Institution of Affiliation
The biological perspective of depression argues that depression is as a result of an imbalance of the brain chemicals, the neurotransmitters. Various compounds are used by the brain as messengers to communicate with other parts of the brain as well as the nervous system. The neurons communicate through the chemical messengers, and they are in constant communication through the exchange of the neurotransmitters. The neurons communication is essential to the brain as it aids the brain to carry out its functions. The imbalance of neurotransmitters can be articulated to the development of depression. The monoamine hypothesis has the suggestion that the lowered levels of the brain chemicals such as serotonin, dopamine, and norepinephrine to which result in the symptoms of depression.
The imbalance of serotonin levels is said to influence a person’s mood and eventually lead to depression. There are possible problems that are associated with the imbalance of the serotonin levels, and this includes reduced brain cell production of serotonin, the inability of the serotonin to reach the receptors and as well can be attributed to the shortage of the chemical trypan from which serotonin is made. In case any of the above biochemical problems do occur, it is believed that one has a high probability of being depressed.
Depression can also be related to abnormalities in the circadian rhythm. Such examples include the rapid eye movement sleep, a stage in which dreaming do occur, may be intense and quick to arrive in people with depression. Rapid eye movement sleep relies on decreased serotonin levels in the brain stem. The serotonin levels are impaired by the compounds such as the antidepressants, to which increase the level of serotonin levels in the brain stem structures. The serotonergic system tends to be least active during sleep and most active during wakefulness. Continued wakefulness due to the deprivation of sleep tend to activate the serotonergic neurons, and this leads to the same effect that is caused by the therapeutic effect of anti-depressants like the selective serotonin reuptake inhibitors (SSRIs). The depressed people exhibit a significant elevation in the moods after deprivation of sleep The selective serotonin reuptake inhibitors may directly depend on the rise of the central serotonergic neurotransmission for their therapeutic effect, the same effect to which alter the cycles of being awake and that of sleep.
According to research, the effects of light therapy on the seasonal affective disorder suggest that light deprivation is related to the lowered activity in the serotonergic system as well as to the abnormalities in the sleep cycle that include insomnia. The exposure to light as well targets the serotonergic system and therefore provide more support for the essential role to which the serotonergic system play to the development of depression. Light therapy and sleep deprivation target the same brain neurotransmitter system and brain sites the same way the antidepressant drugs and therefore, they are also used in the treatment of depression.
The increase as well as the decrease in sleep length also play a significant role and can be a significant risk factor for the development of depression. The patients who are diagnosed with major depressive disorders sometimes may manifest diurnal and seasonal variations of symptoms severity, even during the no-seasonal depression. The daily mood improvement is associated with the activity of the dorsal neural networks, and as well a rise in the mean core temperature is observed. A proposition made by one of the hypothesis indicates that depression is as a result of a phase shift. The exposure to daylight leads to decreased serotonin levels due to reduced transport activity, and this may underlie the seasonal development of depression in individuals. In short, the biological perspective of depression is of the opinion that depression is due to a reduction or alteration of the serotonin levels which result in mood swings to which lead to the development of depression resulting from the abnormalities in the circadian rhythm.
Demirkan, A., Penninx, B., Hek, K., Wray, N., Amin, N., Aulchenko, Y., Middeldorp, C. (2011). Genetic risk profiles for depression and anxiety in adult and elderly cohorts. Molecular Psychiatry, 16(7), 773–783.
Silberg, J., Maes, H., & Eaves, L. (2010). Genetic and environmental influences on the transmission of parental depression to children’s depression and conduct disturbance: An extended children of twins study. Journal of Child Psychology and Psychiatry, 51(6), 734–744.