Winter depression may heed hormonal signal

It’s the most wonderful time of the year, according to a popular holiday song. Yet it’s the most excruciating time for people who endure the biological tidings of discomfort and gloom that are linked to winter’s arrival, according to a new study.

A specific shift of the body’s daily pacemaker, akin to one that regulates seasonal behavior in many mammals, underlies recurring winter depression, contend psychiatrist Thomas A. Wehr of the National Institute of Mental Health (NIMH) in Bethesda, Md., and his coworkers.

“These results vindicate what we suspected about this condition when we first described it in 1984,” says NIMH psychiatrist Norman E. Rosenthal, a coauthor of the new report in the December Archives of General Psychiatry. Conducting a study big enough to probe the condition’s biological bases has taken years, he notes.

Winter depression, or seasonal affective disorder (SAD), includes weight gain, increased sleep, decreased physical activity, and loss of interest in sex. Comparable responses occur in many mammals as sunlight wanes in winter. In these creatures, when the brain detects shortening of day length, it secretes melatonin for a longer time at night. Melatonin is a hormone that regulates sleep.

To see if similar melatonin changes occur in people, Wehr’s group recruited 110 volunteers, half with SAD and half without. The scientists measured melatonin concentrations in blood samples obtained from the participants every 30 minutes for 24 hours in each season.

The researchers found that the duration of melatonin release was steady at 9 hours throughout the year in the participants without SAD. In those with SAD, nightly melatonin secretion lasted, on average, 38 minutes longer in the winter than in the summer, with the greatest durations being about 9 hours. This seasonal disparity was more pronounced in men than in women.

Melatonin secretion began at about the same time in the early evening for people in both groups. For volunteers with SAD, most of their extra melatonin activity in winter occurred at the end of the night. The lengthening of nightly melatonin secretion from summer to winter in SAD may somehow trigger the condition, Wehr and his colleagues theorize.

“This study provides important evidence that winter depression is, at least in part, related to biological rhythms,” says psychiatrist Al Lewy of the Oregon Health Sciences University in Portland. In his studies of SAD patients, Lewy sees a delay in nightly onset of melatonin release. He suspects that it’s caused by the later dawn each morning during the winter. His research suggests that morning doses of bright light dampen winter depression by advancing the start of nightly melatonin secretion by 1 to 2 hours (SN: 10/24/98, p. 260: https://www.sciencenews.org/sn_arc98/10_24_98/Fob1.htm) without necessarily lengthening the duration of that secretion.

Although Wehr’s team has conducted the largest SAD study to date, questions remain about how to interpret the results, comments psychologist Michael Terman of Columbia University in the same journal.

For instance, Terman speculates, among 12 of the 55 SAD volunteers in the NIMH study who experienced euphoria, excess energy, and other manic symptoms in the summer, shorter periods of melatonin secretion may largely reflect early awakening in that season. Their exposure to early-morning light, rather than SAD, would have cut off melatonin secretion, Terman holds.