Depression

Question 1

Define depression

Answer 1

SLOANE+STRAUS 2001; A mood disorder involving emotional, behavioural, physical and cognitive symptoms: often involves a low emotional state characterised by significant levels of sadness, lack of energy and self worth

Question 2

Describe major depression

Answer 2

A psychological problem characterised by relatively extended periods of clinical depression which cause significant distress o the individual and impairment in social or occupational functioning.

Four Domains of Symptoms:

1. Affective: depressed mood, sadness
2. Cognitive: guilt, thinking they’re worthless
3. Behavioural: social withdrawal, restlessness
4. Physical: Changes in sleep patterns, energy levels or appetite

Question 3

Describe the diagnosis of depression

Answer 3

1. Presence of a single major depressive episode (not attributed to other disorders) where 5+ depressive symptoms must be observed during the same 2 week period
2. Too become clinically problematic, a presence of dysfunctional symptoms such as worthlessness is required
3. The symptoms must cause clinically significant distress or impairment in social, occupational or other forms of functioning

Question 4

Issues with diagnosis of depression

Answer 4

1. Test-retest reliability is low for the diagnosis of major depression. Keller et al (1995) carried out a multisite study and diagnosed 500 patients using diagnostic criteria and repeating the process six months later, results showed poor consistency between diagnosis on separate occasions. Zanarini (2000) further evidenced it finding only a 0.61 test-retest correlation. Reasons for this includes that because there needs to be 5 symptoms shown out of 9 for diagnosis to occur, a one symptom disagreement can make the difference in the diagnosis of major depression or a less serious illness.
   Such issues have significant negative implications, as once diagnosed, the label of ‘depressed’ tends to stick in the long term. This has a stigmatising effect as this label can be used to describe the person rather than the disorder.
2. Low validity in diagnosis as for most people a diagnosis is given by their local GP. However, it is suggested that these diagnoses may be less objective as they are based on previous knowledge of patient rather than actual presenting symptoms (VAN WEEL-BAUMGARTEN 2006). Severe implications as the more willing GPs are too diagnose depression, the greater the risk of the medicalisation of normal everyday negative emotions (SHAW 2004).

Question 5

Describe the prevalence of major depression

Answer 5

Major depression is the #1 psychological disorder in the western world. At the rate of increase, it will be the 2nd most disabling condition in the world by 2020, behind heart disease (TYRELL+ELLIOT, 2015)

1. People of all ages, backgrounds, lifestyles, and nationalities suffer from major depression, with a few exceptions.
2. Up to 20% of people experience symptoms of depression.
3. 10 times more people suffer from major depression now than in 1945
4. The average age of first onset of major depression is 25-29

Question 6

Societal impact of depression

Answer 6

GLOBAL BURDEN: COSTS MONEY

Work: at least £8 billion lost productivity in UK annually (Thomas & Morris, 2003).

Treatment: at least £370 million in UK annually, 84% antidepressant meds (

Question 7

Describe neurochemical explanation

Answer 7

MONAMINE HYPOTHESIS: suggests that depression is due to abnormal levels of neurotransmitters in the monoamine group (noradrenaline, serotonin, and dopamine).

Neurotransmitters act at the synapses between neurons in the brain. They facilitate or block nervous transmission. Noradrenaline and serotonin are related to arousal and sleep—high levels of noradrenaline are linked to high levels of arousal, and increases in serotonin generally reduce arousal.

This was expanded upon with the permissive amine theory (Kety, 1975), which proposes that the level of noradrenaline and dopamine are controlled by serotonin, and that low levels of serotonin are inherited. When serotonin is low the levels of noradrenaline fluctuate wildly; low levels are associated with depression and high levels with mania. The biochemical system depends in part on genetic factors and so the genetics and biochemical explanations are inter-linked.

Question 8

Evidence for neurochemical explanation

Answer 8

1. (Teuting, Rosen, & Hirschfeld, 1981) Antidepressant drugs such as the monoamine oxidase inhibitors (MAOIs) increase the levels of noradrenaline and serotonin and alleviate the symptoms of depression, which supports the influence of the biochemicals on mood. Similarly, SSRIs inhibit the re-uptake of serotonin and the resulting increase in the level of serotonin is linked to improved mood.

Question 9

Evaluation of neurochemical explanation

Answer 9

+ Underlying explanation of depression means that fast and easy treatment methods can be developed in result. The proponents of this theory recommend the choice of an antidepressant with mechanism of action that impacts the most prominent symptoms. Anxious and irritable patients should be treated with SSRIs or norepinephrine reuptake inhibitors, and those experiencing a loss of energy and enjoyment of life with norepinephrine- and dopamine-enhancing drugs

• Cause, effect, or correlate. It is difficult to establish whether the low levels of neurotransmitters cause depression, are an effect of having the disorder, or are merely associated. Causation cannot be inferred as associations only have been identified. This is the same for the hormonal imbalances that have been linked to depression.
• Basing evidence on the effects of drug treatments is not sufficient enough: Contemporary neuroscience research has failed to confirm any serotonergic lesion in any mental disorder, and has in fact provided significant counterevidence to the explanation of a simple neurotransmitter deficiency. With direct proof of serotonin deficiency in any mental disorder lacking, the claimed efficacy of SSRIs is often cited as indirect support for the serotonin hypothesis. Yet, this ex juvantibus line of reasoning (i.e., reasoning “backwards” to make assumptions about disease causation based on the response of the disease to a treatment) is logically problematic; Treatment aetiology fallacy. The success of antidepressant drugs as a treatment does not necessarily mean the biochemicals are the cause of the depression in the first place. MacLeod (1998) described this as the treatment aetiology fallacy and used headaches as an example. Aspirin works well as a treatment but this doesn’t mean the headache was due to an absence of aspirin.
• Despite its flaws, the chemical imbalance explanation remains the potentially dominant cultural story of depression etiology in the United States (e.g., Smith, 1999). The chemical imbalance explanation does not reflect the full range of causes of depression, however it is given greater credence by both consumers and practitioners than is supported by sound research, and/or may be understood in an overly simplistic manner. Severe implications to society

Question 10

Describe genetic explanations

Answer 10

In terms of genetic factors depression can be seen to occur due to inherited predispositions that have been passed on from parent to child. Family, twin, and adoption studies suggest the involvement of genetic factors.

FAMILY STUDIES Gershon (1990) reviewed the findings from a number of family studies and found that depression runs in families, as the rate of depression was two to three times higher in first degree relatives of depressives compared to the general population.
TWIN STUDIES: Allen (1976) reported a mean concordance rate of 40% for MZ twins compared to 11% for DZ twins. The high ratio supports the role of genetic factors.
McGuffin et al. (1996) found a concordance rate of 46% for identical twins compared to 20% for fraternal twins.
ADOPTION STUDIES shown that the biological parents of adopted children who develop depression were eight times more likely than the adopted parents to have suffered with depression, which suggests the role of nature over nurture (Wender et al., 1986))

ALSO…A gene-environment interaction (GxE) was hypothesized to explain why life stress is a predictor for depressive episodes in some individuals, but not in others. Caspi et al. suggested that individuals possessing either one or two copies of the short variant of the 5-HTTLPR (serotonin transporter) gene, which is not transcriptionally as effective as the long form, experienced higher levels of depression and suicidality following a recent life stressor. The study has since been supported by a large number of other studies
— the relationship between 5-HTTLPR, stress, and depression in a large birth cohort and found a significant interaction between 5-HTTLPR and both stressful life events (SLEs) and childhood maltreatment in the development of depression. In this cohort, subjects carrying the less functional 5-HTTLPR s allele reported greater sensitivity to stress.

Question 11

Evaluation of genetic explanations

Answer 11

– Nevertheless, although genetics can explain 40% of cases, there must be other factors that must be the cause of the remaining 60%, thus suggesting that a purely biological explanation is reductionist and reduces complex human behaviour down to a purely physiological cause. Thus a more holistic approach is needed; the social/cog approach may better explain Depression as seen later in

Furthermore, the high concordance rates found in MZ twins compared to DZ twins is perhaps not due to their shared genetic makeup but their shared environment. MZ twins, identical in physical appearance are most likely to be treated equally by those surrounding them than DZ twins who are different in looks. Therefore, within research evidence there is an interaction between nature and nurture, which consequently decreases the validity of the study as the cause of the schizophrenia is uncertain.

Question 12

Describe the first cognitive explanation

Answer 12

Cognitive dysfunction in attributional style (Abramson et al.’s attribution model) and view of self, the world, and the future (Beck’s cognitive triad) have been linked to the development of depression.

COGNTIVE TRIAD (BECK 1967)
Individuals are depressed because their thinking is biased towards negative interpretations of the world and have thus acquired a negative schema. Negative schemas develop during childhood as a consequence of critical interpersonal experiences, and are activated when the individual experiences similar situations in later life. 

There are also a set of information-processing strategies that are con- sidered to lead to typical depressive distortions or logical errors in thinking. Negative schemas and cognitive biases maintain a ‘negative triad’ which is a pessimistic view of the self, world and future.
It is maintained as the schemas influence the selection, encoding, categorisation and evaluation of environmental stimuli which leads to a cycle of depressive symptoms.

Question 13

Evidence for the first cognitive explanation

Answer 13

1. A prospective study by Lewinsohn, Joiner, and Rohde (2001) measured negative or dysfunctional attitudes in participants who did not have a major depressive disorder at the outset of the study. They re-assessed the participants 1 year later and found those high in dysfunctional attitudes were more likely to develop major depression in response to negative life events. This supports faulty cognition as a cause rather than an effect of depression.
2. Evans et al. (2005) also conducted a prospective study and found that women with the highest scores for negative self-beliefs during pregnancy were 60% more likely to become depressed subsequently than those with the lowest scores.
3. Abela and D’Alessandro’s (2002) study on college admissions is a good example of this phenomenon. In their study they found that the student’s negative views about their future strongly controlled the interaction between dysfunctional attitudes and the increase in depressed mood. The research clearly backed up Beck’s claim that those at risk for depression due to dysfunctional attitudes who did not get into their college of choice then doubted their futures, and these thoughts lead to symptoms of depression. Therefore, the students’ self-perceptions became negative after failing to get into college, and many showed signs of depression due to this thinking.

Question 14

Evaluation of the first cognitive explanation

Answer 14

+ Beck’s theory is more useful than other cog explanations as in contrast to the laboratory based approaches of Seligman and Bower, has been primarily based on clinical data. Therefore, there are better therapeutic implications that can be based on the theory. CBT for example has been created which has been widely evidenced to be efficacious in reducing symptoms of a wide number of disorders.

• The concept of schemata in the sense used within the theory is extremely vague (Ingram, 1984), and, indeed, the term is frequently considered to be synonymous with beliefs, atti- tudes, and assumptions. This vagueness, although it may satisfa,ctorily express the clinical aspects of depressive vulnerability, is unnecessary given the relatively detailed consideration that the concept has received within cognitive science (Mandler, 1984)
• Cause or effect? The evidence that negative cognitions and dysfunctional beliefs precede the disorder is not convincing but nor has it been disproved. Therefore, conclusions are limited. It may be that the relationship is curvilinear, i.e. negative thinking predisposes depression and depression increases negative thinking

Question 15

Describe Life Events factor of depression

Answer 15

Depression is often preceded by a high number of stressful MAJOR LIFE EVENTS which are suggested to be a trigger for depression in individuals who have a genetic vulnerability or have a presence of a depressive attributional style which acts as a diathesis that predisposes a person to interpret the event that facilitates depression.

Child abuse has been associated with increased risk of developing depressive disorders later in life as it is during the years of development that a child is learning how to become a social being. Abuse by the caregiver is bound to distort the developing personality and create a much greater risk for depression and many other debilitating mental and emotional states. Disturbances in family functioning are additional risk factors.

In studying how stressful events may lead to depression, SELIGMAN (1975) have developed a theory called, “learned helplessness.” This theory states that when people experience chronic or repeated stressful events, they learn to feel helpless. This feeling of helplessness is strengthened when a person believes he or she has no control over the stressful situation.

Question 16

Evidence for life events as an explanation

Answer 16

1. Found that episodes of depression wee almost always preceded by a major life event. Interviews of depressed women showed that 61% of the depressed women had experienced at least one very stressful life event compared to only 19% of the non-depressed women. (BROWN+HARRIS 1978)
2. Kendler et al. (1993) found that women reported significantly more negative life events than men in the past year. It is also possible that women rely on a more emotion-focused approach and so spend a lot of time thinking about their problems and focus excessively on their emotions. Whereas men are more problem-focused, or if they do take an emotion-focused approach they seek distraction from their problems (e.g. drinking alcohol) (Nolen-Hoeksema, 1991
3. Studies compared scores on aggregated stressful life event scales between persons who did and did not report the recent onset of an episode of major depression. (Shrout et al 1989, Williamson et al 1995) and mainly show the following: 1. There is a consistently documented association between exposure to stressful life events and subsequent onset of episodes of major depression. 2. However, the magnitude of this association varies across studies depending on how life events are measured, with associations generally stronger when “contextual” measures are used rather than simple life event checklists.

Question 17

Evaluation for life events as an explanation

Answer 17

• Again the issue of causal relationships come into play, although in evidence of the effects of life events, the majority of depressed people report the occurrence of a stressful event shortly before the onset of their depression, only a minority of those people exposed to such events become depressed. Therefore, it would appear that there are individual differences at play which mediate who becomes depressed.
• Methodological issues with many of the evidence: most of the studies failed to consider that accuracy in reporting life events is associated with depression. These studies failed to adjust for the bias introduced by this possibility. For example, many studies failed to confirm whether events occurred before depression. Because depression can cause some events (Hammen 1991) and because people with a history of depression have more events than others even when not in episodes of depression (Kessler & Magee 1993), there may be a bias toward finding specious associations between life events and depression. Retrospective reports about event exposure might have been biased in these studies by differential recall accuracy or differential willingness to disclose and discuss stressful experiences among currently (at the time of interview) depressed versus nondepressed respondents in such a way that created the appearance that life events cause depression
• If societal factors are cause of depression then treatment is limited

Question 18

Whats the most useful explanation of depression

Answer 18

A psychobiological approach that integrates the different perspectives of depression. BECK 2008

A gene × environment interaction occurs in the onset and maintenance of depression where individuals experience stressful life events. However only those with a genetic predisposition are likely to develop depression as a result - there significant interaction between the 5-HTTPLR genotype and adverse events in determining the likelihood of an episode of major depression in a longitudinal cohort.

Furthermore, a number of studies indicate that negative cognitive processing and negative cognitions are associated with the presence of the 5-HTTLPR short allele.

Question 19

Describe biological treatments for depression

Answer 19

ANTIDEPRESSENTS (DRUG THERAPY)
Based on the concept that depression is caused by imbalances of neurotransmitters of serotonin or noradrenaline being produced in the nerve endings to active neighbouring cells.
1. TRICYCLICS (older) block the transporter mechanism that re-absorbs both sere toning and noradrenaline into the presynaptic cell after it has fired. So, more of these neurotransmitters are left in the synapse, prolonging their activity and making the transmission of the next impulse easier.
– Because of limitations (more side effects), newer drugs were created.
2. SSRIs (Prozac) work similarly but instead of blocking the reuptake of different neurotransmitters, they block mainly serotonin and so increase the quantity available to excite neighbouring brain cells, thus reducing the symptoms of depression.

Question 20

Evaluation for biological treatments for depression

Answer 20

+ EFFECTIVNESS

1. Tryclics are shown to be effective (Gitlin, 2002) where around 60-65% of individuals who took drugs showed improvement when compared to individuals on placebos.
2. Dependent on the severity of the depression individuals suffer from; Kirsch etal. 2008 reviewed clinical trials of SSRIs and concluded that only in cases of severe depression was there any significant advantage of using drug therapy. There was also only a difference found between drug treatment and placebo in those who have severe depression. Thus, even those moderately depressed benefit from the placebo, suggesting that there are psychological causes of depression.

APPROPRIATNESS

1. Less appropriate for children and adolsencts as double blind studies (Gellar etal. 1992) failed to demonstrate the superiority of antidepressant medications over placebo conditions. This is suggested to be due to the developmental differences in brain neurochemistry.
2. There are vast number of side effects associated with antidepressants that make them less beneficial for the individual.
   - Rosen 1999 found that SSRIs have side effects of headaches, gastric disorders and sexual dysfunction.
   - Ferguousen etal 2005 also reported that SSRIs are associated with increased risk of suicide as they increase suicidal thoughts in those susceptible. Compared to other treatments those on SSRIs were twice as likely to attempt suicide. Thus, there is a risk factor in taking these drugs which places a concern for the safety for sufferers.
3. Generally, drugs are a quick and effective method for dealing with symptoms of depression in the short term, however psychological therapies must be explored to improve chances of long term effectiveness.

Question 21

Describe cognitive therapy for depression

Answer 21

(BECK) CBT emphasises the role of maladaptive thoughts and beliefs in the origins of depression such as when people think negatively about themselves and their lives.

Aim: identify and alter maladaptive cognitions as well as dysfunctional behaviours that may contribute to depression. Sessions are brief and are 16-20 times. For depression, two strategies re particularly focused on:

1. THOUGHT CATCHING: individuals taught to seek link between their thoughts and the way they feel. As homework they are asked to record and emotion arousing events and the automatic negative thoughts associated with these events. During therapy they are taught to challenge this association by asking themselves questions such as where is the evidence their thoughts are true. By challenging dysfunctional thoughts and replacing them, they try new ways of behaving.
2. BEHAVIOURAL ACTIVATION: Depressed people often don’t participate in activities they previously enjoyed as they lose sources of reward and reinforcement and this lack of reward generates depressive symptoms. In CBT the therapist and client identity potentially pleasurable activities and deal with any anticipated cognitive obstacles

Question 22

Evaluation of cognitive-behavioural therapy

Answer 22

EFFECTVINESS

1. Behavioural activation has been shown to be very effective as a number of studies have showed that cognitive change is just as likely to occur following this than after cog interventions and so reductions in negative thinking are often observed.
   - Also effective equally to CBT in preventing relapse after 24 months (Gortner et al, 1998).
2. CBT has been shown to be superior in effectiveness than drug therapy: Shelton et al 2005 found that in a comparison of both therapies, CBT had a longer term beneficial effect by preventing relapse compared to medication, however a combination of therapies was most effective off all to either treatment alone.
3. Depends on therapist competence: Kyuken 2000 conclude that as much of 15% of the variance in outcome may be attributable to therapist competence.

APPROPRIATENESS

1. CBT is not appropriate for everyone who is depressed.
   - Not suitable for people who have high levels of dysfunctional beliefs that are rigid and resistant to change as well as to those in situations with high levels stress which therapy will not be able to resolve form their real life.
2. However, appropriate for everyone else. Even though it is a lengthy process, research has shown it can even be admitted online and be equally as effective (Selmi et al 1990) and thus there will be low drop out levels

Question 23

Describe the best therapy for preventing relapse

Answer 23

Many sufferers are prone to relapse: 50% relapse within 1 year (Belsher and Costello, 1988) whilst 70% have further episode(s) within 10 years (Coryell & Winokur, 1992). Thus, interventions which target this is necessary to ensure longevity.

Mindfulness-based cognitive therapy targets this issue and focuses on relapse prevention.

MCBT was created to try combat the link between periods of negative moods and activated negative thinking and aims to get people to become more aware of their negative thinking patterns and view them as purley mental events rather than accurate reflections of reality.
– A key process is “Decentering” which focuses on becoming aware of all incoming thoughts and feelings and accepting them, but not attaching or reacting to them. It aids in disengaging from self-criticism, rumination, and dysphoric mood that can arise when reacting to negative thinking patterns.

It involves CBT and included meditation elements by making clients aware of their thoughts, feelings and bodily sensations.

Question 24

Evidence for mindfulness-based cognitive therapy

Answer 24

1. MA+TEASDALE 2004: Found that MCTB prevents relapse by up to 78% for individuals who have experienced up to 4 bouts of depression compared to all individuals who had drug therapy instead
2. KYUKEN 2016: meta-analysis of studies reviewing the efficacy of MBCT found that in the 1500 patients, this therapy was very effective treatment particularily for relapse prevention for those with recurrent depression, particularly those with more pronounced residual symptoms.

Question 25

General evaluation of depression

Answer 25

1. Research has a long way to go; Research into depression, meanwhile, seems to have floundered: once-hopeful therapies have failed in clinical trials, genetic studies have come up empty-handed. The field is still struggling to even define the disease — and overcome the stigma associated with it.
2. Depression research also gets a great deal less funding than that gobbled up by cancer. The US National Institutes of Health pumped about US$5.3 billion into cancer research in 2013 — a stark contrast to the $415 mil- lion it spent on depression research and the $2.2 billion on mental-health research as a whole. The same pattern holds elsewhere: in its most recently completed funding scheme, the European Union invested about €54.3 mil- lion (US$67.4 million) a year for studies of mental-health disorders, €8 million of which was flagged specifically for depression. The programme allotted €205 million a year for studies of cancer.

Question 26

Evaluation for biopsychological approach

Answer 26

• SUPPORT
  1. In 2003, Caspi and colleagues1 used a prospective, longitudinal design to examine the relationship between 5-HTTLPR, stress, and depression in a large birth cohort and found a significant interaction between 5-HTTLPR and both stressful life events (SLEs) and childhood maltreatment in the development of depression. In this cohort, subjects carrying the less functional 5-HTTLPR s allele reported greater sensitivity to stress.
  2. HAYDEN etal. found that nondepressed children homozygous for the short allele showed greater negative processing on a self-referential encoding task following a negative mood induction than did children with other genotypes. Thus, the accumulating evidence suggests the genetic predisposition to depression is associated with biases in the processing of information.
• • To date, there have been 55 follow-up studies exploring whether 5-HTTLPR moderates the relationship between stress and depression, with some studies supporting the association between the 5-HTTLPR s allele and greater stress sensitivity and others not.
• – Two recent meta-analyses have assessed a subset of these studies and concluded that there is no evidence supporting the presence of the interaction
• — However, only a subset of the studies investigating the relationship between 5-HTTLPR, stress, and depression were included in the meta-analyses
• However, future research efforts may be directed towards determining whether the identification of ‘at-risk’ genotypes can inform treatment decisions concerning psychological or pharmacological therapies to prevent or ameliorate the eventual onset of depression. In addition, there is the equally important question of what can be learned from studying ‘ at-risk’ individuals who are resilient to the effects of adverse life events (Farmer et al, 2005).