Biological explanations of depression
- Created by: rachel cantwell
- Created on: 06-06-14 15:33
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- Biological Explanations
- Serotonin
- AO1
- An imbalance of neurotransmitters can lead to depression
- Serotonin, noradrenalin and dopamine are important in the functioning of the limbic system and amygdala
- Which play a significant role in the regulation of drives such as appetite and the control of emotion
- Depression occurs when there is not enough serotonin in the synaptic gap to bind the receptors
- This causes a chemical imbalence in the dendrite of the next neuron, and depressive symptoms occur
- AO2
- 1) Delgado et al.
- Gave depressed patients a special diet that lowered their levels of one of the precursors of serotonin - tryptophan
- The majority of paitents experienced a return of their depressive symptoms, which disappered after the diet returned to normal
- This suggests that serotonin levels play an important part in the prescence of depressive symptoms
- Correlational - doesn't shown cause and effect
- Ruhe et al.
- Serotonin may play a role but not necessarily a causal one
- Patients who were in remission from depression experienced a brief lapse of symptoms when a tryptophan-deficient amino acid mixture
- However, this was only evident in patients who had a history of depression, ppts. who had never had depression nor a family history experienced no such relapse
- Suggests that lowering serotonin levels does not induce depression in everyone and serotonin may only play a minor role in the development of depression
- Thase et al.
- Claimed that depression was caused by an overall imbalance of several neural transmitters (incl. serotonin, dopamine, noradrenalin and acetylcholine)
- Serotonin appears particularly important because it may act as a neuromodulator (controller) of a variety of brain systems
- When serotonin levels are low, activity in the other systems is disrupted and causes depressive symptoms
- This suggests the serotonin explanation is too simplistic
- 1) Delgado et al.
- AO1
- Genetics
- AO1
- Depression appears to run in families, therefore there may be a genetic cause
- Can be investigated through the use of adoption studies - if there is a genetic link then biological parents should show higher rates of depression than adopted ones
- Also twin studies: monozygotic and diztgotic twins are studied to see if the other twin has been, or might be diagnosed with depression
- If there is a gentic link there should be a higher concordence rate between MZ than DZ twins
- AO2
- Wender et al.
- Studied biological relatives of adopted individuals who had been hospitalised for severe depression
- They found a much higher instance of severe depression in the biological relatives than in the biological relatives of a non-depressed control group
- This suggests that there is a heritable component to depression and implies that gentics are involved in the development of depression
- Bierut et al.
- Carried out a twin study of 2262 twin pairs in Australia, and found concordence rates of 36% and 44% in MZ twins
- They claimed that environmental factors played a larger role
- This is supported by the idea of genes of diathesis, which suggests that people have a genetic disposition for depression that interacts with environmental stressors to produce a depressive reaction
- Kendler et al.
- Found that negative symptoms of depression (sleep disturbance, weight changes etc) seemed to be more influenced by heredity than by stressful events
- However, the actual no. of depressive episodes was linked to life events.
- This suggests that there may be a genetic component operating as a predisposing factor, with additional components (life events) leading to depression
- However, the actual no. of depressive episodes was linked to life events.
- Found that negative symptoms of depression (sleep disturbance, weight changes etc) seemed to be more influenced by heredity than by stressful events
- Concordence rates
- Lack of a 100% concordence rate, which would be present if genetics were the sole cause of depression
- Genetics appear to be a risk factor, but are not sufficient to provide a complete explanation in isolation
- Wender et al.
- AO1
- Serotonin
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