People living in unforgiving climates will testify that the winter blues is a very real phenomenon affecting millions each year as the seasons change and the greens of summer turn white. A recent Canadian study has gone a step further, identifying neurological changes brought on by extreme weather that affect both the level of mood-enhancing hormone serotonin and the mechanism by which it’s transported. A study performed by the Center for Addiction and Mental Health (CAMH) in a country whose citizens report alarmingly high instances of the “winter blues,” confirms the prevalence of Seasonal Affective Disorder (SAD) and identifies its most likely cause: a slowdown in serotonin activity due to a decline in the ability of serotonin transporter genes to bind themselves to target molecules.

The symptoms of SAD very closely resemble those of standard clinical depression. It not only regulates mood but can lead to changes in appetite, energy level, metabolism and sexual functions. All these variables heavily influenced by serotonin levels in different parts of the brain, and the inconveniences brought on by unpleasant weather only contribute to the condition because the winter months make less-active lifestyles necessary in cold climate. Researchers have long known that serotonin levels dip during the winter months but, until now, have not been able to explain why. The answer is a decreased level of serotonin transporter binding. Because these genes are less active in the vulnerable period stretching from late fall to early spring, less serotonin is removed from the affected brain. This fact initially sounds counterintuitive as serotonin deficiencies are often to blame for low moods. But serotonin moves in a cyclical pattern, and these transporters only help to make that cycle move faster, with the brain’s serotonin levels effectively refreshing themselves. When these receptors fail to bind to the serotonin molecules, decreased serotonin movement affects the brain’s ability to regulate mood and results in a greater prominence of depressive symptoms. 

One of the key elements in this equation is light exposure. The main variable in the study was average daily hours of sunlight. Not only is sun exposure compromised by an inability to spend extended periods outside in cold temperatures, but the days themselves of course grow shorter during winter months. There’s simply less light to be had. And trends in the CAMH study showed that levels of depression coincide very closely with average amounts of daily sunshine. But the research goes a step further, using positron emission tomography brain scans to demonstrate particularly notable deficiencies in the binding ability of serotonin transporter genes during these low-sunlight periods.

Researchers do not yet know exactly why transporter binding efficiency is compromised by a lack of sunlight, but further research will certainly illuminate that process. For now, the most important advice that can be drawn from this study is that, true to the age-old mothers’ axiom, time spent in the daylight really does improve the mood even when the temperature outside is 20 below. Fresh air and sunshine may indeed be some of nature’s best medicine.