Within the mysterious depths of our brains and bodies remain the ancient systems that adjust our sleep, energy, mood and behaviors in alignment with the ebb and flow of nature’s seasons. Many moons ago, especially in temperate latitudes, we evolved a genetic makeup that promoted the “winter blues”: eating a lot, sleeping a lot and doing less physically and socially helped conserve valuable energy — an evolutionary advantage for surviving the harshness of winter.
The winter blues is so deeply ingrained in our genetic history that we are now beginning to document human-like winter blues in primates, such as our distant cousin the Rhesus macaque monkey.
Today, many people’s minds and bodies still yearn for settling into a hibernation-like mode that is completely at odds with the unyielding productivity of work and life demands in modern society.
For some, the effects are relatively benign. Being a bit cranky, putting on a few extra pounds and snuggling on the couch at the weekend instead of hitting the town isn’t the hardest cross to bear. For others, the by-product of this mismatch between the demands of modern living and nature includes lethargy, melancholy, withdrawal from life and complete despair, clinically known as seasonal affective disorder (SAD), and also known as seasonal depression, winter depression or the aforementioned, misleadingly sugar-coated term, the winter blues.
Thanks to recent discoveries coming from contemporary research we are at the forefront of understanding both the mechanisms behind SAD and using multi-hit treatments and life tweaks to manage SAD and keep the debilitating effects of the winter blues at bay:
What is SAD?
Seasonal affective disorder (SAD) is considered as a subtype of major depressive disorder (MDD) characterized by recurrent episodes of depression in winter and normal to elevated mood in summer.
What causes SAD?
The causes of SAD are not clear cut and are still being determined. The leading theory is as follows and regards the disruption of systems that have a circadian rhythm. Put simply, circadian rhythms are physical, mental and behavioral changes that follow a roughly 24-hour cycle. They are primarily influenced by light and darkness in order to optimize our bodies and minds differently for daylife and nightlife.
To keep the circadian rhythm system cycling on time we all have a master clock in our brains. This master clock is located in the suprachiasmatic nucleus (SCN) of the hypothalamus. From the brain, it synchronises peripheral biological clocks found in most organs, such as the heart and liver, by changing levels of different hormones in response to external cues such as light/dark, exercise and diet. Processes following a circadian rhythm include sleeping, feeding, body temperature, brainwave activity, hormone production and cell regeneration.
In this way, healthy bodies and minds know the time of the day from light entering the eyes synchronizing the functioning of the master clock in the brain, which in turn synchronizes clocks in the rest of the body.
In SAD, the story goes that shorter lengths of exposure to light in winter puts the master clock and circadian system out of whack, which is associated with the enhanced and untimely production of the hormone melatonin, as well other hormones and neurotransmitters that are part of the circadian rhythm system.
Melatonin production is the fundamental example of a malfunctioning part of the circadian rhythm system in SAD. Melatonin is a hormone produced from serotonin by the pineal gland in response to increasing levels of darkness. Its primary function is to transmit go-to-sleep messages from the brain to other bodily systems, preparing them for sleep.
In people with SAD, with their haywire master clock, they have consistently higher levels of daytime melatonin. Presumably this is due to a delayed response of the pineal gland to the limited morning light in winter that would normally reduce melatonin production in the morning to get the body and mind to wake-up for daytime. Basically, those with SAD often get stuck on sleep-mode in the morning making it very difficult to drag themselves out of bed.
Then in the evening when they should be sleepy, many get stuck on awake-mode. The rather sluggish and seemingly confused pineal gland finally stops making melatonin when it really should be starting. The pineal glands circadian rhythm has been shifted out of its regular beat, known as circadian phase shifting. This keeps some SAD sufferers more alert and awake into the early hours of the morning or simply reduces sleep quality more than in healthy individuals.
It is important to recognize that a limited number of studies have not found strong evidence for circadian dysregulation or a circadian phase-shift in response to light therapy in patients diagnosed with seasonal depression. Some researchers consider the circadian rhythm hypothesis to not adequately account for all episodes of SAD.
SAD risk factors
The causal and contributory mechanisms behind SAD are complex. A large number of factors are involved that influence a large number of genes in the development of SAD.
Within the last decade in which SAD research has been blossoming, a number of biological and psychological mechanisms have been proposed that differentially involve depression, seasonality, circadian rhythms, retinal sensitivity and skin melatonin levels, as well as lifestyle and sleep factors.
A summation of the main interconnected biological and psychological factors that can be involved in the generation of a SAD episode are as follows:
Environmental: Ultimately a short photoperiod in winter coupled with poor weather conditions that limit sunlight is the essential component in the development of SAD.
Genetic: Some gene variations associated with circadian rhythm, photopigments, and serotonin and dopamine synthesis make some people more sensitive to the winter season than others.
Physiological vulnerabilities: Having an enhanced inflammatory response in winter, darker skin and iris pigmentation, a retinal subsensitivity to light or serotonin and dopamine dysfunctions are all considered to be factors that can contribute to SAD.
Psychological vulnerabilities: There are many cognitive factors (dysfunctional attitudes, rumination, core beliefs and negative attributional style) and behavioural factors (behavioural disengagement, emotional and psychophysiological reactivity to light, season and weather types) that can make the chances of experiencing SAD in the winter much higher.
Lifestyle vulnerabilities: Having a largely indoor lifestyle, lack of regular exercise, drug abuse and poor nutrition from diet also contribute to SAD development.
Vitamin D status: Low vitamin D levels have previously been proposed to be a causal factor in a vitamin-D specific sub-mechanism of SAD development. The latest research tentatively suggests that vitamin D plays an important regulative role in many, if not all, of the sub-mechanisms involved in SAD development as well as healthy seasonal changes.
Who has SAD?
Prevalence rates vary dramatically from country to country, with ethnicity, skin tone and of course geographical location all known to influence an individual’s susceptibility to SAD. Rates for chronic presentations of SAD have been found to range from 0-10%, peaking at a high of 33% for sub-syndromal presentations of SAD.
Generally, research suggests that first and second generation darker-skinned immigrants living in higher-latitude areas, menopausal women, indoor workers and those with a family and/or personal history of mental illness are high risk groups for the development of SAD.
However, skin tone is not the primary determinant of SAD development. Using people living in Norway as an example of differences between ethnic groups, men from Sri Lanka have the lowest SAD rates in the country (6%), dramatically less than Iranian men (21%), despite Iranian men being generally lighter in skin color.
Undoubtedly, SAD is more common in women than men of reproductive age, with 60-90% of reported cases being in women. Although kids are more evenly affected across genders until puberty, there is a boom in SAD in women of reproductive age where the gender bias begins, followed by men and women being equally affected again in old age.
While over a third of SAD suffers become mildly hypermanic in spring and summer, when symptoms are turned on their head (which includes excessive excitement, enthusiasm, distractability, talkativeness and a decreased need for sleep), here is a list of symptoms more specific to the far less desirable winter hypomania:
Increased sleep and sleep need (hypersomnia)
Extreme difficulties in waking from sleep
Increased appetite, carbohydrate cravings and weight gain (decreased appetite and weight loss is also reported)
Lethargy and fatigue
Enhanced inflammatory immune response
Loss of motivation and interest in daily activities
Decreased libido (thought to once have been an evolutionary advantage to prevent child birth in autumn/winter months)
Decreased abilities to think clearly, concentrate or make decisions
Feelings of worthlessness and recurrent thoughts of death
In the winter months of this year, scores of high quality studies have been published that contribute actionable findings for improving treatment and prevention of SAD episodes, as outlined below.
Light therapy: Light therapy has been used for decades in the winter months. It was even used in schools as early as the 1960s in the UK, before being officially prescribed for SAD in 1984. Yet up until very recently, despite many studies exploring the benefits of light therapy for SAD, the research has been of relatively poor quality.
While light therapy works via light entering the eye, researchers have found that administering the light directly to the brain through the ear canal is also effective.
A recent meta-analysis of light therapy efficacy studies used high-quality study selection criteria, resulting in data from only eight studies being used despite there being over 586 published studies at the time of the analysis. A moderate to large effect size of 0.54 was found in favour of bright white light therapy successfully lowering SAD symptoms, although the authors do note that even some of these most high quality studies had design issues.
An earlier meta-analysis published in 2005 using less strict selection criteria had a much larger effect size of 0.84. As such, more accurate research in the future may lower the 0.54 effect size even further. This lends to the fact that bright white light therapy alone is simply not enough to treat all SAD sufferers – multi-hit treatment methods and lifestyle changes are more effective.
Dawn simulators: Competing for the limelight as an effective SAD treatment is dawn simulation. A dawn simulator also uses bright white light, however it emulates sunrise by gradually increasing the intensity of light.
Many studies have compared bright white light therapy with dawn simulation since the early 90s, however the results have been mixed and there is no clear victor. The most recent study published this year was the first controlled, randomized crossover design, crossover meaning that each SAD patient and control in the trial tried both of the treatments, half of the subjects using light therapy first, half of the subjects using dawn simulators first, with 3 weeks break between using the two therapies.
From analysis of data from 40 participants, depression scores reduced similarly for light therapy and dawn simulation, 44% and 42% respectively, and the participant’s personal preference was also similar at a respective ratio of 21:19.
Importantly, whichever treatment the individual preferred was the most effective treatment for them. Bright light therapy being most preferred and more effective for those with higher depression scores. Whereas dawn simulation was most preferred and more effective for those with lower depression scores.
The take home message for SAD sufferers is that your preferred strategy, immediate bright light or gradual dawn simulation, is the one likely to be most effective for you — give them both a try and see which makes you feel best.
Psychotherapy: A cognitive behavioural therapy specific for SAD (CBT-SAD) addresses the role of environmental changes as well as cognition and behavior in the onset and maintenance of SAD symptoms. It was recently pitted against light therapy in a randomized head-to-head comparison of the two treatments.
Both treatments were equally effective in reducing ratings for SAD and depression severity one whole year after just 6 weeks of CBT-SAD or light therapy, with only ~17% of participants having a SAD episode.
However, two years later there was a big difference between the two groups. In the second winter twice as many of the participants had SAD rear its ugly head again with light therapy (45.6%) than with CBT-SAD (27.3%). By the second winter, those receiving CBT-SAD also had less severe symptoms on both measures, and a larger proportion of patients in remission (68.3% compared with 44.5%).
It makes a lot of sense really. It’s a power of the mind over matter thing. If someone’s physiology is hardwired to lean towards SAD symptoms in winter, the effects of one light therapy session are unlikely to withstand the test of time year on year. However, being given the psychological tools to mentally and behaviorally protect oneself from letting a SAD episode take over is intuitively a better long-term strategy.
Presumably, light therapy’s physiological approach coupled with CBT-SAD’s psychological approach, will boost therapeutic effectiveness when used in combination. However, no study seems to have addressed this as of yet.
Pharmacotherapy: Just a few short years ago it seemed pretty clear cut that selective serotonin reuptake inhibitors (SSRIs) were the drug of choice for treating SAD. It sounds logical. With the excess melatonin production and related serotonin depletion found in SAD, drugs that help boost serotonin levels like SSRIs sounds like a no brainer right? Well today, the picture is not so clear.
There is extremely limited high quality or even low quality research on the effectiveness of different SSRI medications in treating SAD – the research is sketchy at best. One meta-analysis states that evidence for the effectiveness of second generation antidepressants is limited to one small trial of fluoxetine compared with placebo, which shows a non-significant effect in favour of fluoxetine, and two small trials comparing fluoxetine against light therapy, which suggest equivalence between the two interventions. The researchers concluded that there is not enough to make any claims about efficacy and that more research is needed.
Moreover, chronic SSRI treatment in a mouse model of SAD were recently shown to the opposite of what is intended. They dramatically depleted serotonin in the brain even further, although this was preventable when the mice were given the serotonin supplement, 5-HTP (5-hydroxytryptophan).
Despite this lack of promising SSRI research findings for the treatment of SAD, around the globe those with SAD are still considered good candidates for being prescribed SSRIs. Major depression and SAD are clinically lumped under the same umbrella with little evidence to back it up.
In the US, one atypical non-SSRI antidepressant drug has been specifically approved for the treatment of SAD. Its best known in treating nicotine dependence, and goes under the brand names Prexaton, Zyban, Wellbutrin or Budeprion.
Bupropion is a commonly prescribed antidepressant that is structured similarly to stimulant amphetamine that acts on norepinephrine and dopamine neurotransmission (a norepinephrine-dopamine reuptake inhibitor (NDRI)), although its mechanism of action is very poorly understood. It is considered to be a better choice for SAD than standard SSRIs as it is associated with a lower risk of weight gain, mania, drowsiness and sexual dysfunction.
In all honesty, research shows that with SAD, treatment effects using bubpropion are relatively small compared to placebo. As found in three clinical efficacy trials with bupropion, the overall rate of patients depression-free at the end of treatment was 84% for those on taking Wellbutrin XL compared with 72% for those on placebo.
One published paper insists that more placebo-controlled trials are needed to determine if bubpropion has any real efficacy despite it being FDA approved.
As with all antidepressants, there are well-known adverse side effects, and it’s important to weigh the risks and benefits before starting any medications, especially considering the effectiveness of CBT and light therapy.
Exercise: Exercise is a common non-pharmacological treatment for depression. One study has compared the effects of one week of one hour of daily bright light therapy or one hour of daily stationary bicycling in both seasonally and non-seasonally depressed individuals.
While exercise was considered effective for reducing depression symptoms in both seasonally and non-seasonally depressed individuals, in those with SAD, exercise resulted in the normalization of body metabolism associated with both weight loss and increased oxygen consumption. Light therapy on the other hand had relatively low efficacy for non-seasonal depression and high efficacy for seasonal depression.
Diet: Protein-based nutritional interventions are looking promising. Mice being fed gluten prior to experiencing a short photoperiod showed more depression-like symptoms than those on a casein diet. However, mice that ingested soya protein displayed less depression-like symptoms. This was attributed to the high level of the amino acid tryptophan in soy protein. In the body, tryptophan is converted to 5-HTP, which is then converted to serotonin, which in turn is converted into melatonin.
As this study was not-placebo controlled, and carbohydrate-based drinks were shown to be no different to placebo drinks in improving SAD symptoms (sharing remission rates of around 70%), the conclusions should be taken lightly.
While the research is outdated, there is evidence of L-tryptophan ingestion in humans being similarly effective to light therapy, again this study was not placebo controlled. More commonplace is 5-HTP supplements which have been used clinically for over 30 years for the treatment of depression and a wide variety of conditions. It is generally considered more effective than tryptophan due to bypassing the rate-limiting step in the syntheisis of serotonin, the enzymatic conversion of tryptophan to 5-HTP, which unlike tryptophan, readily crosses the blood-brain barrier.
Unfortunately, most research on 5-HTP is from the 1970s and 1980s before the approval of the SSRI fluoxetine in 1987 shifted researchers’ focus onto the more lucrative SSRI research.
Another amino acid of interest when it comes to SAD is L-serine. The boosting of brain serotonin levels in response to bright light was enhanced by l-serine injections in a mouse model of SAD. Thus, there is an early indication, although not-corroborated in humans as of yet, that eating foods high in l-serine, such as egg and soy, or an l-serine supplement, could improve SAD symptoms.
Vitamin D: If you have heard about SAD before, you have probably heard about Vitamin D supplements. It’s not surprising Vitamin D has been found to improve SAD symptoms. It is produced in the body from exposure to ultraviolet light, it naturally dips in winter, and plays an important part in the synthesis of dopamine and serotonin, neurotransmitters that in low levels are associated with depression.
The most recent research on Vitamin D involved a double-blind randomised placebo-controlled trial of Danish healthcare professionals who had experience with depression symptoms in the past. Researchers found no significant differences between people taking a daily dose of vitamin D or placebo. However, when compared with similar research, the amount used seems to be the lower limit when it comes to improving SAD symptoms, with more robust improvements found only when relatively high doses of vitamin D are used (100 micrograms daily).
Natural light: Additionally, little light-related life tweaks may collectively make a huge difference. Normal circadian rhythms should be promoted by getting as much natural light as possible, and taking natures lead by slowing down at night: Take work breaks outdoors; walk to and from work; plan outdoor activities for days off; and reduce artificial light exposure in the evenings to help kickstart nightime melatonin production.