Neurotransmitter Serotonin Cause Depression Psychology Essay

Neurotransmitter Serotonin Ca go for Depression Psychology Es claim tally to the military man Health Organization, about 121 million people across the globe back up from opinion and the WHO has ranked impression as fourth in a list of most urgent problems worldwide (2). It is the most prevalent psychiatrical disorder and is responsible for nearly 850,000 deaths perpetuallyy year. Supporting this accompaniment, statistics get revealed that the use of anti-depressants has soargond oer 400 per centum in the past two decades (3). According to Kresser, a licensed acupuncturist and practitioner of integrative medicine, several chemically obvious anti-depressants marketed under trade names such as Prozac, Zoloft, and Paxil direct enjoy immense popularity as anti-depressants (4). Amongst the four classes of anti-depressant medication, namely selective serotonin reup affiance inhibitors (selective-serotonin reuptake inhibitors), atypical depressants, tricyclic anti-depressants (T CAs) and monoamine oxidase inhibitors (MAOIs), SSRIs remove been the most widely overconfident medication by physicians. In this essay, the terms SSRI and anti-depressant will be used interchangeably.The current model of SSRIs assumes that a first gear level of extracellular neurotransmitter, serotonin, is primarily responsible for first. Serotonin in our body quarter be found in two places 80 percentage of it in our GI tract spell the rest in our top dog (5). The 80 percent of serotonin function as hormones and they play a role in muscular contractions whereas the 20 percent act as a neurotransmitter in our mentality (6). In our brain in that location atomic number 18 mevery cells called nerve cells, which are separated by small gaps. Messages carried by neurotransmitters are delivered from one neuron to another across the gaps. These messages come in the form of chemical impulses, and give information about mood, behaviour, body temperature, appetite and sleep. Once a neurotransmitter leaves the move neuron, it will latch onto the receiving neuron and relay chemical impulses over. Then the neurotransmitter returns to its displace neuron to be re-used again this process is called reuptake. On the other hand, if in that respect are inadequate centers of neurotransmitters, the next impulse does not fire away and messages will not be relayed. (7) SSRIs break away to block or verbose down the reuptake of serotonin in particular, hence increasing the arrive of extracellular serotonin. As a result, more serotonin are record in the gaps which will addition rate of successful transmission of impulses to the receiving neuron. SSRI is hence engineered on the belief that serotonin is the bugger off of first. However ever since the advent of the medicate and its side- cause exposed, medicine researchers are compelled to re-investigate the skill of SSRIs, in which conflicting results were revealed.The investigation into the serotonin-depress ion connection will not entirely prevent doctors devising inappropriate prescriptions that whitethorn not be in the beaver cheer of their patients health, it also al deplorables a clearer definition of the causes of depression. Ultimately, establishing the proper function of serotonin whitethorn lead to a ground-breaking change in the methodology of treating depression and think disorders in the psychiatric and pharmacology world.While most people harbour with the belief that a deficiency of serotonin is related to depression, some get by that an imbalance in serotonin levels leads to depression. This imbalance theory arises because of the widespread tactual sensation that SSRIs are only effective for patients with moderate to severe depression while it is ineffective for nutsly depressed patients. The basis of the debate surrounding the dexterity of SSRIs in fact boils down to a deeper problem whether or not the neurotransmitter, serotonin, is related to depression at all. Nevertheless, I oppose both claims of the serotonin-depression attach and con turn up that there is no coherence between levels of serotonin and depression. Up till now, there have no substantial evidence that depression is caused by serotonin deficiency, neither is there one that shows that over stimulant do do drugss of serotonin causes depression.Efficacy of SSRIs challenged by small drug-placebo differenceMany studies have shown that the cogency of SSRI drugs in the treatment of depression is challenged by low drug-placebo difference scores. Studies to investigate the efficacy of anti-depressants by giving placebos to a controlled sort have revealed that the recovery rate of patients who alsok a glucose pill was equivalent to patients who consumed the anti-depression drug (8). A 2008 meta synopsis of the efficacy of SSRIs that was published by the Food and medicine Administration (FDA), revealed that these anti-depressants have no clinically authoritative edge over all placebos. By this, it means that it did not meet the drug licensing authority, UK home(a) Institute of Clinical Excellence (NICE) standards. As evident in the meta analysis, the placebo response groups account for up to 75 percent of all positivistic effects of anti-depressant medication (9) which shows that 3 in 4 of all patients who reputationed an increase in heightened emotional well-being were actually consuming sugar pills. some other studies yielded similar results a study by Khan et al. found a 10 percent difference in level of symptoms when patients consume the muddy placebos compared to the active drugs in two separate meta-analyses (10). As the drug-placebo difference is small, it brush aside be seen that regardless of whether SSRI is administered or not, symptoms of depression are electrostatic greatly reduced. This implies that serotonin level may not be related to depression at all.Opponents argue that experiments to trial run the efficacy of SSRIs again st inert placebos may not be accurate because the side effects of SSRIs are not mimicked. They claim that commonly known side effects of SSRIs, such as diarrhoea, nausea, dizziness, headaches or even gastrointestinal bleeding (11) may affect patients mood, which in turn underrate the impact of serotonin in lifting depression. This claim is and rejected by many scientific lits which show counter-evidences. According to Joanna Moncrieff, the co-chair somebody of Critical psychopathology Network, when she used active placebos to simulate the adverse-effects of SSRIs in anti-depressant drug trials, results revealed that differences between active placebo and SSRI were significantly small (12). To measure luridness of depression before and after the drug trials, the accomplished Hamilton Rating weighing machine of Depression (HRSD) was used. Since it did not meet NICE standards of an improvement in evaluation score of 3 points to be defined as clinically significant (8), the above studies involving inert and active placebos clearly show that no affaire which placebo type was administered active or inert, drug versus placebo significance in anti-depressant efficacy is clinically insignificant. Whether or not the level of serotonin is increased, patients reported a reduction in symptoms of depression, therefore there is little evidence to say that a neglect of this neurotransmitter causes depression.Another common belief by proponents of anti-depressants is that initial causticity of depression is directly related to the effectiveness of SSRIs, that SSRIs work best for patients with very severe depression. It is thought that over stimulation of serotonin may cause further chemical imbalance in patients suffering from mild depression, hence rendering SSRIs ineffective (13). Thus in order to test this claim, Kirsch et al moved on to investigate whether initial severity of depression affects the efficacy of anti-depressants. He tested on the hypothesis that an ti-depressants work only for people suffering from moderate to major depression. In this double-blinded study of 35 clinical trials involving 5,133 subjects, both drug administers and subjects were unknown to results of randomized medication (placebo or SSRI) to prevent sampling biasness and subjects severity of depression was heedful by HRSD (14). The test was conducted to see if there is an improvement in the subjects depression, metric against their baseline severity and the closing conclusion is as follows patients with an initial moderate depression did not report a drug-placebo difference, patients with an initial severe depression reported a relatively small drug-placebo difference and only for patients situated at the hurrying end of very severe depression category did the drug-placebo difference pay heed into the clinically significant criterion by NICE standards (8). Although effectiveness of SSRIs may seem to improve with the severity of depression, further research has revealed a interdict coherence between severity and placebo response. As highlighted from Figure 1, the drug-placebo difference reached clinical standards for people with a higher initial severity of depression. Further analysis shows that a higher drug-placebo difference is due to a decrease in improvement of the placebo group rather than due to the effects of SSRIs.Figure 1. tight Standardized Improvement as a Function of Initial ruggedness and Treatment Group, Including Only Trials Whose Samples Had High Initial Severitygraph.pngSource http//www.plosmedicine.org/ term/fetchObject.action?uri=infodoi/10.1371/journal.pmed.0050045.g003representation=PNG_MThis implies that the increased benefit for extremely depressed patients seems credited(predicate) to a response-deficiency to placebos rather than a heightened response to SSRI medication. wherefore efficacy of SSRI does not increase with severity of depression and increasing amount of serotonin did not work for patients w ith all levels of depression. Since SSRIs are designed to mitigate depression by inhibiting the reuptake of serotonin in our brain cells, it shows that there is no relationship between extracellular serotonin and ones mood. Furthermore, it usually take weeks before effects of anti-depressants are expressed and can be measured by testing for serotonin levels in the blood, yet patients often report relief within hours or days of medication. thus this phenomenon demonstrates the lack of coefficient of correlativity between serotonin and depression and gives support to the placebo effect.The lack in correlation is further evidenced by the results of a Force go discharge (FST). FST, also known as the behavioural despair test, is a conventional anti-depressant screening test which involves using rodents as test subjects. In this test, rats are dropped in an enclosed water cylinder and their movements observed. The struggling time of rats is measured based on the precondition that i mmobility of rats is directly proportional to their conjure of depression. For example depressed rats will cease trying and float in the cylinder, which is akin to despair, whereas non-depressed rats will continue to struggle in search of a way out (15). Although it is thought that SSRIs should extend struggling time of rats, final results were inconsistent hence inconclusive (16). The administration of SSRIs in rodents did not scram them less susceptible to depression, displaying no direct relationship between serotonin and depression. Nonetheless, it should be noted that experiments done on mice may not be entirely accurate in predicting responses in humans (17).The bold assumption made by researchersThe serotonin-depression link came about when scientists first discovered that in most depressed patients, the level of serotonin is comparably lower than that in non-depressed people. The amount of serotonin in a humans body was measured by analyse blood samples taken from depress ed and healthy people. afterward the anti-depressant SSRI was invented, which targets the neurotransmitter serotonin and works to stimulate the production of it. This methodology wherefore raises a few doubts. Firstly, the assumption that blood serotonin and brain serotonin are directly proportional can be contested as it is certainly impossible to measure the amount of serotonin in the brain. Patients who have high levels of serotonin in the blood may have low levels of serotonin in the brain and vice versa. As mentioned earlier, 80 percent of the humans body total serotonin is found in our bloodstream and the rest in the brain. While the level of blood serotonin can be measured, current biomedical technology has yet to transcend the brain barrier. In all clinical trials involving SSRIs, the assumption made is that blood serotonin shines brain serotonin, which is a very bold one to make. This then creates a paradox in research methodology the reason for inventing SSRIs instead o f provide serotonin directly to a humans body is due to the blood-brain barrier. viva voce ingested serotonin are ineffective as they do not become flat through bloodstreams into the brain, that is the digestive system is unparallel to the central nervous system. Whereas SSRIs work because they merely seek to enhance an impulse that is already present, but too feeble to cross the gap. Yet scientists conveniently established a link between serotonin and depression by measuring serotonin in patients blood. It is reasonable to say that since blood serotonin is not proven to be a clear indication of brain serotonin, any positive outcomes of anti-depressant drug trials may not be due to the increase in brain serotonin but other unknown factors. This again shows a lack of tangible evidence between the neurotransmitter, serotonin, and depression.Secondly, in all probability that there is a direct attestation of serotonin deficiency in any mental disorder lacking, it is still unclear wh ether low levels of serotonin causes depression or depression causes a dip in serotonin. Evidences supporting the latter(prenominal) can be based on observations of non-depressed people with low amounts of serotonin. In a 1996 investigation of the biochemistry of depression, attempts made to induce depression by minify serotonin levels yielded no consistent results (18). Similarly, researchers found that a surge in brain serotonin, arrived at by administering SSRIs, were ineffective at alleviating depression (19). at that placefore there is little evidence to support serotonin as a mood chemical.Also problematic for the serotonin-depression claim is the expanding field of research comparing SSRIs to other anti-depression drugs that do not target serotonin specifically (20). For instance, the atypical anti-depressant buproprion (21) and St. Johns Wort (22), which do not alter the level of serotonin were proven to be just as effective as SSRIs in the treatment for depression. Theref ore doubts about the serotonin-depression link are acknowledged by many researchers as well as by advocates of SSRIs (23). To supplement my stand, serotonin is not listed as the cause of depression disorder in theDiagnostic and Statistical manual of Mental Disorders (24). The American Psychiatric Press Textbook of Clinical Psychiatry (25) also reiterates that serotonin deficiency as an unconfirmed hypothesis (20). In short, there exists no rigorous corroboration of the serotonin theory, which may draw out the reliability of positive drug trials published by drug companies. oddmentIn addition to what textbooks have to say about serotonin, it is important to olfactory perception at what not being said in scientific literature. There are numerous peer-reviewed articles supporting the disconnect between serotonin and depression however not a single one can be precisely cited to directly endorse claims of a serotonin deficiency in any mental disorders (20). Assuming that blood seroton in is a wide measure for brain serotonin, abundant evidences of high placebo significance in anti-depressant drug trials, the rejection of the claim that efficacy of SSRIs depends on severity of depression, and an inconsistent Force Swim Test results indicate that serotonin may not be the cause of depression. No doubt there may be a positive outcomes from the drug trials, however because blood serotonin may not reflect brain serotonin, these outcomes coupled with the above mentioned proofs against the serotonin hypothesis strongly signal that other factors are involved in depression. The incongruence between the scientific literature and the claims made by proponents are prominent, hence I stand for the fact that there is no direct correlation between serotonin level and depression.