A case of the winter blues- the facts and science behind Seasonal Affective Disorder (SAD) 

By Fatemah Kassamali

Note: this article deals with themes associated with depression- please speak to a trained mental health professional to seek help if you need it.          

As the nights draw in and temperatures plummet, many people report feeling the “winter blues”, but is there more to this story than just feeling a little low? Sufferers from winter-patterned Seasonal Affective Disorder (SAD) often link their emotional state to the seasons, with colder periods being anecdotally correlated to symptoms linked to the onset of depression. As the taboo of mental health is being tackled on a global scale, it is important for us to shine a light on the realities many face and open up such conversations with those around us. This is especially critical at a time as we are entering the aftermath of COVID-19, with increasing diagnoses of depression and related mental conditions1.

The reported symptoms of SAD are highly variable in both nature and severity between patients. In alignment with the symptoms of depression: reported feelings of consistent low mood and difficulties with insomnia, lethargy, loss of appetite, difficulty concentrating, and in some cases suicidal thoughts2,3. Reporting experiences with these symptoms in the colder months (circa October through March) in an annual periodicity is characterised as winter-patterned SAD. Other specific winter symptoms include hypersomnia (oversleeping), social withdrawal (colloquially termed ‘hibernation’), and overeating leading to weight gain2. Meanwhile, sufferers from the less-common summer-patterned SAD have reported feelings of increased anxiety and restlessness2,3. Moreover, it is theorised that some of the symptoms associated with SAD could be the result of underlying, often undiagnosed, mental health conditions4 or associated with hormonal changes especially in young adulthood2, which are exacerbated in certain periods of the year.

Generally, the profile of patients diagnosed with SAD is as variable as the symptoms. In the UK. An estimated 6% of the population is thought to be affected by SAD5. Strikingly, geography influences notably the proportion of the population diagnosed with SAD. In the USA, the statistics have indicated that those living in northern states (e.g. New Hampshire at 10%) have a much higher prevalence compared to southern states (e.g. Florida at 1.4%), whereas the global US average is 5%6. Whilst the easily apparent difference in local climate, conjures up a sensible parallel regarding SAD diagnosis rates, discrepancies in access to mental healthcare and public information campaigns regarding SAD, on both a national and international level, does draw this link into question. On average, women are more likely to be diagnosed with SAD2. However, as with many mental health conditions, the historic hesitance amongst male members of the population to consult with a mental health professional, casts a shadow on this average. The validity of SAD as a mental health condition has been questioned in the field, most notably by Traffanstedt, et al., because their analysis indicates the rate of patients with symptoms of depression does not show seasonal variation and recurrence is in line with natural oscillations in depressive episodes7. However, such arguments have been widely criticised, as they fail to account for a potentially varied lag-time between presentation and diagnosis, the limitation of sunlight exposure as a lone marker for seasonal climate changes, as well as not acknowledging personal case studies of the impact of seasonal variation on patient wellbeing. 

Despite many attempts to understand the causes of SAD, the underlying science is yet to be fully characterised. Suggestions of a link between SAD and circadian rhythms is a widely accepted theory in the field2,3,6, with the seasonal change to our time clocks misaligning with our body clocks. The suprachiasmatic nucleus in the brain is known as the ‘timekeeper of circadian rhythms’, receiving stimulus from Retinal Ganglion Cells upon the detection of sunlight and outputting subsequent signals to the pineal gland, inhibiting melatonin secretion6,8. Melatonin levels are strongly correlated with the night-day cycle, with suppression causing wake signals. The lack of light in the winter months can be the direct cause of hypersomnia, as the body does not receive the cue to wake from sleep8

Other fields of study have suggested that SAD is instead caused by depletion of the neurotransmitter serotonin. Changes in serotonin levels is widely accepted to be associated with fluctuations in mood9 and the regulation of serotonin and precursor tryptophan is thought to be implicated in depression9. Using Positron Emission Tomography (PET)10, brain scan studies indicated that patients diagnosed with SAD have an upregulated level of Serotonin Transporter protein (SERT, 5-HTTLPR) in the winter11. Polymorphisms in 5-HTTLPR have shown to be associated with increased prevalence of SAD12 The increased level of serotonin transportation outside of the extracellular environment of neurones in the cerebral cortex, leads to reduced “happy” stimuli11,12, theoretically causing symptoms associated with depression. Therefore, a plausible cause of SAD could be a synergistic mechanism between melatonin misalignment and serotonin depletion. 

Can we not simulate summer to cure winter-patterned SAD? The use of UV light therapy boxes to mimic natural light has been reported to ameliorate the symptoms of some patients with SAD2,3,5,6. The Swedish government has converted bus stops into light boxes, which failed due to practical limitations6,13. However, trials seem to indicate that this is not a blanket solution for all patients, with 43% of patients reporting remission of symptoms11. Additionally, a link between the deficiency of vitamin D, an endogenous promoter of serotonin associated with skin exposure to sunlight, and SAD has been explored6. However, the efficacy of vitamin D supplements as a prescription to treat SAD had contradictory findings, requiring further research2. Traditional cognitive behavioural therapy has reported success at patient-level2, but it is limited by the shortage of qualified mental health professionals and time commitments of patients, highlighting the need for therapeutics at the molecular level. 


  1. Santomauro, D.F. et al. (2021) “Global prevalence and burden of depressive and anxiety disorders in 204 countries and territories in 2020 due to the COVID-19 pandemic,” The Lancet, 398(10312), pp. 1700–1712. Available at: https://doi.org/10.1016/s0140-6736(21)02143-7
  2. National Institute of Mental Health. U.S. Department of Health and Human Services. Seasonal affective disorder at: https://www.nimh.nih.gov/health/publications/seasonal-affective-disorder  (Accessed: October 22, 2022). 
  3. Mayo Clinic. Mayo Foundation for Medical Education and Research (2021). Seasonal affective disorder (SAD)Available at: https://www.mayoclinic.org/diseases-conditions/seasonal-affective-disorder/symptoms-causes/syc-20364651  (Accessed: October 22, 2022).
  4. Roecklein, K.A. and Wong, P.M. (2013) “Seasonal affective disorder,” Encyclopedia of Behavioral Medicine, pp. 1722–1724. Available at: https://doi.org/10.1007/978-1-4419-1005-9_836
  5. Jinks, L. (2022) The science behind Seasonal affective disorder (SAD)SRG. Available at: https://www.srgtalent.com/blog/the-science-behind-seasonal-affective-disorder  (Accessed: October 21, 2022). 
  6. Pfizer. The Science Behind the Winter Blues. Available at: https://www.pfizer.com/news/articles/the_science_behind_the_winter_blues  (Accessed: October 22, 2022). 
  7. Traffanstedt, M.K., Mehta, S. and LoBello, S.G. (2016) “Major depression with seasonal variation,” Clinical Psychological Science, 4(5), pp. 825–834. Available at: https://doi.org/10.1177/2167702615615867
  8. Rosenthal, N. E., Sack, D. A., Jacobsen, F. M., James, S. P., Parry, B. L., Arendt, J., Tamarkin, L., & Wehr, T. A. (1986). “Melatonin in seasonal affective disorder and phototherapy,” Journal of neural transmission. Supplementum, 21, pp. 257–267.
  9. Magnusson, A. and Boivin, D. (2003) “Seasonal affective disorder: An overview,” Chronobiology International, 20(2), pp. 189–207. Available at: https://doi.org/10.1081/cbi-120019310
  10. Erritzoe, D., Ashok, A. H., Searle, G. E., Colasanti, A., Turton, S., Lewis, Y., Huiban, M., Moz, S., Passchier, J., Saleem, A., Beaver, J., Lingford-Hughes, A., Nutt, D. J., Howes, O. D., Gunn, R. N., Knudsen, G. M., & Rabiner, E. A. (2020). “Serotonin release measured in the human brain: a PET study with [11C] CIMBI-36 and d-amphetamine challenge,” Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology, 45(5), 804–810. Available at: https://doi.org/10.1038/s41386-019-0567-5
  11. Terman, M., Amira, L., Terman, J. S., & Ross, D. C. (1996). “Predictors of response and nonresponse to light treatment for winter depression,” The American journal of psychiatry, 153(11), 1423–1429. Available at: https://doi.org/10.1176/ajp.153.11.142.
  12. Rosenthal, N. E., Mazzanti, C. M., Barnett, R. L., Hardin, T. A., Turner, E. H., Lam, G. K., Ozaki, N., & Goldman, D. (1998). “Role of serotonin transporter promoter repeat length polymorphism (5-HTTLPR) in seasonality and seasonal affective disorder,” Molecular psychiatry, 3(2), 175–177. Available at: https://doi.org/10.1038/sj.mp.4000360.
  13. Sky (2012) Bus stop light therapy dazzles driversSky News. Sky. Available at: https://news.sky.com/story/bus-stop-light-therapy-dazzles-drivers-10462280 (Accessed: October 24, 2022). 

A very good idea, should be included. [GW1]

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