12/19/2025 | Press release | Distributed by Public on 12/19/2025 10:33
For some people, the start of winter can bring the onset of depression, fatigue, and agitation. These symptoms can be severe enough to interfere with day-to-day life. Some people may begin to overeat, especially carbohydrates, resulting in unintended weight gain. They may have a hard time concentrating on regular tasks or not feel joy from their hobbies or favorite activities.1
This may be more than the winter blues; it may be seasonal affective disorder (SAD). There are two primary types of SAD: winter-pattern SAD and summer-pattern SAD. This article addresses the more common type, winter-pattern SAD, in which depressive symptoms begin in late fall or early winter and mostly resolve in the spring or summer.1
The prevalence of SAD depends upon geography. Because less exposure to the sun can negatively affect one's mood and behavior, SAD is more common in higher-latitude areas that experience fewer hours of sunlight during the winter months. For example, SAD has a rate of 9.7% in New Hampshire but just 1.4% in Florida.2SAD also has an association with other mental disorders. People are more likely to develop SAD who have conditions such as bipolar disorder, attention-deficit/hyperactivity disorder, or anxiety.1
Lower Serotonin Levels
During the winter months, people with SAD tend to have lower levels of serotonin, a chemical within the body that manages mood and behavior, among other things. When serotonin levels drop, people may become more susceptible to depression.
Research suggests that sunlight affects serotonin production, and that even healthy adults experience seasonal patterns: higher serotonin levels during sunny, summer months and lower during the darker, winter months. Adults with SAD, however, seem to be especially susceptible to the effects of these seasonal changes.3
Higher Melatonin Levels
During winter, people with SAD tend to have higher levels of melatonin, a hormone that regulates the sleep cycle and signals to our body when it's time to fall asleep or wake up. 4
Like serotonin, the production of melatonin has a connection to light; unlike serotonin, however, the levels of melatonin rise with a lack of sunlight. This increase can disrupt the body's sleep-wake cycle, especially in people with SAD, causing daytime sleepiness.5
Lower Vitamin D Levels
Lower levels of vitamin D have been found in people who have SAD. The body produces vitamin D when sunlight hits the skin, so less daylight can mean lower levels of the "sunshine vitamin."1,6
Research suggests that vitamin D affects how our bodies regulate both serotonin and melatonin. A drop in vitamin D, then, could exacerbate the effects of SAD in those who have it.1,7
[1] Seasonal Affective Disorder. National Institute of Mental Health: National Institutes for Health. 2023. Accessed December 5, 2025. https://www.nimh.nih.gov/health/publications/seasonal-affective-disorder
[2] Seasonal Affective Disorder. National Library of Medicine: National Institutes for Health. April 20, 2024. Accessed December 5, 2025. https://www.ncbi.nlm.nih.gov/books/NBK568745/
[3] Sansone RA, Sansone LA. Sunshine, serotonin, and skin: a partial explanation for seasonal patterns in psychopathology?. Innov Clin Neurosci. 2013;10(7-8):20-24.
[4] Melatonin: What You Need to Know. National Center for Complementary and Integrative Health: National Institutes for Health. May 2024. Accessed December 5, 2025. https://www.nccih.nih.gov/health/melatonin-what-you-need-to-know
[5] Melrose S. Seasonal Affective Disorder: An Overview of Assessment and Treatment Approaches. Depress Res Treat. 2015;2015:178564. doi:10.1155/2015/178564
[6] Vitamin D: Fact Sheet for Professionals. Office of Dietary Supplements: National Institutes of Health. June 27, 2025. Accessed December 5, 2025. https://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/
[7] Yao L, Chen M, Zhang N, et al. The Mediation Role of Sleep Disturbances between Vitamin D and Depressive Symptoms: A Cross-Sectional Study. Brain Sci. 2023;13(11):1501. Published 2023 Oct 24. doi:10.3390/brainsci13111501