DSM IV is used to diagnose unipolar depression, where the patient needs to suffer at least five symptoms for a two week period and find it ‘disabling’. There are many theories for what causes unipolar depression, some physiological (biological influences) and some psychological (environmental influences); therefore a debate between nature and nurture takes place.
One physiological explanation is genetic vulnerability. This is where illnesses that affect mental functioning such as unipolar depression, a mood disorder, can be partially due to genetic influences. Genes code for cells in our bodies, which determine our characteristics and physiology (e.g. neurotransmitter production and the nervous system), which affect behaviour. The theory proposes that people inherit a predisposition to develop unipolar depression. The main way to research genetic influences on behaviour is twin studies.
Identical (monozygotic) twins have the exact same genes, so if the theory of genetic vulnerability is correct, if one twin has the disorder so will the other. This is known as 100% concordance rate. Concordance rates are measured for monozygotic (MZ) and dizygotic (non-identical, DZ) twins to check for a comparison between siblings. Dizygotic twins share 50% of genetic material as opposed to monozygotic twins with
100% shared genetic material.
A case study to support this theory is McGuffin, who sampled 214 pairs of twins where at least one was being treated for unipolar depression and found 46% concordance rate for MZ twins as opposed to 20% for
DZ twins. This research suggests genetics play a role in the development of the disorder, but as there was not found to be any 100% concordance rates, genetics cannot be the only cause; however there was a moderate genetic influence. Kendler et al looked at over 15,000 pairs of twins and concluded unipolar depression was ‘moderately heritable’. They found the influence was greater in women than men (49% to
29% respectively), showing environmental factors may also play an important role. It is likely that genes influence vulnerability to negative life events.
Another physiological explanation is the monoamine theory. Monoamines are a group of neurotransmitters including adrenaline, noradrenaline, serotonin and dopamine. The theory suggests a lack of these neurotransmitters causes unipolar depression as the necessary messages aren’t being relayed. Neurotransmitters work by electrical impulses being sent along a neuron causing neurotransmitters to be released into the synapse. Receptors in the next neuron take up the neurotransmitter and cause it to ‘fire’ as well, passing along the message.
Serotonin is linked to maintaining mood, controlling eating, sleeping and arousal. Dopamine affects movement and attention, as adrenaline and noradrenaline increase alertness. It is possible genetics programmed the levels of neurotransmitters to be lower than normal, linking to the theory of genetic vulnerability. Delgado et al gave depressed patients who were receiving antidepressant medication a special diet that lowered the levels of one of the precursors of serotonin. The majority of patients experienced a return of depressive symptoms, which disappeared again when their diet was returned back to normal, showing support for the idea that serotonin is related to depressive symptoms.
A study by Klimek et al carried out post-mortem studies on dead brains to investigate noradrenaline. They compared fifteen patients’ brains that had all suffered from depression and fifteen controls. They found a significant difference between the structures of the locus coeruleus in the brain – the structure responsiblefor noradrenaline production. This suggests people with depression have low levels of noradrenaline.
Reimold et al