Depression Flashcards

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1
Q

depression

A
  • Nature of ‘depression’ – are we talking about a disorder or phenomenon?
    • The diagnosis of depression is sometimes described as the common cold of psychiatry (Rosenhan & Selifman, 1989).
      ○ does not downplay the importance but highlights commonality as we all go through periods of low mood
    • We all have periods of ‘depression’, or more specifically of sadness and low mood across our lives. These experiences are often understandable reactions to difficult circumstances.
    • “Depression refers to a wide range of mental health problems characterised by the absence of a positive affect (a loss of interest and enjoyment in ordinary things and experiences), low mood and a range of associated emotional, cognitive, physical and behavioural symptoms.” NICE (2022).
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2
Q

positivism

A
  • Positivism assumes depression is a ‘natural kind’ reflecting the natural world rather than human interest.
  • Sadness has been documented for as long as human records have existed (Cromby et al., 2013). Ancient Greeks and religious scriptures reference low mood and sadness.
  • The presence of sadness throughout human history does not mean that the experience has been unchanging. The word ‘depression’ has evolved to capture a cluster of phenomena around sadness.
    Positivism assumes that the explanations we now have are more plausible we are coming closer to discovering truth
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3
Q

validity and reliability

A
  • Depression diagnoses are not distinct from one another. Co-occurrence is higher than chance levels (Andrews et al., 2008; Cromby et al., 2013). Diagnoses are therefore not discrete, separate entities.
  • Variation within diagnostic categories is very common. Depression is heterogeneous.
    • Two people with the same diagnoses may have very different experiences- many different combinations of symptoms but both diagnosed with the same disorder
    • Fried and Nesse (2015) found that combining the symptoms of MDD listed in the DSM can result in over 1000 different combinations of symptoms.
    • So, people with the same diagnosis lack the same experiences (Johnstone, 2013).
  • Depression is limited in predictive validity for treatment plans (NICE, 2007).
    • If mental health conditions are valid medical categories, we should be able to reliably predict outcomes and effective treatments (Johnstone, 2013).
    • Diagnosis does not predict medication response (Kendell, 1988). This is not to say that medication is not useful or that it should not be offered. But it does suggest that positive effects are non-specific and unpredictable.
      Single symptom research might be better than research using psychiatric categories (Cromby et al., 2013).
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4
Q

vitamin d

A
  • Vitamin D has been linked to depression.
  • Would the disorder be deficiency or depression?
  • Some research takes this to mean that supplements would prevent depression (Sangle et al., 2020).
  • Not everyones depression is linked to low levels of vitamin D
  • Someone research suggests we should take supplements to help with depression and lift mood
    Issue- if you present to your gp with symptoms of depression and vitamin d deficiency they will look at different treatments
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5
Q

neurotransmitters

A
  • Monoamine hypothesis:
    • Norepinephrine, dopamine and serotonin.
    • All three are involved in sleep, appetite, and emotion.
  • Antidepressants work by increasing levels of one or more of these monoamines in the brain.
    However, instead of starting with a hypothesis about the neural basis of depression, these explanations have worked backwards from the discovery that drugs that impact upon these neurotransmitter systems can influence mood (Cromby et al., 2013).
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6
Q

serotonin hypothesis

A
  • SSRIs (e.g., Prozac) slow down serotonin reuptake, gradually increasing serotonin levels.
  • No strong evidence for the serotonin or monoamine hypotheses. No evidence of what a typical balance should look like or why some people have an imbalance (Cromby et al., 2013).
    If we could support this hypothesis, should we diagnose depression or a serotonin deficiency/imbalance of some kind?
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7
Q

criticisms of the serotonin hypothesis

A
  • The chemical imbalance model remains the dominant cultural story of depression, particularly in America (France et al., 2007).
  • Many scientists, however, claim that the low serotonin explanation of depression is not substantiated (Kendler & Schaffner, 2011; Kirsch, 2010; Lacasse & Leo, 2005).
  • Joanna Moncrieff
    • proper studies show that anti depressants are only minimally different from a placebo- mind altering drugs that suppress emptions
    • Effects that anti depressants have are not useful- libido taken away etc does not help- makes it more difficult to recover long term
    • Especially in children- more severe side effects as brain is still developing- also giving them the message they need a chemical crutch and cannot manage and control emotions themselves- need to find other ways to help them do that
    • No one thinks about social measures to help- quick fix for patients, appealing to politicians, parents, patients for ease of use. Think about societal level (why do people find modern life difficult, build up communities, provide employment to lead a satisfying life) and individual level (depends on their problems, cannot prescribe a solution for every problem- consider family situations, behaviour, trauma which is different in each case- role for therapy to help individuals find their own solutions and ways of managing their difficulties)
    • Main stream response is to prescribe medication to help cope with problems- not supported by evidence suggesting serotonin abnormalities cause depression
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8
Q

geographical profile of depression

A
  • When you look at the profile geographic of people taking anti-depressants, they are not evenly distributed across the country.
    Places that have higher levels of social deprivation tend to have higher levels of antidepressant prescriptions.
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9
Q

less common biomedical treatments

A
  • Benzodiazepines (e.g., Valium) increase GABA and inhibit neurotransmitter activity leading to calming effects.
    • Linked to dependency and withdrawal.
      Electro-convulsive therapy (ECT) is when electrical currents are passed through the brain. This is now seen as a ’last resort’.
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10
Q

modern ECT guidelines

A
  • According to the NICE guidelines, consider ECT if:
    • Patient preference
    • Rapid response needed. For example, if the depression is life-threatening because the person is not eating or drinking.
    • Other treatments unsuccessful.
  • A person must be fully informed of the risks.
    • Risks include headaches and retrograde amnesia which can lead to longer term or permanent memory loss.
    • Heart irregularities can result.
      Reviews indicate a marked risk of death (Read, 2004).
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11
Q

general criticisms

A
  • Our biology is bound up in other aspects of our lives, such as psychological processes. Evidence suggests biology enables low mood rather than causing it (Cromby et al., 2013).
  • Biological treatments are not without risks, patients should be aware of risks and have a choice over treatment (NICE, 2022).
  • Overlooks depression as a cluster of smaller phenomena that can be clustered together in different ways. Depression is a common symptom of many conditions. Why do we have a BMM of depression but not pain?
    Neurotransmitter hypotheses under-supported and so mechanisms underlying medication effects are not well understood.
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12
Q

the cognitive model

A
  • All about how a person interprets a situation
  • It is not a situation in and of itself that determines what people feel, but rather how they construe a situation (Beck, 1964).
  • For example:
    • Light and dark pixels on a screen vs meaning of the words on the screen.
    • Friend walks past without acknowledging you.
    • Partner says they are feeling too tired for date night.
      The cognitive model of depression suggests that our early life experiences set up some core beliefs about ourselves/some conditional assumptions and these might be hidden (but they can come back). So, the idea is that activating events bring back these core beliefs.
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13
Q

core beliefs

A
  • Beginning in childhood, people develop certain ideas about themselves, other people, and their world.
  • Their most central or core beliefs are enduring understandings so fundamental and deep that they often do not articulate them (even to themselves).
    The person regards these ideas as absolute truths – just the way things are (Beck, 1987).
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14
Q

Beck’s cognitive model of depression

A
  • Beck’s cognitive model suggests that vulnerability to depression arises from certain kinds of schemas/beliefs that a person holds about themselves, the world, and the future (negative cognitive triad).
    When a core belief is activated, we interpret situations through the lens of this belief even though the interpretation may not be valid.
  • The negative triad of views is caused by an underlying negative schema (a collection of interrelated beliefs about the self which are negative and acquired during childhood, usually as a result of adverse life experiences).
  • Because of this negative self-schema, individuals have a set of cognitive biases toward pessimistic, negative or critical interpretations of events or experiences (see next slide for examples).
    As a consequence of these cognitive biases, when faced with adversity, some individuals more readily develop the kinds of reactions that as associated with a diagnosis of depression.
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15
Q

cognitive behavioural therapy

A
  • CBT focuses on how thoughts, feelings and bodily reactions all interact and influence how we behave.
  • Therapy therefore draws upon Beck’s model of depression and focusses on identifying unhelpful thought patterns or biases.
  • In particular, therapy aims to illuminate and question the usefulness of some of our automatic thought processes.
  • Preferred treatment for ‘less severe depression’ (NICE, 2022).
  • Often uses thought diaries and records to help people identify unhelpful and challenge problematic thinking patterns.
    Associated with long term efficacy, and reducing relapse compared to medication alone but not enough long-term research.
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16
Q

criticisms

A
  • Cognitive biases can still risk pathologising difference and risk implying blame on the person with depression.
  • CBT often follows a prescriptive approach and applies logic to emotion.
    When used alone, it does not take account of biological influence and can be seen as downplaying social influences.
17
Q

social inequality

A
  • The association between social inequality and distress has been demonstrated in many different countries, including the UK.
  • Two hypotheses have been put forward:
    • Social inequality causes clinical sadness.
    • As clinical levels of sadness can impair relationships and obstruct employment, this causes downward social mobility.
      Nevertheless, there are many studies suggesting the clinical sadness is caused by social inequality. For example, median household income at age seven was a strong predictor of depression in adult life (Fan & Eaton, 2001).
18
Q

gender

A
  • Women are roughly twice as likely to meet the diagnosis associated with sadness (Cromby et al., 2013).
  • Women more likely to receive clinical intervention for experiences of low mood or sadness (Cromby et al., 2013).
  • One explanation for women’s higher rates of sadness is domestic violence (Cromby et al., 2013).
  • Also, women are still at a relative economic disadvantage (Cromby et al., 2013) with unemployment and low socio-economic status linked to depression and suicidality (Stack, 2021).
  • Post-natal depression draws upon biological explanations. Overlooks the profound change of having a child (Cromby et al., 2013) together with women being more likely to be the primary carer.
    In heterosexual relationships, women often do more nurturing, and are less likely to have their own needs met (Perrons, 2000).
19
Q

adverse life experiences

A
  • Multiple meta-analyses have demonstrated a robust association between traumatic experiences and depression (e.g., Mandelli et al., 2015; Nelson et al., 2017).
  • Research suggests that typical psychological therapies are not as effective for people who have had traumatic life experiences:
    • Increased risk of recurrent and persistent depression (Nanni et al., 2012)
    • A lack of response/remission during depression treatment (Nanni et al., 2012)
      Twice as likely to develop chronic or treatment-resistant depression (Nelson et al., 2017).
20
Q

adverse childhood experiences

A
  • Initially, there were ten different types of adversities such as violence, abuse, neglect, family members with mental health and/or addiction struggles or loss of a parent.
  • Research has since added to this list. For example, bullying is now considered by many as an ACE. Poverty may also be an ACE (Hughes & Tucker, 2018).
  • There is a strong graded relationship between high ACE scores and higher rates of mental distress, including depression.
  • Around 61% of adults have had at least one ACE (CDC, 2023).
  • Meta analysis and review (Hughes et al., 2017) found that four or more ACEs leads to:
    • Moderate risk of smoking, cancer, heart and respiratory disease.
    • Strong risk of sexual risk taking, mental ill health and problematic alcohol use.
  • Briggs et al. (2021) found that 4+ has become a way to define ‘high risk’ but not all ACEs are equal.
    • For example, sexual abuse had a greater association with negative outcomes.
      Sexual abuse linked to diagnoses of depression and PTSD and also with suicidality (Paolucci et al., 2001).
21
Q

general criticisms

A
  • Social models risk overlooking psychological responses.
  • Need to exist within a bio-psycho-social model to effectively consider how we can reduce the impacts of social issues (e.g., ACEs).
    Next steps are around preventing ACEs- moving away from ACEs causing mental distress evidence base and taking a step back to prevent them in the first place to reduce levels of distress in future generations
22
Q

NICE guidelines

A
  • Overview
    • This guideline covers identifying, treating and managing depression in people aged 18 and over.
    • It recommends treatments for first episodes of depression, further-line treatments, and provides advice on preventing relapse and managing chronic depression, psychotic depression, and depression with a coexisting diagnosis of personality disorder.
  • NICE guidelines look dynamically at symptoms, duration and impact on functioning
    Then categorises people as less or more severe- not in terms of symtpoms of comparison but infividually looking at each persons presentation e.g. if it is the first time a person is depressed, not really impacting daily life they would be less severe
23
Q

treatment for a new episode of less severe depression

A
  • Treatment options
  • … consider the least intrusive and least resource intensive treatment first…
  • … reach a shared decision on a treatment choice appropriate to the person’s clinical needs, taking into account their preferences …
  • … recognise that people have a right to decline treatment.
  • 1.4.2
    • Match the choice of treatment to meet the needs and preferences of the person with depression. Use the least intrusive and most resource efficient treatment that is appropriate for their clinical needs, or one that has worked for them in the past.
  • 1.5.3
    • Do not routinely offer antidepressant medication as first-line treatment for less severe depression, unless that is the person’s preference.
  • Recurrence is more likely if:
    • History of recurrent depression especially in the past two years.
    • History of incomplete treatment.
    • Unhelpful coping styles (e.g., avoidance or rumination).
    • Other chronic physical or mental health problems
    • Personal, social or environmental factors that contributed and are ongoing.
  • Treatment guidelines
    • Review what was learnt previously and what was helpful.
    • Make plans to maintain progress.
    • Identify circumstances or signs that can worsen depression.
      Plan for challenging events over the coming 12 months.
24
Q

criticisms

A
  • Still need a research and policy approach to address adverse effects of medication and this should be measured against effectiveness. Important for recommendation guidelines and for informed consent.
  • Although conceptualisation has improved, it can still be argued to centre around pathologised understandings of human experience.
    Lack of homogeneity across depression subtypes is overlooked. Depression is still treated as a valid category without acknowledgement of subjective knowledge creation.