Why Does This Happen?

Through decades of research, SAD was revealed to be quite a complex mood disorder. Several proposed theories regarding the pathophysiology will be broken down in this article. It seems likely that the internal and external factors that have been identified in the following theories all play a role in the pathogenesis of this mood disorder.

The Latitude Hypothesis

The first theory, and perhaps the most well-known, is the latitude hypothesis. This is one of the first causes of SAD to be investigated. It is based on the idea that those at increasing latitudes are more likely to have SAD, due to the decreased amounts of sunlight they are exposed to in winter seasons. A few studies have been performed with results that align with this hypothesis; however, there are exceptions to this theory. The largest study conducted on the latitude hypothesis mailed a validated questionnaire for SAD, the Seasonal Pattern Assessment Questionnaire, to four areas in the United States at different latitudes (n = 1671). It was found that rates of winter SAD and subsyndromal SAD were higher at more northern latitudes (p < 0.001). ⁶ This theory was somewhat questioned when a study analyzed SAD in Icelanders who had migrated to Canada versus the ethnic population that resided there (n = 252). It was found that the rates of SAD in the Icelandic population were much lower than the migrated population (p < 0.001). ⁷ This suggests that, in addition to latitude, there are likely genetic factors at play, or that Icelanders have developed tolerance.

Recent research has added to the understanding of the role of genetics in SAD. Family and twin studies have produced results demonstrating a positive genetic link in SAD. ⁸ Additionally, a genome-wide association study (GWAS) identified genetic variants in individuals with SAD that are involved in adult neurogenesis and circadian rhythm. This suggests that there is a genetic component involved in SAD.

The Phase-Shift Hypothesis

Another potential theory for the development of SAD is the phase shift-hypothesis. It posits that seasonal depression occurs due to phase shifts in internal circadian rhythms relative to the external environment. More specifically, it alludes to disruptions in melatonin and temperature rhythms versus the external clock and sleep-wake cycles. ⁹ These phase shifts can be either delayed or advanced, with phase delay believed to be more relevant to SAD. In a more recent study, it was determined that 71% of the study participants with SAD were phase-delayed, and 29% were phase advanced (n = 68). ¹¹ However, the number of participants in this study was rather small, and larger scale studies are required to further support this hypothesis. This theory has sparked scientific interest in potential treatments to readjust phase delays in individuals with SAD using light therapy, which will later be explored.

Hormone Biochemistry at Work

Other factors that may play a role in the development of SAD are disruptions in melatonin and catecholamine biochemistry.

Melatonin is a hormone that is produced by the pineal gland in response to the dark. It is involved in circadian rhythm regulation and sleep patterns. Several studies performed on melatonin’s involvement in SAD report inconsistent findings. Two studies found no significant differences in melatonin between patients with SAD and controls; however, another study reported higher daytime melatonin levels in those with SAD during depressive episodes (p < 0.05). ^12,13,14 Further research is required to better understand its role in this condition.

Serotonin is a catecholamine that has many actions including mood, memory, and behaviour. It has been extensively researched for its role in depression, and thus its role in SAD remains plausible. The administration of a serotonin agonist, meta chlorophenylpiperazine, has been shown to significantly increase feelings of euphoria in patients with SAD compared to controls, in multiple studies. ^15,16Additional research has demonstrated that individuals with SAD have the SERT protein increased by 5% (n = 15, p = 0.01). ¹⁷ This protein assists with protein-bound serotonin transport, and higher levels of this protein would lead to lower serotonin activity, which could explain low mood and depression.

The precursor of serotonin and other catecholamines, tryptophan, has also been investigated. A study instituted patients already diagnosed with SAD who were in remission on a protocol that depleted them of tryptophan. It was found that active depletion of this amino acid caused a temporary relapse of the depressive symptoms compared to no mood changes in the controls (n = 13, p < 0.001). ¹⁸

The Sunshine Vitamin Theory

Another plausible factor and likely contributor to SAD is vitamin D status. Low vitamin D levels have been consistently correlated with major depression, although the direction of this causality remains incompletely understood. ¹⁹ This is speculated to be relevant to SAD as many individuals at northern latitudes are deficient in vitamin D during winter months. This is due to reduced exposure to sunlight, which is required for vitamin D synthesis. Large-scale studies looking at this direct relationship have not yet been performed and would potentially provide a better understanding of the role of vitamin D in this condition.

Hopefully, you now understand all these theories and potential contributors to SAD. There is likely a complex interplay between several or all of these factors, and it is important to understand them, as they provide a basis for which we can understand what treatments are used and why.

Naturopathic Treatments and Prevention Light Therapy

Bright-light therapy has been used for over 30 years and has undergone many trials, although most consist of small to medium study sizes. This therapy requires retinal light exposure following waking time to assist in correcting possible phase delays. It typically involves artificial light, with a full spectrum lamp at 10,000 lux for 30–90 minutes. A meta-analysis demonstrated that bright-light therapy significantly improved depression scores in SAD patients versus placebo (n = 610, p < 0.05). ²⁰ Another meta-analysis looked at light therapies’ role in the prevention of SAD in patients who had a history of recurrent major depressive episodes in the fall or winter. It was found that both white-light therapy (n = 23, CI 95% 0.3 to 1.38) and infrared light (n = 24, CI 95% 0.50 to 3.28) reduced the incidence of SAD compared to no light therapy. However, the authors were hesitant of the significance of the results, due to the high risk of bias in the studies and large confidence intervals. ²¹ Although larger-scale studies are required, the present research suggests an important role of bright-light therapy in the treatment and prevention of patients with SAD, as it provides an option that is of low cost and has a low adverse-effect profile.

Counselling

Counselling has also been investigated as a potential treatment for this condition. A trial analyzed cognitive-behavioural therapy (CBT) using light therapy as a control (n = 177). Both treatments significantly improved patients’ depressive scores during their depressive episodes (p < 0.0001), and no significance was found between the two treatment groups (p = 0.96). ²² Additionally, they found that CBT and light therapy provided similar remission rates and may be equally effective in supporting these patients. Although it may come at a higher cost, it offers another modality that can be used to help treat this condition.

Physical Activity

Another possible treatment recommendation includes physical activity; this is a common recommendation for other mood disorders and major depression. It is not fully determined what the mechanism of action is, but it likely has multiple effects including influence on neurotransmitters and endorphin release. A review summarized that there were consistent improvements in depressive scores of SAD patients across studies analyzing exercise as a treatment. ²³ The majority of trials that had investigated this treatment lasted one to eight weeks, and mostly involved aerobic exercise. No consensus has been made on the type and amount of exercise required for optimal treatment due to the lack of trials on this topic; however, adding in some form of physical exercise consistently may further improve SAD symptoms during depressive periods.

Diet

There have been some investigations on the role of diet in SAD. A review demonstrated that both vegetarianism and alcoholism were associated with higher rates of SAD. ²⁴ No current data reveals dietary interventions that may help treat SAD, but this does provide some insight into some generic dietary goals that can be utilized, such as reducing alcohol intake and including more protein-rich foods.

Supplementation

Several nutraceuticals have been studied, mostly based on supporting neurotransmitter and catecholamine support. However, more research is needed.

A study was performed on tryptophan administration versus light therapy in a repeated-measures design (n = 13). Both light therapy (p = 0.012) and tryptophan supplementation (p = 0.014) improved symptoms, with no significance between difference in efficacy of either treatment. However, this study was very small, and thus the results should be interpreted with caution.

Hypericum perforatum, also known as St. John’s wort, has been investigated for a potential SAD treatment in combination with light therapy. A controlled, single-blind study administered 900 mg/d of St. John’s wort combined with either bright (3,000 lux) or dim (< 300 lux) light therapy (n = 20) for 2 hours a day over a period of 4 weeks. A significant improvement in SAD symptoms was found in both groups (p < 0.001), with no difference between the two groups. ²⁶

Vitamin D is another nutraceutical that has been studied due to its potential role in depression. A randomized control trial compared vitamin D supplementation to light therapy (n = 15). It was found that after one month of treatment, patient outcomes had improved in the vitamin D group (p = 0.05) but not in the light therapy group. ²⁷ This also correlated with increased vitamin D blood levels, making it a potential treatment option.

Other supplements that have been studied with no significant findings include vitamin B12 and Ginkgo biloba. ^28,29,30

Additionally, as mentioned, pharmacotherapy is an option in jurisdictions where naturopathic doctors have prescription rights. There is substantial research behind fluoxetine in improving patient outcomes. ³¹

Overall, SAD is a complex condition, with multiple players influencing its pathophysiology. Several treatment options have been explored to treat this disorder. Currently, light therapy has the most evidence behind its efficacy, but physical exercise and counselling provide other potential treatment options for patients with this condition. Vitamin D is currently the only nutraceutical with supporting research behind it, but there is a great need for further research with well-conducted, large-scale trials to further investigate the impacts of other supplements and botanicals on the symptoms of SAD.