Euthanasia In The United States Essay Research free essay sample

Euthanasia In The United States Essay, Research Paper Euthanasia in the United States Every twelvemonth two million people die in North America. Chronic unwellness, such as malignant neoplastic disease or bosom disease, histories for two of every three deceases. It is estimated that about 70 per centum of these people die after a determination is made to waive vital intervention ( Choice in Dying ) . In America and all around the universe, the on-going argument is whether patients should hold the chance to implement this critical option of mercy killing. Although controversial, it is imperative that United States citizens are non denied this right to a humane decease. Groups in resistance to euthanasia state that patients who yearn to do this determination are neither in a healthy psychological province of head nor have the God-willing right to make so. These groups feel if mercy killings were to go a publically accepted option to the terminally ill that doctors, household, and even patients may mistreat it. We will write a custom essay sample on Euthanasia In The United States Essay Research or any similar topic specifically for you Do Not WasteYour Time HIRE WRITER Only 13.90 / page They besides strongly back up modern end-of-life intervention, known as alleviative attention, as a more logical and moral option. Possibly the strongest belief that mercy killing is incorrect comes from those who follow the words of the Bible and believe that every facet of life belongs to God. The Old Testament records an incident affecting King Saul of Israel, who became earnestly wounded on the battleground. Fearing the progressing enemy, Saul took his ain blade and tried to fall against it. He cried to a soldier, ? Come and set me out of my wretchedness for I am in awful hurting but life lingers on. ? The soldier acted in conformity with the wants of the male monarch and killed him. The soldier so brought some of Saul? s armour to David and said, ? I killed him, for I knew he couldn? t live. ? David ordered the soldier put to decease ( Eareckson, 111 ) . Those who believe in the Bible clearly see here that, whether a sovereign or a common individual, clemency violent death is perceived as sinful in the Lord? s eyes. To see a more recent illustration of the Catholic Church? s dissension of mercy killing we merely have to look back a few old ages. In 1994, for case, the Dutch telecasting station IKON? s cinematography of the decease of a adult male with Lou Gehrig? s disease in a docudrama, ? Death on Request, ? brought a denouncement from the Vatican ( Branegan, 30 ) . Equally of import to those back uping the anti-euthanasia cause is the idea of any doctor, household member or patient who would mistreat this right if given the opportunity. Naturally, much trust is bestowed in these cardinal participants of our lives if anything were to go on to us. The inquiry in this sense is how do we know that they will do determinations in the best involvement of the patient if they are unable to talk for themselves? Would the fiscal and emotional load on the household of a terminally sick patient do them to do an irrational determination to straight impact the life of the patient? If the emotional emphasis doesn? t get to some people, the fiscal load may decidedly hit some households hard these yearss with the high costs of modern medical intervention. And who couldn? T usage 1000s of dollars in life insurance? The enticement is decidedly at that place. A rough illustration of this can be seen in the experience of a fifty-year-old adult female with malignant neoplastic disease of the castanetss, liver, lungs, and chest. Her physician was a Polish-born oncologist, Dr. Ben Zylicz. Dr. Zylicz explained to the adult female that he could decrease her hurting with drugs, and offered her a infirmary room. Aware of Holland? s policy leting physicians to stop the lives of the terminally ill by such agencies, the adult female stated, ? I am Catholic. My spiritual beliefs would neer let me to accept euthanasia. ? Zylicz assured the adult female that he would take attention of her, and she agreed to take the room. After 24 hours of morphia intervention she was able to see her household ( Eads, 93 ) . Subsequently, a nurse called Zylicz at place with some straitening intelligence. After Zylicz had left the infirmary, another physician entered the patient? s infirmary room and asked her hubby and sister to go forth. He so ordered an addition in her morphia dose, but refused to corroborate the order in authorship. Within proceedingss the adult female was dead. Zylicz demanded an account from his co-worker. The other physician? s answer was, ? It could hold taken another hebdomad before she died. I needed the bed? ( Eads, 93 ) . For grounds like these, if a individual were to go handicapped without antecedently finishing a life will in a clear province of head, they should non be put to decease. Anyone that would genuinely wish to decease in that province would hold taken the enterprise to do his or her purposes clear before the disabling event took topographic point. As in all instances, the duty of the patient? s life should be up to a medical staff in concurrency with the patient and household. Undoubtedly, mercy killing can be ghastly and downright immoral if non managed with utmost duty, but groups in support of mercy killing still back up terminally sick patient? s option to decease with self-respect and regard. Euthanasia can be administered with positive effects every bit long as certain situational factors are ever considered. These factors include: the type of aid, the type of helper, the type of unwellness being dealt with, and the age of the patient. Furthermore, mercy killing or assisted self-destruction should merely be a last ditch attempt after optimum alleviative attention has been administered. Euthanasia, which means? good decease? in Greek, became a universe fame motion launched by a famed 1973 instance of a physician who helped her female parent dice and so was acquitted of condemnable charges ( Branegan, 31 ) . Since so it has been praised and protested all around the universe, the United States is a particular instance though. In the land of life, autonomy, and the chase of felicity, I ab initio assumed that this should non truly be an issue. Regardless of race, faith, colour, or credo, everyone in this state should hold the right to do their ain determinations sing their quality of life and where it is heading. A instance in point of where mercy killing may be accepted comes in the undermentioned narrative: On her eighty-fifth birthday, Virginia Eddy celebrated with her household at a party with all the fixingss. Then, her boy wrote, # 8220 ; She relished her last piece of cocoa, and so stopped eating and drinking. # 8221 ; Her boy arranged for her to be placed on a self-administered morphia trickle to alleviate the hurting of desiccation. She died six yearss subsequently. # 8220 ; This decease was non a sad decease ; it was a happy decease, † Eddy wrote. â€Å"She had done merely what she wanted to make, merely the manner she wanted to make it? ( Euthanasia.com ) . Harmonizing to Eddy, his female parent had chosen the clip and mode of her decease and this had been a positive experience for the full household. # 8220 ; Although we will lose her greatly, her ability to accomplish her decease at the right clip and in her right manner transformed for us what could hold been a desolate and devastating loss into a clip for joy? ( Euthanasia.com ) . Obviously, this adult male genuinely cared for his female parent and her well being, merely as any boy would. Another presentation of where mercy killing worked out in the best involvement of the patient and household can be found a narrative of merely holding the option of mercy killing available to them. When Annemie Douwes Dekker? s hubby Hink was foremost told he had multiple induration in 1978, his household physician agreed to discourse the possibility of mercy killing when the clip of all time came to earnestly see it. ? That was a great aid to us, ? Annemie recalled ( Choice in deceasing ) . Five old ages subsequently Hink, now 50 old ages old, had been in a nursing place for a twelvemonth and was deteriorating quickly, losing his abilities to pass on and command bodily maps. His widow, now sixty-two, says, ? he had a strong bosom ; he could hold gone on life for years. ? When Hink originally requested to be put to decease he was denied, but after multiple months and multiple petitions he came place from the nursing place to be with his household and was administered toxicant by a physician. ? I? m convinced we did the right thing, ? said Annimie, ? He died a good decease? ( Choice in deceasing ) . Personally, I prefer to believe that human factors change society, non that society changes the human factor. The pick of mercy killing is a particular thing, and is a determination that belongs to persons and their effects. Courts and legislative assembly truly have no portion in doing this an illegal or legal issue ( The right to take to decease, 15 ) . Although it is widely believed that mercy killing is incorrect under any conditions due to religion, many people are non spiritually strong plenty to manage a terminal unwellness such as malignant neoplastic disease or multiple induration in its concluding phases. I am personally comfy with the place of my faith, but that does non blind me to the retching worlds and soul-searching involved in mercy killing determinations. If a terminally sick patient in great hurting makes an informed pick to decease and inquire for the aid of a loved one or a long-time personal doctor, that should non be publically viewed as a job. It shouldn? T be incorrect to make it for person? s female parent if it were her deceasing wish. When doing a determination that entails the expiration of a life, it should be left up to the patient or the patient? s life will to show what minimum quality of life would be acceptable to that person. The position this paper has taken is non to state that mercy killing or assisted self-destruction should be level out legal, but instead that it should be accepted by the populace in regard of those who suffer more than they can manage and wish to set it to an terminal. In order to pull off these instances efficaciously there should be restrictions to the types of instances that receive this signifier of intervention. Much like the guidelines put together by the Royal Dutch Medical Association in 1984, the patient? s status should be one of? intolerable agony that can non be relieved, and the patient must freely bespeak to decease. When a patient does inquire, the physician should non continue without confer withing another independent doctor. Then each instance must be reported as an? unnatural decease? to local functionaries? ( Eads, 95 ) . In add-on to these guidelines I propose the patient should besides hold to supply cogent evidence beyond a sensible uncertainty that he or she would hold made this determination in a stable psychological province. I besides feel the patient and immediate household should see a psychologist on at least two separate occasions before the mercy killing takes topographic point to guarantee that the purposes are within acceptable bounds. Finally, physicians who violate these guidelines before supplying their services should hold to confront anything up to first-degree slaying charges. When I foremost chose to look into this subject I was merely concerned that Americans should be given the right to decease if it is their wish to make so. After all of my research and analyzing of resources I have been enlightened that this truly isn? t merely about rights. This issue is truly about the strength of people? s spiritual will to populate. I have seen narratives of people paralyzed from the cervix down, had both of their legs amputated, but have still been satisfied with their quality of life. On the other manus, there are people that could hold been in a comatose province for less than a twenty-four hours and wake up somewhat encephalon damaged but non hold the will to try a recovery. Neither mentality on mercy killing should needfully hold a publically moral significance inferior to the other to anyone on the outside universe, but merely to the patient. Most significantly, irrespective of the concluding determination, the patient should hold the option to do that critical determination and their overall mentality on the quality of life will do the difference between a pick for life or decease. Without this option, the members our ain households may endure someday more than anyone would of all time desire to see them hold to. Branegan, Jay. ? I want to pull the line myself. ? Time. 17 March 1997: 30-31. Choice in deceasing. Partnership for Caring Inc. 12 May 1997. Eads, Brian. ? A licence to kill. ? Reader? s Digest. Sep. 1997: 93-97. Euthanasia.com. 19 January 2000. Not Dead Yet. Ed. Stephen Drake. 12 May 1997. ? The right to take to die. ? The Economist. 21 June 1997: 15-16. Rosenblatt, Stanley M. Murder of Mercy: mercy killing on test. New York: Prometheus Books, 1992. Tada, Joni Eareckson. When is it right to decease? Michigan: Zondervan Publishing House, 1992. Plants Consulted ? Death by Doctor. ? By Mike Wallace. 60 Minutes. CBS. 22 November 1998. MacDonald, William L. ? Situational factors and attitudes toward voluntary euthanasia. ? Social Science A ; Medicine. Jan. 1998: 73-81. ? Mercy or Homicide? ? By John Donovan and Forrest Sawyer. ABC Nightline. ABC. 23 November 1998 Rollin, Betty. ? Last Rights. ? Ms.. Aug./Sep. 1999: 31. Will, George F. ? Life and Death at Princeton. ? Newsweek. 13 September 1999: 80-82.

Free Essays on What Is Humes Problem Of Induction

What is Hume’s problem of induction? How successful is his sceptical solution to the problem? David Hume was born in 1711 and studied at Edinburgh University, his influences were great natural scientists like Isaac Newton and Rene Descartes. Hume first wrote â€Å" a treatise of Human nature â€Å" which as Hume put it â€Å"fell stillborn from the press† it was â€Å"An enquiry concerning human understanding† (from here this will be referred to as â€Å"the enquiry†) in which Hume put forward, in the form we are concerned with, the problem of induction and his own response to that problem. Although as we shall see his own response may be far from adequate. This essay is concerned with explaining Hume’s problem of induction as put forward in the enquiry, and explaining his sceptical solution to this problem. The essay is also concerned with assessing how successful his solution is. Arguably Hume’s most famous contribution to philosophy was the problem of induction. The problem of induction arises from Hume’s belief that propositions fall into one of two categories, relations of ideas and matters of fact. It is in the latter of these two categories, matters of fact that the problem of induction occurs. It was Hume’s view that matters of fact are statements about the world, justification for their validity comes from experience. This is fine for the present or past but it is the future that throws up the problem of induction. How can we justify expectations of the future? Or to put it another way how can we justify the belief that we know what will occur in unobserved events. If we use the same method as for the present and the past i.e. experience then we are assuming that nature will stay the same. But as Hume points out it is conceivable that nature will change in some way, therefore in Hume’s philosophy it is possible that nature will change, therefore you cannot justify beliefs about the future using past experien... Free Essays on What Is Hume's Problem Of Induction Free Essays on What Is Hume's Problem Of Induction What is Hume’s problem of induction? How successful is his sceptical solution to the problem? David Hume was born in 1711 and studied at Edinburgh University, his influences were great natural scientists like Isaac Newton and Rene Descartes. Hume first wrote â€Å" a treatise of Human nature â€Å" which as Hume put it â€Å"fell stillborn from the press† it was â€Å"An enquiry concerning human understanding† (from here this will be referred to as â€Å"the enquiry†) in which Hume put forward, in the form we are concerned with, the problem of induction and his own response to that problem. Although as we shall see his own response may be far from adequate. This essay is concerned with explaining Hume’s problem of induction as put forward in the enquiry, and explaining his sceptical solution to this problem. The essay is also concerned with assessing how successful his solution is. Arguably Hume’s most famous contribution to philosophy was the problem of induction. The problem of induction arises from Hume’s belief that propositions fall into one of two categories, relations of ideas and matters of fact. It is in the latter of these two categories, matters of fact that the problem of induction occurs. It was Hume’s view that matters of fact are statements about the world, justification for their validity comes from experience. This is fine for the present or past but it is the future that throws up the problem of induction. How can we justify expectations of the future? Or to put it another way how can we justify the belief that we know what will occur in unobserved events. If we use the same method as for the present and the past i.e. experience then we are assuming that nature will stay the same. But as Hume points out it is conceivable that nature will change in some way, therefore in Hume’s philosophy it is possible that nature will change, therefore you cannot justify beliefs about the future using past experien...

Naturalism Research Paper Example | Topics and Well Written Essays - 1000 words

Naturalism - Research Paper Example In trying to understand nature and seek explanations of natural processes, naturalists use science as their main resource. Some people believe that science and religion are very different and irreconcilable as science is based on rationality as opposed to faith which is irrationality. Other people believe that naturalism is the home of reconciliation between science and religion with yet some irreconcilable discrepancies showing conflict between naturalism and science. Evolution is the scientific explanation of the origin of life in nature that was proposed by Charles Darwin and it remains one of the most contentious and hotly debated issues in religious naturalism. This paper will explore naturalism in religion with a bias in evolution as put across by science and scientific theory of evolution and natural selection. First, the paper will have a brief description of naturalism and then have a look at evolution and the controversies surrounding the evolutionary theory. Naturalists ca n be described as pragmats who have their basis of reality in empirical logic and do not consider testimony as a source of truth of reality (Anderson 111). All the conscious differentiations of reality are based on the way that human beings identify the various qualities of world experience and how they think and reason about them. The natural world is the centre of the most significant experience and understanding of nature and thus it is the most valuable thing in the assessment of an individual’s well being. The idea of a supreme being is considered to have no grounds and everything is approached from a rational point of view and the harmony of reason and our understanding of the universe as informed by science (Griffin 56). Naturalism is presumably not a religion as such as it stands but it plays a vital role just like a religion does which is that of giving adherent to a world view. It provides explanations of why thing happen the way they happen, it tells us what fundam entally the world is and what is important in the world and the essence of human life and general life in the world. This is to a great extent what other religions do except for a few differences which might arise from worship and rituals which are not necessarily part of naturalism. There have been concerns whether theology is compatible with naturalism which has often elicited different responses and controversies. Theology and naturalism are compatible but not all forms of naturalism are compatible with theology as it is both the science about God and also the science about the human experience of God’s manifestation in individual life, the society or nature (Francis, Robbins & Astley 95). With science being the underpinnings of naturalism as it provides the explanations for the fundamental structure of the universe, one may think that the theory of evolution is one of the major pillars in naturalism. The theory of evolution which was put forward by Charles Darwin stipulat es that all life in the universe is related and share a common ancestry. It further says that life originated from non life with more complex organisms forming out of more simple organisms and that human beings have an animal descent (Smith 3). The theory puts it that more complex organism evolve from simple organisms over a long period of time and that there are mutations that occur on the genetic makeup of organisms that may favour their survival in a process called natural selection (Smith 4). This

Industry Report OR Design of a Performance Essay - 1

Industry Report OR Design of a Performance - Essay Example The improvement is not restricted to any individual employee; a performance management process locates the performance of whole team and ensures versatile improvement. Performance management can reveal the current position and skills of employees and areas where employees need to be developed. The research paper will describe and analyze the performance management system and good business practices of one healthcare organization in UAE, named RAK Hospital. In hospital industry the performance of employees are vital for company’s success. It can ensure good customer satisfaction and create a good image of company. This paper will describe the good business practices of RAK Hospital which is one the reasons for its success. Further, it will recommend the possible solutions which can improve the performance management system in RAK Hospital. ... Office of Personnel Management, n.d.) Performance management is defined as a continuing procedure of communication that is commenced by an employee and his immediate boss. Through performance management an employee can recognize the essential task that the company expects from him and how the task of the employee can contribute to the mission and objectives of the company. Performance management can ensure to improve the performance of employees in case any employee is performing below the desired level of efficiency or replicating similar mistakes (Bacal, 1999). To mange the performance efficiently it requires an understanding of the framework in which the performance management procedure occurs. The performance management procedure must be initiated along with keeping in mind the strategic goals and core values of the company. It is important for any company to select the right employee into the system (Cardy & Et. Al., 2011). The performance management process includes planning, m onitoring, developing, rating and rewarding. Source: (U.S. Office of Personnel Management, n.d.). These five components can make a successful performance management. RAK Hospital RAK is one of the superior hospitals of the Middle East nation UAE. The hospital was established by the joint venture between government of ‘Ras Al Khaimah’ and ‘ETA Star Healthcare’ in Dubai city. ETA Star Healthcare has a medical library in Dubai city and it is active in the business of medicinal, diagnostic and imaging tools. The RAK hospital is sponsored by Arabian Healthcare. The design of the hospital is developed by Eller Becket which is one of the top engineering, interior design and manufacture companies of the US. This hospital provides variety of premium rooms with a capacity of 65 beds,

Production and Cost Relationships Essay Example | Topics and Well Written Essays - 1500 words

Production and Cost Relationships - Essay Example Profit is measured as the difference between the revenue generated deducted with the costs incurred. Thus, in order to maximize profits, the company could either ensure that it is generating the highest revenue possible by increasing price and quantity demanded or minimize the costs that it incurs (Pindyck and Rubinfeld 2005). This paper will focus on the latter. The following chapters will look at the relationship of average cost, marginal cost, and marginal product in the aim of helping a business organization attain its goal of profit maximization. In the course of its operation, a business organization incurs various costs in order to ensure that products are designed, manufactured, and distributed to customers (Cepeda 2005). In order to understand average total cost, it is best to have a comprehension of what comprises the total cost that a business organization faces. In general, the company is faced with two different costs which make up its total cost namely fixed cost and variable cost (Brue and McConnell 2005). Fixed cost, as the name implies is fixed and does not vary with the level of production. An example of fixed cost is the payment for rent of production plant or retailing store. On the other hand, variable costs are those costs which changes when the quantity of production is changed (Cepeda 2005). Examples of these are the cost of materials and labor which are needed in the production of one unit of a product. The sum of the total fixed cost and the total variable cost is the total cost. Dividing the total cost with the number of quantity produced by the business organization will yield the average total cost (Brue and McConnell 2005). Table 1. Numerical Example for Average Total Cost Quantity Total Fixed Cost Total Variable Cost Total Cost Average Total Cost 50 $600 $1250 $1850 $37 100 $600 $2500 $3100 $31 150 $600 $3750 $4350 $29 200 $600 $5000 $5600 $28 250 $600 $6250 $6850 $27.4 300 $600 $7500 $8100 $27 In order to illustrate fixed cost, it is best to come up with a numerical example. Suppose that a company manufactures figurines and incurs fixed cost as follows in a month: $200 for building rent; $300 for administrative expense; and $100 for utilities. On the hand, it incurs the following variable cost per unit: $10 direct material and $15 direct labor. The company's production capacity is 300 units per month. Table 1 shows the company's variable cost and fixed cost at each level of quantity produced. On the other hand, Figure 1 shows the short run average total cost curve. It should be noted that as the quantity produced is increased, ATC declines because of economies of scale, managerial specialization, and use of more efficient labor. Figure 1. ATC Curve in the Short-run However, in the long run, ATC curve will begin to inflect because of the diseconomies of scale as production expands further (Pindyck and Rubinfeld 2005). Thus, the long run ATC curve will tend to slope downward at first and begin to

Analysis of SAMe as an Antidepressant

Analysis of SAMe as an Antidepressant S-Adenosyl-Methionine (SAMe) And Improved Methylation Offer A Serious Alternative To Orthodox Medications Can S-Adenosyl-Methionine (SAMe) and improved methylation offer a serious alternative to orthodox medications in the treatment of depression? Abstract In this dissertation we consider the issues surrounding the use of SAMe as an antidepressant. There are many different aspects to this consideration. We start by a consideration of exactly what depression is on a clinical basis and examine the psychological and physiological changes that characterise the condition. We then consider and examine the evolution of the current forms of antidepressant medication. We explore the fields of neurochemistry and pathophysiology of depressive states with particular emphasis on the chemistry of the methylation reaction and its relevance to the SAMe compound. Consideration is then given to SAMe specifically as a medication and the evidence that there is to support its apparent beneficial effect in depression. This is then expanded with a review of the chemistry of SAMe and its interactions with other biologically active entities. We conclude the exploration with a critical review of the published literature that is relevant to the role of SAMe as an antidepressant agent. Introduction In order to investigate the full extent of the question at the heart of this dissertation we must examine a number of background issues in some detail first. Depression is a complex clinical state. It has been said that there are as many theories about the aetiology and treatments for depression as there are clinicians thinking about the problem. (LeDoux, J. 1996). A brief examination of the literature on the subject tells us that this comment, although clearly intended to be flippant, may not actually be so very far from the truth. Perhaps it is because of the plethora of hypotheses, ideas and theories on the issue that there are also a considerable number of forms of treatment that are commonly employed. It has to be admitted that some are rational and some appear to be completely irrational. In this dissertation we shall examine some of the more rational forms of psychopharmacology in order to understand the place of SAMe in the therapeutic pharmacopoeia. Depression is a commonly occurring illness. It will significantly affect between 10-25% of women and approximately half that number of men during their lifetimes. Approximately 5 million people in the UK will experience significant depression in any given year. (Breggin 1994) If you suffer from an acute or chronic illness you are even more likely to suffer from depressive states with frequencies ranging from 30-50% depending upon the nature and severity of the illness. (Robertson et al 1997) What is depression ? There are many definitions of clinical depression and indeed many different rating scales which purport to try to quantify it. It is important to distinguish between clinical depression and simply feeling down or miserable. Depressive illness typically occurs in episodes although in some cases it can actually last for many months or even years. (Skolnick, P. 1999). One severe depressive episode is a major independent risk factor for getting further episodes. In other words, having had depression once you are statistically considerably more likely to have another attack. (Post RM. 1992). For our purposes we shall consider a practical overview of the nine classic symptoms that characterise classical depression 1. Depressed mood for most of the day 2. Disturbed appetite or change in weight 3. Disturbed sleep 4. Psychomotor retardation or agitation 5. Loss of interest in previously pleasurable activities; inability to enjoy usual hobbies or activities 6. Fatigue or loss of energy 7. Feelings of worthlessness; excessive and/or inappropriate guilt 8. Difficulty in concentrating or thinking clearly 9. Morbid or suicidal thoughts or actions. (After Zuess 2003) The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) states that in order to merit a diagnosis of clinical depression you need to demonstrate at least five of these symptoms and that they represent a change in your life. Mood alterations are commonplace in depressive states. The depressed patient will classically feel despair or sadness. Pleasure becomes an alien emotion as they tend to progressively loose interest in activities that they would have previously enjoyed. Mood swings can also occur although they are more commonly found in bipolar states (manic depression). Subjective feelings of tension or irritability are often described as well as just sadness. (Duman et al 1997) In addition to mood changes, depression can also produce changes in the emotional state as well. Feelings of worthlessness and guilt are perhaps the commonest emotions in the clinical spectrum. This is closely followed by both ineptitude and lack of confidence in ones own abilities or capabilities. It is common for depressed people to take action that avoids them having to take responsibility because of an overwhelming fear of failure. (Altar CA 1999) Somatic manifestations of depression are perhaps easier to quantify as they have a qualitative characteristic about them as opposed to the purely subjective. Changes in appetite are commonly found. Generally it is an anorexic change with a decrease in appetite and a loss of interest in food generally. Less frequently, the converse is observed with a voracious increase in appetite (comfort eating) which is normally associated with weight gain. This weight gain can be quite substantial in extreme cases. Sleep disturbances are commonplace. Insomnia and early waking are perhaps the commonest of this type of symptom. This can occur despite severe subjective symptoms of somatic tiredness and fatigue. Some people will find that fatigue is a prominent symptom and may find that this is translated into excessive sleeping and motor retardation generally. Fatigue is actually more difficult to quantify, but it is commonly experienced by the depressed patient. It can either be an overwhelming tiredness (lack of energy) or perhaps lack of stamina (tiring too easily). Associated with this is often a reduction in libido and, if severe, impotence can also occur. It is not unusual to find sexual avoidance behaviours developing in these circumstances. (Janicak et al 1989) Concentration is commonly impaired. Generally speaking the greater the degree of depression, the greater is the degree of concentration impairment. Thinking and reasoning processes slow down and the attention span is often markedly reduced. Students find they can have an inability to study and if severe, patients report an inability to even sit and watch television. (Bazin et al 1994) Somatic symptoms can occur without the psychological elements of the depression being apparent or obvious. This is a common clinical dilemma. Patients may enter a phase of denial or minimisation where they will not accept that they are actually depressed. They can try to rationalise their physical symptomatology into other disease processes. This can be mistaken for hypochondriasis. (De Vanna et al 1992) If depression is severe (or occasionally part of a symptom complex of another underlying pathology), then psychosis can be found. Delusional states are not uncommon in severe depression. Hallucinations can occur, but they are comparatively unusual. Patients can state that they hear voices telling them that they are worthless or perhaps instructing them to kill themselves. Although this is consistent with a depressive diagnosis, one should note that other illnesses such as schizophrenia must clearly be considered and excluded before a confident diagnosis of depression can be made. The actual basis or specific triggering factors for depression are not yet clearly defined but we do know that a number of different biological factors are relevant. Environmental factors, together with both genetic and neurobiological elements are all capable of influencing the overall clinical picture. (Kendler KS, 1998). Depression is broadly divided into endogenous and reactive types. In general terms endogenous depression is thought to be influenced the genetic and neurobiological factors whereas reactive depression may well have environmental factors as being relevant. This has considerable implications in our considerations of the possible actions of SAMe. (Gold et al 1988) Pharmacology of depression This is a vast subject and is generally considered to be a sub-speciality in its own right. It has long been recognised that certain substances appear to be able to exert a mood elevating effect. The advent of modern psychopharmacology allowed us to develop an understanding into just how some of these substances work. The drugs and medicines that are in common use today are the result of a process of evolution that, arguably, began with the uses of herbs at the beginning of recorded history and progressed to the chemically and biologically sophisticated compounds that are in use today. (Peinell and Smith 2003) In order to put the SAMe compounds into their appropriate place in the continuum we need to look at some of the evolutionary developments in the field. Most of the currently used antidepressants work by interfering in some way with the actions of the various neurotransmitters in the brain. Many work by slowing down the biological processes of degradation or destruction of these neurotransmitters. In purely simplistic terms, this results in a greater concentration of the neurotransmitter at the critical synaptic interfaces within the brain. (Levine et al 1998) The first real breakthrough with what could be considered to be a major therapeutic agent for depressive states came with the discovery of the MAOI (Monoamine Oxidse Inhibitors), group of drugs. Three were commonly used in clinical practice isocarboxazid, phemelzine and tranlcypromine. For a while they were used extensively but it became obvious that they had serious drawbacks including some potentially fatal side effects. (Saarelainen et al 2003), Headaches dizziness and tremor were not unusual accompaniments of the drug. They also had the ability to interact with other medications and certain types of food (tyrosine containing foods such as cheese could cause hypertensive crises). Despite these drawbacks, many patients were willing to take them because they indisputably worked. (Skolnick 1999) In time, the MAOis were superseded by the Tricyclic group of drugs. There were four in common use, namely amitriptyline, desipramine, imipramine and nortriptyline. These were generally speaking, marginally more effective than the MAOIs but they were without the worst of the side effects. Despite that, they were still able to cause dry mouth and blurred vision in some people. Constipation and drowsiness were not unusual and they were not commonly used if a person also had hypertension. The pharmaceutical industry then produced a number of different categories of medication in fairly quick succession. SSRIs (Selective Serotonin Reuptake Inhibitors), SNRIs (Serotonin and norepinephrine reuptake inhibitors) and NDRIs (Norepinephrine and dopamine reuptake inhibitors) all emerged into the market place. (Smith et al 2004) It is probably fair to say that they all had their niches in the therapeutic spectrum but the SSRIs were seen to corner the biggest share of the clinical market with citalopram, escitalopram, fluoxetine, paroxetine and sertraline as examples of the group. Fluoxetine was probably the most widely used and its trade name, Prozac was accepted almost as a household word. The side effect profile of this particular group was certainly less significant than their predecessors, but nausea and headaches were not uncommon. (Stewart et al 2000), The SNRIs fell into disuse largely because of their reputation in raising cholesterol levels and the NDRIs were found to cause unacceptable agitation in certain groups. There was then an emergence of a group of drugs which not only blocked the mechanisms that removed the trophic neurotransmitters from the synapse they also had an effect which effectively enhanced their action by blocking the action of the inhibitory neurotransmitters at the same time. There are several types of medication in this category, but perhaps the best known is maprotilene. Like most of the other types of effective medication, it is not without side effects. Drowsiness, nausea, dizziness and a dry mouth are common accompanying symptoms of a therapeutic dose of this medication. (Harmer et al 2003) Neurochemistry and pathophysiology of depression So far we have take a brief and admittedly comparatively simplistic tour of the nature and pharmacology of depression. We shall now look at the neurochemistry and pathophysiology of certain relevant aspects of the subject in more detail. In general terms, stress and antidepressants appear to have reciprocal actions on neuronal growth and to some extent, on their activity (see on). This appears to be through the mediation of various neurotrophins and the action of synaptic plasticity mainly in the region of the hippocampus and some other brain structures (Reid et al 2001). Various stresses appear to disturb and disrupt the activity, both of individual neurones and also larger functional groups, or networks of neurones whereas antidepressants appear to antagonise this disruptive ability. (Henke 1990) There is a large body of opinion which agrees with the hypothesis that regulation of synaptic activity is a major key to the pathophysiology of depression and related disorders. (Drevets et al 1997) The discovery of the MAOI group of drugs (above) led researchers to speculate that the monoamine group of neurotransmitters were central to the aetiology of depression. As more research is done it is becoming apparent that this may not actually be the case. It is now considered more likely that the fundamental problems lie further along the metabolic cascade from the monoamine oxidase activity. It is also considered likely that the pathology may well not be just a chemical imbalance, but may well involve other functions of neural tissue such as various cellular changes in physiology, genetic factors and the ability of neuronal network to change their characteristics. (Czyrak et al 1992) Observational studies have suggested that early life experiences, the impact of stress and the presence or absence of social support or interactions all have an influence on the development of a depressive state. (Gould et al 1998).Consideration of the monoamine chemistry clearly does not account for all of these factors although it is clearly acknowledged that it does play an important contributory role. Some recent work relating to the chronic use of different classes of antidepressants (Duman et al 1997), has appeared to show that they all are able to increase the production of the neuroprotective groups of proteins which, amongst other actions, play a central role in the plasticity of neurones. Current thinking is that this may well be a common function of a number of different pathways that the different antidepressants exploit. It is known that increases in monoamine levels in the synaptic region result (by a number of different mechanisms) and are associated with the induction of enzyme systems that control gene expression within the neurone. This can be inferred from the finding of increases in the levels of messenger RNA which codes for the cAMP response element binding protein (CREB). These levels slowly increase with chronicity of administration of antidepressants and this mechanism may well account therefore for the commonly observed slow and progressive onset of action of most of the antidepressant drugs. It is proposed that CREB triggers the production of BDNF (Brain Derived Neurotrophic Factor). This is significant since other work has shown that stress antagonises the levels of BDNF which is opposed by the actions of the antidepressant drugs. (Smith et al 1995). Further credence is given to this theory with the discovery that placing BDNF directly into the brain of experimental animals appeared to relieve many of the behaviour patterns that are associated with depression (Siuciak et al 1997) Some authors have suggested that depression may represent a particularly subtle form of neural degenerative disorder as it has been shown that the hippocampus becomes progressively atrophic in chronic depressive states. This is particularly significant as BDNF is thought to reverse such findings. (Shah et al 1998). There is associated supporting evidence in the form of a study by Vaidya (et al 1999) which shows that ECT treatment (which was always assumed to be detrimental to the neural structure and physiology) is associated with both increased levels of BDNF and trophic changes in the hippocampal neurones. A paper by Czyrak (et al 1992) looked at the antidepressant activity of SAMe in mice and rats in a way that clearly is not possible in humans. It is not always possible to directly extrapolate findings from animals to humans, but there are some pieces of evidence in this work which strongly implicate SAMe in the pathogenesis of depression. The paper itself is extremely long and complex but the relevant parts to our considerations here are the fact that normal geographical exploratory behaviour in rodents tends to diminish if a depressive state is induced. To some extent, exploratory behaviour is therefore considered a marker for the depressive state. It was found that SAMe tended to increase exploratory activity in mice. This, and other more sophisticated testing of the pharmacological interactions of SAMe showed that it tended to have the same psychopharmacological profile as many of the mainstream antidepressants. Many of the neurotransmitters and for that matter some neuroactive hormones have been variously implicated in the aetiology of depression (eg thyroid hormones and noradrenaline). (Nemeroff, 1998). Modern research has most consistently found that alterations in the levels of serotonin (5-HT) (Melzter H, 1989), system and the chemicals of the Limbic Hypothalamic-Pituitary-Adrenal (LHPA) axis. (Kathol et al 1989), as the most consistently implicated mechanisms that appear to be associated with the control of the mood stabilising and regulating mechanisms. It is in fact very likely that both these mechanisms are in some way interlinked as part of the regulatory mechanism of mood. We have already referred to the role of stress in the aetiology of depression. We know that the adrenal glucocorticoid hormones subtly interact with the 5-HT system and these are produced in direct response to stress. (Lopez et al 1999) (I). We also know that the glucocorticoids have a number of direct effects on the Limbic Hypothalamic-Pituitary-Adrenal (LHPA) axis. It may be that this is the mechanism by which stress antagonises the changes brought about by SAMe. (Lopez et al 1999) (II) We do not need to consider the effects of the corticoids on the LHPA axis in detail as it is only of peripheral relevance to our considerations here. The important consideration in this regard is that the LHPA axis is intimately connected to the hippocampus. It is this structure that is the intermediate step and connection between the bodys hormonal response to stress and the response of the higher functions of the brain. (Dallman et al 1987). The immediate relevance of all this to the actions of SAMe are that hyperactivity of both the hippocampus and the LHPA axis are both well documented in cases of clinical depression. This has been shown to also be associated with high levels of corticosteroid production (Kalin et al 1987), but one study has shown that in suicide cases who have had profound depression the hippocampus has fewer corticosteroid receptor sites than one might normally expect (Lopez et al 1998). One further piece of clinical evidence in the role of the corticosteroids in depression is that patients with Cushings disease have a high incidence of depression. This incidence returns to normal when their hormonal over-activity is treated and returned back to physiological levels. (Murphy 1991) SAMe as a medication SAMe was discovered in Italy in 1952 during research into the chemistry of neurotransmitters. It was not, however, introduced in a useable form for patient benefit until 1974 (as SAMe sulphate-paratoluene-sulphonate). It is for this reason that the majority of the early papers and work on the subject are almost exclusively Italian in origin. (De Vanna et al 1992) SAMe has been used clinically in a number of conditions including cholestasis, osteoarthritis and depression. (Carney et al 1987) Although there is a wealth of literature on the first two elements it is not relevant to our considerations here. We shall therefore restrict this discussion to the spectrum of its use in the field of depression. A number of studies have shown that SAMe has useful activity in depressive illness. Studies that have compared it to placebo have found that it can consistently produce about a 6 point increase on the Hamilton rating scale after about three weeks of optimum treatment. This finding is approximately in line with the results that are found with most of the other clinically effective antidepressant medications. (Cooper et al 1999) (De Vanna et al 1992) Some studies have found that using SAMe in a large dose has produced an unusually rapid onset of beneficial effects (Kagan 1990) One could argue that, because it is a naturally occurring substance, it would not be likely to have a high side-effect profile. Although these two statements do not always follow, it is generally true. A study by Bressa (1994) on the issue showed that it did have a particularly low side-effect profile, particularly when compared to the other antidepressants (Tricyclics). To demonstrate this point further, we can point to the study by Caruso (et al 1987) where there were a greater number of patient withdrawals due to the side effects of the placebo than withdrew because of the SAMe drug. For the record, that particular trial was in its use as an antiarthritic rather than an antidepressant, but the point is made. The two major unwanted clinical effects are nausea and hypomania. The nausea is not a local effect on the gut lining but appears to be a centrally mediated effect and is possibly caused by the same phenomenon of over-stimulation of the neuronal networks which causes the other major clinical manifestation of hypomania. For this reason it is generally not used in cases of bipolar disorder. (De Vanna et al 1992) It is probably not strictly accurate to refer to SAMe as a drug as it is normally found in the cellular matrix. It has been found to be effective in patients who have been unable to tolerate other forms of antidepressants or, for that matter, have had minimal response to them. (Reynolds et al, 1984) Young (1993) produced a particularly interesting review of dietary treatments for depression. A lot of his article is not relevant to our considerations here, but he makes a number of interesting and relevant observations. Low serotonin levels are known to be associated with depression even though low levels on their own do not appear to cause the condition. It appears that it needs to be in combination with a low level of folic acid. We know that low levels of folic acid are also often found in combination with depressive illness and that low levels of folate are often associated with low levels of SAMe. The evidence points to the fact that the low levels of serotonin are more likely to be a result of the low SAMe levels in neural tissue and that this is more likely to be nearer to the root of the main anomaly that causes depression. Pregnancy is known to be associated with low levels of folate and post natal depression is a well recognised clinical entity. Salmaggi (et al 1993) considered the effects of SAMe in the postnatal period. This was a well considered and constructed study. It was a double blind placebo controlled trial over a 30 day period and had an entry cohort of 80 women. The degree of depression was assessed before, during and after the trial on the Hamilton Scale. The results showed a statistically significant improvement in the SAMe group when compared to the placebo group. The authors comment that there were no significant side effects of the medication encountered. Because we know that any beneficial effect that SAMe is likely to have on a patient tends to be seen more quickly than with the other antidepressants, and also, by virtue of what we suspect about its probable mode of action in the hippocampus and elsewhere in the brain, it seems a logical step for someone to look into the effects of giving SAMe alongside a conventional antidepressants to see if there is either any synergistic effect or possibly a speeding up of the clinical onset of the secondary medication. The study by Berlanga (et al 1992) did exactly that. Unfortunately the trial was not particularly rigorous in its design as although it was double blind, it was not placebo controlled, which would appear to have been the method of choice in this type of investigation. Its other problem as that it only had an entry cohort of 40 patients. Despite these limitations it was indeed shown that depressed patients who took SAMe in conjunction with other antidepressant medication found that the depressive symptoms resolved faster with the SAMe added to their normal treatment regime. There are one or two other less important papers which we shall only mention in passing. Kagan (et al 1990) ran a small trial on 15 inpatients (with very severe depression) and found SAMe to be a safe, effective antidepressant with few side effects and a rapid onset of action. This particular trial is notable as it was the first to report the side effect of mania in a patient who didnt have a previous history. Another is the trial by Rosenbaum (et al 1990). This particular trial is notable for the demonstration of the fact that about 20% of other treatment resistant patients experienced benefit with SAMe. Faya (et al 1990) (II) considered the fact that SAMe is thought to exert its effect through its action in increasing dopamine levels in the synaptic cleft. It is known that dopamine inhibits the production of both Thyroid stimulating hormone (TSH) and Prolactin from the pituitary gland. Faya considered measuring the levels of both TSH and Prolactin during treatment with SAMe. His findings constituted something of a surprise insofar as in the men in the trial group had their levels of TSH and Prolactin reduced which is consistent with the hypothesis that SAMe increases the dopamine levels in the brain. Much to everybodys surprise, this effect was not seen in the female group. The authors do not offer any explanation of this fact. For the record, there is another trial (Thomas et al 1987), which obviously considered the same phenomenon and their trial did not show any sex linked difference in the suppression of the Prolactin levels With regards to efficacy, a trial by Carney (et al 1986) suggests that the beneficial action of SAMe is restricted to endogenous depression and it does not appear to have any action above placebo on reactive depression. As far as we can ascertain, this is the only trial published that has made this suggestion, although from a first principles basis, one can see the biochemical rationale for believing that it might well be the case. On a purely empirical grounds, some authors have recommended (on the basis of scant hard evidence), that SAMes action can be maximised by the addition of B12, B6 and folic acid. It is known that SAMe is required to convert these agents into their active form as a coenzyme. (Morrison et al, 1996). The same author also recommends the simultaneous adminstration of Trimethylglycine (TMG) which is necessary for the intracellular conversion of methionine into SAMe by the provision of the necessary methyl- groups. Comment has to be made that again, this appears to be a completely empirical (and logical) suggestion, but we cannot find any hard evidence to substantiate its clinical use. Chemistry SAMe is a basic component of cellular biochemistry. It occurs in every living cell and is second in importance only to ATP in both the number variety and significance of the reactions in which it serves as a cofactor. (Stramentinoli 1987). It is central in the chemistry of the transmethylation reactions. In essence its cellular function is to transfer the active methyl group form carrier molecules to a multitude of other molecules. In general terms, this methylation makes inert molecules biologically active. In addition to the transmethylation reactions it also plays a central role in transsulfuration and aminopropylation reactions It is involved in the synthesis of proteins including the nucleic acids, fatty acids, lipids and phospholipids, porphyrins and polysaccharides. In terms of our considerations here, perhaps the most significant reaction type that SAMe is involved in is the generation of the neurotransmitter amines. In this regard it is considered to be the most biologically significant provider of methyl groups within the cell. (Baldessarini 1987). Significantly it is also involved in the pathways to produce a number of other neurologically active compounds such as adrenaline, the neuronutrients acetyl l-carnitine and phosphatidyl choline (Mathews et al 1990) It is also to be found in the metabolic pathways of both serotonin and dopamine. Oral administration has been shown to increase the metabolites of these compounds in the CSF (implying increased turnover). It is thought to exert its antidepressive effect partly through the mechanism of increasing the levels of both dopamine and serotonin as neurotransmitters, but it also appears to have some form of trophic action on some of the neurones in the brain cortex. (Baldessarini 1987) It has been demonstrated that the tissue levels of SAMe tend to diminish with age and blood levels are also found to be low in some cases of clinical depression (Baldessarini 1987) A methyl group (CH3) is a group of three hydrogen atoms bound to one carbon atom. It does not exist in a stable isolated form and is transported between molecules by intermediaries such as SAMe. Methylation is the process by which this group is transferred from the methyl donor molecule to the recipient molecule. In general terms this process is central to the control of many of the intracellular pathways. Giving a methyl group to an enzyme is often the key to activating it, and thereby beginning a synthesis or degradation process elsewhere in the cell. Equally removing the methyl group will render the enzyme inactive and stop that particular pathway. Similar mechanisms are involved in the expression of genes and therefore the production of proteins within the cell. Some specific methylation reactions include the methylation of phenols which detoxify them and thereby aid in their excretion. (Stramentinoli 1987) In the context of this dissertation, methylation is also central to the metabolic chemistry of serotonin (and therefore also melatonin). The activity of both these compounds is effectively regulated by the presence of a methyl group. SAMe is synthesised from methionine, a naturally occurring amino acid. As the name implies (METH-ionine), it contains a methyl group. By utilising the energy supplied by ATP and in the presence of magnesium, it is converted into SAMe. The process is catalysed by the intervention of the enzyme MAT (methionine adenosyl Analysis of SAMe as an Antidepressant Analysis of SAMe as an Antidepressant S-Adenosyl-Methionine (SAMe) And Improved Methylation Offer A Serious Alternative To Orthodox Medications Can S-Adenosyl-Methionine (SAMe) and improved methylation offer a serious alternative to orthodox medications in the treatment of depression? Abstract In this dissertation we consider the issues surrounding the use of SAMe as an antidepressant. There are many different aspects to this consideration. We start by a consideration of exactly what depression is on a clinical basis and examine the psychological and physiological changes that characterise the condition. We then consider and examine the evolution of the current forms of antidepressant medication. We explore the fields of neurochemistry and pathophysiology of depressive states with particular emphasis on the chemistry of the methylation reaction and its relevance to the SAMe compound. Consideration is then given to SAMe specifically as a medication and the evidence that there is to support its apparent beneficial effect in depression. This is then expanded with a review of the chemistry of SAMe and its interactions with other biologically active entities. We conclude the exploration with a critical review of the published literature that is relevant to the role of SAMe as an antidepressant agent. Introduction In order to investigate the full extent of the question at the heart of this dissertation we must examine a number of background issues in some detail first. Depression is a complex clinical state. It has been said that there are as many theories about the aetiology and treatments for depression as there are clinicians thinking about the problem. (LeDoux, J. 1996). A brief examination of the literature on the subject tells us that this comment, although clearly intended to be flippant, may not actually be so very far from the truth. Perhaps it is because of the plethora of hypotheses, ideas and theories on the issue that there are also a considerable number of forms of treatment that are commonly employed. It has to be admitted that some are rational and some appear to be completely irrational. In this dissertation we shall examine some of the more rational forms of psychopharmacology in order to understand the place of SAMe in the therapeutic pharmacopoeia. Depression is a commonly occurring illness. It will significantly affect between 10-25% of women and approximately half that number of men during their lifetimes. Approximately 5 million people in the UK will experience significant depression in any given year. (Breggin 1994) If you suffer from an acute or chronic illness you are even more likely to suffer from depressive states with frequencies ranging from 30-50% depending upon the nature and severity of the illness. (Robertson et al 1997) What is depression ? There are many definitions of clinical depression and indeed many different rating scales which purport to try to quantify it. It is important to distinguish between clinical depression and simply feeling down or miserable. Depressive illness typically occurs in episodes although in some cases it can actually last for many months or even years. (Skolnick, P. 1999). One severe depressive episode is a major independent risk factor for getting further episodes. In other words, having had depression once you are statistically considerably more likely to have another attack. (Post RM. 1992). For our purposes we shall consider a practical overview of the nine classic symptoms that characterise classical depression 1. Depressed mood for most of the day 2. Disturbed appetite or change in weight 3. Disturbed sleep 4. Psychomotor retardation or agitation 5. Loss of interest in previously pleasurable activities; inability to enjoy usual hobbies or activities 6. Fatigue or loss of energy 7. Feelings of worthlessness; excessive and/or inappropriate guilt 8. Difficulty in concentrating or thinking clearly 9. Morbid or suicidal thoughts or actions. (After Zuess 2003) The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) states that in order to merit a diagnosis of clinical depression you need to demonstrate at least five of these symptoms and that they represent a change in your life. Mood alterations are commonplace in depressive states. The depressed patient will classically feel despair or sadness. Pleasure becomes an alien emotion as they tend to progressively loose interest in activities that they would have previously enjoyed. Mood swings can also occur although they are more commonly found in bipolar states (manic depression). Subjective feelings of tension or irritability are often described as well as just sadness. (Duman et al 1997) In addition to mood changes, depression can also produce changes in the emotional state as well. Feelings of worthlessness and guilt are perhaps the commonest emotions in the clinical spectrum. This is closely followed by both ineptitude and lack of confidence in ones own abilities or capabilities. It is common for depressed people to take action that avoids them having to take responsibility because of an overwhelming fear of failure. (Altar CA 1999) Somatic manifestations of depression are perhaps easier to quantify as they have a qualitative characteristic about them as opposed to the purely subjective. Changes in appetite are commonly found. Generally it is an anorexic change with a decrease in appetite and a loss of interest in food generally. Less frequently, the converse is observed with a voracious increase in appetite (comfort eating) which is normally associated with weight gain. This weight gain can be quite substantial in extreme cases. Sleep disturbances are commonplace. Insomnia and early waking are perhaps the commonest of this type of symptom. This can occur despite severe subjective symptoms of somatic tiredness and fatigue. Some people will find that fatigue is a prominent symptom and may find that this is translated into excessive sleeping and motor retardation generally. Fatigue is actually more difficult to quantify, but it is commonly experienced by the depressed patient. It can either be an overwhelming tiredness (lack of energy) or perhaps lack of stamina (tiring too easily). Associated with this is often a reduction in libido and, if severe, impotence can also occur. It is not unusual to find sexual avoidance behaviours developing in these circumstances. (Janicak et al 1989) Concentration is commonly impaired. Generally speaking the greater the degree of depression, the greater is the degree of concentration impairment. Thinking and reasoning processes slow down and the attention span is often markedly reduced. Students find they can have an inability to study and if severe, patients report an inability to even sit and watch television. (Bazin et al 1994) Somatic symptoms can occur without the psychological elements of the depression being apparent or obvious. This is a common clinical dilemma. Patients may enter a phase of denial or minimisation where they will not accept that they are actually depressed. They can try to rationalise their physical symptomatology into other disease processes. This can be mistaken for hypochondriasis. (De Vanna et al 1992) If depression is severe (or occasionally part of a symptom complex of another underlying pathology), then psychosis can be found. Delusional states are not uncommon in severe depression. Hallucinations can occur, but they are comparatively unusual. Patients can state that they hear voices telling them that they are worthless or perhaps instructing them to kill themselves. Although this is consistent with a depressive diagnosis, one should note that other illnesses such as schizophrenia must clearly be considered and excluded before a confident diagnosis of depression can be made. The actual basis or specific triggering factors for depression are not yet clearly defined but we do know that a number of different biological factors are relevant. Environmental factors, together with both genetic and neurobiological elements are all capable of influencing the overall clinical picture. (Kendler KS, 1998). Depression is broadly divided into endogenous and reactive types. In general terms endogenous depression is thought to be influenced the genetic and neurobiological factors whereas reactive depression may well have environmental factors as being relevant. This has considerable implications in our considerations of the possible actions of SAMe. (Gold et al 1988) Pharmacology of depression This is a vast subject and is generally considered to be a sub-speciality in its own right. It has long been recognised that certain substances appear to be able to exert a mood elevating effect. The advent of modern psychopharmacology allowed us to develop an understanding into just how some of these substances work. The drugs and medicines that are in common use today are the result of a process of evolution that, arguably, began with the uses of herbs at the beginning of recorded history and progressed to the chemically and biologically sophisticated compounds that are in use today. (Peinell and Smith 2003) In order to put the SAMe compounds into their appropriate place in the continuum we need to look at some of the evolutionary developments in the field. Most of the currently used antidepressants work by interfering in some way with the actions of the various neurotransmitters in the brain. Many work by slowing down the biological processes of degradation or destruction of these neurotransmitters. In purely simplistic terms, this results in a greater concentration of the neurotransmitter at the critical synaptic interfaces within the brain. (Levine et al 1998) The first real breakthrough with what could be considered to be a major therapeutic agent for depressive states came with the discovery of the MAOI (Monoamine Oxidse Inhibitors), group of drugs. Three were commonly used in clinical practice isocarboxazid, phemelzine and tranlcypromine. For a while they were used extensively but it became obvious that they had serious drawbacks including some potentially fatal side effects. (Saarelainen et al 2003), Headaches dizziness and tremor were not unusual accompaniments of the drug. They also had the ability to interact with other medications and certain types of food (tyrosine containing foods such as cheese could cause hypertensive crises). Despite these drawbacks, many patients were willing to take them because they indisputably worked. (Skolnick 1999) In time, the MAOis were superseded by the Tricyclic group of drugs. There were four in common use, namely amitriptyline, desipramine, imipramine and nortriptyline. These were generally speaking, marginally more effective than the MAOIs but they were without the worst of the side effects. Despite that, they were still able to cause dry mouth and blurred vision in some people. Constipation and drowsiness were not unusual and they were not commonly used if a person also had hypertension. The pharmaceutical industry then produced a number of different categories of medication in fairly quick succession. SSRIs (Selective Serotonin Reuptake Inhibitors), SNRIs (Serotonin and norepinephrine reuptake inhibitors) and NDRIs (Norepinephrine and dopamine reuptake inhibitors) all emerged into the market place. (Smith et al 2004) It is probably fair to say that they all had their niches in the therapeutic spectrum but the SSRIs were seen to corner the biggest share of the clinical market with citalopram, escitalopram, fluoxetine, paroxetine and sertraline as examples of the group. Fluoxetine was probably the most widely used and its trade name, Prozac was accepted almost as a household word. The side effect profile of this particular group was certainly less significant than their predecessors, but nausea and headaches were not uncommon. (Stewart et al 2000), The SNRIs fell into disuse largely because of their reputation in raising cholesterol levels and the NDRIs were found to cause unacceptable agitation in certain groups. There was then an emergence of a group of drugs which not only blocked the mechanisms that removed the trophic neurotransmitters from the synapse they also had an effect which effectively enhanced their action by blocking the action of the inhibitory neurotransmitters at the same time. There are several types of medication in this category, but perhaps the best known is maprotilene. Like most of the other types of effective medication, it is not without side effects. Drowsiness, nausea, dizziness and a dry mouth are common accompanying symptoms of a therapeutic dose of this medication. (Harmer et al 2003) Neurochemistry and pathophysiology of depression So far we have take a brief and admittedly comparatively simplistic tour of the nature and pharmacology of depression. We shall now look at the neurochemistry and pathophysiology of certain relevant aspects of the subject in more detail. In general terms, stress and antidepressants appear to have reciprocal actions on neuronal growth and to some extent, on their activity (see on). This appears to be through the mediation of various neurotrophins and the action of synaptic plasticity mainly in the region of the hippocampus and some other brain structures (Reid et al 2001). Various stresses appear to disturb and disrupt the activity, both of individual neurones and also larger functional groups, or networks of neurones whereas antidepressants appear to antagonise this disruptive ability. (Henke 1990) There is a large body of opinion which agrees with the hypothesis that regulation of synaptic activity is a major key to the pathophysiology of depression and related disorders. (Drevets et al 1997) The discovery of the MAOI group of drugs (above) led researchers to speculate that the monoamine group of neurotransmitters were central to the aetiology of depression. As more research is done it is becoming apparent that this may not actually be the case. It is now considered more likely that the fundamental problems lie further along the metabolic cascade from the monoamine oxidase activity. It is also considered likely that the pathology may well not be just a chemical imbalance, but may well involve other functions of neural tissue such as various cellular changes in physiology, genetic factors and the ability of neuronal network to change their characteristics. (Czyrak et al 1992) Observational studies have suggested that early life experiences, the impact of stress and the presence or absence of social support or interactions all have an influence on the development of a depressive state. (Gould et al 1998).Consideration of the monoamine chemistry clearly does not account for all of these factors although it is clearly acknowledged that it does play an important contributory role. Some recent work relating to the chronic use of different classes of antidepressants (Duman et al 1997), has appeared to show that they all are able to increase the production of the neuroprotective groups of proteins which, amongst other actions, play a central role in the plasticity of neurones. Current thinking is that this may well be a common function of a number of different pathways that the different antidepressants exploit. It is known that increases in monoamine levels in the synaptic region result (by a number of different mechanisms) and are associated with the induction of enzyme systems that control gene expression within the neurone. This can be inferred from the finding of increases in the levels of messenger RNA which codes for the cAMP response element binding protein (CREB). These levels slowly increase with chronicity of administration of antidepressants and this mechanism may well account therefore for the commonly observed slow and progressive onset of action of most of the antidepressant drugs. It is proposed that CREB triggers the production of BDNF (Brain Derived Neurotrophic Factor). This is significant since other work has shown that stress antagonises the levels of BDNF which is opposed by the actions of the antidepressant drugs. (Smith et al 1995). Further credence is given to this theory with the discovery that placing BDNF directly into the brain of experimental animals appeared to relieve many of the behaviour patterns that are associated with depression (Siuciak et al 1997) Some authors have suggested that depression may represent a particularly subtle form of neural degenerative disorder as it has been shown that the hippocampus becomes progressively atrophic in chronic depressive states. This is particularly significant as BDNF is thought to reverse such findings. (Shah et al 1998). There is associated supporting evidence in the form of a study by Vaidya (et al 1999) which shows that ECT treatment (which was always assumed to be detrimental to the neural structure and physiology) is associated with both increased levels of BDNF and trophic changes in the hippocampal neurones. A paper by Czyrak (et al 1992) looked at the antidepressant activity of SAMe in mice and rats in a way that clearly is not possible in humans. It is not always possible to directly extrapolate findings from animals to humans, but there are some pieces of evidence in this work which strongly implicate SAMe in the pathogenesis of depression. The paper itself is extremely long and complex but the relevant parts to our considerations here are the fact that normal geographical exploratory behaviour in rodents tends to diminish if a depressive state is induced. To some extent, exploratory behaviour is therefore considered a marker for the depressive state. It was found that SAMe tended to increase exploratory activity in mice. This, and other more sophisticated testing of the pharmacological interactions of SAMe showed that it tended to have the same psychopharmacological profile as many of the mainstream antidepressants. Many of the neurotransmitters and for that matter some neuroactive hormones have been variously implicated in the aetiology of depression (eg thyroid hormones and noradrenaline). (Nemeroff, 1998). Modern research has most consistently found that alterations in the levels of serotonin (5-HT) (Melzter H, 1989), system and the chemicals of the Limbic Hypothalamic-Pituitary-Adrenal (LHPA) axis. (Kathol et al 1989), as the most consistently implicated mechanisms that appear to be associated with the control of the mood stabilising and regulating mechanisms. It is in fact very likely that both these mechanisms are in some way interlinked as part of the regulatory mechanism of mood. We have already referred to the role of stress in the aetiology of depression. We know that the adrenal glucocorticoid hormones subtly interact with the 5-HT system and these are produced in direct response to stress. (Lopez et al 1999) (I). We also know that the glucocorticoids have a number of direct effects on the Limbic Hypothalamic-Pituitary-Adrenal (LHPA) axis. It may be that this is the mechanism by which stress antagonises the changes brought about by SAMe. (Lopez et al 1999) (II) We do not need to consider the effects of the corticoids on the LHPA axis in detail as it is only of peripheral relevance to our considerations here. The important consideration in this regard is that the LHPA axis is intimately connected to the hippocampus. It is this structure that is the intermediate step and connection between the bodys hormonal response to stress and the response of the higher functions of the brain. (Dallman et al 1987). The immediate relevance of all this to the actions of SAMe are that hyperactivity of both the hippocampus and the LHPA axis are both well documented in cases of clinical depression. This has been shown to also be associated with high levels of corticosteroid production (Kalin et al 1987), but one study has shown that in suicide cases who have had profound depression the hippocampus has fewer corticosteroid receptor sites than one might normally expect (Lopez et al 1998). One further piece of clinical evidence in the role of the corticosteroids in depression is that patients with Cushings disease have a high incidence of depression. This incidence returns to normal when their hormonal over-activity is treated and returned back to physiological levels. (Murphy 1991) SAMe as a medication SAMe was discovered in Italy in 1952 during research into the chemistry of neurotransmitters. It was not, however, introduced in a useable form for patient benefit until 1974 (as SAMe sulphate-paratoluene-sulphonate). It is for this reason that the majority of the early papers and work on the subject are almost exclusively Italian in origin. (De Vanna et al 1992) SAMe has been used clinically in a number of conditions including cholestasis, osteoarthritis and depression. (Carney et al 1987) Although there is a wealth of literature on the first two elements it is not relevant to our considerations here. We shall therefore restrict this discussion to the spectrum of its use in the field of depression. A number of studies have shown that SAMe has useful activity in depressive illness. Studies that have compared it to placebo have found that it can consistently produce about a 6 point increase on the Hamilton rating scale after about three weeks of optimum treatment. This finding is approximately in line with the results that are found with most of the other clinically effective antidepressant medications. (Cooper et al 1999) (De Vanna et al 1992) Some studies have found that using SAMe in a large dose has produced an unusually rapid onset of beneficial effects (Kagan 1990) One could argue that, because it is a naturally occurring substance, it would not be likely to have a high side-effect profile. Although these two statements do not always follow, it is generally true. A study by Bressa (1994) on the issue showed that it did have a particularly low side-effect profile, particularly when compared to the other antidepressants (Tricyclics). To demonstrate this point further, we can point to the study by Caruso (et al 1987) where there were a greater number of patient withdrawals due to the side effects of the placebo than withdrew because of the SAMe drug. For the record, that particular trial was in its use as an antiarthritic rather than an antidepressant, but the point is made. The two major unwanted clinical effects are nausea and hypomania. The nausea is not a local effect on the gut lining but appears to be a centrally mediated effect and is possibly caused by the same phenomenon of over-stimulation of the neuronal networks which causes the other major clinical manifestation of hypomania. For this reason it is generally not used in cases of bipolar disorder. (De Vanna et al 1992) It is probably not strictly accurate to refer to SAMe as a drug as it is normally found in the cellular matrix. It has been found to be effective in patients who have been unable to tolerate other forms of antidepressants or, for that matter, have had minimal response to them. (Reynolds et al, 1984) Young (1993) produced a particularly interesting review of dietary treatments for depression. A lot of his article is not relevant to our considerations here, but he makes a number of interesting and relevant observations. Low serotonin levels are known to be associated with depression even though low levels on their own do not appear to cause the condition. It appears that it needs to be in combination with a low level of folic acid. We know that low levels of folic acid are also often found in combination with depressive illness and that low levels of folate are often associated with low levels of SAMe. The evidence points to the fact that the low levels of serotonin are more likely to be a result of the low SAMe levels in neural tissue and that this is more likely to be nearer to the root of the main anomaly that causes depression. Pregnancy is known to be associated with low levels of folate and post natal depression is a well recognised clinical entity. Salmaggi (et al 1993) considered the effects of SAMe in the postnatal period. This was a well considered and constructed study. It was a double blind placebo controlled trial over a 30 day period and had an entry cohort of 80 women. The degree of depression was assessed before, during and after the trial on the Hamilton Scale. The results showed a statistically significant improvement in the SAMe group when compared to the placebo group. The authors comment that there were no significant side effects of the medication encountered. Because we know that any beneficial effect that SAMe is likely to have on a patient tends to be seen more quickly than with the other antidepressants, and also, by virtue of what we suspect about its probable mode of action in the hippocampus and elsewhere in the brain, it seems a logical step for someone to look into the effects of giving SAMe alongside a conventional antidepressants to see if there is either any synergistic effect or possibly a speeding up of the clinical onset of the secondary medication. The study by Berlanga (et al 1992) did exactly that. Unfortunately the trial was not particularly rigorous in its design as although it was double blind, it was not placebo controlled, which would appear to have been the method of choice in this type of investigation. Its other problem as that it only had an entry cohort of 40 patients. Despite these limitations it was indeed shown that depressed patients who took SAMe in conjunction with other antidepressant medication found that the depressive symptoms resolved faster with the SAMe added to their normal treatment regime. There are one or two other less important papers which we shall only mention in passing. Kagan (et al 1990) ran a small trial on 15 inpatients (with very severe depression) and found SAMe to be a safe, effective antidepressant with few side effects and a rapid onset of action. This particular trial is notable as it was the first to report the side effect of mania in a patient who didnt have a previous history. Another is the trial by Rosenbaum (et al 1990). This particular trial is notable for the demonstration of the fact that about 20% of other treatment resistant patients experienced benefit with SAMe. Faya (et al 1990) (II) considered the fact that SAMe is thought to exert its effect through its action in increasing dopamine levels in the synaptic cleft. It is known that dopamine inhibits the production of both Thyroid stimulating hormone (TSH) and Prolactin from the pituitary gland. Faya considered measuring the levels of both TSH and Prolactin during treatment with SAMe. His findings constituted something of a surprise insofar as in the men in the trial group had their levels of TSH and Prolactin reduced which is consistent with the hypothesis that SAMe increases the dopamine levels in the brain. Much to everybodys surprise, this effect was not seen in the female group. The authors do not offer any explanation of this fact. For the record, there is another trial (Thomas et al 1987), which obviously considered the same phenomenon and their trial did not show any sex linked difference in the suppression of the Prolactin levels With regards to efficacy, a trial by Carney (et al 1986) suggests that the beneficial action of SAMe is restricted to endogenous depression and it does not appear to have any action above placebo on reactive depression. As far as we can ascertain, this is the only trial published that has made this suggestion, although from a first principles basis, one can see the biochemical rationale for believing that it might well be the case. On a purely empirical grounds, some authors have recommended (on the basis of scant hard evidence), that SAMes action can be maximised by the addition of B12, B6 and folic acid. It is known that SAMe is required to convert these agents into their active form as a coenzyme. (Morrison et al, 1996). The same author also recommends the simultaneous adminstration of Trimethylglycine (TMG) which is necessary for the intracellular conversion of methionine into SAMe by the provision of the necessary methyl- groups. Comment has to be made that again, this appears to be a completely empirical (and logical) suggestion, but we cannot find any hard evidence to substantiate its clinical use. Chemistry SAMe is a basic component of cellular biochemistry. It occurs in every living cell and is second in importance only to ATP in both the number variety and significance of the reactions in which it serves as a cofactor. (Stramentinoli 1987). It is central in the chemistry of the transmethylation reactions. In essence its cellular function is to transfer the active methyl group form carrier molecules to a multitude of other molecules. In general terms, this methylation makes inert molecules biologically active. In addition to the transmethylation reactions it also plays a central role in transsulfuration and aminopropylation reactions It is involved in the synthesis of proteins including the nucleic acids, fatty acids, lipids and phospholipids, porphyrins and polysaccharides. In terms of our considerations here, perhaps the most significant reaction type that SAMe is involved in is the generation of the neurotransmitter amines. In this regard it is considered to be the most biologically significant provider of methyl groups within the cell. (Baldessarini 1987). Significantly it is also involved in the pathways to produce a number of other neurologically active compounds such as adrenaline, the neuronutrients acetyl l-carnitine and phosphatidyl choline (Mathews et al 1990) It is also to be found in the metabolic pathways of both serotonin and dopamine. Oral administration has been shown to increase the metabolites of these compounds in the CSF (implying increased turnover). It is thought to exert its antidepressive effect partly through the mechanism of increasing the levels of both dopamine and serotonin as neurotransmitters, but it also appears to have some form of trophic action on some of the neurones in the brain cortex. (Baldessarini 1987) It has been demonstrated that the tissue levels of SAMe tend to diminish with age and blood levels are also found to be low in some cases of clinical depression (Baldessarini 1987) A methyl group (CH3) is a group of three hydrogen atoms bound to one carbon atom. It does not exist in a stable isolated form and is transported between molecules by intermediaries such as SAMe. Methylation is the process by which this group is transferred from the methyl donor molecule to the recipient molecule. In general terms this process is central to the control of many of the intracellular pathways. Giving a methyl group to an enzyme is often the key to activating it, and thereby beginning a synthesis or degradation process elsewhere in the cell. Equally removing the methyl group will render the enzyme inactive and stop that particular pathway. Similar mechanisms are involved in the expression of genes and therefore the production of proteins within the cell. Some specific methylation reactions include the methylation of phenols which detoxify them and thereby aid in their excretion. (Stramentinoli 1987) In the context of this dissertation, methylation is also central to the metabolic chemistry of serotonin (and therefore also melatonin). The activity of both these compounds is effectively regulated by the presence of a methyl group. SAMe is synthesised from methionine, a naturally occurring amino acid. As the name implies (METH-ionine), it contains a methyl group. By utilising the energy supplied by ATP and in the presence of magnesium, it is converted into SAMe. The process is catalysed by the intervention of the enzyme MAT (methionine adenosyl

Creative Story: In Short :: essays research papers

Creative Story: In Short   Ã‚  Ã‚  Ã‚  Ã‚  It all started not so long ago. In fact, though I can't be completely sure about it, I think it was only five months ago. My name is Jeff Washburn and I am a surgeon. Not that long ago my life under went a huge change. Unfortunately a huge misfortune had to take place first. Not that long ago, I had a terrible thing happen to me. A misfortune led to my being expelled from the hospital and my medical license being revoked. Two patients died on me. I might have gotten away with only one but the board of directors are good at finding patterns. Don't get me wrong, I want these people to die. I just happened to be drunk at the time. Now I drink even more just to soften the constant hangover. The hearing were probably the worst part of whole ordeal. Three weeks of being put in the spotlight. Every inch of my life was put under a big magnifying glass. Every mistake I made in the last fourteen years was read bunch of know-nothings who sit and pretend to run a hospital. The mistakes weren't very frequent, at least, not until I started to drink.   Ã‚  Ã‚  Ã‚  Ã‚  I suppose you want to know the reason I started to drink. Well, I mess up big time during a triple bypass and killed a patient. That's when the drinking started and the drinking lead to the death of another patient. Now I drink even more and remember even less which means its working.   Ã‚  Ã‚  Ã‚  Ã‚  About a month ago I left England, which is where I worked, and moved here to a small fishing island off the coast of France. There is no doctor on the island so they welcomed me, sort of. I scare them I suppose. They're afraid they might catch me when I'm to drunk to work properly.   Ã‚  Ã‚  Ã‚  Ã‚  But now things are different. About three weeks ago I had a big wake-up call. I was sitting in my normal Sunday drunken stupor when a man was brought in to my office. This man had been seriously injured by gun shot wounds. Apparently he had be found in the ocean by a group of fishermen. I knew that I could not perform the necessary surgery in my present condition. I bandaged him up and stooped the major bleeding. Then I took two hours and did all I could to dry out. With my condition a little better I performed the most delicate surgery of my life. For another hour I scrubbed at the wound in his head.

Modernization in Filipino Women Essay

For centuries, Filipino women have thought themselves of being dominated by men. From the Spanish era to the American colonization, they were brought up to believe that men are leaders in society and that they are subordinate to them [men]. This therefore affects their views on femininity. It has been said in Johanna Francisco’s Essence of a Filipino Woman that women in the Philippines are luckier among women of other countries in Asia. This has been so because men in Philippine society appreciate and honor them. In fact, it is being shown on how they [women] are permitted to educate themselves, work, and possess belongings which are prohibited [or not normal] in other Asian countries. But above all, it is primarily because of their character or â€Å"role† as a [loving] mother. How would one know what a Filipina is? Well, a Filipino woman is described as shy, reserved, prim, and discreet. She is cautious, bashful, charming, and meek. She could either be â€Å"Mestiza†, â€Å"Chinita†, or â€Å"Morena†. She is a lover, and, at times of trouble, a fighter. She, by nature, possesses a strong faith. She may not admit her being religious, but deep inside, she trusts in God’s loving power. It is being seen on how she always puts herself in the care of the Lord and prays for everybody she loves. She thinks of other people first before herself. She plays different roles in the society. According to Francisco, â€Å"she is a considerate daughter, a loyal friend, and a supportive and loving wife?. She is the driving force in the family, in a marriage, or in a relationship?. But for the most part, she is dignified†. Francisco also describes her as being humorous. She laughs a lot, making it one of her best asset. She is also an optimistic person who always finds â€Å"positive† things in â€Å"dire situations†. This paper talks about how Filipino women morality has been changed or influenced by modernization, therefore losing the real Filipina within. It tackles and touches on issues that are degrading to Filipino women. It has five major parts. The first would be the definition of morality and modernization, with an explanation of the connection between the two. Next is the evolution of Filipino women which starts from the very beginning of Philippine history. This would include mainly Filipino women of yesterday, and Filipino women of today. The third would be the beginning of modernization in the Philippines. This part discusses how modernization entered our country. The fourth would be Filipino women’s response to the fast growing modernization, and the last talks on the effects it [modernization] has given to Filipino women, specifically, their morality. The last pages of this paper would include a researched survey on what young adults of Silliman University of Dumaguete City, specifically from the College of Business Administration, thinks about modern Filipina morals as influenced by fast westernization of the Philippines. Modernization in the Philippines The Philippines has not been considered different from other countries. Like the countries in Africa and Asia (particularly southeast Asia), it has gone through experiences that deeply influenced Filipino customs and beliefs. It all began from the Spanish colonization to the American era to the commonwealth years and to the decades of independence that the Philippines has slowly changed its people due to factors of modernity such education, mass media, technological advancement, and the like. These changes are seen most commonly in the urban areas such as the cities and larger towns. It is in these areas where westernization is concentrated brought about by television, radio, and news papers. The impact of modernization in the Philippines has been â€Å"persuasive† since the first ever colonizer stepped into its lands. The Philippines’ attempt to compete in the highly modernized world can greatly affect the attitude of women today. However, according to a Filipino psychologist, the Filipinos have this â€Å"split-level personality. † This personality explains that some values of a Filipino remain the same even though some of his or her outlooks and aspects have been modernized. But this greatly depends on how well a person weigh things over. If he/she prefers modernization more than tradition, the â€Å"split-level personality† thing dissolves. This has been evidenced by Filipino women’s responses to modernization.

Workforce Diversity

Organization Culture/Workforce Diversity Abstract Different organizations are defined by the unique characteristics displayed by their workforce. Developing unique behavior enables workers to share responsibilities and attain a strong bond that helps the company to realize its corporate goals. This paper will analyze organizational culture and workforce diversity and evaluate their contribution towards organizational success.Advertising We will write a custom essay sample on Organization Culture/Workforce Diversity specifically for you for only $16.05 $11/page Learn More Organization Culture Organization culture is defined as a unique and different way of thinking and behaving that is demonstrated by workers from the same organization. It is a characteristic pattern that is distinctive and recognizable, one that enhances the operations carried out in a particular organization (Moffat, McLean, 2010). For an organization to develop its unique culture, there must be shared understanding between the w orkers. The shared understanding is derived from the executives, who encourage joint operations. Through the shared understanding, organizations are able to perform better. The coordination that is created within organization’s workforce increases productivity and encourages workers to focus on organizational objectives. In the development of an organizational culture, workers must be given an opportunity to express their views, present proposals and engage in debates that are all geared towards realizing the organization’s goals. When the workers are given the freedom of expression, they develop a coordinated and shared understanding, which is unique for all organizations. Organizational culture can also be defined as an invisible web that enhances decision-making, and employees’ behavior and thinking (Schein, 2010). The routine and common practices seen in every organization is the culture that is sometimes taken for granted. In the development of these unique characteristics, there must be agreements between the executives and the junior members on how to proceed. The culture is not forced into the employees, but rather, it is nurtured and slowly developed to perfection. The nurturing process allows the employees to fully understand their responsibilities and develop shared interests for enhanced coordination (Moffat, McLean, 2010). Some of the tools that can be used by organizations to enhance culture are the social networking sites. The main objective of a culture is bringing together employees’ behaviors and ways of thinking to one common and shared characteristic that is geared towards achieving the company’s goals. Communication is the key to realizing this objective and social networking sites provide a good framework on which workers can communicate, give their views and consent on certain issues in the company (Tan, Lee, Chiu, 2008).Advertising Looking for essay on business economics? Let's see if we can help you! Get your first paper with 15% OFF Learn More The possibility of communication and sharing ideas increases the commonality among employees and shapes up a shared way of thinking (Moffat, McLean, 2010). Conversations within an organization are the most effective ways of ensuring that ideas and interests are shared. Without proper communication, employees would be disintegrated and this would lead to varying behaviors and thinking. The leaders must make the most sensitive decisions for a company. However, through the social networking sites, ideas can be generated from the rest of the workers and help in establishing the best decision for the company. These tools are effective in developing the ‘both-and’ strategy that allows for contained debate from all the employees within an organization. Ambiguity can cause the company to collapse. However, all the information concerning the company that is in circulation can be verified through social netw orking sites. Through conversations and communication, any ambiguity detected in an organization can be discussed and this can lead to new possibilities (Schein, 2010). The social networking sites are frameworks on which corporate members and employees can meet and discuss the issues affecting the company. In addition, the tool can be used to come up with development ideas from the workforce despite the fact that the executive management has to approve them. Shared interests and understanding shape up organizations and enhance communication between workers and executives. While this feature goes undetected in many organizations, it is present through common behaviors and unique characteristics (Tan, Lee, Chiu, 2008). All organizations have their unique characteristics and any new employee is expected to study and be connected with the existing culture for shared understanding to exist. New employees can learn about the existing culture by observing, or following the conversations i n the social networking sites. The expectations from the organization are defined in the sites and they assist in determining the best strategy to be adopted by the company. The management has to set up effective communication channels that are to be used by the workers in developing a unique culture (Moffat, McLean, 2010).Advertising We will write a custom essay sample on Organization Culture/Workforce Diversity specifically for you for only $16.05 $11/page Learn More While social networking sites are some of the best communication channels, other ways may be considered provided they enhance dialogue and allow all workers to express their views. With increased freedom and opportunities to contribute to organizational matters, a culture is formed that streamlines all employees’ thoughts and behaviors towards realizing corporate goals. Productivity is increased when the workers and the organization develop common interests. Development of opportuniti es by the managers increases the efforts from the workforce and ensures that corporate objectives are prioritized. Workplace Diversity The concept of workplace diversity can be defined as the existing differences between workers in an organization. It is a wider definition of the employees in an organization in terms of gender, race, age and ethnic background. In addition, it also encompasses personal behavior, cognitive styles and experiences among others. In workforce diversity, there are various benefits and challenges present. One of the benefits is increased adaptability in the workforce (Herring, 2009). Employees with different characteristics will provide different solutions to the problems within an organization. For a company to be successful, the employees must have the potential to embrace diversity. Since employees possess different and unique characteristics, they provide the required skills and experiences that are required to realize corporate goals. The other benefit is the availability of many viewpoints to a problem. In a company with same employees, the viewpoints and ideas for solving corporate problems are limited. However, in a diverse workforce, there are different ideas and viewpoints that help in reducing the problems in an organization. Efficiency and effective execution of requirements is realized only amid a diverse workforce. This is due to the potential held by each of the workers, which helps them utilize their unique traits to the company’s benefit. Each employee acts as a representation of a larger group and hence offers his/her best (Kundu, 2003). A young worker would want to prove that young employees are competent and perfect, while an old worker would like to prove that experience brings about perfection. Through such competition, an organization increases its output.Advertising Looking for essay on business economics? Let's see if we can help you! Get your first paper with 15% OFF Learn More A diverse workforce also ensures that there is a broader service range. In a multi-cultured workforce, offering services on a global basis becomes an easy task. Barriers to communication and other issues are dealt with by the diversity present within the organization. With a diverse workforce, a company can allocate specific employees to specific tasks depending on the nature of the job and customers’ expectations. A company can exploit languages, cultural understanding and experiences possessed by members of its workforce (Kundu, 2003). This helps in ensuring that there is equal representation and improving service delivery. There are various challenges that are associated with a diverse workforce. One of the challenges is communication (Herring, 2009). The diverse workforce may bring about cultural, language and perceptual barriers that may hinder effective communication. Whether intentional or unintentional, employees may develop certain perceptions about certain factions and hence limit openness and coordination. Without proper coordination, the company may reduce productivity and record losses. The other challenge in workforce diversity is that some of the workers may be resistant to change. When joining a new company, employees must be willing to change and adapt to the culture and expectations of the company. However, people from different regions may bring into the company different beliefs that may compromise its organizational culture. Workers with different beliefs may fail to change and comply with the organizational expectations. Bringing along experiences and strategies and sticking to them, even when they are not workable, are some of the common characteristics of a diverse workforce (Corinne, DiTomaso, 2004). The other challenge of workforce diversity is experienced in the implementation of policies to cater for it. All the employees must feel appreciated and represented in the best way possible by the company. The company must ensure t hat all its policies are fair and just and that there is no discrimination and prejudice against any employee (Herring, 2009). The implementation process is very tricky as it can compromise certain values hitherto held by the company. In addition, it may favor some employees at the expense of others. To prevent the challenges from affecting an organization, the management should frequently assess their diversity process to determine whether there is need for change. Assessment allows the management to determine all possible challenges at an earlier stage so that solutions can be easily developed. Training of the workforce should also be prioritized to prevent some workers from resisting change. The training is meant to help the workers learn about the existing culture and the expectations of the company and its customers. Workforce diversity is therefore beneficial to a company, but can also affect the operations if not properly handled. The workers should work together with the man agement to ensure that all challenges are addressed and that corporate goals are not compromised. References Schein, E. H. (2010). Organizational Culture and Leadership (4th ed.). San Francisco, CA: Jossey-Bass. Moffat, A., McLean, A. (2010). Merger as conversation. Leadership Organization Development Journal, 31(6), 534-550. Kundu, S. C. (2003). Workforce diversity status: a study of employees’ reactions. Industrial Management Data Systems, 103(4), 215 – 226. Herring, C. (2009). Does Diversity Pay? Race, Gender, and the Business Case for Diversity. American Sociological Review, 74(2), 208-224. Corinne, P., DiTomaso, N. (2004). Workforce Diversity: Why, When, And How. Research in the Sociology of Work, 14, 1-14.