Leave it to researchers in Denmark, home of long, dark winters, to find the cause of seasonal affective disorder, or the aptly named SAD.

In a study presented earlier this month at a European College of Neuropsychopharmacology meeting in Berlin, researchers from the University of Copenhagen confirmed why, come winter, some people are hit with seasonal blues.

SAD is a condition that can result in depression and is normally tied to seasonal change. About 5 percent of the population suffers from SAD. If you have ever lived in a northern region where the days shrink come November and you don’t feel the heat of the sun until March, chances are you’ve met someone with SAD. The most popular treatment for SAD is exposure to ultraviolet light. 

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SAD most commonly affects women, teens, and young adults. It turns out that the brain chemical serotonin and the serotonin transporter (SERT) protein may be to blame.

Serotonin is a neurotransmitter made in the brain and in the gut that is thought to affect mood, social behavior, sleep, appetite, memory, sexual desire, and more. Serotonin levels are associated with depression, but whether low serotonin levels cause depression or vice versa is still unclear. Medications like selective serotonin reuptake inhibitors (SSRIs) are prescribed as antidepressants to help maintain serotonin levels in a person’s brain.

Researchers speculate that lack of exposure to sunlight is the cause of SAD, but this study may help pin down why SAD is so tied to the changing seasons. Using PET brain scans, researchers studied 11 people with SAD and 23 without. “We found that healthy individuals with no [SAD] actually have lower SERT in winter,” said lead researcher Dr. Brenda Mc Mahon.

While shorter days and cold weather are enough to make anyone stay inside with a cup of hot cocoa, for some, SAD is much more than just a couple days of feeling down. What Mc Mahon and her team found is that for people affected by SAD, compared to the general population, SERT levels are significantly higher.

During the winter, the SAD population experiences an uptick in SERT, which carries serotonin into nerve cells where it is inactive. So, the more SERT, the less active serotonin in the brain.

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Mc Mahon and her team focused on SERT because previous studies have shown that SERT levels fluctuate in healthy subjects.

“We would like to see if the SERT is susceptible to light changes in a controlled setting using … bright light therapy,” Mc Mahon said. “Genetic studies of the gene 5-HTTLPR that codes for the SERT are implicated in regulating the response to bright light therapy.”

These findings point to a genetic reason why some people are affected by SAD and some aren’t, as well as why some people respond to UV light therapy while others don’t.

However, there is still the chicken-and-egg issue of whether changes in SERT levels cause SAD or are simply a side effect of the condition. “We would like to investigate if these SERT changes are the primary event or a secondary compensatory mechanism,” Mc Mahon said.

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At this point, the research is still in its infancy. Before these findings can be applied, researchers need to determine how SERT can be used to diagnose and treat SAD.

“This is basic research, aimed [at explaining the] neurobiological underpinnings of SAD,” Mc Mahon said. “Future research must clarify how this can be used.”

For those living in colder climates under a thick blanket of SAD, there may be a bright light at the end of a long winter tunnel.