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Psychology > Biological Explanaions For Mood Disorders > Flashcards

Biological Explanaions For Mood Disorders Flashcards

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1
Q

What is the main argument of the neurochemistry explanation?

A

An IMBALANCE in the levels of the neurotransmitters NORADRENALINE and SEROTONIN has been found to be involved in both unipolar and bipolar depression

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2
Q

How might an imbalance of the neurotransmitters noradrenaline and serotonin cause depression, according to the neurochemistry explanation?

A

DEPRESSION was associated with LOW levels of NORADRENALIN and SEROTONIN

MANIA was associated with HIGH levels of NORADRENALIN

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3
Q

What are the 3 biological explanations for mood disorders?

A

Neurochemistry

Hormones

Genetics

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4
Q

Who conducted the study to support the neurochemistry explanation of mood disorders?

A

Teuting et al.

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5
Q

In what year did Teuting conduct his study?

A

1981

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6
Q

What was the aim of Teuting’s study?

A

To investigate the ROLE of NORADRENALINE and SEROTONIN in depression

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7
Q

What was the method used by Teuting?

A

A COMPOUND, produced when noradrenaline and serotonin are BROKEN DOWN by ENZYMES, is present in URINE

Teuting ANALYSED and COMPARED urine samples from DEPRESSED and NON-DEPRESSED adults

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8
Q

What were the results from Teuting’s 1981 study?

A

DEPRESSED patients’ urine had LOWER levels of the COMPOUND COMPARED to the NON-DEPRESSED adults

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9
Q

What conclusion can Teuting make form the results of his 1981 study?

A

Supports the idea that depression is associated with low levels of noradrenaline and serotonin, as lower levels of the compound, produced when noradrenaline and serotonin are broken down by enzymes, were found in depressed of patients

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10
Q

The neurochemistry explanation ignores other factors. Why is this a weakness?

A

OTHER FACTORS must be involved other than faulty biochemistry - ANTIDEPRESSANTS IMMEDIATELY RAISE LEVELS of the neurotransmitters but it can take SEVERAL WEEKS for the depressive symptoms to ease

Suggests other factors are also involved

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11
Q

What is the support for the neurochemistry explanation from antidepressants?

A

Antidepressant medication, which INCREASES levels of NEUROTRANSMITTERS, EASES DEPRESSED SYMPTOMS

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12
Q

What is the support from Reserpine for the neurochemistry explanation?

A

Reserpine (a drug which reduces blood pressure) LOWERS the levels of SEROTONIN and NORADRENALINE in the brain and is KNOWN to CAUSE DEPRESSION

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13
Q

What is the support for the neurochemistry explanation from the manic phase?

A

In the manic phase, levels of NORADRENALINE have been found to be HIGH whilst levels of SEROTONIN LOW

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14
Q

Why is CAUSE AND EFFECT a weakness of the neurochemistry explanation?

A

INCOMPLETE

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15
Q

Why is CONTRADICTORY RESEARCH a weakness of the neurochemistry explanation?

A

Thase et al (2002) found that DEPRESSED patients had INCREASED levels of NORADRENALINE, rather than reduced

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16
Q

Why does the role of social factors weaken the neurochemistry explanation?

A

Some evidence suggests that mood disorders may be CAUSED or TRIGGERED by SOCIAL FACTORS e.g. STRESS

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17
Q

Why might the neurochemistry explanation by described as REDUCTIONIST?

A

Reducing such a complex disorder down to levels of GENES or CHEMICALS may be an OVERSIMPLIFICATION

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18
Q

What three hormones are believed to be involved with causing depression?

A

Cortisol

Oestrogen and Progesterone

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19
Q

What is the link between cortisol and depression?

A

People with UNIPOLAR depression have been found to have unusually HIGH levels of the STRESS HORMONE cortisol in their body

Cortisol is released during times of stress

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20
Q

What did evidence did Southwick et al (2005) find to support the cortisol hormone link to mood disorders?

A

Found that people with depression MAINTAINED HIGH levels of CORTISOL AFTER a STRESSFUL situation had disappeared

This means that DEPRESSIVE EPISODE CONTINUES in the absence of any obvious external stressful event

If an individual feels unable to cope with stress they may RESPOND MALADAPTIVELY and become DEPRESSED

21
Q

What is the link between Oestrogen and Progesterone and depression?

A

There is limited evidence that post-natal depression and pre-menstrual syndrome (PMS) in women may be linked to hormonal changes of oestrogen and progesterone

22
Q

What did Baker et al (1982) find as evidence to support the oestrogen and progesterone hormone cause of depression?

A

Studied the FEMALE ADMISSIONS to one psychiatric hospital and found that 41% entered on the day before or the first day of their menstrual period

23
Q

Why is contradictory evidence a weakness of the Hormone explanation for mood disorders?

A

Research linking post natal depression to oestrogen and progesterone has NOT STRONGLY SUPPORTED the idea that FLUCTUATIONS of these hormones cause the disorder

24
Q

What evidence did Hendrick et al (1988) find to weaken the hormone explanation?

A

Some research into post natal depression suggests it is due to SOCIAL FACTORS such as life events, marital problems and ‘difficult’ babies rather than hormones

25
Q

Why does CAUSE AND EFFECT weaken the hormone explanation?

A

Unable to determine whether hormone fluctuations cause mood disorder or are a symptom of

26
Q

Why does the history of PMS patients weaken the hormone explanation?

A

It is usually the case that most individuals with PMS have a history of depression, suggesting it is not linked to levels of oestrogen and progesterone

27
Q

What is he belief that genetics plays a role in causing depression?

A

Research on genetic factors in depression has found evidence that depression, especially BIPOLAR, has a GENETIC FACTOR and RUNS IN FAMILIES

28
Q

What is generally identified in a GAMILY STUDY?

A

Generally, in family studies a PROBAND is identified and then INFO regarding CLOSE FAMILY RELATIVES of the person diagnosed with a mood disorder is GATHERED

29
Q

Outline Gershon’s 1990 family study

A

Reviewed 10 studies of adult UNIPOLAR depressed probands and found the RATES of DEPRESSION in FIRST DEGREE RELATIVES was between 7%-30% - much higher figure then would be found in the general pop (5%)

30
Q

Outline Winokur et al’s 1995 family study

A

In a large scale study (900 patients and controls) by Winokur et al the rate of UNIPOLAR depression was 10.4% in the FIRST-DEFREE RELATIVES of the probands, compared to 4.9% of CONTROLS’ relatives

31
Q

What is the evidence to support the idea that depression runs in families?

A

CHILDREN of DEPRESSED PARENTS seem to be particularly at RISK of DEVELOPING DEPRESSION

Weissman et al (1987) found approx 50% of the offspring of depressives DISPLAY DEPRESSIVE SYMPTOMS themselves

32
Q

Why is more evidence needed from family studies to support the genetic explanation?

A

It is DIFFICULT to DRAW CONCLUSIONS specifically about the genetic components of depression from family studies alone and therefore twins have been investigated too

33
Q

Why is it difficult to attribute results of studies investigating probands to genetics alone?

A

ENVIRONMENT

not close to expected figures (50/100%)

34
Q

What is the argument that twin studies support a genetic factor?

A

If mood disorders are genetically inherited then the CONCORDANCE RATE for MZ twins SHOULD be HIGHER than that for DZ twins

35
Q

Why is it suggested that BIPOLAR depression has more of a genetic link?

A

Concordance rates for BIPOLAR depression are HIGHER than those for UNIPOLAR depression

36
Q

What was the aim of McGuffin et al’s 1996 twin study (UNIPOLAR)?

A

To investigate the genetic component of UNIPOLAR depression

37
Q

What was the method used by McGuffin et al for their 1996 UNIPOLAR depression twin study?

A

Looked at 177 SAME SEX twin PAIRS (68 MZ pairs and 109 DZ pairs) of which ONE of the pair had SUFFERED from UNIPOLAR depression

38
Q

What were the risk its of McGuffin et al’s 1996 UNIPOLAR depression twin study?

A

MZ - 46% concordance rate

DZ - 20% concordance rate

39
Q

What could McGuffin et al conclude form their 1996 UNIPOLAR depression twin study?

A

UNIPOLAR depression has a genetic link as HIGHER in MZ twins who SHARE 100% GENES

NOT 100% rate, so OTHWR FACTORS influencing

40
Q

What was the aim of Price’s 1968 BIPOLAR depression twin study?

A

To provide evidence of a genetic cause of BIPOLAR depression

41
Q

What was the method used by Price in the 1968 BIPOLAR depression twin study?

A

Looked at 109 pairs of MZ twins and 119 pairs of DZ twins

SOME of the MZ twins (97 pairs) had been RAISED in the SAME FAMILY whilst others (12 pairs) had been RAISED APART

42
Q

What could Price conclude from the 1968 BIPOLAR depression twin study?

A

These rates INDICATE a GENETIC COMPONENT for BIPOLAR depression

43
Q

What were the results from Price’s 1968 BIPOLAR depression twin study?

A

MZ reared TOGETHER - 68%

MZ reared APART - 67%

DZ - 23%

44
Q

What is the evidence from Wilhelm et al (2006) that supports the genetic explanation?

A

Suggests that an ABNORMAL SEROTONIN TRANSPORTER (SERT) gene COULD play a key role in depression

45
Q

The genetic explanation is based of indirect evidence. Why is this a weakness?

A

Much of the genetic evidence requires INFERENCE from INDIRECT EVIDENCE eg when depression appears to run in families it is attributed to genetic transmission

46
Q

What is an issue with TWIN STUDIES?

A

While research shows that genetic factors are important in bipolar depression, we CANNOT say that it is PURELY GENETICS as CONCORDANCE RATES would be 50 and 100%

47
Q

What is the contradictory evidence presented by Brown and Harris (1978) that weakens that genetic explanation?

A

There is contradictory evidence for the role of genetics in UNIPOLAR depression

Brown and Harris (1978) found that OTHER SOCIAL FACTORS such as unemployment, divorce or caring for small children in difficult circumstances, may be MORE IMPORTANT in determining depression

48
Q

No SINGLE GENE had been found. Why is this a weakness of the genetic explanation?

A

There appears to be MANU DIFFERENT SUBTYPES of UNIPOLAR depression making the search for a gene/genes responsible VERY DIFFICULT

Psychology (9 decks)

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