Abnormal (MDD) Flashcards
(15 cards)
Biological Aetiologies Theory? Including key words? What two studies support this?
BIOLOGICAL AETIOLOGIES of MDD focus on the role of GENETIC PREDISPOSITIONS, NEUROCHEMICAL IMBALANCES, and BRAIN STRUCTURE ABNORMALITIES in increasing vulnerability to depression. The SEROTONIN HYPOTHESIS proposes that a deficit in the neurotransmitter SEROTONIN contributes to low mood, lethargy, and other depressive symptoms. Research on the 5-HTT GENE, particularly the presence of the short allele, suggests a GENE–ENVIRONMENT INTERACTION whereby individuals with this genetic variant may be more sensitive to STRESSFUL LIFE EVENTS, leading to a higher risk of developing MDD. This is supported by the DIATHESIS–STRESS MODEL, which posits that a genetic VULNERABILITY FACTOR interacts with environmental stressors to produce the disorder. Protective factors such as social support, coping mechanisms, or resilience traits may buffer genetically at-risk individuals. There are also other examples of pinning MDD symptoms on specific hormone concentrations, such as Videbech and Ravnkide’s (2004) study proposing the Cortisol Hypothesis.Findings from TWIN STUDIES and CROSS-CULTURAL GENETIC RESEARCH further support the idea that biology plays a key role in the development of depressive disorders, though it does not act in isolation.
Linked studies: Caspi et al. (2003), Kendler et al. (2006), Chiao & Blizinsky (2010)
What is MDD?
MAJOR DEPRESSIVE DISORDER (MDD) is a mood disorder characterised by a persistent low mood and a loss of interest or pleasure in most activities, lasting for at least two weeks and accompanied by cognitive, emotional, and physical symptoms. These may include feelings of worthlessness, fatigue, changes in appetite or sleep, difficulty concentrating, and, in severe cases, suicidal ideation. MDD is diagnosed according to classification systems such as the DSM-5 or ICD-11, which require a minimum number of symptoms to be present. It is one of the most common mental disorders globally and can range from mild to severe, often with significant impacts on functioning and quality of life. The disorder is influenced by biological, cognitive, and sociocultural factors, making it a complex and multifaceted condition.
Cognitive Aetiologies Theory? Including key words? What two studies support this?
COGNITIVE AETIOLOGIES of MDD propose that maladaptive patterns of THINKING and INFORMATION PROCESSING underlie the development and maintenance of depressive symptoms. According to BECK’S COGNITIVE THEORY, individuals develop NEGATIVE SCHEMAS during childhood, which manifest in AUTOMATIC THOUGHTS and COGNITIVE DISTORTIONS such as CATASTROPHISING, OVERGENERALISATION, and PERSONALISATION. These contribute to the NEGATIVE COGNITIVE TRIAD—pessimistic views about the SELF, WORLD, and FUTURE. COGNITIVE VULNERABILITY refers to the enduring tendency to interpret experiences through these biased thought patterns, which can be triggered by stress or failure. The HOPELESSNESS THEORY expands on this by suggesting that individuals who attribute negative events to INTERNAL, GLOBAL, and STABLE causes are more likely to develop depressive symptoms. Protective cognitive factors such as optimism, problem-solving ability, or emotional regulation may mitigate these risks. Cognitive aetiologies are well supported by longitudinal and prospective studies and form the basis for interventions such as COGNITIVE BEHAVIOURAL THERAPY (CBT).
Linked studies: Alloy et al. (1999), Joiner et al. (1996)
Sociocultural Aetiologies Theory? Including key words? What two studies support this?
SOCIOCULTURAL AETIOLOGIES of MDD focus on the influence of ENVIRONMENTAL STRESSORS, SOCIAL STRUCTURES, and CULTURAL NORMS in shaping mental health outcomes. According to the VULNERABILITY MODEL developed by Brown and Harris, depression is more likely when individuals experience SEVERE LIFE EVENTS (e.g., bereavement, abuse, financial strain) in the presence of VULNERABILITY FACTORS such as lack of social support, unemployment, or role conflict. Sociocultural models also emphasise the role of PROTECTIVE FACTORS, such as close relationships, community integration, and cultural coping mechanisms, which may buffer against depression. CULTURE shapes not only the experience and expression of symptoms (e.g., somatic vs affective presentations) but also access to diagnosis and treatment. COLLECTIVIST CULTURES may have lower reported rates of MDD due to stigma and alternative idioms of distress, or due to the gene–culture coevolution hypothesis, which suggests cultural values may interact with genetic predispositions. GENDER differences are also significant, with women more likely to be diagnosed due to both biological sensitivity and gendered social stressors.
Linked studies: Brown & Harris (1978), Parker & Amenson (1987)
Prevalence Rates Theory? Including key words? What two studies support this?
PREVALENCE RATES refer to the frequency of a disorder within a population and can be measured as point prevalence, period prevalence, or lifetime prevalence. In the case of MDD, rates vary widely across gender, culture, and socioeconomic status. For example, MDD is more prevalent in women, possibly due to increased exposure to interpersonal stress, societal roles, or biological sensitivity to hormonal fluctuation. This is supported by the ARTEFACT HYPoTHESIS, stating that women are disproportionately diagnosed with MDD due to their tendency on average to share their emotions more. Cross-cultural comparisons show variation in how depression is reported, experienced, and diagnosed, with somatic symptoms (e.g., fatigue, sleep disturbance) being more common in non-Western cultures, and affective symptoms (e.g., sadness, hopelessness) more prominent in Western settings. These patterns are influenced by stigma, diagnostic criteria, and healthcare access. The gene–culture coevolution hypothesis suggests cultural values (such as collectivism) may offer protective buffering against genetic vulnerabilities (e.g., the short allele of the 5-HTT gene). Epidemiological data, while useful, must be interpreted cautiously due to issues of cross-cultural validity and diagnostic bias.
Linked studies: Lewinsohn et al. (1988), Chiao & Blizinsky (2010), Parker & Amenson (1987)
Treatment (SSRIs) Theory? Including key words? What two studies support this?
TREATMENT of MDD using SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIs) is based on the biomedical model, which attributes depressive symptoms to neurochemical imbalances, particularly low levels of serotonin. SSRIs function by blocking the reuptake of serotonin in the synapse, increasing its availability and potentially alleviating symptoms of low mood and lethargy. While SSRIs are widely prescribed and effective for many individuals, their success may be moderated by genetic factors, such as 5-HTT gene polymorphisms, which affect sensitivity to the medication. Some patients experience side effects, treatment resistance, or relapse, especially when SSRIs are used without adjunct psychotherapy. Placebo effects are also significant, particularly in cases of mild to moderate depression. The effectiveness of SSRIs is best evaluated through double-blind clinical trials, meta-analyses, and longitudinal follow-ups. While SSRIs remain a first-line treatment, many treatment models now favour multimodal approaches, integrating CBT, lifestyle interventions, and social support.
Linked studies: Caspi et al. (2003), Kirsch et al. (2008)
What is the APFC for Caspi et al (2003), and what theories does it support?
Aim - To determine whether there is evidence for a gene-environment interaction (G x E) for a mutation of the serotonin transporter gene - 5-HTT.
Procedure - A sample of 847 new Zealand 26-year olds. All were members of a cohort that had been assessed for mental health on an every–other year basis until they were 21. Participants were divided into three groups, having two short alleles of the 5HTT gene, having one short and one long and having two long alleles.
Findings - Participants with at least one copy of short allele exhibited more depressive symptoms, diagnosable depression and suicidal ideation in relation to stressful life-events.
Conclusion - Short alleles could indicate vulnerability to developing depression after undergoing stressful life-events. However, those who are genetically predisposed to depression does not mean they will develop depression. THIS STUDY CAN BE USED FOR GENES, GENETIC SIMILARITIES, MDD TREATMENTS AND BIOLOGICAL AETIOLOGIES
What is the APFC for Kendler et al (2006), and what theories does it support?
Aim - To investigate the heritability of MDD using twin studies.
Procedure - 15000 from the Swedish Twin Registry were called. They were tested by trained psychologists using DSM-IV criteria. They compared the concordance for MDD between MZ and DZ twins, being genetically different. Data on depression diagnoses were also obtained from clinical records.
Findings - MZ twins had a 44% concordance rate, whereas DZ twins had a 17% concordance rate.
Conclusion - MDD has a significant genetic component, but environmental factors also play a role, as MZ concordance is not 100%. THIS STUDY CAN BE USED FOR GENES, GENETIC SIMILARITIES AND BIOLOGICAL AETIOLOGY
What is the APFC for Chiao & Blizinsky (2010), and what theories does it support?
Aim - To explore the association between cultural values of individualism and collectivism, and the frequency of the mutated 5HTT S allele. And how this association impacts the prevalence of mood and anxiety disorders globally
Procedure - Data was gathered from 29 countries, from which 50,000 participants were examined for the frequency of the 5HTT S allele, cultural values based on the Hofestede individualism collectivism scores. They also studied historical pathogen prevalence.
Findings - The study found a strong correlation between collectivist cultures and higher frequencies of the S allele of 5-HTTLPR. Nations with high pathogen prevalence historically tended to have higher collectivism and more S allele carriers. This genetic-cultural adaptation was associated with lower reported rates of anxiety and mood disorders in these populations.
Conclusion - The results supports the culture-gene coevolution hypothesis, suggesting that collectivistic cultural values may buffer genetically susceptible populations (those with the S allele) against higher rates of affective disorders by promoting social harmony and reduced life stress. This cultural adaptation appears to have evolved as a protective mechanism against both environmental and mental health challenges. THIS STUDY CAN BE USED FOR PREVALENCE RATES AND BIOLOGICAL AETIOLOGY.
What is the APFC for Brown & Harris (1978), and what theories does it support?
Aim - Investigate how depression is linked to social factors and stressful life events in women.
Procedure - 458 women in South London surveyed about daily life and depressive episodes. Life events were rated for severity by independent researchers.
Findings - 8% of women (37) became clinically depressed; 33 of them experienced adverse life events.
Social class played a role; working-class women with children were 4x more likely to develop depression than middle-class women. From this, 3 key factors were deduced:
Protective factors - High intimacy with husband, leading to higher self-esteem.
Vulnerability factors - Loss of mother before age 11, lack of confiding relationships, unemployment, and having more than 3 children under 14.
Provoking agents - Stressful life events leading to grief and hopelessness.
Conclusion - Social factors, particularly life stress and social class, are linked to depression. Low social status is associated with higher exposure to vulnerability factors and provoking agents, while high social status is linked to more protective factors. THIS STUDY CAN BE USED FOR SOCIOCULTURAL AETIOLOGIES.
What is the APFC for Alloy et al. (1999), and what theories does it support?
17 - 1 - 27 - 6
Aim - To investigate the role of negative thinking patterns in the development of MDD symptoms.
Procedure - Non-depressed Uni student participants with no other diagnosed mental disorders were clinically assessed for their cognitive thinking styles, and regularly assessed for MDD symptoms. Half of them had a history of clinical depression, and yet at the beginning of the study they possessed no symptoms at the start of the study. The cognitive thinking style test consisted of identifying participants as HR (High Risk) or LR (Low Risk) for depression based thinking patterns, and every 6 weeks for 2.5 years these students were assessed for the development of MDD symptoms (and every 4 months for the 3 years after). The study’s questionnaires and structured interviews were designed to identify stressful life events, cognitive styles and symptoms.
Findings - In the group with no previous MDD history, 17% of HR participants developed MDD symptoms, compared to only 1% of LR. 29% of the HR groups showed minor signs of MDD, compared to 6% in the LR group. In comparison, in the group with MDD history, 27% of the HR group relapsed in comparison to 6% of the LR group. Additionally, 50% of this HR group showed minor MDD symptoms, and for the LR group it was 26.5%. On top of that, the rate of suicidality was higher in HR groups (28% ) compared to LR groups (12.6%). Negative cognitive styles were significantly associated with onset and relapse MDD. Participants were also asked, after all of this, to do a word association test, where it was found that HR group participants had better word recall and processing for negative information than positive information.
Conclusion - Negative thinking patterns are shown to be more associated with negative thinking patterns. THIS STUDY CAN BE USED FOR COGNITIVE AETIOLOGIES
What is the APFC for Joiner et al. (1999), and what theories does it support?
Aim - To determine the role of depressive and anxious thinking patterns on the development of depressive symptoms. They hypothesized that negative thinking patterns, but not anxious cognitions, would play a role in the onset of symptoms related to depression.
Procedure - The sample was made of 119 American university students, all taking an abnormal psychology course. The mean age of the students was 19 years old.
The stressor that the researchers would observe was mid-term examinations. The students were assessed two weeks before and two weeks after their mid-term examinations. As the administration of the exams was naturally occurring in the university setting, this study was a natural experiment.
To assess the students, there were three tests that were given.
1. The Dysfunctional Attitudes Scale [DAS] This test measures thinking patterns such as vulnerability, need for approval, perfectionism and the need to impress. This was taken only before the mid-term exams.
2. The Cognitive Checklist [CCLJ. Half of the questions determine automatic thoughts linked to depression; the other half, linked to anxiety. This test was taken both before and after the exams.
3. The Beck Depression Inventory [BDI] - A standardized assessment to measure levels of symptoms linked to depression. This test was also taken both before and after the exams.
Findings - The researchers found an increase in the scores on the BDI only in students who had higher scores on the DAS and who had failed an exam. Students who had a higher score on the DAS but did well on the exams showed no significant increase in their BDI score. For the students who had lower scores on the DAS, even if they received low grades, they did not experience depressive reactions.
Conclusion - When looking at the scores for the CCL, there was a correlational between having higher scores on the depressive thinking patterns questions and the increase in the BDI scores if a student failed an exam. There was no significant correlation between the anxiety scores and an increase in BDI scores. THIS STUDY CAN BE USED FOR COGNITIVE AETIOLOGIES
What is the APFC for Parker et al. (2001), and what theories does it support?
Aim - To compare the extent to which depressed Chinese patients in Malaysia and Caucasian patients in Australia identified both cognitive aspects of depression and a range of somatic symptoms as a sign of their depression and the reason that they sought professional help.
Procedure - The sample was made up of 50 Malaysian participants of Chinese heritage and 50 Australian participants of Caucasian, Western heritage. Whereas the Australians all had English as their first language, the Chinese were a mix of Chinese (80%) and English (20%) as their first language, All participants were out-patients who had been diagnosed with Major Depressive Disorder, but who did not have other diagnoses as well, such as drug addiction or schizophrenia. The questionnaire was based on two sets of symptoms. First, a set of mood and cognitive items common in Western diagnostic tools for depression. Secondly, a set of somatic symptoms commonly observed by Singaporean psychiatrists. The questionnaire was translated into Malay and Mandarin Chinese. It was back-translated to establish credibility.
The patients were asked to judge the extent to which they had experienced each of the 39 symptoms in the last week. They had only four options: all the time, most of the time, some of the time and not at all. They were also asked to rank the symptoms that they experienced in order of how distressing they were. Through the assistance of their psychiatrists, it was also noted what the primary symptom was that led to them seeking help.
Findings - When looking at which symptom led them to actually seek help, 60% of the Chinese participants identified a somatic symptom, compared to only 13% of the Australian sample.
distress they cause. However, when comparing the lists of which symptoms each group acknowledged experiencing, something rather interesting happened. There was no significant difference in the number of somatic symptoms indicated by each group as being linked to their depression. However, the Chinese participants were significantly less likely to identify cognitive or emotional symptoms as part of their problem. They were less likely to rate feeling helpless and hopeless, a depressed mood, having poor concentration, or having thoughts of death than the Australian participants.
The role of culture is evident here; in Western culture it is more appropriate to discuss one’s emotions and depression is seen as linked to a lack of emotional well being; whereas in Chinese culture, it is less appropriate and even stigmatised if one speaks about a lack of emotional health. THIS STUDY CAN BE USED FOR PREVALENCE RATES
What is the APFC for Amenson and Lewinsohn (1981), and what theories does it support?
Aim - To evaluate the validity of the artefact hypothesis under naturalistic conditions.
Procedure - The sample was made up of 998 participants who were recruited through an announcement mailed to 20,000 residents of Eugene and Springfield, Oregon. The names were randomly selected from the county voter registration list. Participants were told that they would be part of a study of “the understanding of psychological health and its relationship to what people do, think and feel.” There were two times that the participants were assessed for depressive symptoms. First, they were asked to fill out a 20-item questionnaire and mail it back to the researchers. The second time was about 8 - 9 months later when they were interviewed at the clinic. The interview was a 2-hour semi-structured interview. The interviewers were blind to the questionnaire data. Part of the questionnaire was the Centre for Epidemiological Studies Depression Scale (CES-D), which measures the intensity of depressive symptoms. o test the artifact hypothesis, men and women were divided into high, medium, and low symptom level groups based on their CES-D scores. Each group had a similar mean score. When asked about how they labelled their own behaviour and whether they had sought help, there were no significant differences between the genders in any of the three groups. In addition, they compared the CES-D scores based on self-reported symptoms with the clinical diagnosis from the two-hour interview.
Findings - The analysis found that men and women with equal reported symptom levels were equally likely to be diagnosed as depressed, regardless of whether the interviewer was male or female. Self-labelling and clinical diagnosis were in agreement for 81% of the female and 92% of the male participants.
Conclusion - This study supports the argument that there are actual differences in the prevalence of depression in males and females and that is not the result of reporting or clinical biases. THIS STUDY CAN BE USED FOR PREVALENCE RATES
What is the APFC for Kirsch et al. (2008), and what theories does it support?
Aim - To evaluate the efficacy of SSRIs in the treatment of MDD and assess whether their therapeutic effects were greater than placebo, particularly across levels of depression severity.
Procedure - This was a meta-analysis using clinical trial data obtained through the Freedom of Information Act from the US Food and Drug Administration (FDA). The researchers examined data from 35 randomised, placebo-controlled trials involving 4 widely used SSRIs, including fluoxetine (Prozac) and paroxetine (Paxil). The analysis included 5,133 patients diagnosed with depression and assessed using the Hamilton Depression Rating Scale (HAM-D), which measures the severity of depressive symptoms. The trials compared changes in symptom severity from baseline to after SSRI or placebo treatment. Importantly, the FDA data included unpublished trials, allowing the researchers to overcome publication bias—the tendency for positive results to be published more often than negative or null results. Participants were grouped by initial severity of depression (mild, moderate, severe) to investigate whether SSRI efficacy was consistent across all levels of symptom intensity.
Findings - The results showed that, across most trials, SSRIs were only marginally more effective than placebo, especially in cases of mild to moderate depression. The mean difference in HAM-D score between the SSRI and placebo groups was below the threshold considered clinically significant by the National Institute for Health and Care Excellence (NICE). Significant effects were only observed in participants with severe depression, where the placebo effect was notably lower, making the drug effect appear larger. This led the researchers to propose that the majority of the benefit seen in SSRI use could be attributed to the placebo effect rather than the drug’s pharmacological action.
Conclusion - SSRIs provide minimal clinical benefit over placebo for most people with depression, particularly those with mild or moderate symptoms. This study challenges the effectiveness and ethical justification of widespread SSRI prescription and supports a move toward more personalised or combined treatments for MDD. THIS STUDY CAN BE USED FOR TREATMENTS
