Looking closer at DNA the gene SERT, occurs 10 to 12 times. However, people with depression have only 9 repeating sections, linked with serotonin. Fact that serotonin is strongly implicated in depression and new drugs interacts with serotonin leads us to think that genes may be involved in depression.
Looking at biochemical influences as a biological factor, Schilknats proposed that too little noradrenaline causes depression. Evidence to support this is when non humans were given drugs that limit noradrenaline being released, they became sluggish and inactive, two clinical characteristics of depression. However, lower levels of serotonin are also found in mania therefore cannot be the case of excess or deficient amounts of neurotransmitters.
Many drugs used to treat medical conditions e.g. TB produce elation that increased levels of noradrenaline and serotonin levels. Teuting et al (1981) found by using urine samples of depressed people, there were lower levels of compounds produced when noradrenaline and serotonin are broken down by enzymes, this suggesting lower than normal activity or noradrenaline and serotonin secreting neurons in the brain. Kety theory states that serotonin plays a role in limiting noradrenaline levels, when this is deficient noradrenaline levels fluctuate leading to both mania and depression. However, antidepressant drugs take time to take effect, therefore suggestion that depression cannot be explained simply by neurotransmitter levels. Also as not everyone responds to the drugs to alleviate depression.
Looking at the psychological explanations of depression two main parts of the behavioural and cognitive ideas. Ferster proposed that depression is a result of a reduction of reinforcement. Lewinsohn expanded this theory by suggesting that certain events induce depression because they reduce positive reinforcement. Depressed people causes of other people to be concerned for them which reinforce the depressed behaviour. However, after a while concern wears out and reduced reinforcement exacerbates the depression. People lacking social skills are prime candidates for depression as social ineptness is unlikely to bring reinforcement from others. Consequently there is a correlation between greater depression with fewer pleasant experiences. However, depression might precede a reduction in pleasant experiences therefore cause and effect cannot be assumed.
Looking at cognitive explanations, Seligman’s research represented a link between the behavioural and cognitive perspective. An experiment conducted in which dogs were restrained so that they could not avoid electric shocks, appeared to become passively resigned the shocks. Later the dogs were introduced to a new situations were they were allowed to escape, the dogs made no attempt. The behaviour shown is similar to depressed humans. Depressed people, like the dogs, learn from experience to develop expectancy that their behaviour will be fruitless in bringing about change. When people feel helpless to influence their encounters with pleasurable and unpleasurable stimuli they become depressed. However this theory fails to address the issue why some people blame themselves whilst others blame the outside world.
Explaining depression as either biological or psychological alone is limited as many explanations do not explain everything. To understand the causes, psychologist have to combine explanations to gain a wide range of answers.
