As fall transitions into winter, all animals, including humans, must acclimate to colder weather, shorter days, and less sunlight. In many northern latitudinal regions across the globe, winter is often characterized by overcast skies and snowy days, in which little to no sunlight reaches life on the ground. Colloquially, some people report having the “winter blues” each year once winter briskly enters the picture. However, what many people don’t know is that winter depression actually has a biological basis and is classified as a medical condition, called seasonal affective disorder (ironically, abbreviated SAD). Better yet, scientists are diligently working to tease apart the biological mechanisms underlying SAD, which will ultimately allow for the development of novel treatments.
The Diagnostic and Statistical Manual of Mental Disorders, which describes the standard criteria for classifying mental disorders, defines SAD as “depression that begins and ends during a specific season every year, in which no episodes of depression occur during the season in which you experience a normal mood.” Specifically, winter SAD is a subtype of depression that is characterized by the recurrence of major depressive episodes in the fall and/or winter months and remission of these episodes during the following spring or summer. In addition to depression, SAD is often accompanied by atypical depressive symptoms, including lethargy; increased sleep, or hypersomnia; overeating, or hyperphagia; craving for carbohydrates; weight gain; and loss of libido. Interestingly, although SAD is a relatively common condition, which affects about 5% of adults in the United States; SAD is four times more common in women than in men. Overall, SAD prevalence and severity tend to be inversely related to photoperiod, or day length, such that SAD is more common at higher (i.e., northern) latitudes.
So, what causes SAD, and why is SAD such a problem during the winter months? To answer these questions, we need to look deeper into the physiological mechanisms that underlie SAD. More specifically, we must examine the processes that are responsible for maintaining the body’s circadian, or daily, rhythms. In all mammals, including humans, light information is converted into a neural signal by specialized photosensitive, or light-sensitive, neurons in the retina of the eye. The activity of these nerve cells, called photosensitive retinal ganglion cells, is inhibited by sunlight and is activated by darkness; thus, photosensitive retinal ganglion cells are, counterintuitively, more active during the nighttime hours. Information about the activity of these specialized cells is transmitted to a brain region called the suprachiasmatic nucleus (SCN). The SCN is also called the central pacemaker, since this brain region is responsible for regulating most circadian rhythms in the body, including the sleep/wake cycle and daily shifts in physiology and behavior. Then, this signal passes through a series of nerve cells in the brain and spinal cord and is transmitted to its ultimate destination: the pineal gland. This gland translates the neural signal into an endocrine message by secreting the hormone melatonin during the night. Thus, this mechanism culminates in the release of melatonin into circulation, and melatonin then communicates with the rest of the body to relay photoperiodic information.
While a few different theories have been proposed to explain the psychological symptoms associated with SAD, one hypothesis in particular, the phase-shift hypothesis, has garnered the most support from scientists. The phase-shift hypothesis suggests that SAD patients have delayed circadian rhythms relative to their sleep/wake cycle. In other words, because dawn occurs later during the winter months, our circadian rhythms also naturally shift later, causing our internal clock to be out of sync with our actual sleep/wake cycle, which stays the same throughout the year. Indeed, a recent study showed that patients whose melatonin production begins too many or too few hours prior to going to sleep at night tend to have the highest rates of SAD. Some studies also suggest that other factors may contribute to SAD, including abnormal melatonin secretion from the pineal gland; irregular retinal sensitivity to sunlight, which may result in atypical activity of photosensitive retinal ganglion cells; decreased vitamin D levels; and deviations in daily cycles of core body temperature and metabolic (i.e., energy-releasing) hormones, such as cortisol. Furthermore, there is evidence that SAD is a consequence of reduced synthesis or dysfunction of serotonin, a chemical messenger that modulates mood and regulates physiological processes related to cognition, reward, learning, and memory.
Although the physiological irregularities that result in SAD are still being explored, several treatments are effective in alleviating its symptoms. To date, light therapy has been one of the most successful treatment options for patients with SAD. Light therapy is a natural, non-invasive treatment that involves sitting close to a special broad spectrum, fluorescent “light box” for about 30 minutes each day, typically during the early morning hours. This treatment is particularly effective for patients that have a phase shift in their circadian rhythms during the winter months, since light therapy corrects phase-shifting by synchronizing your natural circadian rhythms with your actual sleep/wake cycle. In fact, this treatment is so successful that universities and public libraries in parts of the northern U.S. and Canada offer free light therapy stations to people suffering from SAD. Furthermore, recent work suggests that cognitive-behavioral therapy and medication may also be effective options for treating SAD. In particular, antidepressants and selective serotonin reuptake inhibitors (SSRIs), which increase serotonin levels in the brain, have had some success in relieving the psychological symptoms associated with SAD. With these treatments and the promise of others on the horizon, there is a chance of relief for the hundreds of thousands of people that experience SAD each winter.
For more information about seasonal affective disorder and its potential treatment options, check out my recommendations for further reading below!
References and Recommendations for Further Reading:
Cotterell, D. (2010). Pathogenesis and management of seasonal affective disorder. Progress in Neurology and Psychiatry, 14, 18-25.
Koch, B. C. P., Nagtegaal, J. E., Kerkhof, G. A., & ter Wee, P. M. (2009). Circadian sleep-wake rhythm disturbances in end-stage renal disease. Nature Reviews Nephrology, 5, 407-416.
Melrose, S. (2015). Seasonal affective disorder: an overview of assessment and treatment options. Depression Research and Treatment, 178564.
Rohan, K., & Rough, J. N. (2017). Seasonal affective disorder. In R. J. DeRubeis & D. R. Strunk (eds.), The Oxford Handbook of Mood Disorders (pp. 254-262). Oxford: Oxford University Press.
Tam, E. M., Lam, R. W., & Levitt, A. J. (1995). Treatment of seasonal affective disorder: a review. Canadian Journal of Psychiatry, 40, 457-466.