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Biological Explanations for Depression

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Submitted By acur1
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Genetic factors
A01 – Family studies
>having a 1st degree relative (parent or sibling) with depression appears to be a risk factor for depression >the studies select people who already have depression (probands), and then examine whether other family members have been, or might be, diagnosed with depression
-if there is a genetic link for this disorder, the probands’ relatives should show higher rates of depression than the rest of the population

Harrington et al (1993)
>found that around 20% of proband’s close relatives have depression compared to 10% for the general population

A01 – Twin studies
>basis is that identical (monozygotic) twins are clones of each other and have all the same genes
-fraternal (dizygotic) twins share just half of their genes
-we assume that the environment shared by the twins is roughly the same for both types of twin

McGuffin et al (1996)
>studied 177 probands with depression with their same-sex co-twins

>concordance rate was 46% for identical twins and 20% for fraternal twins

>suggest that depression has a large heritable component

A01 – Adoption studies
Wender et al (1986)
>studies the biological relatives of adopted individuals who had been hospitalised for severe depression

>found a much higher rate of severe depression in the biological relatives of the depressed group than in the biological relatives of a non-depressed control group (nature may be a stronger component than nurture)
Genetic factors
A01 – Family studies
>having a 1st degree relative (parent or sibling) with depression appears to be a risk factor for depression >the studies select people who already have depression (probands), and then examine whether other family members have been, or might be, diagnosed with depression
-if there is a genetic link for this disorder, the probands’ relatives should show higher rates of depression than the rest of the population

Harrington et al (1993)
>found that around 20% of proband’s close relatives have depression compared to 10% for the general population

A01 – Twin studies
>basis is that identical (monozygotic) twins are clones of each other and have all the same genes
-fraternal (dizygotic) twins share just half of their genes
-we assume that the environment shared by the twins is roughly the same for both types of twin

McGuffin et al (1996)
>studied 177 probands with depression with their same-sex co-twins

>concordance rate was 46% for identical twins and 20% for fraternal twins

>suggest that depression has a large heritable component

A01 – Adoption studies
Wender et al (1986)
>studies the biological relatives of adopted individuals who had been hospitalised for severe depression

>found a much higher rate of severe depression in the biological relatives of the depressed group than in the biological relatives of a non-depressed control group (nature may be a stronger component than nurture)
Biological explanations of depression
Biological explanations of depression

Genetic factors
A02 – Research support
Zhang et al (2005)
>a mutant gene that starves the brain of serotonin has been found to be 10x more prevalent in depressed patients than in control individuals
>the mutant gene codes for the brain enzyme, tryptophan hydroxlase-2, which makes serotonin, and can result in an 80% reduction in normal serotonin levels in the brain

Caron et al

Genetic factors
A02 – Research support
Zhang et al (2005)
>a mutant gene that starves the brain of serotonin has been found to be 10x more prevalent in depressed patients than in control individuals
>the mutant gene codes for the brain enzyme, tryptophan hydroxlase-2, which makes serotonin, and can result in an 80% reduction in normal serotonin levels in the brain

Caron et al

A01 – Genes as diatheses
>Diathesis-stress model = the view that individuals inherit a susceptibility for a disorder (diathesis) which develops only if the individual is exposed to certain environmental conditions (stress)

>suggests that genes predispose an individual to depression, when they are in specific situations

Kendler et al (1995)
>found that women who were the twin of a depressed sibling were more likely to have become depressed than those without a depressed twin >the highest levels of depression were found in the group who were exposed to significant negative life events and were most genetically at risk for depression

A01 – Genes as diatheses
>Diathesis-stress model = the view that individuals inherit a susceptibility for a disorder (diathesis) which develops only if the individual is exposed to certain environmental conditions (stress)

>suggests that genes predispose an individual to depression, when they are in specific situations

Kendler et al (1995)
>found that women who were the twin of a depressed sibling were more likely to have become depressed than those without a depressed twin >the highest levels of depression were found in the group who were exposed to significant negative life events and were most genetically at risk for depression

Neurotransmitter dysfunction
A01 – Noradrenaline
>low levels of noradrenaline in certain brain circuits were associated with depression (in the 60s)

Bunney et al (1965)
>low levels of by-products of noradrenaline were found in depressed individuals

>post-mortem studies of suicides found increased noradrenaline receptors in the brain as a compensatory mechanism for the lack of noradrenaline and to attempt to pick up whatever signals are available (process known as ‘up-regulation’)

A01 – Serotonin >link between low synaptic serotonin levels and depression

McNeal and Cimbolic (1986)
>low levels of serotonin by-product (signifying reduced levels of serotonin in the brain) found in depressed and suicidal patients

>the introduction of Prozac and other antidepressant drugs (SSRIs) that selectively block serotonin re-uptake confirmed the association between low serotonin and depression

Delgado et al (1990)
>gave depressed patients who were receiving antidepressant medication a special diet that lowered their levels of tryptophan (ancestor of serotonin)
>the majority of patients experienced a return of their depressive symptoms, which disappeared again when their diet was returned to normal
Neurotransmitter dysfunction
A01 – Noradrenaline
>low levels of noradrenaline in certain brain circuits were associated with depression (in the 60s)

Bunney et al (1965)
>low levels of by-products of noradrenaline were found in depressed individuals

>post-mortem studies of suicides found increased noradrenaline receptors in the brain as a compensatory mechanism for the lack of noradrenaline and to attempt to pick up whatever signals are available (process known as ‘up-regulation’)

A01 – Serotonin >link between low synaptic serotonin levels and depression

McNeal and Cimbolic (1986)
>low levels of serotonin by-product (signifying reduced levels of serotonin in the brain) found in depressed and suicidal patients

>the introduction of Prozac and other antidepressant drugs (SSRIs) that selectively block serotonin re-uptake confirmed the association between low serotonin and depression

Delgado et al (1990)
>gave depressed patients who were receiving antidepressant medication a special diet that lowered their levels of tryptophan (ancestor of serotonin)
>the majority of patients experienced a return of their depressive symptoms, which disappeared again when their diet was returned to normal

A02 – Depression and adolescents
>limited data on the relationships between adolescent depression and heritability

Glowinski et. al (2003)
>sampled 3416 female adolescent twins for MDD with a structured telephone interview
Risk of MMD due to genetic factors was 40% (similar to adult samples) rest due to environmental factors
>GENDER BIAS only female participants so cannot be generalised to the wider population.
A02 – Depression and adolescents
>limited data on the relationships between adolescent depression and heritability

Glowinski et. al (2003)
>sampled 3416 female adolescent twins for MDD with a structured telephone interview
Risk of MMD due to genetic factors was 40% (similar to adult samples) rest due to environmental factors
>GENDER BIAS only female participants so cannot be generalised to the wider population.
Neurotransmitter dysfunction
A02 – Noradrenaline and depression
Leonard (2000)
>drugs that lower noradrenaline levels bring about depressive states, while those that increase noradrenaline levels show antidepressant effects

Kraft et al (2005)
>studied 96 patients with major depression who were treated for 6weeks with a dual serotonin-noradrenaline re-uptake inhibitor (SNRI)
>the patients showed a significantly more positive response than those treated with a placebo = suggesting that both of these neurotransmitters are responsible for the development of depressive symptoms

A02 – Serotonin and depression
>the link between the two is not that straightforward

Ruhe et al (2007)
>Patients in remission were given a mixture that temporarily decreases serotonin levels in the brain by reducing tryptophan.
>however patients suffer from a relapse of their symptoms when tryptophan was reduced
>suggests that a lowering of serotonin levels results in depression
>however, individuals had never been depressed or never had a family history of depression did not show any mood changes when tryptophan was reduced = lowering serotonin levels does not induce depression in all people

Rot et al (2009)
>suggests that it is possible that a depressive episode alters the serotonin system in such a way that a person becomes more vulnerable to the effects of future changes in serotonin levels
Neurotransmitter dysfunction
A02 – Noradrenaline and depression
Leonard (2000)
>drugs that lower noradrenaline levels bring about depressive states, while those that increase noradrenaline levels show antidepressant effects

Kraft et al (2005)
>studied 96 patients with major depression who were treated for 6weeks with a dual serotonin-noradrenaline re-uptake inhibitor (SNRI)
>the patients showed a significantly more positive response than those treated with a placebo = suggesting that both of these neurotransmitters are responsible for the development of depressive symptoms

A02 – Serotonin and depression
>the link between the two is not that straightforward

Ruhe et al (2007)
>Patients in remission were given a mixture that temporarily decreases serotonin levels in the brain by reducing tryptophan.
>however patients suffer from a relapse of their symptoms when tryptophan was reduced
>suggests that a lowering of serotonin levels results in depression
>however, individuals had never been depressed or never had a family history of depression did not show any mood changes when tryptophan was reduced = lowering serotonin levels does not induce depression in all people

Rot et al (2009)
>suggests that it is possible that a depressive episode alters the serotonin system in such a way that a person becomes more vulnerable to the effects of future changes in serotonin levels

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