One of the most basic facts of life on earth is the daily rhythm of light and dark. As earthly creatures, we come equipped with brains prewired to this rhythm. Our own internal pacemaker tunes our mental and physical energy levels more or less to the cycles of sunlight.
At least that's the general plan. Sometimes the system is a little off and night just won't quit the brain.
As the seasons turn, in response to the waxing and waning of the sun, most people respond to the change in environmental light—a pronounced shortening of the period of light—with a shift in energy. The body seems to slow down, we feel fatigue, we are slow to wake in the dark of the morning—a faint echo of seasonal patterns of response among other animals. In one survey, conducted in the state of Maryland, over 90% of those surveyed reported that they felt some difference in mood, energy or behavior with the change of seasons.
But for some people the change in energy level is so extreme they have trouble functioning. These people—some estimates say 11 million in the U.S.—have seasonal affective disorder (SAD), or winter depression.
SAD is probably as old as patterns of human migration to latitudes distant from the equator. The disorder is rare in those living within 30 degrees of the equator, where daylight hours are long, constant, and extremely bright. But only recently has it become clear how the disorder emerges from seasonal change.
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Research now underway suggests that SAD may come about through the collision of two vulnerabilities—one to depression, the other to seasonality. People with SAD seem to be unique in that they have a kind of "biological calendar;" they generate a distinct biological signal of lengthening nights, and that sets off a cascade of responses resulting in depression.
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Carefully timed exposure to specific types of light early in the morning constitutes the most specific therapeutic approach to SAD now available. But in the near future it may be possible to prevent the disorder before it starts. Research already in progress is testing whether seasonal administration of an antidepressant drug in advance of symptoms can ward them off entirely.
That makes Norman E. Rosenthal, M.D. very happy. Clinical professor of psychiatry at Georgetown University and researcher at the National Institute of Mental Health (NIMH), he coined the term Seasonal Affective Disorder—over two decades ago. "Finally," he says, "pharmaceutical companies are getting interested in SAD. That will help focus public attention on it as a real problem, not just an inconvenience."
After all, he points out, the disorder takes up half the year. The average duration is five months at 39 degrees latitude. "And we're not talking about the Arctic Circle here." But geography counts.
Location, Location, Location
In the United States, the symptoms of SAD usually begin in October or November, are most pronounced in January and February, when days are shortest, and subside in March or April. As the days shorten, those afflicted are drained of energy, sleep excessively (sometimes needing as much as four hours more per day than in summer), crave carbohydrates and overeat, and become increasingly sluggish. Sufferers engage their environment less and withdraw socially; they also lose interest in sex. They feel sad, empty, or anxious.
Such symptoms qualify as SAD only if they resolve in the spring and summer, and mood then returns to normal. And it isn't SAD unless the symptoms recur for two or more consecutive winters.
Generally, the symptoms of SAD are mild to moderate and the condition is more prevalent with distance from the Equator. SAD is up to eight times more common in the northern U.S. and Canada than in Florida. However, regular consumption of fish rich in omega-3 fatty acids may prevent the disorder. Last year researchers reported that northerly countries where fish consumption is high—Iceland and Japan, for example—are spared the expected high rates of seasonal affective disorder.
As with major depression, those most at risk of developing SAD are women in their 20s. And as is common among people subject to depression, more than two thirds of them report at least one close relative with the disorder. In one study, six percent of suffers had such severe symptoms they required hospitalization.
A Matter of Melatonin
The disorder, says research psychiatrist Thomas Wehr, M.D., chief of the Section on Biological Rhythms at NIMH, has its roots in a mechanism that is ubiquitous among animals. Most animals (and plants) detect changes in seasons by registering day length. Production of the hormone melatonin is a chemical signal of that change.
The changes of SAD are so reminiscent of changes in animals' seasonal cycles—changes in sleep, appetite, activity levels, social contact and sex—that "it was only reasonable to investigate whether SAD was governed by that same melatonin mechanism," Dr. Wehr explains. Indeed, he and colleagues reported in the Archives of Psychiatry, patients with SAD register an abnormality in melatonin secretion that healthy controls do not.
Normally, our bodies produce the hormone melatonin while we sleep. Melatonin has a slowing effect on the nervous system and induces sleep, summer and winter.
