Serotonin Essay

Abstract

The research question addressed in this paper is premised on the relationship between high serotonin levels and depression. Depression and other mood disorders are among the common illnessesthat are known to cause high morbidity and mortality rates.The research was done from the perspective of healthcare professionals and is aimed at collecting and analyzing data that would be useful in informing health practitioners on the relationship between serotonin and depression. The development of modern anti-depressants being the target,SERT aims at achieving popularity over the other transporters.Several pieces of research have shown the Serotonin uptake inhibitors are considered useful in depression treatment.However, they are known to disrupt sleep and causing a slow-onset of action nausea.Depression being a polygenic and high complex psychiatric discarder and society burden, research on it is very crucial.The experimental study design was used in this research where a group of 100 individuals was recruited into the study. After obtaining their consent, 100 patients from the Johns Hopkins Hospital were recruited to intro the study. Out of the 100 participants, 50 were exposed to high levels of serotonin while the other 50 were presented to the usual body serotonin requirement of 101-283 Nanograms per millilitre (ng/ml) /. The selection procedure involved randomly choosing the participants with the aim of reducing bias and also to give them an equal 50 % chance of being selected. The evidence that link serotonin and its receptors to depression will be discussed in detail in this paper

Introduction

Serotonin is a chemical that is mostly found in the digestive system. Its role is to send signals between the body’s nerve cells.It was discovered in the late 1940s, and it was found to be existing in the central nervous system of animals and its neurotransmitter function a decade later.It is made from the essential Amino acid known as tryptophan.The amino acid enters the body through the food we eat and is commonly found in foods such as red meat, cheese and nuts.If the body is experiencing Tryptophan deficiency, lower serotonin levels may result therefore leading to mood disorders such as depression and anxiety. Serotonin is known to impact every part of the body and is considered a natural mood stabilizer.It helps in body functions such as digestion, sleeping, reducing depression, maintaining bone health, healing wounds only to mention a few.When the levels of serotonin in the body are healthy, an individual may feel happier, more focused and less anxious.Recent studies have shown that people with low levels of serotonin are at higher risk of depression compared to those with normal levels. However, there have been minor disagreements on the role of serotonin in mental health.According to an animal study conducted in 2016, it was found that the mice that lacked serotonin autoreceptors exhibited less anxiety and other depression-related behaviours.The reason for this is that since the mice lacked the serotonin autoreceptors, they had higher levels of serotonin in their brains.The serotonin depression relationship is almost 50 years old.The hypothesis proposes that the activity of serotonin pathways play a casual role in clinical depression. The theory, later on, was rejected by some researchers whose primary purpose was to increase the sales of SIRS to the public.

Serotonin deficiency is a situation where the body does not produce enough serotonin.It can happen due to both physiological and psychological symptoms.However, its role in these processes is not fully understood.For instance, the serotonin and depression relationship has been in discussion for over 50 years now. Researchers have a different perception of that topic.The most common one is that low serotonin increases the risk of depression although no such evidencesupports that theory. However, most people seem to agree on the fact that the function of serotonin in the body is more complicated than previously thought. Diagnosing it is nonetheless hard because accurately measuring the amount of serotonin is impossible.However, measuring the amount of serotonin in the blood is possible, and it is used to check for serotonin-producing tumours.

According to the article titled The Serotonin Theory of Depression, the breakdown of serotonin (5-hydroxytryptamine; 5-HT) is a signalling process that is involved in the symptoms and the treatment of clinical depression using drugs.Recent studies have shown that decreased levels of 5-HT in the brain, is the leading cause of depression for almost half a century.This may be due to a lack of receptors sites, low brain production of serotonin or a shortage in tryptophan. In as much as 5-HT deficiency is known to alleviate depression, it is not the primary cause of depression.Depression can arise from diverse neurological conditions such as Parkinson’s and Alzheimer’s.

Moreover life situations such as job environment, personal loss and trauma are known to cause depression. Besides the twin and adoption studies have also indicated a crucial genetic component in depression.Studies involving tryptophan deficiency, have proved that it induces the recurrence of mild n-depression especially in patients who have recovered following the treatment of serotonergic antidepressants due to the lowered levels of 5-HT. Out of all the tryptophan consumed in the diet, less than 1% is converted into 5-Ht while the rest is metabolized via the indoleamine 2, 3 dioxygenase pathway.         Depletion of Tryptophan in the body affects the brain since it starves metabolism.About 50% of the patients who are treated with interferon end up developing depression.Researches have found that depletion of tryptophan does not produce clinically significant changes in mood in healthy individuals who are not at risk of depression.The same is also true for individuals who have recovered from depression who undergo depletion of catecholamine. Generally, these pieces of evidence prove that impairing the secretion of serotonin in the body can cause distress in some clinical circumstances. However, it is not sufficient since association does not necessarily lead to causation. The effect of tryptophan on depression is more evident in individuals who have experienced earlier episodes of depression as compared to those with no depression history. Therefore, lowering the serotonin function compromises the mechanisms involved in depression recovery.

The fact that SSRIs are antidepressant drugs that are widely used givesresearchers the opportunity to research more on the serotonin-depression relationship.Some of them are Prozac, Paxil and Celexa only to mention a few.These anti-depressants help to keep the serotonin produced in the body in circulation but do not increase the serotonin supply in the brain. Most neurophysiological studies have proved that the administration of SIRS in both the depressed and healthy patients leads to positive shifts in the way the brain the brain responds to emotionally –valenceinformation. Emotions are short –lived and most of the times they are negatively biased in depressed patients. Therefore, from this viewpoint, it is right to say that increasing the serotonin levels does not influence mood directly but acts as a secondary consequence of a definite shift in the emotional responses. However, the nature of serotonin deficiency has proved to be elusive, and it is still unclear how its signalling effects may alter the neurophysiological process to bring about atrelaxed depression mood. Among the individuals with severe depression, around 40-60 percent of them report Improvements after taking the SSRIs for eight weeks.This statement shows that increasing the serotonin levels does not treat the underlying depression. Moreover, researchers have found that SSRIs have an inflammatory effect on the body.

Studies have shown that by inducing the indoleamine 2,3 dioxygenase by the interferon and depletion of tryptophan and the decreased 5-HT synthesis are involved in depression in those patients.The reserpine inhibitor is also known to cause a 5-HT deficiency, therefore, precipitating depression symptoms. However, high doses of reserpine not only depletes the 5-HT storage but the noradrenaline and dopamine as well. However, there is a contentious link between the treatment of chronic reserpine and depression. Common anti-depressant drugs that are designed to boost serotonin levels help in kicking off the production of new cells which in turn makes a depression to lift. Generally, there is a strong association between 5-HT deficiency and depression.

Alzheimer’s disease which is a  progressive generative brain disorder has a strong link to the serotonin amountin the body.Studies have proved that low levels of serotonin production are a risk factor of Alzheimer’s disease.Additionally, some studies have produced that a loss in the neurons that produce serotonin in the brain can lead to an excessive build-up of amyloid plaque in the brain which a hallmark of Alzheimer’s disease.A new study from the Johns Hopkins University school of medicine has indicated that serotonin does play a vital role in the development of Alzheimer’s disease.The research suggests that the chemical may drive the condition rather than merely being its by-product.

Alzheimer is the most common form of dementia and affects 5% of people older than 65 years.It is characterized by progressive impairment of memory, cognitive function, language, judgement and activities of daily living. Ultimately, the patient cannot perform self –care activities and become dependent on caregivers. Its onset is subtle and insidious.Initially, there is a gradual decline in cognitive function from a previously high level.Short term memory impairment is the first characteristics in the early stages.The patient may also seem to experience forgetfulness and also difficulty in learning and retaining new information. They also have trouble planning meals, managing finances or even using a telephone. The disease is characterized by complications such as injury due to lack of insight, pneumonia and other infections, malnutrition and dehydration due to inattention to mealtime and hunger or theinability to prepare meals.It can be diagnosed through scanning (CT scans, MRI or SPECT scans ), genetic testing, laboratory tests, mental status assessment and detailed patient history information. In as much as there is no definitive medical treatment for it, it can be managed by administering cholinesterase inhibitors; these inhibitors improve the cholinergic neurotransmission to help delay decline function over time.

Serotonin levels in the body can not only be reduced through medication but natural methods as well. Some of the natural serotonin level booster methods are; regular exercise, exposure to bright light, healthy diets and meditation.Meditation helps in relieving stress and promoting a generally positive outlook.The bottom line is that serotonin affects every part of the body and it is essential to maintain it at a balanced state.Serotonin imbalance may meansomething serious, and it is necessary for individuals to talk to their doctors in case of any concerns.

Conclusion

The study upheld the hypothesis since it was found that the patients who had were exposed to high levels of serotonin showed reduced anxiety as well as other depression-related behaviours compared to those with the average level of serotonin.Therefore it is entirely right to say that there is an association between serotonin levels and depression. However, assuming that low serotonin causes depression is not correct. From this research, it is evident that there is a vast amount of information concerning the relationship between serotonin and various body functions over the last two decades. Researchers are still trying to find the exact cause of depression since the role of serotonin in distress is still not clear.

Reactions

The serotonin depression relationship is worth researching on because as researchers, we need to come up with the best correlation between serotonin and depression. Prescribing an antidepressant for a patient may not be so useful because the antidepressants do not entirely treat depression.

 

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