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Winter makes me SAD: The biological story behind seasonal affective disorder and its potential treatments

Posted on by Kat Munley

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.

A barren hillside with a few large boulders and trees scattered in the background. The trees pictured have no leaves, and there are a few small patches of grass growing on the side of the hill. The sky above is overcast, and no visible sunlight is shining through the clouds.
In the northern latitudes, winter is commonly characterized by overcast skies, in which little to no sunlight is visible from the ground. This lack of light exposure during the day is thought to be the major cause of seasonal affective disorder. Image credit: Petr Horák.
A young adult woman is hunched forward and covering her face with both of her hands. The photograph is in black and white.
People that have seasonal affective disorder (SAD) often experience depressive episodes during the fall and/or winter months. In addition, patients often report symptoms such as fatigue, increased sleep, loss of libido, overeating, carbohydrate craving, and weight gain. Image credit: Peter vd Ham.

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.

Profile of a drawing of a human head, colored in blue. The human head drawing contains an eye and a brain, in which specific structures are highlighted in different colors. The front of the head is facing a drawing of a sun, which is located to the left of the head. A solid black line is drawn from the sun to the eyeball on the human head, with the word “Inhibition” written above it. A thick tan, tubular structure connects the back of the eye to a small circular red structure near the middle of the brain, and a black dotted line runs along the middle of the tan structure and points to the red structure. The tan structure is labeled “Retinohypothalamic tract,” and the red structure is labeled “Suprachiasmatic nucleus.” Another thick tan, tubular structure runs down the base of the brain to a tan circular structure, which is located slightly below the human head drawing. A black dotted line runs along the middle of this tan tubular structure and points towards the tan circular structure, which is labeled “Superior cervical ganglion.” A black dotted line is drawn from the superior cervical ganglion back along the thick tan, tubular structure at the bottom of the human head drawing, and this dotted line points to a small green, circular structure located near the center of the brain and to the left of the suprachiasmatic nucleus. This small, green structure is labeled “Pineal gland.” A solid black arrow points from the pineal gland to a yellow box located to the right of the human head, which contains a drawing of a chemical structure that is labeled “Melatonin.”
Schematic of the physiological mechanisms underlying seasonal affective disorder (SAD). In all mammals, including humans, light information is transmitted into a neural signal via specialized photosensitive ganglion cells in the retina. Specifically, sunlight inhibits the activity of these photosensitive ganglion cells, whereas darkness activates these cells. This signal is then transmitted to the suprachiasmatic nucleus, a brain region that is responsible for regulating circadian (i.e., daily) rhythms, via the retinohypotahalmic tract. Interestingly, this neural signal leaves the brain and travels to the superior cervical ganglion in the spinal cord, and then re-enters the brain and is transmitted to the pineal gland. This small endocrine gland ultimately translates this neural signal into an endocrine message by secreting the hormone melatonin, specifically at night. Studies suggest that the physiological and psychological symptoms displayed by SAD patients are the result of circadian phase shifting during the winter months, in which patients’ natural circadian rhythms, which are modulated by melatonin, are delayed relative to their actual sleep/wake cycle. Image credit: Koch et al. 2009 (Nature Reviews Nephrology).

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.

A young man is sitting at a wooden desk at a library, and a textbook, notebook, cup of coffee, and a glowing rectangular screen are sitting on top of the desk. He is holding a pen in his hand, looking up from his notebook, and smiling at the camera. Other cubicles and workstations are visible in the background of the image.
A student studying at a light therapy station in the Red River College library. This university, which is located in Winnipeg, Manitoba, Canada, recently added light therapy stations to their libraries for students experiencing seasonal affective disorder (SAD). Light therapy is one of the most common treatments recommended to SAD patients. Image credit: Red River College.

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.

Edited by Riddhi Sood and Taylor Nicholas

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