The Symptoms And Potential Treatments Of The Depression
Depression is a mood disorder which leads those individuals who suffers from it a range of potential symptoms. The current paper will look into how serotonin can be a factor of low moods, with physiological changes happening in a range places in the brain, such as the hippocampus; this is because serotonin receptors are not restricted to one part of the brain. Another symptom we will be looking into is sleep and circadian disturbance amongst depressed patients, which affects the glucose metabolism.
The first symptom is low moods which is a major symptom of depression, affecting over 20% of the population. A major treatment for depression is antidepressants, mainly SSRI’s which is argued to increase synaptic levels of monoamines, mainly serotonin and noradrenaline and through activating serotonergic and noradrenergic postsynaptic and autoreceptors. Serotonin receptors are known to come from the 5-HT1 to 5-HT7 family, and have projection across the brain, such as in the hippocampus, amygdala, hypothalamus or thalamus. Investigating the effect serotonin has on moods is done through tryptophan depletion. This is where tryptophan levels are lowered to create low levels of serotonin, creating an opportunity to study serotonin-dependent behavior (Young, 2013). Tryptophan depletion studies on participants who hadn’t suffered from depressed prior had varying results, but ultimately there was no significant effect made on mood altering. However with another set of participants who have not suffered from depression but do have a potentially high risk for depression through genetics, tryptophan depletion did succeed in creating lower moods. Finally, in patients with a history of depression, by temporarily lowering tryptophan levels a depressive relapse was caused with an increase of symptoms associated with serotonergic antidepressants (Booji et al, 2005). Therefore, it can be argued that low levels of serotonin can factor into a lowered mood, although this cannot be the sole factor, there must be an interaction with the reduced serotonin lower our mood levels.
Another symptom of depression is sleep disturbance. Studies have shown that disturbance in the circadian rhythm and sleep disturbances among depressed patients show different patterns in their brain. There is a variation of regional brain glucose metabolism compared to people not suffering from depression. Sustained activity in the brainstem and hypothalamic regions were also found in relation to maintaining wakefulness across times of day (Buysse et al., 2004). It’s also been found that oscillations in plasma cortisol and norepinephrine are advanced in depressed patients compared to healthy individuals. Sleep disturbance complaints are common within depressed patients, with 90% of patients reporting finding it difficult to fall asleep, stay asleep, and early mornings. Depressed patients have shown a latency from sleep onset and the first REM sleep being shortened in comparison to a healthy person. Due to the findings of consistent circadian rhythm and sleep disturbance amongst depressed individuals, hypotheses have been proposed to understand why. The past-shift hypothesis argues that when there is a delay of the central pacemaker which is linked to circadian rhythms that regulate temperature, cortisol, melatonin, and REM sleep relative to other circadian rhythms; a mood disturbance will occur.
In terms of treatments for depression which also help alleviate sleep disturbances, antidepressants also seem to be a common treatment. Neurotransmitters, including serotonin and noradrenergic systems, have prominent effects on the circadian process, and especially sleep. A common drug used to target sleep in particular amongst depressed patients are tricyclic antidepressants (TCAs). These are used to shorten sleep latency and improve the general quality of sleep continuity in depressed patients. Most TCAs main quality is to suppress REM sleep, and lower the percentage of REM sleep, therefore trying to normalize the disturbance in sleep archetypes found in depressed patients. Furthermore these results have led to the understanding that is the key target action for these types of antidepressant drugs.
The monoamine deficiency theory argues that depressive symptoms are a result of the lack of monoamine neurotransmitters (Delgado, 2006). This was discovered when compounds developed for non-psychiatric conditions had been found to have antidepressant effects in human were found to enhance the levels of central serotonin or noradrenaline. Today antidepressants still are designed to increase the transmission of monoamine by either by inhibiting neuronal reuptake, through the use of selective serotonin reuptake inhibitors (SSRIs) or by inhibiting degradation. Whilst the use of monoamine base drugs are useful antidepressants it cannot fix depression immediately. The use of Monoamine oxidase inhibitors and SSRIs do provide an immediately higher level monoamine transmissions, the actual mood altering effect requires weeks of treatment to show results. However, the depletion in monoamines can cause in mild mood disturbance in unmedicated depressed patients, but the same treatment in healthy patients doesn’t yield the same effect. Therefore, this shows that monoamine has got to be a factor in depression, however the treatment method while affective does take time to show results and so does come with low remission rates (Rush, et al,. 2006).
Overall it seems that an individual who is suffering from depression will experience a number of physiological changes within their brain in comparison to a healthy person, which will lead to a number of potential symptoms. In terms of treatment, the current paper see antidepressants as the main method to alleviate symptoms, however they are not fool proof and do have side effect and undesirable qualities such as taking time to actually yield results.
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