Better known by its Anglo-Saxon acronym SAD (‘sad’ in English), seasonal affective disorder or winter depression refers to the severe mood swings that some people experience during the fall and winter , when there is less exposure to sunlight. Common symptoms include sadness and anxiety, pessimism, feelings of guilt or helplessness, irritability and restlessness, loss of interest in activities you used to enjoy, social withdrawal, tiredness and decreased energy, difficulty concentrating and remembering details, changes of weight, insomnia in some cases and excess of drowsiness in others, and suicidal thoughts.
Emotional affective disorder has been associated with melatonin , a hormone related to sleep that occurs in greater proportion when the days are shorter and darker. Some studies suggest that the further a person lives from the equator, the more likely they are to develop this disorder.
Half of those affected respond positively to light therapy treatments ( phototherapy ).
A new study used a seasonal affective disorder model to find out why some people don’t develop depression despite being genetically predisposed to it. The findings also shed light on possible new treatments for seasonal depression.
The symptoms of seasonal affective disorder or seasonal / winter depression are so similar to those of depression that it can sometimes be difficult to distinguish between the two.
It usually affects women. In fact, 4 out of 5 people with the condition are women, and the reasons for this predisposition are likely genetic.
However, although some people are genetically prone to the disease, they resist the environmental factors that could trigger it.
The new work set out to examine the neurobiology of seasonal affective disorder in an attempt to understand what actually makes some people more resistant to the development of depression.
The results of the study were published in the journal European Neuropsychopharmacology.
The key role of serotonin transporters
As the researchers explain, seasonal depression is caused by a lack of daylight, which makes the disease more widespread in countries that are farther from the equator.
“Daylight is indeed a natural antidepressant. Like many medications currently used against depression, more daylight prevents serotonin from being removed from the brain,” explains Brenda McMahon, leader of the work.
Previous studies have shown that winter depression tends to affect people with a gene called 5-HTTLPR. This gene encodes a brain serotonin transporter, a protein that regulates how efficiently serotonin, the so-called happiness neurotransmitter, is removed from the brain.
Most antidepressants work by lowering the levels of serotonin transporters to slow the clearance of serotonin between nerve cells.
For the new study, the experts recruited 23 participants, 13 of them women, who had not developed depression despite having the 5-HTTLPR gene.
The scientists used a positron emission tomography (PET) scanner once in summer and twice in winter to examine the participants’ levels of both serotonin and serotonin transporter.
“We found,” explains McMahon, “that the level of serotonin transporter protein dropped by an average of about 1% between summer and winter, with a markedly greater drop in women.”
“We found that some people who we would expect to have winter blues because of their genetic disposition could, however, control the amount of serotonin transport that is produced, which means that they were able to regulate the amount of serotonin removed from their brain,” he adds. “In this way they become more resistant to depression.”
This is the first time anyone has used PET scans to look at resistance to winter blues.
