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Outline and evaluate biological explanations of depression. 8 + 16 marks One biological explanation of depression is genes. This suggests that depression is inherited. Research shows that individuals with a depressed relative (parent/sibling) are 1.5. to 3 times more likely to develop depression than those without a depressed relative. Twin studies show a concordance rate of 46% for MZ (identical) compared with 20% for DZ (non-identical) twins. This suggests that genes have a role in whether people develop depression or not. However, concordance rates are never 100% for identical twins so this suggests that genes can’t be a full explanation because MZ twins share 100% of their genes and so if genes were the only cause of depression there would be a 100% concordance. This means that there must be other factors involved for example environmental ones such as upbringing and interaction with parents and family members. Higher concordance rates for MZ twins could be explained by the fact that being identical, they are more likely to share a more similar life experience than non-identical twins. It makes sense to take a mixed approach; the diathesis-stress model shows how there can be a genetic predisposition which is triggered by environmental cues such as life experience. Research has shown that women who were genetically predisposed to depression (had an identical twin suffering with depression) were more likely to develop depressive symptoms when faced with negative life experiences than women who were at less risk, i.e. not genetically predisposed. A methodological problem with twin studies is sample size because it can be difficult to find depressed twins which leads to a problem of inappropriate overgeneralisation. The relatively small number of participants available may not always be representative of people generally. Furthermore, it would take a longitudinal study over many years to establish accurate concordance rates as, while one twin may not be depressed at the time of the study, they may on to develop depression later on. Biochemistry can also explain depression. The amine hypothesis suggests that an imbalance of neurotransmitters in the synapses in the brain may bring about low mood. For example, it was discovered by accident, during drug trials, that the neurotransmitter noradrenaline may be involved in depression. Reserpine (used to treat high blood pressure) resulted in lowered levels of noradrenaline and patients in the drug trial suffered acute depression. Evidence for the amine hypothesis comes from the effectiveness of medications which raise the levels of this neurotransmitter. MAOIs and Tricyclics, work by either inhibiting the flushing away of noradrenaline from the synapse or blocking its reuptake into the presynaptic neuron. This ensures that more noradrenaline remains available in the synapse to bind with the receptor sites on the post-synaptic neuron. Such drugs seem to be effective in relieving symptoms of depression. However, while the drugs raise levels of the noradrenaline immediately the symptoms of low mood take a couple of weeks at least to be relieved. This suggests that there must be other factors involved. As Tricyclics work on serotonin as well as noradrenaline, it was considered that serotonin may have a part to play in regulating mood which led to another group of drugs being produced – SSRIs which specifically target serotonin and block its reuptake. The effectiveness of these drugs and the lack of side effects made them a popular alternative to MAOIs and Tricyclics. However, they do not work for everybody and if depression was simply caused by amines we would expect to see less variation in how people respond to them. Furthermore, it isn’t even certain whether these chemicals are the cause of depression or whether it is the depression which brings about changes in their levels.