Depression: Mental Ailment, Antidepressants and Major Impairment - Essay Sample

Introduction

Depression is a mental ailment that affects how individuals think, feel, and handle their daily errands. In most instances, antidepressants are prescribed by physicians to alleviate symptoms of depression. The antidepressants are equally used to assist the brain in processing some chemicals which regulate stress or moods (Erb, Schappi, & Rasenick, 2016). Unfortunately, an occurrence of a significant depression can impair the ability to eat, sleep, or work. Major depression can also cripple an individual. In severe cases, depression can lead to a mood disorder, which may lead one to commit suicide. Some drugs have been availed to treat both mild and severe depression, which affects one in six of the American citizens in the course of their lives (Frazer & Benmansour, 2002). Sadly, the current depression medication usually takes a long time of usage before patients start responding. Hence, this paper will examine the possible reasons why there is a delay of several weeks in the alleviation of depression symptoms after initiation of antidepressant medication.

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The antidepressants are medicament being used to treat some anxiety disorders, certain chronic pain conditions, major depressive disorder, and even assist in managing specific addictions (Frazer & Benmansour, 2002). The antidepressants equally have cumulative side effects, which include sexual dysfunction, the gain of weight, dizziness, dry mouth, and headaches (Frazer & Benmansour, 2002). Most of them are safe to take. When a person is under severe depression, they are introduced to antidepressants by physicians. A major concern is that these antidepressants take a long time to alleviate depression symptoms after initiation. A lot of reasons as to why they take longer have been documented and include neuropharmacological actions, mechanism of serotonin inhibitors, and lack of adherence to practitioner instructions.

The neuropharmacological actions of the antidepressants are documented to be one of the causes of a delayed alleviation of depression symptoms. We all know how antidepressants work, but our comprehension of how they improve depressed moods is still an emerging issue. All negative emotional bias is highly connected with despair and downheartedness. Converging results indicate that antidepressants, in most instances, increase positive emotional processes and modulates the emotional processing capability much earlier than it does on the moods (Frazer & Benmansour, 2002). The alterations in emotional processing are thus associated with the neural modulation in the prefrontal circuitry and limbic. Usually, antidepressants work in a manner that is dependable on cognitive theories related to depression. The antidepressants prescribed by the physician does not act as a direct mood activator or enhancer but somewhat changes the virtual balance of the positive emotional processing to a negative processing one, hence providing an excellent platform for subsequent psychological and cognitive reconsolidation thus this entire neuropharmacological action takes so long to work.

The mechanism of serotonin inhibitors also plays a role in delaying the alleviation of depression symptoms after a patient has been given medication. All this process of serotonin inhibitors takes place in the peripheral cells and brain of a patient diagnosed with depression where the diminution of cyclic adenosine monophosphate (cAMP) are responsible (Erb et al., 2016). The adenosine monophosphate is recognized as the second messenger. In most instances, the conventional antidepressants treatment of the patient's serotonin inhibitors receives activations signaling passageways which leads to an increase in the accumulation of regulated transcription cAMP genes and cyclic adenosine monophosphate that incorporates genes for the growth factor and neurotransmitters used in alleviating the symptoms for depression (Erb et al., 2016). The work of antidepressants is to increase the concentration of the brain through its many neurotransmitters, such as serotonin, norepinephrine, noradrenaline, dopamine, and adrenaline. Many researchers have submitted that the antidepressant effects possibly will be interceded through the induction of the system, which generates the cyclic adenosine monophosphate (Grillon, Levenson, & Pine, 2007).

Rasenick researched glioma cells, a site with many antidepressants (Erb et al., 2016). The glioma cells lacked serotonin reuptake proteins and monoamine transport proteins. The research demonstrated in the absenteeism of SERT that antidepressants accumulated steadily on the plasma membrane microdomains of the glioma cells. The team of Rasenick further shown that a sustained medication with drugs of antidepressants known as escitalopram moved the G-protein from the lipid rafts (Erb et al., 2016). The lipid rafts are specialized areas of the plasma membrane. These specialized regions indicated that they could inhibit the generation of the cAMP cascade. Rasenick and his team passed a gas through the lipid rafts to other nonraft areas in the glioma cells. The gas passed through the nonraft, which in return heightened its signaling ability(Grillon et al., 2007).

Rasenick's observation on the association of antidepressants with lipid rafts made them investigate further the amassing of representative drugs of other classes of antidepressants, which they passed through the lipid rafts. Their research indicated that a buildup of drugs in the lipid raft hanged on the classes of antidepressant drugs a patient took (Erb et al., 2016). For instance, only selective serotonin receptor and monoamine oxidase inhibitors like escitalopram exhibited a connotation with lipid rafts in the long run. Hence, this phenomenon corresponds with the evidence as mentioned earlier that medications such as escitalopram, phenelzine, and fluoxetine mediate all the movement of cyclic adenosine monophosphate from the lipid rafts to the non-raft areas of the plasma membrane. In contrast, anti-anxiety and anti-psychotic drugs do not mediate any movement (Erb et al., 2016).

Rasenick and his team conducted further analysis of escitalopram. They further wanted to investigate the composition of antidepressants, which especially gets accumulated in the lipid rafts. Rasenick and the team tracked all the amassing of the escitalopram in the fractions of the lipid raft from the glioma cells. They discovered that the escitalopram bit by bit accumulated in the lipid rafts over time and concentration was dependent on the accumulations. In contrast, the R-citalopram and non-therapeutic enantiomer of the escitalopram did not accumulate in the lipid rafts (Erb et al., 2016).

Therefore, Rasenic and his colleagues' research indicates that antidepressants possibly have diverse mechanisms of actions. Despite the different mechanisms depicted by these antidepressants, they all translocate the inside gas out of their lipid rafts. This process of translocating the gases out of the lipid rafts is a gradual process that is in line with the delayed therapeutic undertakings. Besides, there are specific monoamine oxidase inhibitors and selective serotonin receptors that completes this phenomenon through a slow accumulation of the lipid rafts (Erb et al., 2016). The discovery of Rasenic and the team has recognized a famous novel of a biochemical hallmark for most of the antidepressants' action that makes available a new molecular target for these antidepressant actions alongside a fast-tracked timescale (Grillon et al., 2007). Thus, specific monoamine oxidase inhibitors and selective serotonin receptors may be the probable reasons why there is a delay of several weeks in the alleviation of depression symptoms after initiation of antidepressant medication.

Depression is a mental ailment that affects how individuals think, feel, and handle daily errands. For patients who partake, the prescribed drugs are deemed to be mentally ill; hence, their adherence to practitioner instructions can be questioned. As of the year 2003, 30 to 60% of people suffering from depression did not heed to the practitioner's simple instructions on the usage of the antidepressants (Hafizi, Chandra & Cowen, 2007). As of 2013, 50% of the depressed patients in the United States did not follow the regulated antidepressant directions given by the respective physicians (Hafizi, Chandra & Cowen, 2007). It is a fact that when patients fail to comply with the underwritten prescription on how to take the antidepressants, there is a greater peril that the medication given to them might not work correctly or will take a bit longer before the desired effect is evident. In some instances, the depression symptoms may take longer to be alleviated or may even get worse (Kent, Coplan & Gorman, 1998). Hence, lack of adherence to laid down procedures or instructions of the practitioner may be the probable reason why there is a delay of several weeks in the alleviation of depression symptoms after initiation of antidepressant medication.

Conclusion

All in all, depression is a mental ailment that affects how individuals think, feel, and handle daily errands. Major depression can cripple an individual. In severe cases, depression can lead to mood disorder, which may lead one to commit suicide. Antidepressants are prescribed by physicians to alleviate related symptoms of depression. The antidepressants can also be used to assist the brain in processing some chemicals that regulate stress or mood. Unfortunately, the current medication of antidepressants characteristically takes a long time before patients start responding. The possible reasons why there is a delay of several weeks in the alleviation of depression symptoms after initiation of antidepressant medication can be attributed to neuropharmacological actions, mechanism of serotonin inhibitors, and lack of adherence to practitioner's instructions.

References

Erb, S. J., Schappi, J. M., & Rasenick, M. M. (2016). Antidepressants accumulate in lipid rafts independent of monoamine transporters to modulate redistribution of the G protein, Gas. Journal of biological Chemistry, 291(38), 19725-19733. DOI: 10.1074/jbc.M116.727263

Frazer, A., & Benmansour, S. (2002). Delayed pharmacological effects of antidepressants. Molecular psychiatry, 7(S1), S23. https://www.nature.com/articles/4001015.pdf?origin=ppub

Grillon, C., Levenson, J., & Pine, D. S. (2007). A single dose of the selective serotonin reuptake inhibitor citalopram exacerbates anxiety in humans: a fear-potentiated startle study. Neuropsychopharmacology, 32(1), 225. https://www.researchgate.net/publication/6818947_A_Single_Dose_of_the_Selective_Serotonin_Reuptake_Inhibitor_Citalopram_Exacerbates_Anxiety_in_Humans_A_Fear-Potentiated_Startle_Study

Hafizi, S., Chandra, P., & Cowen, P. J. (2007). Neurokinin-1 receptor antagonists as novel antidepressants: trials and tribulations. The British Journal of Psychiatry, 191(4), 282-284. https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/neurokinin1-receptor-antagonists-as-novel-antidepressants-trials-and-tribulations/9E49C9DFF929C8E46C7AD116C84796C6/core-reader

Kent, J. M., Coplan, J. D., & Gorman, J. M. (1998). Clinical utility of the selective serotonin reuptake inhibitors in the spectrum of anxiety. Biological psychiatry, 44(9), 812-824. https://www.ncbi.nlm.nih.gov/pubmed/9807637