Seasonal Affective Disorder: Actual or Just an Excuse - Coursework Example

Seasonal Affective Disorder Actual or Just an Excuse? A clinical subtype of mood disorder which consists of recurrent episodes of major depression that have a seasonal pattern is called as Seasonal affective disorder (SAD). It is characterized by depressed mood, sleep disorder, fatigue and anxiety (Shen et al, 2005). The symptoms of SAD also include, hypersomnolence, loss of interest in sex, increased carbohydrate consumption, and weight gain Some individuals in an extreme stage also experience a manic state. Cognitive function might also be affected by the seasons (Miller, 2005). There are two types of SAD. Winter depression or fall onset is one, which consists mainly symptoms closely related to atypical depression. Symptoms tend to appear in late fall and remit during early spring and summer months. Another pattern of SAD is the spring onset pattern or summer depression , where the depressive symptoms begin in late spring or early summer and lasts through early fall. This pattern of depression is much less common than winter depression (Jepson et al., 1999). SAD or recurrent winter depression criteria in the 4th edition of Diagnostic and Statistical Manual of Mental Disorders are similar to other definitions of SAD, specifying a recurrent pattern of major depressive episodes during winter and remission of symptoms during summer, in the absence of seasonal psychosocial stressors as stated by Lam & Levitan (2000). Areas of North America in the higher latitudes have greater, and sometimes drastic, differences in yearly seasons. In contrast, the areas of the world in latitudes closer to the equator have fewer seasonal changes than geographic areas further from the equator. Some species gather food for winter, while other species go into hi­bernation, in the fall and as winter approaches, when days shorten and temperatures drops. Though, most humans are not seriously affected by the shorter days and longer nights of fall and winter; some individuals experience severe changes in mood, energy, and appetite to be di­agnosed with SAD. The mechanisms by which SAD symptoms arise from the seasonal changes are not fully understood. Certain mechanisms may apply to specific genetic types. Literature reveals that individuals with SAD have a longer period of melatonin synthesis at night in the winter. Compared to those without SAD, daytime melatonin levels may be higher in SAD sufferers in the winter. Melatonin synthesis peaks in darkness. Studies have shown that blood levels of melatonin are very low during the daylight. The light entering the retina stimulates the suprachiasmatic nucleus of the hypothalamus which in turn inhibits the pineal gland from converting serotonin to melatonin. This results in the diurnal and circadian rhythm of this secretion of melatonin. This inhibitory mechanism is no lon­ger present in the dark and the pineal gland begins synthesizing melatonin. Melatonin is formed by acetylation and methylation of serotonin. SAD patients show a delayed nocturnal onset of melatonin secretion in winter. The period of nocturnal melatonin secretion in women with SAD is increased as compared to sum­mer whereas, women without SAD symptoms do not show this seasonal variance in melatonin synthesis. The blood levels of melatonin are also raised during the daytime in patients with SAD. It was also proved that the onset of melatonin secretion may be delayed in SAD pa­tients and controls. The SAD patients may have some other hormonal response or other as yet unknown negative reaction to this normal phase shift. In addition to melatonin, other hormones and the nocturnal body temperature are also phase-delayed in SAD. Low brain levels of serotonin also contribute to symptoms of SAD. SAD patients also demonstrate hyperphagia and carbohydrate cravings, symptoms typical of inadequate brain sero­tonin (Miller, 2005). Epidemiology Epidemiological studies have reported the incidence of SAD in 4-10 percent of general population, with a higher incidence in women than men. Seasonal Pattern Questionnaire (SPAQ) and the Structured Interview Guide for the Hamilton Depression Rating-Seasonal Affective Disorder (SIGH-SAD) are the most commonly used diagnostic research tools for SAD. These diagnostic tools help to differentiate between SAD and sub-syndromal SAD (S-SAD). The sub-syndromal form of SAD is milder, clinically significant and seasonal affective symptoms. Together, the occurrence of SAD and S-SAD is 11-21 percent, which indicates that a significant portion of the population suffers from varying degrees of seasonal depression. Seasonal Health Questionnaire (SHQ) is another sensitive and specific diagnostic means of SAD. Studies have demonstrated an increase in the incidence of SAD and S-SAD in populations in higher latitudes com­pared to the lower latitude of Florida. Populations in Alaska and other areas of the world close to the arctic show an increased incidence of SAD. A SAD prevalence of 13.1 percent for women and 6.5 percent for men was noted in a study of U.S. Army soldiers. Another study of Fairbanks residents who had lived there for more than three years reported an overall incidence of 9.2 per­cent, with a 3:2 female-to-male ratio. The risk of SAD increases in people who move from southern latitudes to north, as it ap­pears some individuals develop a tolerance to seasonal changes over time. Studies provide ample evidence for a “latitude theory” of SAD incidence that the de­creased exposure to sunlight in the winter in northern climates increases the risk of SAD. There was a pos­sible genetic adaptation to the low light of winter in the arctic north in populations native to Iceland. Direct descendants of Icelandic emigrants and people living in an area of Manitoba, Canada (lat. 50° N) had SAD and S-SAD at a prevalence of 1.2 and 3.3 percent, respectively. There appears to be a genetic component that protects Icelanders from SAD, compared to other populations; but within Icelandic populations there is still an increased occurrence in northern latitudes. SAD runs in families as it has been found to occur more often in relatives of those who have SAD. Studies have confirmed that genetic effects accounted for 29 percent of the variance in seasonality in 3,331 twins in Aus­tralia with SAD (Miller, 2005). There may be a genetic component to susceptibility as found by twin studies. The authors also suggested several genes code for serotonin transport, but the overall pattern of heritability likely is complex and polygenomic. The overall lifetime prevalence of SAD was reported to range from 0 to 9.7 percent. A U.S. study using DSM-IV–based criteria found the lifetime prevalence of major depression with a seasonal pattern was 0.4 percent. Prevalence may be higher at northern latitudes, and it may vary within ethnic groups at the same latitude (Lurie et al, 2006). Its prevalence in Canada is 1%–3%, as compared with 1.3%–3% in Europe and less than 0.9% in Asia. SAD begins insidiously, appears in people aged 20 to 30 years as mild to moderate depressive episodes (Weir, 2001). Treatment Light Therapy Light therapy is the least invasive, very natural, and most re­searched treatment of SAD. Light therapy causes a normalization of the phase-shift delay in SAD. It was also thought to lengthen the photoperiod in winter in those with SAD. It suppresses the production of melatonin by the pineal gland. Light therapy has been proved to be an effective method of treatment of SAD. Light therapy is not associated with any side effects and it has an overall positive treat­ment response of up to 70 percent. There has been a positive clinical response bright light (3300 lux), medium light intensity, and dim light. Morning, midday, and evening application are most effective timings for light therapy. Full spectrum with ultraviolet (UV), full spectrum without UV, cool white, red spectrum, and blue/green/yellow spectrum has been used with success. A four-week study by SIGH-SAD showed morning bright light therapy (2500 lux cool white light box) for two hours (6-8 am) normalized body temperature, cortisol, and mood. SIGH-SAD scores were significantly better in the treatment group, where full spectrum or cool white light was administered from 6-8 am for seven days, with no significant difference be­tween cool white and full spectrum therapy, suggest­ing treatment with a light spectrum similar to the sun is not necessary in SAD. Positive clinical results were obtained in both groups in a study comparing morning and evening bright light therapy (10,000 lux x 30 min), using the SIGH-SAD scale. Regardless of morning or eve­ning administration, light therapy caused an antidepressant effect. Sit­ting in front of a bright light box for 30 minutes to two hours each day, was a problem for many patients with SAD. Researchers in Basel, Switzer­land, therefore, studied the effects of artificial bright light (2800 lux x 30 min/day) or a daily one-hour walk outdoors in natural light. They found that the natural light group performed significantly better than the artificial light group on the SIGH-SAD after one week. “Dawn simulation” in SAD patients was another aspect of light therapy. This treatment improved the phase delay of mela­tonin, the difficulty in awakening, and morning fa­tigue experienced by SAD patients. Dawn simulation demonstrated a greater response (p Read More