiatrist and 19 by one member of staff and then one psychiatrist.
What were the findings of the mini-experiment?
4% of pseudo-patients received an answer from a psychiatrist and 0.5% form a nurse. 100% of people on campus stopped and talked.
What were the findings of the mini-experiment?
4% of pseudo-patients received an answer from a psychiatrist and 0.5% form a nurse. 100% of people on campus stopped and talked.
What was the conclusion of Rosenhan’s study?
‘We cannot distinguish the sane from the insane in psychiatric hospitals’
The hospital environment created situational factors leading to depersonalisation and segregation. Overdiagnosis occurred because clinicians avoided calling a sick person healthy. But in the follow-up study, staff erred in the opposite direction to avoid calling a healthy person sick.
What is the strength of Rosenhan’s study (in terms of design)?
Used covert participant observation and collected both qualitative and quantitative data. Staff were unaware the pseudo-patients were researchers, so their behaviour would have been more natural. Therefore, the data had high ecological validity, enhanced by the wealth of the data collected by naturalistic observation.
What is a counter-argument to the strength of Rosenhan’s study?
It could be argued that the validity of the study is poor. Pseudo-patients may have only recorded instances of negative interaction between staff and patients as they were all supporters of Rosenhan. Only one pseudo-patient per hospital so there is no way to check the reliability of the data collected.
What is a weakness of Rosenhan’s study?
Demand characteristics may explain the diagnosis. Psychiatrists admitted pseudo-patients on flimsy evidence because they didn’t expect someone to fake symptoms. They would assume anyone seeking admission must have a good reason to. This may challenge some on the validity of the conclusions.
What is the strength of Rosenhan’s study (in terms of support for the anti-psychiatry movement)?
Szasz (1960) argued that mental illnesses are problems in living not diseases, and therefore it is inappropriate to use a medical model for the diagnosis of mental illness. Rosenhan supports this as it showed that the diagnosis of mental state was invalid. He also argued that labels for mental illness, once given, were ‘sticky’ so patients would forever be labelled ‘schizophrenic’. Shows that psychiatry needs to be reformed, to avoid the misuse of diagnostic labels. A behavioural approach to avoid labels.
What is the issues and debates that relates to Rosenhan’s study?
Ethics- long-term benefits to society but there were risks to the pseudo-patients, clinicians and real patients. For example, the clinicians were made to feel incompetent and real patients may have been discriminated against if clinicians believed they were fake (psychological harm)
What is the application of Rosenhan’s study?
Spitzer saw the DSM-III revision as an opportunity to address the issues raised by Rosenhan, It arguably paved the way for critical reform to the diagnosis process, though it was not Rosenhan’s intention.
What was the aim of the contemporary study: Carlsson et al. (2000)?
Review evidence for and against the dopamine hypothesis. Consider other neurotransmitters (glutamate, serotonin). Explore new antipsychotics (help with treatment resistance)
What was the first point Carlsson made (contemporary study) - dopamine hypothesis revisited?
Evidence still supports this hypothesis, e.g. studies using PET scans show how amphetamine (dopamine agonist) enhances psychotic symptoms. But still doesn’t apply to all people with schizophrenia.
What was the second point Carlsson made (contemporary study) - beyond dopamine?
Glutamate -PCP (‘angel dust’) induces schizophrenia symptoms, an antagonist (stops glutamate) of NDMA (glutamate) receptors. This leads to increase dopamine activity (acts as an accelerator).
What was the third point Carlsson made (contemporary study) - glutamatergic control of dopamine?
Glutamate also affects the release of GABA, with the opposite effect (a ‘brake’, reducing dopamine activity). Therefore low glutamate (hypo glutamatergic) may cause an increase or decrease in dopamine. Normally, there is a balance between ‘accelerator’ and ‘brake’ but the distribution of either can produce schizophrenia-like symptoms
What was the fourth point Carlsson made (contemporary study) - glutamate-dopamine interaction?
Hypo-glutamatergic in cerebral cortex –> negative symptoms
Hypo-glutamatergic in basal ganglia –> positive symptoms
Dopamine + glutamate pathways interact and affect the striatum.
What was the fifth point Carlsson made (contemporary study) - thalamic filter?
It is suggested that the psychotogenic pathway the thalamus may be ‘turned’ on or off depending on which pathway is activated. Normally the inhibitory glutamate pathway dominates.
What was the sixth point Carlsson made (contemporary study) - comparing two experimental schizophrenia models?
- Hyperdopaminergic model - the traditional view of dopamine (increase produces psychotic symptoms) is not challenged by the second model, merely extended.
- Hypoglumatergic model - glutamate can increase or decrease dopamine activity, depending on whether an accelerator or brake is applied.
Haloperidol tackles hyperdopaminergic, and M100907 tackles hypoglutamatergia (affecting GABA via serotonin). People with different symptoms could be treated with different drugs. Or use combined drugs to tackle both problems.
What was the seventh point Carlsson made (contemporary study) - is the therapeutic exhausted?
Understanding mechanisms that moderate dopamine activity may show new ways to stabilise the dopamine system. May avoid some negative effects of current antipsychotics.
What was the eighth point Carlsson made (contemporary study) - concluding remarks?
More attention could be focused on other neurotransmitters (e.g. acetylcholine) and other pathways in the brain.
What is the strength of Carlsson’s study (2000) - research?
Carlsson and Carlsson (1989) gave mice a drug to reduce motor activity followed by MK-801 (reduces glutamate and increases serotonin and dopamine in the nucleus accumbens) MK-801 restarted motor activity but continued to use highly abnormal, psychotic-like behaviour. This suggests that schizophrenia may be caused by glutamate irregularity and also implies that glutamate agonists may be effective treatments.
What is the counterargument for the strength of Carlsson’s study (research)?
This is not the full story. Since the study, two further neurotransmitters (anandamide and nitric oxide) have been identified as important in psychosis and may lead to new treatments (Crippa et al. 2015). It has also been suggested that neurotransmitter imbalances may arise from autoimmune problems (Severance et al. 2018) - this means even glutamate is not the end of the story.
What is a weakness of Carlsson’s study (culture)?
Luhrman (2015) showed that the US participants were more likely to hear violent and frightening voices whereas Ghanaian and Indian people had more positive experiences. It may be that the review didn’t include cultural factors because of conclusions in the reviews are based on animal models. Thus animal models may fail to capture holistic lived experience of schizophrenia, which includes other people’s reactions to their symptoms (truer reflection)
What is a weakness of Carlsson’s study (experiences)?
Some evidence of the dopamine hypothesis was based on people with schizophrenia during acute periods. But people with chronic schizophrenia may respond differently to drugs when they are between episodes (e.g. more side effects). Therefore, research should consider all the phases of the disorder so better conclusions can be made about efficiency and adherence.
What are the issues and debates related to this study?
Gender. On the average most onset of schizophrenia is later in women than it is for men and the prognosis is generally more positive. The main female sex hormone oestrogen has a neuroprotective role, which helps regulate glutamate, serotonin and dopamine (Gogos et al. 2015). This suggests that gender-related oestrogen-based medications may provide yet another pathway for treating schizophrenia.
What is the application of Carlsson’s study?
Development of new drug treatments. Serotonin antagonists and glutamate agonists are effective in reducing both positive and negative symptoms. By tackling more precisely the disturbances of neurotransmitter systems, their action is less likely to have detrimental effects. These advances have helped people who were treatment-resistant or who experienced side effects (e.g. tardive dyskinesia)
What is the strength of the diagnosis of Anorexia nervosa?
DSM-5 is reliable. Sysko et al. (2012) assessed participants by telephone interview using the DSM-5 criteria for AN and repeated this with a different assessor a few days later. The extent of agreement across the two occasions (test-retest reliability) was described by the researcher as ‘excellent’. This suggests that trained assessors can reliably diagnose AN using the DSM-5 criteria.
What is the counterargument for the strength of the diagnosis of Anorexia nervosa?
This does not necessarily support the view that the DSM-5 criteria for AN are reliable. Thomas et al (2015) point out that many studies go beyond the DSM-5 criteria defining AN. Many use a researcher-defined cut-off point for ‘significantly low weight’ because none is specified in the DSM-5. This means that reliability estimates in research studies are likely to be higher than they would be in real-life clinical practice.
What is the weakness of the diagnosis of Anorexia nervosa?
Smith et al. (2017) looked at the validity of the four severity specifiers. In 109 adults diagnosed with AN, high BMI (low severity) was linked to greater eating disorder psychopathology- the opposite of the expected outcome. This is an issue for the DSM-5 severity specifiers, as they fail to distinguish accurately between people and therefore lack validity.
What is DAT1 and how does that link with explaining Anorexia nervosa?
DAT1 gene codes for a protein called the dopamine transporter (regulates the movement of dopamine in reuptake). Mutation in the DAT1 gene disrupts this process, leaving abnormally high dopamine for transmission. Dysregulates the brain’s reward system (mesocorticolimbic dopamine circuit) so eating’s normal rewarding function is impaired.
How does the 5-HTR2A gene link with explaining Anorexia nervosa?
Codes for a subtype of postsynaptic serotonin receptor called the 5-HT2A. The mutation affects the structure of the 2A receptor- less binding between serotonin and receptor (appetite-related information is not transmitted normally). Kaye et al. (2005) found significantly decreased 5-HT2A activity in the serotonergic system throughout the brains of people with AN (especially in the cingulate cortex).
What is the strength of the biological explanation for Anorexia nervosa?
Holland et al. (1988) found AN concordance rates of 56% for MZ and 5% for DZ twins. This study was replicated by Treasure and Holland (1995) and confirmed the earlier findings, with MZ concordance of 65% and 32% for DZ. This provides good support as the twin study method is a convincing means of demonstrating genetic influences on disorders such as AN.
What is a weakness of the twin studies as a use for biological explanations of Anorexia nervosa?
Assume that MZ and DZ twins were treated the same. Joseph 2002 argues that MZ twins are more likely to be treated the same as DZ twins. MZs look more similar to each other and have similar personality traits, so they elicit more similar behaviours from parents. The greater environmental similarity means heritability estimates are inflated and genetic influences are not as great as studies suggest.
What is the counter argument for the weakness of twin studies for the explanation of Anorexia nervosa?
There is little evidence that the equal environments assumption is violated in twin studies. Klump et al (2000) found that MZ twins were no more likely to have similar attitudes towards eating than non-identical family members. The researchers concluded that their findings support the equal environment assumption for AN.
What is a weakness in the biological explanations for Anorexia nervosa (genes)?
AN is polygenetic - many genes make modest but important contributions. It is likely that genes contribute to the various symptoms of AN to differing degrees. This shows that the true picture of the causes of AN is complex, and any theory that seeks to explain the disorder in terms of one cause risks oversimplification.
What are the issues and debates that relate to the biological explanations for Anorexia nervosa?
Nature and nurture. Abraham (2008) argues that genes may create a diathesis (vulnerability) to AN that is only expressed when an individual tries to lose weight (a stressor). Perhaps the diathesis (genes) makes the person vulnerable to disordered eating, but environmental factors influence the exact type of disorder. Thus the effects of genes (nature) must be seen in the context of wider social, cultural and psychological influences (nurture).
What is the application of the biological explanations for Anorexia nervosa?
Knowing someone’s genetic profile could mean that prevention and treatment are targeted more effectively at people most vulnerable to developing AN. This is a long way in the future, but recent findings are a step n this direction and may help to improve current treatments. May improve the quality of life, reduce distress and avoid needless deaths.
What are the cognitive explanations for anorexia nervosa (AN)?
Core cognitive psychopathology is a distorted perception of body shape/weight. Gives rise to all clinical features. (Murphy et al. 2010)
What are the cognitive distortions and biases?
People with AN are critical of their own bodies and misinterpret emotional states as ‘feeling fat’- due to distorted body schema (Gadsby 2017).
-Mental representation of body size, shape, position
-Internal cognitive structure, continually updated.
-Central to self-image but distorted AN because it represents the body as bigger than it really is- affects how a person with AN interacts with their environment.
Guardia- AN participants imagined walking through a door, compared control group and overestimated their body size. Imagined the researcher they were accurate.
What irrational beliefs for non-biological explanations for Anorexia nervosa?
Irrational beliefs and attitudes are common features of AN- automatic negative thoughts.
All-or-nothing thinking and catastrophising
For a minority of those who have AN the fear of gaining weight is so extreme it is ‘delusional’
What is impaired global processing in non-biological explanations for AN?
The ability to integrate details into a meaningful overall pattern is impaired in people with AN. They find it hard to see the bigger picture, i.e. how details fit together- so they cannot perceive overall body shape accurately.
What is enhanced local processing as an explanation for AN?
At the same time, people with AN have a superior eye for detail, an advantage in some situations, but this works against people with AN as they focus on the small ‘flaws’.
Weak central coherence:
- Combination of impaired global processing and enhanced local processing
- Cognitive deficit which may be inherited vulnerability to developing AN, especially alongside other deficits.
What is the strength of the non-biological explanations for AN (research)?
Sachdev et al. (2008) used fMRI scanning techniques to show that the same brain areas were activated with AN and non-AN participants when they were shown images of other people’s bodies. But when shown pictures of their own bodies, AN participants experienced less activation in areas of the brain thought to be involved in attention. This confirms Gadsby’s prediction that cognitive distortions are limited to the individual’s body image and do not extend to bodies in general.
What is a weakness of the non-biological explanations for AN (causes)?
Lang et al. (2016) found no difference between recovered AN participants and non-AN controls on the ROCFT, a local and global processing measure. Weak central coherence could be a result of starvation in AN (not cause), hence why it persists after recovery. Cognitive theory lacks validity because it cannot explain the causes of AN.
What is a counterargument to the weakness of non-biological explanations (causes) for AN?
Hamatani et al. (2016) found that AN participants’ poor performance on the ROCFT remained even when the researchers statistically controlled for the effects of the symptoms (starvation, depression). So weak central coherence was not a consequence of the symptoms and could be a cognitive cause of AN.
What is ROCFT?
Rey-Osterrieth Complex Figures Test
What is another weakness of the non-biological explanations (findings) for AN?
Cornelissen et al.’s (2013) participants adjusted a computerised image of themselves until it matched their estimated body size. There were no significant differences between AN participants and non-AN participants, so having AN did not worsen the ability to estimate body size. This challenges the central role of body image distortions in cognitive theories of AN.
What is the application of non-biological explanations for AN?
Cognitive-behavioural treatments (CBT) change the client’s distorted cognitions and irrational beliefs about food, eating, weight loss and body size/shape. Dalle Grave et al. (2014) found that enhanced CBT led to a large increase in weight and a decrease in concerns about body shape in hospitalisation AN participants. This demonstrates the validity of predictions derived from the cognitive theory of AN as an explanation of the disorder.
What are the issues and debates involved in the non-biological explanations for AN?
Psychological understanding has developed. In their research, psychologists initially focused attention on body image distortions. They eventually tried to explain them in terms of underlying cognitive processing deficits (like weak central coherence). The next step is to formulate theories that integrate these factors and show how they are affected by non-cognitive influences (mood)
What is the drug treatment for Anorexia nervosa (AN)?
Biochemical mechanisms underlie AN (e.g. abnormal levels of dopamine and serotonin), therefore altering neurotransmitter activity may benefit AN symptoms.
What do antidepressants do for the treatment of AN?
As serotonin levels are low in AN, the drug increases serotonin in the synapse.
What do selective serotonin reuptake inhibitors (SSRIs)- antidepressants- do for the treatment of AN?
Low serotonin may be a direct cause of AN or maybe because AN is co-morbid with depression. Serotonin molecules remaining in the synapse are normally removed by the process of reuptake. They are taken back into the presynaptic neurone through the serotonin transporter. The process is blocked by SSRIs- therefore excess serotonin is not recycled, instead, it stays in the synapse and repeatedly binds with postsynaptic receptors. Extends the appetite-enhancing effects of serotonin.
What do serotonin-noradrenaline reuptake inhibitors (SNRIs)- antidepressants- do for the treatment of AN?
Work in a similar way to SSRIs but target noradrenaline as well as serotonin (inhibiting reuptake of both). Suggests that low serotonin is not the only neurotransmitter dysfunction in AN.
What do antipsychotics do for the treatment of AN?
Dopamine is abnormally high in AN and the drug decreases dopamine in the synapse. Mostly dopamine antagonists, e.g. chlorpromazine block postsynaptic dopamine receptors without activating them, reducing overall dopamine activity.
- counter distorted cognitions about fatness
- counter reduced appetite resulting from disrupted dopamine system
What do atypical second-generation antipsychotics (SGAs)- antipsychotics- do for the treatment of AN?
- causes weight gain when used to treat schizophrenia and bipolar disorder
- may reduce ‘anorexic ruminations’ in people with AN (obsessive thoughts about food, body size and shape)
- is a powerful dopamine antagonist but also a weak serotonin antagonist.
- may influence AN symptoms by blocking D2 or D3 dopamine receptors and serotonin 5-HT2A receptors.
- May increase secretion of the hormone ghrelin (increased linked with a decreased feeling of fullness after eating, encouraging further food intake)
What do atypical second-generation antipsychotics (SGAs)- antipsychotics- do for the treatment of AN?
- causes weight gain when used to treat schizophrenia and bipolar disorder
- may reduce ‘anorexic ruminations’ in people with AN (obsessive thoughts about food, body size and shape)
- is a powerful dopamine antagonist but also a weak serotonin antagonist.
- may influence AN symptoms by blocking D2 or D3 dopamine receptors and serotonin 5-HT2A receptors.
- May increase secretion of the hormone ghrelin (increased linked with a decreased feeling of fullness after eating, encouraging further food intake)
What is the supporting evidence for SGAs (antipsychotics) for the treatment of AN?
Boachie et al. (2003) used olanzapine to treat four children with AN. They gained weight (an average of under one kilo per week) and also experienced less anxiety at mealtimes, with few side effects. This highlights the potential of olanzapine, suggesting an effective drug treatment may finally be within reach.
What is the counterargument for the strength of SGAs (antipsychotics) for the treatment of AN?
Case studies are limited because they have no control group. The gold standard for effectiveness testing is the randomised controlled trial (RCT). The findings from RCTs have been mixed. Kafantaris et al. (2011) found that 15 adolescents given olanzapine gained weight and showed improved eating attitudes. But so did the control group, at the same rate.
What is a weakness of the use of the biological treatment for AN (effectiveness)?
Lebow et al. (2013) found that people with AN who takes SGAs showed increases in BMI and body satisfaction. But the AN participants didn’t significantly differ from the placebo participants. The drugs were linked with greater anxiety and overall worse symptoms. These negative symptoms cast doubt on the effectiveness of the most promising class of drugs to treat AN.
What is another weakness for drugs to treat AN (causes)?
Drugs may reduce AN symptoms by stabilising neurotransmitter systems in the brain. But a temporary and reversible reduction in symptoms is not the same as treating the cause. So, CBT may be preferable.
What is the application of drugs for treating AN?
Most side effects are moderate, some are serious. Side effects can be controlled and/or reduced through monitoring, adjustment of does and in some cases additional medication. This knowledge of side effects increases the acceptability of medication for people with AN, so they are more likely to continue treatment.
Issues and debates that are related to the biological treatment for AN
Important ethical considerations. Encourages the perception that AN is a medical disorder and not a result of psychological weakness. This ethical benefit is that the disorders become less stigmatised as more people realise that the symptoms of AN are not the person’s ‘fault’. Encourages more individuals to seek treatment without fear of being blamed.
What is CBT?
It is the leading evidence-based therapy of choice for AN. Makes sense as the core psychopathology of AN is cognitive (an overvaluation of the importance of body shape and weight)
What is enhanced CBT (CBT-E) for the treatment of AN (non-biological)?
Broad type- treats the core pathology of AN (over-evaluation of shape/weight) plus other symptoms ‘external’ to the core. (suitable for clients with low-self esteem)
Focus type- does not tackle external symptoms (default treatment for most clients)
Two intensives:
- 40 sessions over 40 weeks for BMI <17.5
- 20 sessions over 20 weeks for BMI >17.5
What are the stages of CBT-E by Murphy et al. (2010) for the non-biological treatment of AN?
-Stage 1- intensive- client and therapist identify the main AN-related cognitions and behaviours and two elements introduced- ‘weekly weighing’ and ‘regular eating’- times made for eating
- Stage two- Review- identify the barriers and plan stage 3 and switch to broad CBT-E if ‘external’ symptoms appear.
- Stage three- self-evaluation- client learns to focus on other areas of their lives, dietary rules are identified (what food are being avoided) and the therapist helps to break down the rules using behavioural experiments (breaking the rules doesn’t lead to weight gain)
- Stage four- end well- maintaining progress and prevent relapse- weekly weighing continues, plan the next 20 weeks before follow up, and the client continues rule breaking and avoiding body checking, realistic about relapse (inevitable but can overcome)
What is the strength of CBT-E as a non-biological treatment for AN?
Fairburn et al. (2015) randomly allocated 130 participants with eating disorders to either CBT-E or interpersonal psychotherapy (IPT). After 20 weeks, 65.5% of CBT-E and 33.3% of IPT participants were ‘in remission’. After 60 weeks, 69.4% of CBT-E and 49% of IPT. CBT-E is more effective (and quicker) for the majority of people with AN than the well-established IPT.
What is the counterargument for the strength of CBT-E for the non-biological treatment of AN?
All the participants in Fairburn’s study had a BMI above 17.5 so they were not seriously underweight. It is unclear whether CBT-E is as effective for severely underweight people. On the other hand, the UK’s National Institute for Clinical Excellence (NICE 2017) considered CBT-E effective enough to recommend it for adults with AN.
What is a weakness of the non-biological treatment for AN (cognitive element)?
Soderstern et al. (2017) compared CBT to the ‘normalisation of eating’ procedure of clients’ feedback at mealtimes to encourage normal eating behaviour. The remission rate was 75% and relapse was just 10% over 5 years for normalisation (compared to the remission rate of 45% and relapse of 30% for CBT). This strongly implies that the behavioural elements of therapy are sufficient and the cognitive element is not necessary to improve AN symptoms.
What is a weakness of the non-biological treatment for AN (adherence)?
CBT dropout rates are high because it is a demanding therapy, especially the intensive form of CBT-E (in terms of attendance and homework). Clients have to make difficult changes to their behaviour and thought processes. Carter et al. (2012) found a 45% dropout rate for a CBT-E programme. This means that the effectiveness of the therapy is considerably enhanced in research results as only ‘completers’ are included in any research sample.
What is the title of the key question?
Are drug treatments being overused to treat mental health disorders in society?
What is the AO1 for the key question?
- In 1998, 44% of people with mental health disorders were without psychotherapy and this increased to 57% in 2007.
- 1 in 4 people waiting for 3 months or more for in-person talkative therapy
- Side effects of antidepressants- decreased alertness, headache, and nausea
What is in the first paragraph of the key question (AN)?
Boachie et al. (2003) used olanzapine to treat four people with AN and found that the children had gained weight (1 kilo per week) and experienced less anxiety at mealtimes and improved sleeping. However, Kafantaris et al. (2011) found that 15 adolescents given olanzapine gained weight with improved eating habits, but so did the control group at the same rate.
What is the second paragraph of the key question?
Patel et al. note that 20% of people with schizophrenia show negligible improvement after multiple FGA trials and around 45% experienced only partial or inadequate improvement and unacceptable side effects. Kapur et al. (2000) raised caution over generalisation using animal studies as high doses could cause side effects not yet known and may not be shown.
What is the application of the non-biological treatment of AN?
Understanding the experience of AN helps researchers to support vulnerable participants taking part in research
What are the issues and debates linked to the non-biological treatment for AN?
Research participants (diagnosed with AN) are nearly always female, so there are too few males for any meaningful conclusions to be drawn about gender differences. For example, in Fairburn et al.’s (2015) study 3 out of the 130 participants were males. There are implications for therapy because the female therapist is better for female clients (provides role models), but this may be problematic for male clients.
What was the aim of Guardia et al. (2012) as the contemporary study for AN?
To see if people with AN overestimate body size even in action. To see if AN overestimation of body size extends to bodies in general or is limited to their own.
What was the procedure of Guardia et al. (2012) as the contemporary study for AN?
Parental consent for participants aged under 18 years old. There are two groups of people- people with AN and controls. People were matched on their age and educational level. Laboratory experiment. Independent variable= participants imagining their body action from their perspective or the experimenter’s perspective.
What was the first measure in Guardia et al.’s (2012) contemporary study for AN?
Body weight was measured 6 months before, one month before and at the start of the experiment. Each participant completed 2 questionnaires: Body-Shape questionnaire (BSQ), measuring body dissatisfaction and Eating Disorder Inventory-2 (EDI-2), weight and shape concerns. ‘Drive for thinness’ and body dissatisfaction. Then an image of a 2-metre-high door was projected on a wall and the width varied from 30-80 cm with 51 images altogether, each shown four times
What was the first perspective (procedure) in Guardia et al.’s (2012) contemporary study for AN?
Participants stood 5.9m from the wall and imagined them walking through a ‘door’ (decided if they could walk through at normal speed without turning sideways)
What is the third perspective (procedure) in Guardia et al.’s (2012) contemporary study for AN?
The experimenter soot 5.9m from the walk and the participant decided if they could walk through the door without turning sideways.
How was the perceived passability ratio (PPR) calculated?
Divide the perceived aperture by the participant’s shoulder width. Higher ratio= larger apparent body size
What were the findings of Guardia et al.’s (2012) research as the contemporary study for AN?
No significant difference between the groups in age, educational level and height. Mean BMI and median shoulder width were significantly greater in controls. The 1PP (rated own body) was significantly higher than the control group (1.321 vs. 1.106) and the 3PP condition for the AN group was not significantly higher than the control (1.227 vs. 1.137). This was a mean perceived passability ratio.
What were the conclusions of Guardia et al.’s (2012) research as the contemporary study for AN?
AN participants feel their body is bigger than it is but this did not affect their judgement of others and didn’t distort other bodies. AN has an overestimation of their body size.
What is the strength of Guardia et al.’s (2012) research? (supporting)
Case et al. (2012) studied the size-weight illusion (if you compare two objects of equal weight but of different sizes, people tend to judge smaller objects as heavier). This is the result of the normal integration of two senses, visual and tactile (touch). But people with AN are less affected by the illusion. Supports Guardia by concluding that integrated information from multiple senses is disrupted in AN.
What is the competing argument for the strength of Guardia et al. (2012) research?
Eshkevari et al. (2012) showed that participants with AN had a stronger rubber hand illusion than controls. Perception of rubber hand illusion depends on the ability to integrate information from multiple sensory inputs but there is no sign of an AN-related impairment in this study.
What is a weakness of Guardia et al.’s (2012) research for the contemporary study of AN? (ecological validity)
It is a simulation in which participants imagine performing the actions involved in passing through an aperture. The researchers recognise that this is not identical to the real activity of passing through a doorway and changing position if necessary. The perceived passability ratio is not an ecologically valid measure of the participant’s true behaviour.
What is a weakness of Guardia et al.’s (2012) research for the contemporary study of AN? (confounding variable)
The experimenter’s body in the 3PP condition more closely resembles the size of the control participants’ bodies than the AN participants’ bodies. This makes it easier for the control participants to imagine the experimenter passing through the door or not. This variable may effect the experience of the AN and control participants in the 3PP condition, so differences between the groups may not be valid
What is the application of Guardia et al.’s (2012) research for the contemporary study of AN?
The findings imply that a cognitive impairment underlies AN (disrupted self-body schema). If true, forms of cognitive therapy could be more effective. For instance, virtual reality could be used to counter distorted cognitions by demonstrating ‘own’ and ‘other’ body sizes passing through doorways. This is especially valuable because such treatment would address an underlying cause of AN.
What are the issues and debates of Guardia et al.’s (2012) research for the contemporary study of AN?
The researchers acknowledged that visual perception in the real world is influenced by psychological and social factors. But these influences have been stripped away in the experimental procedure used in the study. This is an issue because reductionist explanations do not account for the complexity of the causes of AN and thus may be misleading.
What is cognitive behavioural therapy?
In order to change behaviour you must change how you think
What is CBTp?
Cognitive behavioural therapy for psychosis. NICE recommends at least 16 sessions of CBTp when being used for schizophrenia.
What is the social causation hypothesis for the social explanations for schizophrenia?
The human world (people around you) is a major cause of schizophrenia (or at least relapse). Many environmental risk factors contribute (e.g. family dysfunction, childhood trauma), the four main ones are social adversity, urbanicity, social isolation and immigration and minority status.
What is social adversity as a social explanation for schizophrenia?
All humans have the same basic physical, e.g. physical but also intellectual, emotional, and social needs. Some children grow up in unfavourable environments, making them vulnerable to mental health disorders in the future (e.g. unemployment and poverty expose some families to stress). People from lower socioeconomic groups may not be able to access treatment. This makes their problems worse,
What is urbanicity as a social explanation for schizophrenia?
City life is more stressful than rural life- noise, light pollution, criminality, faster pace, and anonymity. Long-term exposure may make a person more vulnerable to having an episode of schizophrenia. High population density makes life more competitive, which may increase the experience of chronic social defeat (a stressor that occurs when a person is exposed to hostile confrontations from another individual, such as bullying)
What is social isolation as a social explanation for schizophrenia?
People with schizophrenia find contact with others stressful (Faris 1934). Self-imposed isolation cuts them off from feedback about what behaviours or thoughts are inappropriate- they begin to behave ‘strangely’ without this corrective feedback.
What are immigration and minority status as an explanation for schizophrenia?
Immigrants are at greater risk of schizophrenia than the general population. Research shows the greater risk for first and second-generation immigrants in many countries. The risk decreases as the number of people from the same ethnic background increases- minority or outgroup status is key, not belonging to a particular ethnic group. This implies that the marginalisation of outgroups may leave people vulnerable to schizophrenia. Veling (2008) suggests schizophrenia may be a reaction to the chronic experience of prejudice and discrimination. Second-generation immigrants are at a greater risk that the first generation because:
- they have a weaker cultural identity
-they have learned to fit in with the norms of the indigenous society
- their beliefs and expectations may be at odds with those of their parents and extended family.
This creates stress which worsens vulnerability to schizophrenia.
What is the application of the causation hypothesis (evaluation for a non-biological explanation for schizophrenia)?
It enables the provision of community-level treatment. Housing projects draw attention to factors which affect mental health. This reduced overcrowding and encourage neighbourhood cohesion and celebrated cultural diversity should foster courage, fortitude and resilience which will help communities arm themselves against mental breakdown. It develops a sense of collective social responsibility for, not only their mental well-being but also that of other people. This is important for the real world as it can help protect others as well as themselves from mental breakdowns.
What is the supporting research for social adversity (evaluation of non-biological explanation for schizophrenia)?
The impact of the social environment has been a significant factor. Tienari et al (1994) looked at adoption studies of those who had biological mothers with schizophrenia. None of those who were brought up in healthy families or even mildly disturbed families didn’t develop schizophrenia but 37% of those who had mothers who didn’t have schizophrenia but were raised in a severely disturbed family were classed as severely mentally disturbed.
However, there may be confounding variables.
What is the supporting research for the urban city (evaluation of non-biological explanation for schizophrenia)?
Vasso et al (2012) used a meta-analysis of data from studies from Sweden, Denmark, and the Netherlands and includes 24,000 cases of schizophrenia. They correlated location with schizophrenia risk and found a link. The risk was 2.37 times higher for people living in urban areas than the most rural environments.
The diathesis-stress model explains this as we have a predisposition and stress that is caused in life.
What is the supporting research for immigration and minority status (evaluation for a social explanation for schizophrenia)?
Veling et al. (2010) found that people marginalised and assimilated were at greater risk of schizophrenia than people classed as integrated. Strong ethnic identity may be a proactive factor against schizophrenia. However, this is correlation research and doesn’t show causation.
What is CBTp?
Cognitive Behavioural Therapy for psychosis. NICE recommends at least 16 sessions of CBTp when being used for schizophrenia.
How does CBTp deal with irrational thoughts?
- identification (maladaptive and cognitive-based)
- coping skills (teaching to cope with hallucinations)
- decompensation- prevent schizophrenics from retreating into their delusions- more realistic.
How does CBTp encourage tracing the origins of their symptoms?
Ellis- ABC model (irrational or rational)
A= activating events
B= beliefs
C= consequences
How does CBTp deal with the behavioural experiment?
- evaluate the content
- reality testing- disputing- empirical (evidence/information), logical
How does CBTp deal with behavioural activation?
- homework- therapist set tasks for the client and feedback on like keeping a diary
What are the strengths and weaknesses of CBTp (directive)?
Strengths- Non-directive- If the patient would complete the homework and the level of engagement the patient has.
Weakness- Directive- Which behavioural treatments are undertaken. Expert power to determine which thought process is maladaptive/irrational
What are the strengths and weaknesses of CBTp (effectiveness)?
Strengths- NICE (2014) conducted a meta-analysis of high-quality studies with randomised controls showing that CBT reduced rehospitalisation rates for up to 18 months and reduced the amount of time in hospital (8.26 days on average). Symptom severity and psychosocial functioning also improved.
Weaknesses- Jauhar et al (2014) conducted a large-scale meta-analysis that found a small therapeutic effect on key symptoms. These effects disappeared when the study was blind. (single-blind- the doctors didn’t know if the patient was getting the CBT or not)
If the researchers knew the treatment they would positively report on CBT, which would make it biased as they were researching CBT.
What are the strengths and weaknesses of CBTp (side effects)?
Strengths- Kuipers et al (1997) conducted a randomised control of CBT and found that drug-resistant clients improved when given CBT. It was able to not have the same side effects as drug therapies.
Weaknesses- Behavioural experiments may cause undue stress and anxiety. If these are not done correctly they may reinforce irrational beliefs especially if someone is a paranoid schizophrenic. In extreme cases, they could cause violent outbursts.
What are the strengths and weaknesses of CBTp (expense)
Strengths- Compared to other talking therapies it is time limited. It is a long-term therapy and is less likely to have a relapse, for a longer recovery.
It treats the cause, unlike drugs which treat the symptoms.
Weaknesses- Haddock et al (2013) conducted research in the North West of England surveying 187 randomly selected participants only 13 (6.9%) were offered CBTp.
It is more expensive due to the high levels of training and how long you have the therapist.
What are the strengths and weaknesses of CBTp (reasons)?
Strengths- Activating the event and identification look at the underlying causes and how the thought processes have come about. There is more of a long-term effect.
Weaknesses- It is reductionist as it looks at the thought process controlling behaviour but not all thought processes are conscious and don’t look into the biological factors that could have caused schizophrenia.
What are the strengths and weaknesses of CBTp (types of people)?
Strengths- Addington and Addington (2005)
When patients are in the acute phase (severe- high schizophrenic symptoms) of schizophrenia self-reflection is not appropriate. Once stabilised group-based CBTp can normalise experiences. The greater the realisation the more benefits patients experience.
As they may not be able to realise or understand/ rationalise their thoughts.
Weaknesses- Kingdon and Kirschen (2006)
Investigated 142 schizophrenic patients within a psychiatric hospital many were not deemed suitable to have CBT as it was believed that they would not be able to fully participate in the treatment this was particularly true for older patients. This only happens if people are willing to change, which is particularly true for older patients.
What is the biological explanation for schizophrenia?
Heritability: how well people’s genes can account for differences in their traits or behaviour
Hilker et al. (2018): 79%
The heavy influence of genes on schizophrenia
AN is linked to genes= 70%
OCD linked to genes= 30%
Wright (2014) indicates as many as 700 genes might be linked to schizophrenia
What is the DISC-1 gene and how does this correlate with schizophrenia?
Dysregulation in this gene. People with the abnormality in this gene are 1.4x more likely to develop Schizophrenia (Kim et al. 2012). This gene codes for the regulation/creation of GABA a neurotransmitter that regulates other neurotransmitters (dopamine and glutamate). Hyperdopaminergic which is the excess of dopamine causes positive symptoms of schizophrenia. In a review of 14 studies, Tarik Dahoun et al (2017) concluded DISC-1 is associated with presynaptic dopamine dysregulation which is a key factor for schizophrenia
What is the COMT gene and how does this correlate with schizophrenia?
It codes for an enzyme that breaks down dopamine in the prefrontal cortex. Less dopamine regulation and hyperdopaminergic have been linked to schizophrenia symptoms
Research:
Egon et al. (2001) found a link between decreased dopamine in the prefrontal cortex and the ‘Val’ allele (a form of COMT)–> 2 copies can increase the risk of schizophrenia by 50%
What is a diathesis-stress model and how does this correlate with schizophrenia?
The condition of schizophrenia is triggered by other environmental and biological factors. The original model showed it was triggered by harsh parenting. Today= anything can trigger this
Cannabis –> is 7x more likely to develop schizophrenia.
Tienar, 21-year-long longitudinal adoption studies supporting model children whose biological mum has schizophrenia were more sensitive to family dysfunction. Stress
What are epigenetics and how does this correlate with schizophrenia?
Our environment can switch genes on and off. So environmental stressors actually have an affect on the way our genes express themselves. Susser and Lin (1992) who found that women who were pregnant during the Dutch Hunger Winter (a famine) gave birth to low birth weight babies who were 2 x as likely to develop Sz than normal
What are the strengths (support) of the genetic explanation for Schizophrenia?
- Gottesman and Shields (1966) identified a concordance rate of 42% for MZ twins and 9% for DZ twins. The greater rate for MZs shows that schizophrenia is not entirely a genetic disorder biology certainly plays a role
- Dahoun et al. (2017) concluded that DISC1 is associated with presynaptic dopamine dysregulation, a key factor in schizophrenia.
- Egan et al. (2001) found a link between decreased dopamine activity in the prefrontal cortex and one form of the COMT gene- the ‘Val’ allele (inheriting two copies increases the risk of schizophrenia by 50%)
What are the weaknesses of the genetic explanations for schizophrenia?
- Should be cautious when interpreting the findings of twin studies. MZs not only share more DNA than DZs but they are also treated more similarly. This may also be due to shared environment as shared genes. Shared environment assumption. Reduces the validity of the conclusion that the greater shared DNA is responsible for the similar pathology
- Concordance rates in twin studies are far from 100% even for MZ twins, suggesting the significant role of the environment. Pedersen and Mortensen (2006) show the risk of developing schizophrenia increases with greater exposure to city life and higher population density. This suggests that rural dwellings may help protect a person from developing a disorder to which they are genetically predisposed.
What is the application of the genetic explanation for schizophrenia?
- when a family member receives a diagnosis of schizophrenia, the family may want more information about heritability. ‘Recurrence risk’ can be calculated and the counsellor will then help the family to interpret this information. This can provide support, help allay fears about developing schizophrenia and inform choices about family planning
What are the types of drugs used to treat Schizophrenia?
Atypical (second generation) and typical (first generation)
What are antipsychotics to treat schizophrenia?
- Convectional and first-generation (FGA)
- chlorpromazine
- combat positive symptoms (hallucinations, delusions, disordered thinking and thought insertion
- a product of overactive dopamine (hyperdopaminergic)
- antagonist - reduces the availability of dopamine
What are atypical antipsychotics to treat schizophrenia?
- clozapine
- combat positive and negative symptoms
- claims to have beneficial effects on negative symptoms
- act on dopamine and block serotonin receptors
- works on both dopamine and serotonin
- rapidly dissociate
What are the strengths and weaknesses of drug treatments to treat schizophrenia (in terms of directionality)?
positive:
- the patient will decide if and when they take the drug (compliance)
negative:
- the psychiatrist decides the drug and the dosage. Expert power. The patient may have no choice and consent if sectioned (by the Mental Health Act 2003)
What are the strengths and weaknesses of drug treatments to treat schizophrenia (in terms of effectiveness)?
positive:
- Zhao et al. (2016)- meta-analysis compared 18 antipsychotics from 56 randomised control trials with 10,000 people. 17 of them had significantly lower relapse rates than placebos
negatives:
- Patel et al- 20% of people with schizophrenia show improvement after multiple FGA trials and 45% only partial or inadequate improvement with unacceptable side effects. Failed to function well in everyday life and the vast majority were unemployed. There is also a reliance on animal studies and caution of overgeneralising the findings
What is a weakness of the drug treatments to treat schizophrenia (in terms of side effects)?
- Hill (1986) large amount of court settlements due to side effects of conventional antipsychotics - Tardive dyskinesia- an uncontrolled movement of lips, tongue, faces, hands, and feet and that affects 30% of patients with 75% irreversible. People may not comply due to this.
What are the strengths and weaknesses of drug treatments to treat schizophrenia (in terms of expense)?
strengths
- does not take a long time for the effects of the drug to show and may increase compliance
weaknesses
- make take time to get the correct drug and dosage. If the patient stops taking them, the symptoms will come back
- expensive as the medication is long term
What are the weaknesses of drug treatments to treat schizophrenia (in terms of reasons)?
- only treats the physical symptoms and not the underlying reasons, so if medication is stopped they may see a recurrence and relapse of symptoms.
What are the strengths and weaknesses of drug treatment to treat schizophrenia (in terms of types of people)?
strengths
- anyone could take it (all types)
weaknesses
- some individuals are drug-resistant (symptoms not treated). Carlsson et al. were interested in serotonin antagonists and glutamate agonists - which are effective in reducing positive and negative symptoms. By tackling precise neurotransmitters- less likely to have detrimental effects.
what is the dopamine hypothesis (schizophrenia)?
excitatory neurotransmitters increase the likelihood of the next neurotransmitter firing.
Hyperdopaminergic is when there is excess dopamine. Schizophrenia patients have too much dopamine and are firing too easily and too often.
What do amphetamines do (schizophrenia)?
increased dopaminergic energy and is a drug. It has the mode of action as dopamine. If ‘normal’ (non-schizophrenic) people take amphetamine they would experience similar symptoms to schizophrenia which is the result of excess dopamine
What do antipsychotics do (schizophrenia)?
they decrease dopamine activity. This binds to the postsynaptic receptors neurone which then dopamine can’t binding to the receptors and is then taken up by the reuptake channel. This means the action potential can’t be triggered. The dopamine is displaced, left in the synaptic cleft.
How does beta-hydroxylase link to schizophrenia?
- reduced beta-hydroxylase (the enzyme that breaks down dopamine) is more likely to bind to the post synaptic receptors and then cause more action potential
What do D2 receptors have to do with schizophrenia?
The proliferation of the D2 receptors on the postsynaptic cell means that there are more receptors and is, therefore, more likely to fire.
What did Davis et al conclude about dopamine and schizophrenia?
Hyperdopaminergic- causes positive symptoms (adding to someone’s normal function). Delusions, disordered speaking, hallucinations, thought insertion. In the Mesolimbic pathway (reward pathway)
Hypodopaminergic- causes negative symptoms (taking away someone’s normal function) flat effect- reduce the range of emotions. Alogia- poverty of speech= catatonic schizophrenia in the mesolimbic pathway
What is serotonin and how does this link with Carlsson (schizophrenia)?
Inhibitory neurotransmitter
Carlsson et al did a meta-review analysing the findings of research on neurotransmitters (secondary data). Clozapine binds to the D1 and D4 receptors but only weakly to the D2 receptors to reduce positive symptoms. Based on existing knowledge D2 is important for schizophrenia. This study suggests that it is reductionist as D2 doesn’t work with clozapine. Clozapine also binds to serotonin reducing positive and negative symptoms and focusing on the interaction between neurotransmitters.
Serotonin regulates dopamine in the mesolimbic pathway (reward pathway)
What are the strengths of the neurotransmitter explanation for schizophrenia?
- supporting research- Tenn et al (2003) found that rats given amphetamine injections over 3 week period resulted in negative symptoms and were reversed by a dopamine antagonist
- Practical application and drug therapies. Zhao et al(2016) conducted a meta-analysis comparing 18 antipsychotics tested and had significantly lower relapse rates than placebos but it is limited due to the treatment aetiology fallacy as it treats the symptoms but not the cause
- Snyder (1985) found that chlorpromazine is an antagonist at many dopamine receptors (D1 and D2) and has an antipsychotic effect. He also found that the dopamine antagonist haloperidol is more effective even though it has a narrower range of biochemical effects. This finding suggests that the excess activity at specific dopamine receptors is implicated in the development of symptoms
What are the weaknesses of the neurotransmitter explanation for schizophrenia?
- Departie and Lai (2001) administered a dopamine agonist, apomorphine, and found that non-psychotic participants did not show psychotic symptoms. Furthermore, the drug did not exacerbate the symptoms of schizophrenia- the lack of external reliability of findings suggests that the role of dopamine in schizophrenia may not be causal.
-Veling et al (2008) found that Moroccan immigrants were more likely to be diagnosed with schizophrenia than Turkish immigrants. Social adversity and social isolation as a consequence of discrimination are significant in explaining the different experiences of the cultural groups - biological explanations are low-level and reductionist. Schizophrenia is a complex disorder with patients experiencing a wide range of symptoms, so it is unlikely that one neurotransmitter can cause all the symptoms. Animal research is reductionist as animals are given much higher doses blocking the role of dopamine.
What was the aim of the clinical practical?
The aim was to be able to determine if mental health is portrayed more negatively in tabloid newspapers than in broadsheets. This would help to determine how likely media is to impact the perception of mental health. This could impact how people seek diagnosis and treatment and how others treat people with mental health disorders.
What was the procedure of the clinical practical?
This was done using a content analysis of two news articles (with one being a tabloid, which is more exaggerated and the other being a broadsheet which is more factual). Summative content analysis involves counting the frequency of keywords/terms. These keywords can be determined before or during the analysis of the raw data. Once we looked at one article we tried to decide what key terms are frequent in the Sun (tabloid) for example mental health and schizophrenia (ic) were frequent. Then we used a computer system to find the word and try to find out how many each of the words was present in the article. We then repeated this for the second article and found that other words were more common here and some in article 1 weren’t used in article 2. Once we had found out the frequency of each of the words/phrases in each article we counted all of them up to give us an overall total. Then for each word, we decided if the context in that word was used was either positive, negative or neutral. From this, we calculate how many neutral, positive, and negative terms were used for each article and then determine how many of the articles were neutral, positive, or negative. This would allow for a comparison between how many neutral, positive, and negative terms were used.
What were the findings of the clinical practical?
Schizophrenia is used differently in Article 1 than in Article 2. This is shown as schizophrenia was more distributed across neutral, positive, and negative, while Article 1 used schizophrenia more negatively. Another finding from this experiment was that ‘dangerous’, ‘murder’, and ‘violence’ was not used in article 2 but were used in article 1, which was the tabloid. This suggests that the tabloid uses more negative language than the broadsheet article. Another finding from this experiment was that article 1, which was the tabloid, uses more negative language than article 2, which was the broadsheet. The tabloid had 83.2% negative words while the broadsheet had 56.5% negative words.
What were the conclusions of the clinical practical?
From this study, we can determine that articles do portray mental health negatively overall. However, tabloids like the Sun are more likely to exaggerate mental health and more likely to make negative comments, while the broadsheet still makes negative comments about mental health, it is less than the tabloid and is more factual.
What are the strengths of the clinical practical
- High internal reliability as everyone who was repeating the experiment was replicating it in the same way. Each person was using a computer system to locate the frequency of words instead of having different people find the words.
-High reliability as you can experiment as many times as you need and by different people. This means that it has high external reliability as anyone can take a tabloid and broadsheet about schizophrenia and compare the neutral, positive, or negative language.
-High validity as we used a computer system to find the frequency of each of the words. This increases objectivity and decreases the chance of human error. This makes the findings more accurate than if they were counted by hand using a tally by different people as people are more likely to miss words in longer articles and would therefore find different frequencies for the same word.
-High ecological validity. This is because the articles that are found can be accessed by anyone and used by anyone, and has not been created (made up) for this experiment. Also, this means that each of the findings within the articles was real data findings.
What are the weaknesses of the clinical practical?
-Reduced validity when each of the words was chosen. This is due to it being subjective as each person may interpret different words more or less positively or negatively. This makes it inaccurate as when determining if the word in context is neutral, negative, or positive is up to the interpretation of each person and it is placed in each category is subjective.
-Reduced generalisability as only 2 articles were used, which won’t include the wide range amount of articles about mental health. The other articles not discussed may be more positive or negative about mental health. This means that our sample is not representative of all target articles, which include all tabloids and broadsheets on schizophrenia.
What is the application of the clinical practical?
This applies to the wider media as if they are found to comment more negatively on mental health then there could be laws or changes put in to help it to become more positive. This could then help the number of people seeking a diagnosis and therefore treatment, which will help them and stop their mental health disorder to deteriorate.
