By IANS,
Washington : Seasonal affective disorder or SAD can be a debilitating depression that begins in the autumn and continues through winter. A new study indicates that SAD may be linked to a genetic mutation in the eye that makes a patient less sensitive to light.
The affliction makes you feel sad, grumpy, moody or morose. You crave carbohydrates, gain weight, sleep more and feel drowsy during daytime.
Though not not well understood, SAD is often treated with “light therapy”, where a patient spends time before a bank of bright lights in an effort to trick his brain into believing that the days are bright.
“These individuals may require brighter light levels to maintain normal functioning during the winter months,” said Ignacio Provencio, University of Virginia biology professor who studies the genetics of the body’s biological clock, or circadian rhythms.
Provencio and his colleagues have discovered that melanopsin, a photopigment gene in the eye, may play a role in causing SAD in people with a recently discovered mutation.
“We believe that the mutation could contribute to increasing the amount of light needed for normal functioning during winter for people with SAD,” Provencio said. “Lack of adequate light may be a trigger for SAD, but not the only explanation for the disorder.”
The study was conducted with several other institutions, including the National Institute of Mental Health. It involved 220 participants, 130 of whom had been diagnosed with SAD and 90 participants with no history of mental illness, according to a Virginia university release.
Using a genetics test, the study authors found that seven of the 220 participants carried two copies of the mutation that may be a factor in causing SAD, and, strikingly, all seven belonged to the SAD group.
“While a person diagnosed with SAD does not necessarily carry the melanopsin mutation, what we found strongly indicates that people who carry the mutation could very well be diagnosed with SAD,” Provencio said.
The researchers found that a person with two copies of the gene is five times more likely to have symptoms of SAD than a person without the mutation.
The findings were published in the online edition of the Journal of Affective Disorders.