SAD-Seasonal Affective Disorder

Seasonal affective disorder is a disease which effects between 0.4-9.7 percent of the population (2). SAD was originally defined by Norman Rosenthal in 1984 as “the occurrence in autumn and/or winter of at least two episodes of serious depression, which disappear in the spring and summer, and where there are no clear-cut, seasonal, psychosocial precipitating factors” (1). It is characterized by episodes of major depression which often correspond to the winter months. The episodes may vary in duration and severity but must occur at the same time each year. For people suffering from SAD there is no escape from winter. This paper will explore the causes, symptoms and possible treatments for seasonal affective disorder.

The DSM (Diagnostic and Statistical Manual of Mental Disorders) does not give SAD a distinct diagnosis, but characterizes it as a type of depression. Symptoms include major depressive or bipolar episodes that repeatedly occur at the same time of year (2). Broadly, depression is characterized as an intense sadness or loss of pleasure in activities that once brought pleasure (2).

Although the exact causes of SAD are unknown, research has indicated that there may be a genetic component. “Patients with SAD are more likely to have family members with SAD, although this may be subject to reporting bias. Twin studies have found that there may be a genetic component to susceptibility. Several genes code for serotonin transport, but the overall pattern of heritability likely is complex and polygenomic” (2). In addition, prevalence rates differ with latitude and ethnic groups (2).

Some of the same tools used to diagnosis depression are also used to diagnose SAD. “There are several instruments for detecting depression in primary care, ranging in length from one to thirty items with an average of two to six minutes…Some standardized instruments focus more narrowly on SAD” (2). The Seasonal Pattern Assessment Questionnaire (SPAQ) is used to diagnose SAD specifically and has relatively high specificity rates. The Seasonal Health Questionnaire is also used and may be more specific. Quality of Life (QOL) scores show that QOL significantly increases during the summertime and significantly decreases during the winter months (3).

After diagnosis, there are a few treatments available to the patients. Light therapy is viewed by some as the best therapy available (1) and is used to regulate circadian rhythms. It has been shown to be about as effective as drugs in clinical studies. In addition to shifting circadian rhythms, light therapy also alters serotonin levels. It has been shown that early morning exposure to light therapy is more effective than light therapy later in the day (2). “Light therapy generally is most effective when administered earlier in the day. Early morning light therapy regulates the circadian pattern of melatonin secretion, whereas the use of light in the evening delays the normal melatonin phase shift” (2). The reason light therapy is effective could be linked to human biology. “In the body, photoperiodic information is translated as changing patterns of the secretion of melatonin…Humans exposed to artificially long or short nights and days also who altered patterns of melatonin secretion. Artificially increasing the length of exposure to bright light to match that of a summer day curtails melatonin secretion in winter” (1). Through this reasoning, it is clear why light therapy is the most effective treatment currently available for SAD.

Drug therapy is also used to treat SAD. Most studies have found that drug treatment is more effective than placebo treatment, but not enough research has been done to compare the difference between light therapy and drug use (2). “Pharmacological treatments of SAD have been successful, particularly with drugs that selectively inhibit the uptake of the neurotransmitter serotonin and the newer dual-action antidepressants, which act on both the serotoninergic and catecholaminergic systems” (1). Studies need to be done in the future to test the effectiveness of using drugs and light therapy together. Coupling these two marginally effective treatments may offer a cure for individuals suffering from SAD.

Clearly, there is not enough known about the causes of SAD to design a treatment that would fully cure seasonal affective disorder. The treatments currently available offer some help for those suffering each winter, but there is no fully effective treatment plan. Different ethnicities have different prevalence rates of SAD leading me to believe the school of thought that there must in fact be a genetic component. Perhaps those individuals who have ancestors descended from higher latitudes (i.e. longer winters) suffer less from SAD while those who’s ancestors are from equatorial roots suffer more from SAD. How did the human body evolve to prevent SAD in higher latitudes? If researchers are somehow able to uncover how the human body naturally regulated the serotonin levels in those people from high latitude places maybe a treatment can be derived. Not only is seasonal affective disorder an interesting area of research to explore, but also a debilitating disease that affects people each winter.

Works Cited

1. Arendt, Josephine. "Taking the SADness Out of Winter." Nature 415 (2002): 838-839. Bryn Mawr College, Bryn Mawr. 4 May 2007.

1. Lurie, Stephen J., Barbara Gawinski, Deborah Pierce, and Sally J. Rousseau. "Seasonal Affective Disorder." American Family Physicians 74.9 (2006): 1521-1524. Psych Info. Bryn Mawr College, Bryn Mawr. 3 May 2007.

1. Michalak, Erin E., Edwin M. Tam, Cv Manjunath, Anthony J. Levitt, Robert D. Levitan, and Raymond W. Lam. "Quality of Life in Patients with Seasonal Affective Disorder: Summer Vs Winter Scores." Canadian Journal of Psychiatry 50.5 (2005): 292-295. Bryn Mawr College, Bryn Mawr. 3 May 2007.