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The evidence suggests that losing a parent in childhood increases the risk of depression in adulthood.
False
People with depression often display high levels of premorbid anxiety.
True
A sociotrophic personality is associated with a decreased risk of depression following adverse life events.
False
Genome Wide Association Studies (GWAS) have identified convincingly replicated loci for depression.
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Non-caring and overprotective parenting styles are associated with melancholic depression in adulthood.
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The serotonin transporter gene is not associated with major depression.
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GWAS studies rely on hypothesized candidate genes.
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Dysthymia is no longer classified as a depressive personality.
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Mothers with postnatal depression are more likely to manifest a nurturing and emotionally expressive rearing style.
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The SIRT1 gene is associated with severe recurrent depression in men.
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The 12-month prevalence of major depression in the community is highest among individuals born before 1945.
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The lifetime prevalence of dysthymia is higher in men than in women.
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The prevalence of major depression is lower in the unemployed than in the employed.
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Older people tend to over-report past episodes of depression.
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The mean age of onset of major depression is 40 years.
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The 12-month prevalence of recurrent brief depression is 1.3%.
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Major depression is less common in women than in men.
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The aetiology of depression is not well understood in terms of genetic epidemiology and childhood experiences.
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According to Freud, depression occurs when feelings of disgust and hostility are present at the same time.
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Melanie Klein believed that the loss of the breast during weaning represents a major symbolic loss for the infant.
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Cognitive distortions include arbitrary inference and overgeneralization.
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Beck suggested that depressed patients characteristically have recurrent and intrusive positive thoughts.
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Selective abstraction is a cognitive distortion that involves focusing on a detail and ignoring more important features of a situation.
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John Bowlby showed that the rearing abilities of the main caregiver play an unimportant role in giving the infant a secure emotional 'attachment'.
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Freud suggested that depression results from the loss of a 'good object'.
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Cognitive theories propose that depressive cognitions are the primary cause of depression.
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Schemas established early in life can become activated by 'matching' life experiences.
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Taylor's 2008 review focused on the cognitive-behavioral model of depression.
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The brain's synthesis of 5-HT is dependent on the availability of its precursor amino acid, 1-phenylalanine.
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Decreased plasma tryptophan levels are seen in all types of depression.
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Blunted 5-HT neuroendocrine responses are a characteristic of noradrenaline activity.
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Studies have consistently shown that drug-free patients with major depression have a significant reduction in CSF concentrations of 5-hydroxyindoleacetic acid (5-HIAA).
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Low CSF 5-HIAA levels are specifically associated with depression.
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Post-mortem brain studies have consistently shown a direct link between 5-HT levels and depression.
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Neurochemical brain imaging studies have shown a widespread increase in 5-HT1A-receptor binding throughout the cortical and subcortical regions.
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Neuroendocrine tests have consistently shown a strong correlation between 5-HT function and cortisol levels.
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Clinical relapse after tryptophan depletion is a characteristic of noradrenaline activity.
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The pharmacological effects of antidepressant drugs are not considered in Chapter 25.
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Stressful events always cause depressive disorders that succeed them.
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Life events are important antecedents of all forms of depression.
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Poor social support is associated with a decreased risk of depression.
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Genetic factors play no role in how life events are perceived by individuals.
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Remission from depression is often linked to 'fresh-start' life events.
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Depressive episodes can occur without major environmental precipitants once a depressive disorder is established.
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The perception of stressful events may change over time based on a person's mental state.
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All life events have the same level of impact on depression regardless of their nature.
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The need for a major environmental stressor to trigger depression is unchanged by a family history of depression.
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Peer victimization through bullying can lead to feelings relevant to the onset of depression.
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A transient lowering of plasma tryptophan can rapidly alter brain 5-HT function.
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Low brain 5-HT function is sufficient to cause depression independently of other factors.
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In depressed patients, noradrenaline function does not show any consistent alterations.
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Tryptophan depletion has significant clinical effects on unmedicated individuals with a personal history of mood disorders.
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Drugs that target noradrenaline pathways are always ineffective as antidepressants.
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Normal sadness is defined as being indistinguishable from depressive disorders.
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Anxiety disorders and mild depressive disorders can be difficult to distinguish from one another.
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Schizophrenia can usually be distinguished from depressive disorders based solely on cognitive dysfunction.
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Adjustment disorders related to stressors can present symptoms similar to major depression.
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Cognitive impairment in elderly patients with depressive disorders can be easily differentiated from dementia.
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Depressive disorders often co-occur with various other disorders such as anxiety and eating disorders.
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The prevalence of depressive disorders is clearly defined and universally measured.
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Careful history-taking and physical examination are vital for diagnosing depressive disorders.
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Schizoaffective disorders are characterized by symptoms of both schizophrenia and depressive disorder appearing in equal measure.
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Recent surveys applying DSM criteria indicate that major depression is more prevalent in non-industrialized countries.
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Dysfunctional assumptions are formed during critical incidents.
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The monoamine hypothesis associates mood disorders with abnormalities in monoamine neurotransmitter systems.
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Negative automatic thoughts contribute to a positive mood.
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Biases in facial expression recognition can occur in individuals at high risk for depression.
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The prognosis of mood disorders improves with an increasing number of episodes.
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Critical incidents do not play a role in activating dysfunctional assumptions.
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Changes in brain neurochemistry can be developmental in origin.
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The cognitive model of depression includes five categories of depressive symptoms.
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Depression has a higher concordance rate in dizygotic twins compared to monozygotic twins.
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The heritability of major depression is estimated to be around 37%.
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Individuals with relatives suffering from unipolar depression are at increased risk for bipolar disorder.
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The familial segregation of depression follows a clear Mendelian inheritance pattern.
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Adverse early life experiences have no impact on the development of the HPA axis.
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Polygenic inheritance suggests that multiple genes with large effects contribute to genetic liability for depression.
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The impact of life events on depression is solely determined by genetic inheritance.
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The monoamine theory of depression posits that allelic variations in genes related to neurotransmitter synthesis contribute to mood disorders.
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Meta-analyses provide consistent heritability estimates for men and women regarding depression.
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Changes in the activity of monoamine neurons are related to episodes of depression.
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Dopamine neurons in the mesolimbic system are primarily responsible for cognitive functions rather than incentive behavior and reward.
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Research indicates that lowering 5-HT and noradrenaline is sufficient to cause clinical depression.
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Magnetic resonance spectroscopy has been instrumental in measuring only dopamine levels in the brain of depressed patients.
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Decreased levels of glutamate in the anterior brain regions have been linked to anxiety disorders rather than mood disorders.
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About 50% of patients with Cushing's syndrome do not experience major depression.
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Abnormalities in endocrine function suggest a potential causative relationship with mood disorders.
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In depressive disorders, plasma cortisol secretion is decreased throughout the 24-hour cycle in most patients.
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Patients in recovery from depression show increased dopamine receptor density in striatal regions.
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Study Notes
Here are the study notes for the text:
Differential Diagnosis of Depressive Disorders
- Depressive disorders must be distinguished from normal sadness, adjustment disorder, anxiety disorders, schizophrenia, and organic brain syndromes.
- Comorbidity with other disorders, such as anxiety disorders, eating disorders, substance misuse, and personality disorder, is common.
- Accurate diagnosis is crucial, as misdiagnosis can lead to incorrect treatment.
Epidemiology of Depressive Disorders
- Prevalence of major depression:
- 12-month prevalence in the community: 2-5%
- Lifetime prevalence: 4-30%
- Mean age of onset: 27 years
- Twice as common in women than men
- Higher rates in people born after 1945
- Higher rates in the unemployed and divorced
- Prevalence of dysthymia: 4%
- Prevalence of brief depression: 2.6%
Aetiology of Depression
- Genetic factors:
- Substantial knowledge about genetic epidemiology and the role of childhood experiences
- Certain personality traits may be associated with a predisposition to mood disorders
- Early environment:
- Parental deprivation and separation may not increase the risk of depression in adulthood
- Family discord and lack of care may predispose individuals to depression
- Gross disruption of parent-child relationships, such as physical or sexual abuse, is a risk factor for depression
- Non-caring and overprotective parenting styles are associated with non-melancholic depression in adulthood
- Gene-environment interactions:
- Individuals carrying a particular allele are more likely to experience an episode of major depression during childhood adversity
Personality and Depression
- Certain personality traits, such as neuroticism, may be associated with a predisposition to mood disorders
- Personality features, such as sociotrophic personality, may influence how someone responds to adverse events and make depressive disorders more likely
Vulnerability Factors and Life Difficulties
- Life events, such as loss and humiliation, may precipitate depression
- Genetic factors may be involved in individual liability to experience life events
- Remission from depression is often associated with "fresh-start" life events
Genetic Causes
- Family and twin studies:
- Depression tends to run in families
- Environmental influences are also important in the etiology of depression
- Twin studies confirm that the aggregation of depressive disorders in families is in part due to genetic factors
- Mode of inheritance:
- The familial segregation of depression does not fit a simple Mendelian pattern
- The female preponderance of depression is well established
- Molecular genetics:
- The monoamine theory of depression suggests that allelic variation in genes coding for monoamine synthesis or metabolism or specific receptors may contribute to the risk of mood disorders
Cognitive Model of Depression
- Early experience lays down dysfunctional assumptions, which are activated by critical incidents, leading to a vicious cycle of negative thinking and depressed mood
Neurobiological Approaches to Etiology
- Monoamine hypothesis:
- Suggests that depressive disorder is due to an abnormality in a monoamine neurotransmitter system in the brain
- Changes in brain neurochemistry are associated with mood disorders
- Other neurobiological approaches:
- Biases in facial expression recognition can be found in both recovered depressed patients and those at high risk for depression
Psychological Approaches to Aetiology
- Concerned with the psychological mechanisms by which recent and remote life experiences can lead to depressive disorders
- Psychoanalytic and cognitive-behavioral theories are the main approaches to the problem### Cognitive Theories of Depression
- Depressed patients exhibit recurrent negative thoughts, termed "automatic thoughts."
- Beck proposed that these thoughts reflect negative self-perceptions and pessimistic views about the world and future.
- Cognitive distortions contribute to the persistence of these automatic thoughts, including:
- Arbitrary inference: Drawing conclusions without evidence, or against contrary evidence.
- Selective abstraction: Focusing on less significant details while ignoring relevant context.
- Overgeneralization: Making broad claims based on single events.
- Personalization: Relating external events unwarrantedly to oneself.
Psychoanalytic Theory of Depression
- Freud correlated mourning with melancholia, suggesting similarities in their causes.
- Melancholia can arise from non-physical losses, leading to a loss of an internal representation or "object."
- Depressed patients often engage in self-criticism, redirecting hostile feelings toward themselves from lost loved ones.
- Melanie Klein emphasized early mother-infant separation as a significant emotional loss, resulting in guilt and anxiety.
- John Bowlby identified the importance of secure attachments in childhood, linking them to adult psychopathology, including depression.
Neurotransmitter Abnormalities in Depression
- Monoamine neurotransmitters, especially serotonin (5-HT), noradrenaline, and dopamine, show significant abnormalities in depressed patients.
Serotonin (5-HT) Function
- 5-HT synthesis relies on the availability of 1-tryptophan; low plasma tryptophan levels correlate with melancholic depression.
- Studies indicate dietary weight loss can further decrease plasma tryptophan levels, influencing 5-HT function.
- Evidence shows multiple neurochemical impairments related to 5-HT in depression, including:
- Decreased plasma tryptophan and 5-HT neuroendocrine responses.
- Reduced 5-HT1A receptor binding and reuptake sites in the brain.
Noradrenaline and Dopamine in Depression
- Depressive symptoms linked with:
- Blunted noradrenaline-mediated hormone release.
- Decreased homovanillic acid (HVA) levels, indicating dopamine dysregulation.
- Clinical relapses observed after catecholamine depletion.
CSF and Post-Mortem Studies
- Inconsistent evidence regarding reduced levels of 5-hydroxyindoleacetic acid (5-HIAA) in major depression.
- Low CSF 5-HIAA levels observed in patients with a history of impulsive behaviors, which may indicate a broader tendency towards hostility rather than a direct correlation with depression.
Neurochemical Imaging Studies
- Brain imaging techniques reveal decreased binding of 5-HT1A receptors and reductions in 5-HT reuptake sites across brain regions in depressed individuals.
Neuroendocrine Dysfunction
- 5-HT function assessed via neuroendocrine challenge tests, measuring responses like growth hormone and prolactin release.
- Dysregulations in the hypothalamic-pituitary-adrenal axis, particularly cortisol, are common in depression.
Role of Other Neurotransmitters
- Developments in magnetic resonance spectroscopy have highlighted:
- Decreased glutamate levels in the anterior brain regions of depressed patients.
- Interest in amino acid neurotransmitters like GABA and glutamate in mood regulation.
Endocrine Abnormalities and Depression
- Approximately half of patients with Cushing's syndrome experience major depression.
- Depression also linked to Addison's disease, hypothyroidism, and hyperparathyroidism, suggesting an interplay between endocrine disorders and mood regulation.
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Description
This quiz explores the key aspects of differentiating depressive disorders from other similar conditions. It focuses on understanding the symptoms and comorbidities relevant to proper diagnosis. Get ready to test your knowledge on this important topic in mental health.
