Explanations of Depression - Biological

The genetic basis is strongest for bipolar disorder where almost 60% of MZ twins will develop the same bipolar disorder as their co-twin. Research has been less consistent for unipolar disorder but, using the Maudsley Hospital Twin Register, concordance rates of 46% were found in MZ twins and 20% in DZ twins (McGuffin 1996) - Both rates are higher than for the lifetime risk of developing depression that apply to the general population. However, the concordance rates are never 100% and twins usually share very similar psychosocial experiences. The Diathesis-Stress Model suggests that certain individuals have a genetic predisposition which makes them more susceptible to developing depression when they are exposed to environmental stressors. Kendler 1995 provided support for this model in their Virginia twin study. They found that when women who were genetically predisposed to depression i.e a twin diagnosed with the disorder, were far more likely to develop depressive symptoms when faced with negative life events than women who were at less risk of depression i.e. they had a twin who did not have the disorder.

It is suggested that depression is caused by low activity of certain monoamine neurotransmitters - particularly noradrenaline, serotonin and to a lesser extent, dopamine. These act like chemical messengers in the nervous system and are known to be particularly active in the rewards and punishment areas of the brain. They help to regulate the hypothalamus, which is a crucial link between the nervous system and the endocrine system and is involved in sleep, appetite, sexuality and physical movement - some of the key areas affected in depressive disorders.Support for this comes from drug therapies:

• Tricyclics and MAOIs which increase the available amount of noradrenaline and 5HT in the brain which were found to be effective in alleviating the symptoms of depression.
• Depression is an unwanted side effect of reserpine, a drug used to treat high blood pressure, which also acts by depleting levels of noradrenaline. Similarly, antidepressants such as Prozac, which are effective in providing relief from depression works by increasing the availability of serotonin (but have negligible effects on noradrenaline).

It was thought that depression was caused by neurotransmitters but there are other effects the drugs have so we cannot be sure that it is the change in neurotransmitter levels that accounts for the effectiveness of the drug. A problem is tat they have an immediate effect on NTM levels but take several weeks to have an effect on mood.