But uniquely in people with SAD, the period of nightly melatonin secretion is prolonged—and then, only in the winter months. Melatonin production fails to shut off on time. In the summer months people with SAD produce the same amount of melatonin for the same amount of time as healthy controls. But in the winter, melatonin production persists. Healthy controls show no such seasonal change in nightly melatonin production.
A Big Half Hour
The winter-summer difference in melatonin production among SAD sufferers is only 38 minutes long—but that's 38 important minutes. That same amount of prolonged melatonin secretion in winter, says Dr. Wehr, is "sufficient to elicit behavioral changes in other mammals."
While the changes in melatonin secretion occurred only among the SAD-susceptible, we all have the capacity for it. Dr. Wehr found that normal non-SAD volunteers could be pushed into prolonged melatonin secretion after enduring very tightly controlled cycles of exposure to light and dark.
"We all have the capacity to show changes in melatonin secretion, but in the modern environment that response does not occur," says Dr. Wehr. The modern environment, of course, is full of artificial light, and for most people the body reads it as dim daylight well enough for it to impact melatonin production.
"It could be that SAD patients are less sensitive to light. They are not perceiving artificial indoor light as sunlight." And healthy individuals, because they are sensitive to indoor light, do not biologically perceive changes in day length during winter.
In the Dark
"People with SAD are literally in the dark," explains Dr. Rosenthal. "They don't take artificial light seriously biologically. They get a seasonal signal that is not overridden by artificial light" as it is among the non-SAD. "As a result, people with SAD need supplemental light."
Nightly melatonin production takes place in the pineal gland, which gets its orders from an internal pacemaker, a cluster of nerve cells deep in the brain's hypothalamus that registers light conditions and controls rhythms of alertness. The hypothalamus, in turn, gets its information about light and dark via a dedicated nerve pathway, a kind of light superhighway that runs between the retina and the hypothalamus.
Neuroscientists know that the photoreceptors involved in this pathway are special, different from the rods and cones that regulate everyday vision. It may be that genetic variation in these receptors may render some people susceptible to SAD.
Bright light also affects the emotional brain, reports Dr.. Rosenthal. "We now know—it has been recently demonstrated in imaging studies—that bright light of suitable duration affects the parts of the brain known to be involved in mood regulation."
However they get there, it isn't just that SAD-sufferers exhibit a seasonality in melatonin production, says Dr Wehr. They are also susceptible to depression. "If melatonin increases, most normal people do not become depressed. That points to a second difference in those with SAD. They respond to the change in melatonin with other changes."
While we call these changes "depression," the term does not "do justice to the range of changes" people experience, Dr. Wehr insists. The changes affect fundamental bodily functions, shifts that are at least as much physical as psychic—in energy, drive, weight, sexual desire. These are collectively referred to as "reverse vegetative" changes, and point to disturbances far deeper than mood but perceived as mood.
A Whole New Approach
The depression of SAD is unusual in yet another way. Sufferers can predict when it will strike. And that is opening the door to attempts to prevent onset of the disorder.
Trials are now underway of one or more antidepressant drugs in once-a-day formulations started a month before the usual onset of SAD and continued throughout the season of risk. While the results are not in yet, the study is premised on the idea that patients may not need to take the medication all year if they start ahead of time to ward off symptoms. With any luck, the study will demonstrate that they can discontinue medication in the spring and resume it early in the fall.
One drug now under study for such a use is Wellbutrin. Zoloft is another.
Researchers at the National Institutes of Health are also exploring the feasibility of a totally different pharmacologic approach to SAD, administering the beta-blocker propranolol. It acts at the pineal gland to shut off the signal of melatonin production. A single dose in the morning mimics the effect of morning light. Reports Dr. Wehr, "The studies are promising."
"Light will always be an important element in the treatment of SAD," says Dr. Rosenthal. "And it provides an important clue to what is going on in the illness."
But he is optimistic that drugs may play a role in the future. Light therapy is sometimes not sufficient to banish SAD. Or people are not willing to undergo it.
The search for sensible drug therapy for SAD will have other benefits, he believes. "The connection with light is well-known," he observes. "And much research in SAD has been focused on light therapy. But still the condition is neglected."
Dr. Rosenthal thinks that drug therapy will help put SAD on the map, squarely above the thirtieth parallel but definitely somewhere under the sun.
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