If chosen as second disorder: one biological theory/explanation
A2 Option: Biological explanations of depression: genetic and neurochemical
Neurotransmitters: The Monoamine Hypotheses
- Serotonin: responsible for regulation of mood, appetite and sleep
- Noradrenalin: Responsible for concentration and alertness
- Dopamine: Responsible for movement, memory, pleasure and a host of other functions.
You may have heard about serotonin’s role in depression before. One of serotonin’s main roles is the regulation of other neurotransmitters, so low levels of this neurotransmitter can lead to erratic brain functioning and thus distorted thinking. Low levels of serotonin also lead to imbalances in noradrenaline; another neurotransmitter implicated in depression. Low levels ofserotonin can lead to changes in mood, appetite and sleep, whilst low levels of noradrenalin may lead to poor concentration and alertness. High levels of noradrenalin, on the other hand, has been implicated in mania (Schildkraut, 1965) thus suggesting that it may have a role in the highs of bipolar depression also. Low levels of dopamine can also result in sluggishness, lack of motivation and lack of alertness and focus.
Low levels of these monoamines have been implicated in depression, hence drug treatments are often used to correct these imbalances. A clinician will thus attempt to match the drug treatment to the symptoms shown by the patients, however several drug treatments may need to be tried for effectiveness, since different anti-depressants target different monoamines.
- + Teuting et al (1981) examined the urine of depressed patients and found chemicals that suggest lowered levels of both serotonin and noradrenalin.
- + The amino acid tryptophan is an essential pre-cursor of serotonin. A mutant gene that reduces levels of tryptophan, and results in an 80% reduction in serotonin levels, is ten times more likely to be found in depressed patients.
- – Drug therapies for Depression alter neurotransmitter levels almost immediately, yet it can take up to 6 weeks for patients to see a reduction in their symptoms. This indicates that neurotransmitter levels may be an indirect contributory factor. [The most recent theory for this is that high levels of cortisol in depressed patients kills off cells in the hippocampus, whilst SSRIs release neural growth hormone; it takes 4-5 weeks to repair this damage to the hippocampus (Nestler et al. 2001)
Studies have indicated that there may be a genetic link for depression. McGuffin (1996) studied 214 pairs of twins, where at least one of each twin pair was being treated for unipolar depression. It was found that 46% of the identical twins shared the disorder, and only 20% of fraternal non-identical twins shared the disorder. This indicates a genetic link, since DZ twins only share 50% genetics, yet are likely to also share the same environment.
This research support Allen (1976), who reported the following concordance rates for Unipolar Depression in twins:
- MZ (identical) twins 40%
- DZ (non-identical) twins 11%
Whilst genetic makeup may predispose somebody to develop depression, a stressful life event might be needed to act as a trigger for that depression (diathesis-stress).
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