Genetic factors

In approximately 25% of cases genes are thought to play a role in predisposing an individual to unipolar depression. This hypothesis has identified unipolar depression as an endogenous depression as genetic studies have shown a link with unipolar depression however there is no clear cause.

Studies conducted by Keller et al 1986 have suggested that first-degree relatives of individuals suffering from unipolar depression are 2-5 times more vulnerable in acquiring this disease in contrast to those of the general population. However this study fails to differentiate whether the possibility of suffering from unipolar depression is due to genetic factors or through environmental influence. Kendler et al 1992 illustrated that out of 1000 participants, 48% concordance rate was found amongst monozygotic twins in comparison to the 42% concordance rate present amongst dizygotic twins, suggesting that genetic factors may play a moderate role in underlying the onset of unipolar depression.

This is view is partly concordant with the diathesis-stress model which suggests that pre-existing vulnerability is only triggered when the individuals is exposed to stressful life events and therefore stating that depression arises through interaction of nature and nurture.

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Psychological and Social factors

An individuals personalities has been associated with depression, those with low self-esteem and distorted thinking are more vulnerable to acquiring unipolar depression.

Social factors’ including poverty and social isolation increases the likelihood of an individual suffering from depression. Early child abuse and consistent exposure to stressful situations are also factors, which increase the likelihood of suffering from unipolar depression.

Unipolar depression caused by environmental factors are also known as reactive depression.

Hypothalamic-pituitary-adrenal axis (HPA-axis)

Studies showing an increase in the size of the pituitary and adrenal glands whilst also noting the high levels of cortisol amongst depressed individuals has lead researchers to suggest that dysfunctioning of the endocrine system is involved with regulating the onset of unipolar depression.   

Biochemical theory of unipolar depression

The monoamine theory- This biological theory was originally proposed by Schildkraut (1965), who suggested that depression was attributable to the functional deficiencies of certain monoamine neurotransmitters within the cerebrospinal fluid in localised regions of the brain. These include the following neurotransmitters:

• Noradrenaline (Norepinephrine)
• Serotonin (5-HT)
• And to a certain extent dopamine

This theory has been established by monitoring the clinical effects of drugs which cause or lessen the symptoms associated with depression; through understanding the pharmacological activity of these drugs on monoaminergic transmission in the brain researchers are able to understand the causes of neurotransmitter imbalance associated with unipolar depression. For instance, drugs such as reserpine and methyldopa, which diminished monoamine levels, have expressed symptoms similar to those found in depressed individuals. In addition, antidepressant drugs, which specifically raise the concentration of neurotransmitters present within the synaptic cleft such as serotonin and noradrenaline, have alleviated the symptoms associated with depression, suggesting that these neurotransmitters are the key players underlying depression. However the following points have suggested that the monoamine theory is oversimplified and in fact a combination of factors is associated with depression.    

 ·         Direct measurements in monoamine metabolism in depressed patients, quantitative measurements of monoamine receptors present amongst some post mortem brain tissue studies and examinations through functional tests on monoaminergic pathways activities have all demonstrated inconsistencies with the monoamine theory.

·         Studies on cocaine and amphetamine, which increase the levels of monoamine transmitters, have failed to have antidepressant actions.

·         Antidepressant drugs have shown rapid biochemical effects on the synapse however their therapeutic effects takes weeks to develop; this delayed response is consistent with the view of an apparent inhibition rather than the view that antidepressants aid monoaminergic transmission.

·         Antidepressants such as tianeptine and opipramol effectively reduce depression without targeting monoamine transmission.

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