Biology 103
2002 Second Paper
On Serendip

The winter blues. Cabin fever. These terms bring to mind that glum feeling that overcomes many people during the winter months. Does this seasonal depression have any validity or do we just get antsy when the temperature turns from scorching to frigid? About twenty years ago, Herbert E. Kern noted in himself regular seasonal emotional cycles, which he hypothesized might be related to seasonal variations in environmental light. He then learned from the findings of Alfred J. Lewy et. al that bright environmental light could suppress the nocturnal secretion of melatonin by the pineal gland in humans. In 1980-1981, Dr. Norman Rosenthal admitted Kern to his psychological unit and treated his symptoms of depression with bright light. Amazingly, the treatment worked. The follow-up study, in which the original results were replicated, lead to the description of Seasonal Affective Disorder (SAD) in 1984 (1). Further research over the past two decades has led to a better understanding of SAD, including possible causes, the symptoms associated with SAD, and treatment options.

SAD affects four women four every one man, with an overall incidence ranging from 2% to 10%, with more people effected at higher latitudes, in North America. The frequency of SAD in North America was double that in Europe, "suggesting that climate, culture, and genetics may be more important factors" (2). The differences in the epidemiology of SAD may cause one to pause. How can gender and cultural difference be accounted for in relation to SAD, and do gender differences as a result of culture explain both the epidemiology and etiology of the disease? Have populations in which women hold traditional gender roles, as opposed to many American and European women who are rapidly blurring gender boundaries, been studied?

General Cultural differences between the United States and Europe are also another important point to consider. Do the two cultures place different emphasis on certain events, which in turn lead to a larger prevalence of SAD in America, such as the stresses associated with the winter holiday season? Are post-holiday blues the result of our culture, and do they lead to SAD? Do periods of economic decline contribute to the overall stress of one region, which then leads to more incidents of SAD? These questions, among many, may cause one to wonder what causes this disease; the environment, biology, culture?

The etiology of SAD remains a topic of great debate. Rosenthal notes that "winter changes often involve energy conservation...many SAD symptoms can be seen as conserving-overeating, oversleeping and low sexual ability...Seasonal adaptations are adaptive in some circumstances, but not in humans, who must function at the same level all year" (3). One might wonder if his explanation is a bit shortsighted. Humans are not excluded from their fellow mammals, birds, fish, reptiles, etc. when it comes to conserving energy in the winter. Perhaps the necessity to conserve energy is not as obvious as it once was before modern technology provided Gortex jackets, Polar-fleece gloves, or Smart-Wool socks. Before these luxuries, humans probably considered the importance, and indeed necessity, of keeping warm and conserving energy during the winter months. This may have taken the form of eating more food to add more fat to one's body, remaining in bed or next to a fire, and participating in as little physical exertion as possible. Not only is Rosenthal's explanation insufficient for these reasons, he also does not take into account other factors, such as other biological influences or a genetic component.

Another theory states that excessive or inadequate levels of neurotransmitters, such as serotonin, may cause depression. Interestingly, serotonin is known to decline in the autumn and throughout winter, a fact that might allow for correction by appropriate medications. Disturbed circadian rhythms have also been pointed to as the cause of SAD. At night, circadian rhythms lower body temperature and trigger the production of melatonin, a hormone that enhances sleep. If these are not functioning properly, it is theorized, one might experience symptoms associated with SAD (2).

A genetic factor might also provide an explanation. In a study of monozygotic and dizygotic twins, seasonality was shown to be a heritable trait (4). This area of research leads to interesting questions. For example, further research might attempt to determine what specific genetic factors are responsible for SAD. Also, one might ask if SAD is the result of genetic differences and environmental influences. A study that examines monozygotic twins and dizygotic twins both separated at birth and raised in different environments, and data regarding the frequency of both twins having SAD, would be useful to determine what the effects culture and genetics may have on this disease.

It is plausible that the environment, biological, and cultural factors combine to determine the occurrence of SAD among certain populations. For example, do people who live in northern latitudes have an better chance of having SAD than people who live in southern latitudes, merely as a result of geographic and environmental differences? Do people inherit genes from their ancestors who made physical adaptations, in order to survive in a northern climate, that carry a SAD related gene? If physical adaptations did occur, did those adaptations lead to cultural differences, which in turn increased the likelihood of SAD? As of now, these questions remain just theories, and despite the general success of treating SAD, its etiology remains elusive.

The standard US manual of psychiatric diagnoses, the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), lists SAD as a subtype of major clinical depression. It is called a "specifier" because it refers to the seasonal depressive episodes that can occur within major depression and bipolar disorders. Specifically, the criteria for SAD are as follows:
A. Regular temporal relationship between the onset of major depressive episodes and a particular time of the year (unrelated to obvious season-related psychological stressors).
B. Full remission (or a change from depression to mania or hypomania) also occurs at a characteristic time of the year.
C. Two major depressive episodes meeting criteria A and B in the last two years and no non-seasonal episodes in the same period.
D. Seasonal major depressive episodes substantially outnumber the non-seasonal episodes over the individual's lifetime (5).
SAD is classified into two distinct types: fall-onset SAD, also called winter depression, and spring-onset SAD. Winter depression usually begins in late autumn and lasts through the spring or summer. Symptoms of this type of SAD include increased sleep, increased appetite, craving for carbohydrates, weight gain, irritability, and interpersonal conflict. The symptoms of spring-onset depression include insomnia, weight loss, and poor appetite, and typically begin in late spring or early summer and end in early fall (2). Patients with SAD report that their symptoms improve in lower latitudes, and worsen if they travel to an area with great winter cloud cover (4).

What can be done to help SAD patients. The most widely prescribed treatment is the use of a light box, a device that emits fluorescent light of approximately 2,500 to 10,000 lux. Lux is defined as "a unit of illumination intensity that corrects for the photopic spectral sensitivity of the human eye." Bright sunshine can be over 100,000 lux, a brightly-lit office is less than 500 lux, and an indoor light at night is only 100 lux (4). This treatment, which is 60% to 90% effective, rarely produces side effects. If they do occur, they may include: photophobia, headache, fatigue, irritability, hypomania, insomnia, and possible retinal damage. A typical treatment includes shining the light at a downward slope, while aiming at the eyes, for a period of 10 to 90 minutes daily, depending on the severity of SAD (5). The use of a light box is not effective with all SAD patients, for whose cases selective serotonin reuptake inhibitors (SSRIs) are prescribed. These medications generally are most effective when used in combination of light therapy. For practical reasons, some patients choose not to use light therapy because of the large time commitment. For this reason, the treatment of SAD must be considered on an individual basis (4).

The questions raised in this essay point to the necessity of considering differences in the epidemiology of SAD in terms of culture, biology, and environmental influences. It may be that none of these factors is the cause of SAD, but it is clear that these factors are thoroughly related and sometimes difficult to distinguish. For this reason, the etiology of this disease may be found by looking at these factors as a unit, instead of their individual parts.

References

1)Two decades of research into SAD and its treatments: A Retrospective , an article written by Dr. Rosenthal

2)Seasonal Affective Disorder: Autumn Onset, Winter Gloom, a clinical review of SAD

3)Modern Solutions to Ancient Seasonal Swings, from the November 2000 edition of Psychology Today

4)SAD: Diagnosis and Management, an article written by Raymond W. Lam, with general information about SAD

5)Seasonal Affective Disorders , an article


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