This explain why people suffer from depression, by stating

This essay will begin by looking briefly at the discoveryfor the first antidepressant, and how these findings led to the introduction ofADMS (antidepressant medication) and SSRIs (selective serotonin reuptakeinhibitors) and explain how the concept of the monoamine hypothesis works. Itwill then follow on to how the biological mechanisms of action of currentlyavailable antidepressant medications work on neurotransmitters within thesynapses in the brain. It will discuss alternative hypothesise such as theendorphin hypothesis and the neurotropic hypothesis and will explain bothbriefly, finishing on the effectiveness of treatment for depression usingantidepressant medication and cognitive therapy and how the evidence given inthis essay would show that the stated hypothesis are outdated.

The discovery that the drugReserpine, caused depression in some of its paitents, led to the finding thatthe drug causes monoamine neurotransmitters to decrease, a few of theseneurotransmitters are noradrenaline, dopamine and serotonin. It was also foundthat some paitents prescribed Isoniaxid who previously had depression, findthat their depression lifted. The reason for this is that isoniaxid breaks downmonoamines by inhibiting the enzyme monoamine oxidas (MAO) (GIVE CITATION (examplefigure 2.

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9 p59)). The monoamine hypothesis of mood disorders trys to explainwhy people suffer from depression, by stating that the reduced levels ofmonoamine are the primary cause, and if these levels can be increased,depression or symptoms of depression will be reduced. It is believed that”monoamine molecules are released and bind to receptors on the postsynapticneuron.

In depression, fewer monoamine molecules are available for binding toreceptors on the postsynaptic neuron, leading to a mood disorder.” (GIVECITATION (example of figure 2.10 p60.

Book 2) ). This hypothesis originallygave what seemed like a ‘simple’ explanation and treatment course for thosesuffering with depression, but as time has moved forward, and furtherdiscoveries have been made the monoamine hypotheses of mood disorders isoutdated and the overall understanding of depression and how it words is farmore complex. The biological mechanisms of action of currently availableADMS (antidepressant medications) is that they inhibit the reuptake ofmonoamines, in particular the likes of noradrenaline and serotonin. Reuptakeinhibitors have become the most widely prescribed medication for depressionacross the western societies often believed by the sufferers of depression tobe a ‘quick fix’. You can see in figure ….

. in (CITATION(book 1 section 2.4.

1,p50) ) how ADMS effect neurotransmitters and the reuptake of the likes ofserotonin and noradrenaline with a more detailed explanation. One commonlyknown ADM is that of Prozac. Prozac works by blocking the reuptake of theneurotransmitter serotonin, and is termed as a Selective Serotonin ReuptakeInhibitors (SSRIs) as seen in figure 2.24b (CITATION (example figure 2.24 p50book 1)). However the exact cause of Prozac behaving in this manner towardsserotonin levels is unclear an although it would make sense that altering theselevels to the correct amount would elevate and ease depression and the time itwould take would be short almost a “quick fix”, this has not proven to be the case.There are many alternatives hypotheses’ for the biologicalbasis of mood disorders which include that of the endorphin hypothesis in whichthe concept is that “elevated levels of neurochemicals termed endorphins in thebrain form them basis of the effect on mood.

” (CITATION) another good exampleof the endorphin hypothesis is presented in figure 3.7 (CITATION  (book 1 chapter 3, section 3.3.2, p 71/72)).Another alternative is that of the neurotrophic hypothesis, where after doingpost mortems on patients that had suffered with major depression they foundthat their levels of Brain-Derived Neurotropic Factor (BDNF) were abnormallylow. The concept was that the BDNF levels were a factor in causing depressionand if these were elevated the depression or depressive thoughts again wouldlift. This is further explained in (CITATION (book 2, chapter 2, p 63/64).

There is also the likes off the network hypothesis, stating that neurons thatprocess and send information around, to and from a healthy brain are damaged orhave died in those suffering from depression with the belief with the likesof  ” anti depressant medication,electroconvulsive therapy, exercise and psychotherapy” (CITATION (book 2chapter 2, section 2.3.3, p68) can gradually over time promote and enhanceplasticity and in turn allowing the damaged neurons to network as they should. The effectiveness of ADMS as a treatment for depression islimited as not every person with depression will find that they work, and manymay find that they end up with adverse side effects from their prescribedmedication. Currently less than “50 % of patients will achieve full recovery(defined as 6 months symptom-free) after using a ADM” (CITATION) although manymay find that their symptoms of depression will ease over a period of timeafter taking different medications or a combination of those that are availableand a waiting period of several weeks is recommended as “the therapeutic effect(if any) is not seen for 3-5 weeks” (CITATION (book 2 chapter 3, p 98) andfigure 3.

8 (CITATION (example figure 3.8 chapter 3 section 3.3.

2 p100) showshow paitents responded to ADM and Cognitive therapy (CT) in the long term.These results seem impressive especially when you consider the fact that CT hasno known side effects unlike ADMS, but the bare reality of depression treatmentis that its not advancing aswell as it should be. ” in the UK only 1 in 4people with depression are receiving any kind of treatment and it is claimedthat most episodes resolve without treatment.” (CITATION (example table 3. 2, chapter 3, section 3.3.2 p101) even though those that suffer fromdepression are extremely likely to have further episodes thought their lives. In conclusion neither anti-depressant medication with theirbiological limitations and side effects or cognitive therapy with the vairyingexperience and understanding of therapists, will successfully combat and curedepression on their own,  but acombination of the two allowing for the medication and the therapy to takeeffect, symptoms of depression, can be, at least for the moment, be keptsomewhat under control.

The realms of scientific research into the causes ofdepression with the likes of the monoamine hypothesis, the endorphinehypothesis are becoming outdated and adjusted as we progress in ourunderstanding of the causes of depression and depressive thoughts where it is notjust medically but socially and psychologically concerned.