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Winter Seasonal Affective Disorder (SAD): How It Makes Us Sad

It is cold, dark, and gloomy. It is winter.
Those words are the exact representation of my very first winter experience after
moving to Taiwan. As a resident of a tropical country for my whole life, experiencing winter
would be very exciting, I thought. After first-hand experience with winter season, do I still
think that it will be an exciting period? Nope, I was totally wrong. I would like to rectify my
statement, winter is not exciting at all. I was cold, lethargic, and depressed almost all the time
during this season. Despite of having 7 to 8 hours of sleep, I would still feel sleepy in the
morning, as if there are magnets in my eyelids making it difficult to open. At the beginning I
thought it was only me because I came from a country with no winter season, but it turned
out that several of my local acquaintances also experience the same thing. Was it possible
that we were experiencing seasonal affective disorder (SAD)?
SAD was first described in 1984 by Norman E. Rosenthal, a scientist and psychiatrist
at National Institute of Mental Health in United States, as he and his colleagues conducted a
study involving 29 people recruited through advertisement in newspaper. “SAD is a form of
major depressive disorder (MDD); in other words, patients with SAD can be just as depressed
as patients with MDD and are often more so. The only distinction between these depressive
disorders is the timing of the episodes, which occur during the short, dark days of winter in
patients with SAD.” – Rosenthal N. E. These individuals stated that they experienced
sadness, lower physical activity, anxiety, increased appetite resulting in weight gain, increase
sleeping period, drowsiness and never felt well-rested. This study also revealed strong
correlations between the depression and average temperature as well as photoperiod, in which
lower average temperature and shorter photoperiod were recorded in months with higher
number of depression cases (Rosenthal et al. 1984).
In 1989, S. Kasper, professor at University Clinic for Psychiatry and Psychotherapy at
the Medical University of Vienna, along with N. E. Rosenthal described a sub-group of the
SAD. This group posed similar symptoms as SAD but in milder condition, named as
subsyndromal SAD (S-SAD) (Kasper et al. 1989). The S-SAD is widely known as winter
blues.
Rosenthal and his colleagues also developed a screening method to determine whether
someone has developed SAD. The technique involved a questioner known as Seasonal
Pattern Assessment Questionnaire (SPAQ). This questionnaire assesses any changes and the
severity of the changes in mood, weight gain, social interaction, sleep duration, appetite and
energy level throughout the year (every month), and several related questions. The reliability
and validity of this questionnaire have been determined by Peter Paul A. Mersch, a researcher
at Department of Psychiatry in University of Groningen, Netherlands, and his colleagues.
According to his study, the SPAQ demonstrated a high specificity and high classifying
capability (distinguishing the SAD patients from non-SAD patients). However, the sensitivity
of the questionnaire was relatively low. Therefore, the author suggested that the SPAQ was a
suitable screening method but was inappropriate for diagnostic (Mersch et al. 2004). To date
there are several questionnaires that have been developed in order to give better result in
diagnosing individuals with SAD, for instance Shastun’s questionnaire (Blagonravov. 2017)
and seasonal health questionnaire (SHQ) (Thompson & Cowan. 2001).
Prevalence of SAD has been studied and reported in several areas. As study
conducted in Iceland revealed that 38 people in 1000 people (3.8%) suffered from SAD and
75 people in 1000 people (7.5%) suffered from S-SAD (Magnússon & Stefánsson. 1993).
Prevalence of SAD was also determined in New York, which demonstrated that at least 1 in
22 people (4.7%) experience SAD and at least 1 in 77 people (1.4%) felt the same in Florida.
This report might suggest that the latitude could have some effects on the susceptibility to
SAD, which people in lower latitude might experience less SAD and vice versa (Rosen et al.
1990).
After assessing some basic information regarding SAD, then come the million-dollar
question: What are the factors that lead to SAD in winter as the days become shorter and
sunlight exposure decreases?
First and foremost, the efficacy of bright light therapy (BLT) to reverse the depression
effect caused by winter season in SAD patients suggested that the mood disorder might occur
due to lack of light exposure. A literature study which compared 19 studies regarding BLT
and SAD supported the conclusion that BLT was an effective countermeasure to treat SAD
compared to controlled group treated with dim-light. The BLT occupied light ranging from
1300 to 10000 lux, while dim-light ranging from 500 to less than 300 lux (Pjrek et al. 2020).
For reference, sunrise or sunset on a clear day equals to 400 lux and bright sunlight would
range from 100000 to 120000 lux. What are the mechanisms that can explain this therapeutic
effect of light against depression?
Your eyes could tell your brain about the presence of the light through a special
photoreceptor called intrinsically photosensitive retinal ganglion cell (ipRGC), due to a
photopigment melanopsin that make this special cell sensitive to light. According to a study,
this photopigment was more sensitive towards blue light (excessive in day) and less sensitive
towards the red one (Brainard et al. 2001). This special photoreceptor cells were directly
connected to several parts of the brain (reviewed in Li & Li. 2018). It is like your eyes and
brain are connected via a highway with several exits to various districts in the brain.
One part of the brain that was affected by the light is suprachiasmatic nucleus (SCN).
The SCN controls the circadian rhythm which is the molecular clock of your body. We can
say that the circadian rhythm is the clock that set the daily schedule of your brain. The
circadian rhythm is heavily regulated by the presence of the light that will cause a cascade of
regulatory action in the brain. In the presence of light, circadian locomotor output cycle kaput
(CLOCK) and muscle ARNT-like protein 1 (BMAL1) activate the production of period
protein (PER1, PER2, and PER3), crytochrome protein (CRY1 and CRY2), RORα as well as
REV-ERBs, along with thousand other proteins, which are involved in many biological
processes. Accumulation of these PER and CRY proteins (usually occurs at night) could turn
off CLOCK and BMAL1, decreasing the activity level of CLOCK and BMAL1 until the light
appears in the morning and reactivated the CLOCK and BMAL1 (reviewed in Takahashi.
2015).
Studies of CLOCK and BMAL1 protein regulation in individuals with SAD showed
that their circadian rhythm was shifted in regards to their sleep-wake cycle suggesting that
their molecular clock did not match their real-life clock (Figure A). Due to the dysregulation
of the circadian rhythm, many biological processes in the brain were also dysregulated
resulting in lower mood (reviewed by Campbell et al. 2017). One direct example was the
synthesis of dopamine, a neurotransmitter, by RORα (reviewed by Albert. 2017).
To understand how it works, we need to know that mood is controlled by our brain
and it is regulated by various neurotransmitters, such as serotonin, dopamine, melatonin,
endorphin, as well as norepinephrine (reviewed by Dfarhud et al. 2014). These
neurotransmitters will travel from neuron to neuron in order to regulate diverse biological
processes, which might affect mood. This communication process in the brain looks like the
word relay game, in which the word is a set of orders passed from one person to another until
it reaches the last person. Only it happens in a much higher success rate and lower error rate
in the brain compare to the word relay game in real world.
It is widely known that dopamine has been linked with reward effect that correlated
with increased mood (Nestler & Carlezon. 2006). However, RORα protein also regulates
another protein that can decrease dopamine level (Hampp et al. 2008). Therefore, dopamine
theory is not a one-way street theory, there were other lines that need to be taken into
consideration for determining the role of dopamine in SAD development.
Another neurotransmitter known to be linked with depression is serotonin. It has been
demonstrated that the activity level of serotonin transporter (SERT) was elevated during
winter season leading to the development of mood disorder. In this case, the SERT would
transport the serotonin back into the presynaptic neuron (serotonin reuptake) resulting in
termination of the signalling process. The higher level of SERT activity during winter would
directly cause a higher reuptake rate of the serotonin in our brain that induce lower mood
(reviewed by Campbell et al. 2017). It seems like in winter season you are trying to supply
enough serotonin to regulate your mood but have a lot of drainage resulting in constant loss
of available serotonin to control your mood.
BLT has shown a good efficacy to ease the SAD symptoms (Pjrek et al. 2020). It has
been shown that this therapy can resynchronized the circadian rhythm back to normal in
people diagnosed with SAD (Figure B), which might increase the mood. It was kind of
turning your watch to match local time when you were travelling through different time zone,
so you did not mess up your schedule. The BLT has also been demonstrated to lower the
activity of SERT (Figure C), removing the drainage that cause loss of available serotonin
(reviewed by Campbell et al. 2017). The figure below is taken from Campbell et al. 2017.
A B

C
 It is likely that mood disorders, such as SAD, are not simple diseases that can be
solved with simple solution. There are multiple processes and various factors that play roles
as the causative agent of this disease. More observations and researches are needed to fully
understand the reasoning and other factors that contribute to the development of SAD. Then
we can develop more effective and efficient therapeutic or even prevention method to help us
fight SAD in the future.

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