Sad Patients example essay topic

Running Head: SYMPTOMS, CAUSES AND TREATMENTS Critical View of Seasonal Affective Disorder Ashley C. Kort Illinois CollegeAbstractThis paper is intended to be a critical view of Seasonal Affective Disorder. In order to understand fully the biological and psychological components of the disease, as well as its possible causes and treatments, it is necessary to compile and interpret previously conducted research. Such is the purpose of this paper. First, the symptoms of Seasonal Affective Disorder will be explained and illustrated using data and case studies. Second, the possible causes of the disease will be outlined. Third, proposed treatments will be presented as possible solutions to this debilitating disease.

A Critical View of Seasonal Affective Disorder Norman E. Rosenthal and his colleagues were the first to highlight a pattern of cyclical unipolar depression that was linked to the changing of the seasons, most often from fall to winter months through to the springtime, specifically November to March. His observations of case studies led to a rediscovery of SAD and a modern definition on the disease. In one particular case study, Rosenthal explained, "The patient's tendency to overeat, feel fatigued and lethargic, oversleep, crave carbohydrates, and gain weight - depressive symptoms that have all been designated 'atypical' in the literature on depression - are actually common in SAD, although a significant minority of patients report the more 'typical' vegetative symptoms of eating less, sleeping less, and losing weight" (Rosenthal, 1993). Thus, the symptoms of the majority of patients diagnosed with SAD were characteristic, and when linked to a cyclic pattern, could be identified. However, Rosenthal's "significant minority" left room for confusion between SAD and simple unipolar depression. Often, other diseases must first have been ruled out, and a pattern of SAD symptoms over several years been established before proper diagnosis could occur.

Despite this, Rosenthal's work laid the foundation of any future studies conducted to determine the characteristics of SAD. Although Rosenthal's findings have been deemed accurate over the past 15 years, their validity was proven only through many other case and mass studies. For instance, Ybe Meesters conducted a very poignant case study in 1997 with a nine-year-old boy. According to the study, "The parents reported a considerable difference in the child's mood and behavior between summer and winter. The two winters before referral [, when the boy was three, ] the patient complained of fatigue and apathy from October onward.

He had been easily irritated, suffered from anxiety, and avoided his friends. He had needed more sleep than previously and have been difficult to awaken in the morning. His teachers described him as dreamy and absent-minded during the winter but energetic during the summer" (Ybe Meesters, 1998) The symptoms of the boy were published, and struck a chord with the psychological community. Not only were they consistent with Rosenthal's findings, but also their detailed description allowed for a greater amount of patients to identify with the disease, thus making SAD a clear and applicable diagnosis.

After Meesters modified Rosenthal's definition, it was possible to diagnose correctly many more patients under the umbrella of SAD. Thus, as greater numbers of people were diagnosed, observed trends began to develop. Three in particular were noticed early on, and continue to prove true today. They included an overall lower rate of SAD in children compared to the general population, an increasing diagnosis rate in adolescents, and a much higher rate in adult females versus males. One study that became instrumental in establishing concrete evidence for the rates in children and adolescents was conducted after the inherent trends were noticed throughout the general population. Susan Swedo and her colleagues found that 3.3% of children fit the criteria for SAD, this being considerably lower than the accepted adult value of approximately 6%.

The children also showed patterns in the data as their ages increased (1.7%-5.5% for 9 to 19-year-olds). Thus, Swedo concluded that there was a link between puberty and the rate of diagnosis in SAD patients (Swedo, Richter, Hoffman, Cara, 1995). It was this conclusion, as well as further studies on women, that led to the proposed hormonal explanation of SAD later discussed. In 1998, Low and Feissner were interested in following up Swedo's findings by conducting an experiment to determine a point at which post-puberty individuals fell into the same general statistical patterns as middle-aged adults. By testing a group of college-aged students, they came to several conclusions, which they published in their 1998 article.

According to their results, "Of those who were classified as having SAD, 70% were women" (Low, Feissner, 1998). This was characteristic of an adult population in which women are much more likely to develop SAD than girls in a population of children. Although their SAD rate of 13.2% within the studied population was comparably higher than the accepted 6%, nevertheless, it showed that college students not like children who tend to be below the adult rate. The causes of SAD are still not firmly identified for children or adults.

However, a few major hypothesized theories have gained credit over the last decade. One such theory is the hormone theory. After Swedo's study of SAD in adolescents, the suggestion of hormonal shifts producing stress and mood swings that triggered depressive episodes was proposed. According to the theory, those whose hormone levels were in flux would be more susceptible to the depressive affects of SAD. Rohan's 2003 study confirmed this theory by determining that women had cognitive-behavioral SAD correlations with their monthly cycles. The hormonal shifts over the course of each month also had an affect on the SAD symptoms of the female patients (Rohan, Sigmon, Dorhofer, 2003).

Throughout the study, women were asked to fill out a series of questionnaires to determine their moods and general interest level during daily activities. Based on Rosenthal's previous data, Swedo did not expect to find many women within the study who experienced a major depressive episode. Instead, as expected, the women were down about themselves and the activities in which they participated, but still could function normally. Also, their feelings of sadness and / or apathy were dependent on what point they were at in their menstrual cycle.

Therefore, the cycles had a definite but not severe impact on the intensity of SAD in women. Another explanation for the presence of SAD had its roots in neurobiology. This model, suggested in an article by Lam and Levitan in 2000, implied the affect if some of the crucial hormones within the human brain, but did not center on their fluctuation. Instead, a pattern was suggested that dealt with Circadian rhythms, or the body's internal clock. This clock is set based on the duration and intensity of light that the body receives throughout the day. According to the theory, our bodies adjust hormone levels in the brain by applying this subconscious light meter in order to prepare for the coming winter or summer months.

The hormone levels then affect our mand neurotransmitter function as a result. The article also suggested that there is a genetic component that determines the severity of the circadian rhythms on the brain in every individual, making some (especially women) more likely to develop symptoms of SAD (Lam, Levitan, 2000). A third possible hypothesized cause for SAD was published in the Journal of Abnormal Psychology. Interestingly, it included both the biological and hormonal shift theories, but suggested that they were dependent on a person's geographical placement on the world. Their 1997 study attempted to show a solid connection between the rates of SAD diagnosis and the latitudes of those studied.

Generally, the more towards the poles a community was, the higher their rate of SAD prevalence would be (Young, Meaden, Fogg, Cherin, Eastman, 1997). According to the article, however", [The] results failed to find a relationship between risk of SAD onset and hours of sunshine, mean daily temperature, or total daily radiation based on latitude" (Young, et al., 1997). So, despite the strong previous evidence that suggested higher rates of SAD in regions closer to the poles, the risk was not tied to the amount of light a patient received. The authors of the article felt that more research was needed to explain the findings of their study. The latitude study was interesting in that it contradicted the reasoning behind traditional treatments used to counteract the onset and symptoms of SAD. Phototherapy, or the therapeutic exposure to set varying intensities of light, has been used from the very beginning.

In 1997, Toru Sato took these contradictory findings into account, and attempted to critically analyze the process of phototherapy in order to determine ways in which it could be modified to make the treatments more effective (Sato, 1997). Within his article, Sato included clinical guidelines that were based on his findings. The guidelines were meant to assist psychologists in the efficient administration of phototherapy to patients. According to Sato, "The patient's eye should be exposed to light that is sufficiently intense for a sufficiently long time (e.g. 2,500 lux for 2 hr)... Morning treatments are preferable, although evening treatments may also be effective" (Sato, 1997). Though he could not explain why the latitude findings were not light-based, he did see real results using the traditional method of phototherapy treatment, and even perfected on it for future patients.

While phototherapy with artificial light is an excellent tool for treating SAD sufferers in the winter months, it has not shown to be nearly as effective as natural light, especially light that is absorbed during the summer months. According to another phototherapy study conducted by Postlache, Hardin, Myers, Turner, and Erick, it is an effective treatment, but does not provide the dramatic relief as that of an oncoming spring or a vacation to a place with a high intensity of natural light. Postlache, et al formally documented this difference for the first time. Their documented results were in the form of data, and were as follows:" Eight out of ten patients responded to 2 weeks of light treatment, and 13 of 15 patients responded in summer...

Light treatment consisted of a standard regimen of 10, 00-lux cool-white fluorescent therapy for 45 minutes twice daily... We then recorded the patients' depression levels in summer by using the Friedman's two-way analysis of variance with conditions" (Postlache, et al., 1998). Once again, the latitude Hypothesis remained unexplained, and thus likely refuted. Based on the research, it seems probable that the causes for SAD are light-based, and thus a deficiency of light produces biological responses in the human brain.

Chemicals such as serotonin, norepinephrine, epinephrine and dopamine have been indicated by various researched studies as being triggered by the presence of light, and thus affecting the biological responses of the body. There is one chemical, however, that is just now being implicated in the workings of SAD. According to Neumister and his colleagues, Tryptophan is a chemical that greatly affects the severity of SAD, and is this one chemical not deterred by phototherapy (Neumister, Praschak-Rieder, Hesselmann, Vitouch, Oliver, 1997). Because of this, if SAD because unbearable in a patient, the sole treatment is that of Tryptophan depletion, or the removal of Tryptophan from the brain by way of medications a alteration of diet. Thus, because the drugs were still crude, depletion through medication had little to no effect despite lowered Tryptophan levels in the blood.

However, persons whose diets were altered lowered their Tryptophan levels drastically, and received numerous benefits. It will be a while before enough research is done to claim Tryptophan depletion as an effective treatment, but because of its effectiveness and simplicity, it may one day rank with phototherapy as viable option for SAD treatment. After only a maximum of thirty year's discovery, Seasonal Affective Disorder has been identified, classified, and effectively treated thanks to the work of contributors listed in this paper, as well as many others. Yet, there are still many possible routes future psychologists to study in order to fully elevate the symptoms of all SAD patients. The clear methods for diagnosis, combined with an understanding of the causes of the disease and promising experimental treatments will all likely lead to future breakthroughs in the study of SAD. It is a field of great opportunity for the acquisition of scientific knowledge and the assistance of those in pain.

Bibliography

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Pathophysiology of seasonal affective disorder: a review. Journal of Psychiatry and Neuroscience. 25,469-474. Low, K.G., & Feissner, J.M. (1998).
Seasonal affective disorder in college students: prevalence and latitude. Journal of American College Health. 47,135-137. Meesters, Y. (1998).
Case study: dawn simulation as maintenance treatment in a nine year-old patient with seasonal affective disorder. Journal of the American Academy of Child and Adolescent Psychiatry. 37,986-988. Neumister, A., Praschak-Rieder, Hesselmann, N., Vitouch, B., Oliver, & et al. (1997).
Rapid tryptophan depletion in drug-free depressed patients with seasonal affective disorder. American Journal of Psychiatry. 154, 1153-1155. Postlache, T.T., Hardin, Myers, T.A., Turner, F.S., & Erick, H. (1998).
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