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The monoamine theory of depression holds that depression is associated with
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Since the discovery of monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants in the 1950s and its affect on depressives, Schildkraut first proposed the Monoamine Theory. The theory states that depression is caused by an imbalance of monoamine transmitters (neurotransmitters) in certain areas of the brain, such as noradrenaline, serotonin and dopamine (Schildkraut, 1965). This led to the introduction of antidepressant medication in the treatment of depression, known as pharmacotherapy. However, ongoing research suggests that the theory is “inadequate, as it does not provide a complete explanation for the actions of antidepressants, and the pathophysiology of depression itself remains unknown.”(Hirschfeld, 2000) A few of the main reasons for this inadequacy are because it is difficult to measure the level of neurotransmitters in an individual’s brain (P. L. Delgado, 2000) and that evidence is indirect on whether monoamine function is impaired in individuals with depression as the causes of depression appear to be more complex than simply a reduction in levels of monoamine or diminished function in these systems. (P. Delgado & Moreno, 1999) However, a more direct investigation of the role of monoamines can be used through the neurotransmitter depletion model that can be seen in an experiment with tryptophan depletion and alpha-methylparatyrosine, which is used to lower levels of serotonin and induce catecholamine depletion, respectively, in the brain (Salomon, Miller, Delgado, & Charney, 1993). Results from this experiment show that, depending on the antidepressant used, such depletion rapidly reverses antidepressant responses in the majority of patients and that depletion in unmedicated patients with depression did no... ... middle of paper ... ...d that in four treatment trials, cognitive therapy for depression is superior to pharmacotherapy in reducing relapse, or the need for further treatment. (Blackburn, Eunson & Bishop, 1986; Simons, Murphy, Levine & Wetzel, 1986; Evans, Hollon, De Rubeis, Piasecki, Grove, Garves & Tuason, 1992; Shea, Elkin, Imber, Sotsky, Watkins, Collins, Pilkonis, Leber, Krupnick, Dolan & Parloff, 1992). Therefore, it can be seen that many qualitative and quantitative reviews now conclude that cognitive therapy effectively treats depression, or is at least comparable, if not, superior to medication treatment, and may have lower rates of relapse in comparison to medication treatments. As a result, the implications of the cognitive theory and the treatment used to process Beck’s theory, cognitive therapy, has been a successful treatment in regarding depression, and many other diseases.
Can there ever be scientific theories in psychology, medicine, or psychiatry? I argue that one approach to answering this question consists of investigating the nature of such purported theories and I focus on the monoamine hypothesis of clinical depression. (1) By a careful examination of a typical experiment involving the action of drugs and placebos for the cure of clinical depression-an experiment founded upon the monoamine hypothesis-I raise a number of methodological and conceptual problems that may lead one to conclude that rigorous scientific theories in these three disciplines may never be forthcoming, or at least that the state of scientific research in these areas is still in very rudimentary shape and in need of much logical and philosophical analysis. In addition, because no such biomedical theories may be forthcoming, I also undercut Adolf Grünbaum's analysis of the concept of a placebo, an analysis that makes the definition of "placebo" relative to a biomedical theory in the first place.
Treating depressive and bipolar disorders with antidepressants remains a popular option in clinical practice. Most clinicians choose the drug or class of drugs, usually selective serotonin reuptake inhibitors, SSRI's, that is most effective and best tolerated with fewer severe side effects. These drugs are beneficial because they specifically target serotonin-based areas of the brain without affecting other neurotransmitter systems. SSRI's largely replaced tricyclic antidepressants which work by blocking the absorption (reuptake) of the neurotransmitters serotonin and norepinephrine, thereby increasing the levels of these two neurotransmitters in the brain. Tricyclic antidepressants present severe side effects and thus are usually only used when other treatments have failed. If SSRI's or tricyclics are not effective Monoamine oxidase inhibitors may be prescribed. MAOI's, enhance tyramine to increase norepinephrine and serotonin. While taking MAOI's you must abstain from foods and alcohol that contain tyramine such as, yogurt, aged cheese, and substances such as cold medications. This is because a potential toxic reaction could occur. Additionally, other antidepressants may be utilized such as Wellbutrin (bupropion) an NDRI-
Basically, serotonin levels will provide various benefits regarded to health and mental. It is also called feel good chemical which will apply benefits to both biological and psychological functions. Most of this supplement’s application is found primarily in digestive tract and blood plates. Only small amount of this supplement will be served for its purpose in central nervous systems and brains. If users says that they are in way to achieve serotonin levels, then it is clearly understood that the small percentage will exists in the brain. It is capable of delivering various benefits regarding to mental function and maintenance of serotonin levels of the brain. The neurotransmitter has various things to do
Cognitive Behavioral Therapy appears to be a new treatment, although its roots can be traced to Albert Ellis’s Reason and Emotion in Psychotherapy, published in 1962. Cognitive therapy assumes that thoughts precede actions and false self-beliefs cause negative emotions. It is now known that most depression treatments have cognitive components to them, whether they are recognized or not. In the 1970’s many psychologists began using cognitive components to describe depression. From there, they developed cognitive forms to treat depression with impressive results (Franklin, 2003).
Since Bipolar Disorder involves the cycling between two different states of mania and major depression, there are many different etiological factors in play. The neurotransmitters that are involved in this disease are serotonin, norepinehrine and dopamine. There has been some preliminary research involved with glutamate as well. In patients with the depressive portion of Bipolar Disorder, Serotonin levels were found to be lower than healthy, non-depressed patients (Young, Warsh, Kish, Shannak & Hornykeiwicz, 1994). Young et. al. (1994) found reduced amounts serotonin’s metabolite, 5-HIAA, in frontal and parietal lobes of deceased bipolar disorder patients. Norepinehphrine was also found to be lower as well. During the depressed state of bipolar disorder, the concentration of norepinehphrine ‘s synthesis enzyme, tyrosine hydroxylase, was lower in the locus coeruleus than patients who only had depression and not Bipolar Disorder (Wiste, Arango, Ellis, Mann, & Underwood, 2008). Although in the mania cycle of Bipolar Disorder, Norepinephrine is found to be elevated in the brain (Manji & Lenox,2000). Furthermore, Dopamine was also found to be lower in the brain as well during the depressed state of Bipolar disorder. According to a study by Vawter, Freed, Kleinman (2000), the concentration of the metabolite of dopamine, homovanillic acid, was found to be significantly lower in the parietal lobe of the brain. Dopamine Agonists, while they can treat the depression cycle of the disorder, can also bring about the mania in the disorder; therefore, the pharmacological treatment of the Bipolar disorder must be regulated heavily so that the treatment itself doesn’t exacerbate the disorder instead of treat the disorder (Manji et. al. 2003). ...
Hollon, S. D. & Beck, A. T. (2004). Cognitive and cognitive behavioral therapies. Bergin And Garfield’S Handbook Of Psychotherapy And Behavior Change, 5 pp. 447--492.
Approximately 5% of the United States' population experiences a depressive episode that requires psychopharmacological treatment; in any one year, 10-12 million Americans are affected by depression, with the condition twice as common in females than in males. It has been estimated that 15% of patients hospitalized for depression will commit suicide. These figures are incredible, so finding the root of the problem when it comes to depression is extremely important. "Alterations in serotonin metabolism may be an important factor in the etiology and treatment of depression." (7).
The notion of an individualized chemical imbalance founded in the brain as the explanation of depression, whether it is norepinephrine and serotonin, is a theory which is built on a particular kind of logic that attempts to isolate a causal neurochemical abnormality as giving rise to or generating depressive symptoms. The drugs which are utilize to treat these abnormalities, were shown in the last chapter to be a crucial component in the creation of depressive pathology insofar as they were reasoned or designed to correct them. Within a society that values the biomedical intervention of psychopharmaceuticals in the treatment of depression there is an in...
The end product of these variable factors do, however, provide some common biochemical alterations in the brain that lend insight into understanding the reality and possible treatment of the disease. So, in the spirit of "working backwards," I will explore this end product. Perhaps the most popular end-product of depression is the monoamine depletion or disturbance that is commonly detected in depressed persons. Serotonin, norepinephrine, and dopamine have been identified as the main culprits, with serotonin and norepinephrine being the most suspect. " Among the findings linking impoverished synaptic norepinephrine levels to depression is the discovery in many studies that indirect markers of norepinephrine levels in the brain-levels of its metabolites, or by-products, in more accessible material (urine and cerebrospinal fluid)-are often low in depressed individuals.
Antidepressant are a form of pharmacotherapy treatment developed to treat the symptoms of major depression. Antidepressants are used for many other types of conditions including anxiety disorders, obsessive compulsive disorder, dysthymia, eating disorders, sleeping disorders, and substance abuse, pain syndromes, gastrointestional disorders. Antidepressants usually require several weeks to notice significant effects. There are no antidepressants or any medication that is completely free of adverse effects. This article explains that the adverse effects of antidepressant can decrease compliance and slow down the rate of recovery. It is important for one to take note of potential side-effects before choosing the best antidepressant to suit their personalized needs. Statistics show that about 28 percent of patients sto...
Beck, A. (1978). Cognitive therapy of depression (The Guildford Clinical Psychology and psychopathology series). New York, N.Y : Guildford Press.
Rupke, S., Blecke, D., & Renfrow, M. (2006, January 1). Cognitive therapy for depression. National Center for Biotechnology Information. Retrieved March 10, 2014, from http://www.ncbi.nlm.nih.gov/pubmed/16417069?dopt=Abstract
Depression is a mental illness, which affects millions of Americans each year. Currently there are many prescription drugs, called anti-depressants that have been proven to successfully treat it. The causes of depression are somewhat of a medical enigma, however, it is known that depression is associated with a change in the brains chemistry involving the function of neurotransmitters (Reichert). This chemical change occurs in healthy brain’s, which experience sadness, but ends after the unpleasant stimulus is removed. In people suffering from depression this chemical change does not correspond to any particular stimulus. Symptoms of depression are often incapacitating and include severe and extended sadness, feelings of worthlessness, feelings of emptiness, irritability and anxiety (Reichert, Spake).
Depression disorder is characterized by several impairments in different functions. This paper is aimed to provide an overview of the impairments of depression.
The cause of Clinical depression has long been a mystery to physicians and researchers. Many different theories have been proposed, but no conclusive evidence has been put forth. However, most of what we know about depression stems from the results of certain drugs which have been successful in treating the clinically depressed. These anti--depressants have led to the assumption that depression is most likely due to a chemical imbalance (of neurotransmitters) which somehow leads to the symptoms of depression. To try and write a paper on all the theories of depression would be endless, as would be a study on all the different types of anti-depressants. Therefore I have tried to focus my paper on the serotonin hypothesis for depression, and more specifically how the serotonergic anti-depressants have backed up this theory. Of course, Any paper on serotonin-based anti-depressants must include the popular Prozac. Because of the excitement And controversy surrounding Prozac, I decided to channel most of my paper into the action of this so-called "wonder drug".