Seasonal Affective Disorder (SAD)

🧠 Overview — When “Sunlight” Is Linked to “Emotion”

Seasonal Affective Disorder (SAD) is a type of depressive disorder with a distinctive pattern: symptoms recur in the same period of the year, especially during times when daylight decreases, such as from late autumn to winter, and then gradually improve on their own as spring and summer arrive.
Because of this, it is often called “winter depression” or “seasonal depression” — reflecting the fact that changes in season genuinely affect both the brain and mood.

Medically, SAD is not considered a stand-alone disorder separate from depression, but is defined in the DSM-5-TR as a specifier: “with seasonal pattern.”
This means that people with Major Depressive Disorder (MDD) or Bipolar Disorder can have depressive episodes that “recur in the same season every year.”
For example, becoming depressed every winter, or having abnormally elevated mood every summer.

SAD is therefore a clear example of how “environment” and “brain biology” work together —
even a simple change in the amount of daylight per day can disrupt our biological clock (circadian rhythm), altering the secretion of melatonin and the neurotransmitter serotonin, both of which directly influence energy and mood.

During late autumn–winter, when daylight hours shorten:

• The brain produces more melatonin → causing sleepiness, fatigue, lack of motivation, and slowed movement.
• At the same time, serotonin levels tend to decrease → leading to feelings of sadness, gloom, and low motivation.
• Combined with cold weather, spending more time indoors, and reduced outdoor activity → the mood cycle steadily spirals downward.

Many people might casually call themselves “a bit winter lonely” or “seasonally blue,” but in those who truly have SAD, the symptoms are far more severe —
to the point that they clearly lose psychological and physical balance, such as having no energy to get out of bed, losing appetite or overeating, reduced concentration, and beginning to have thoughts of wanting to die.

Global statistics show that:

• Around 5% of the U.S. population meets full diagnostic criteria for SAD, and another 10%+ may have milder symptoms known as subsyndromal SAD.
• Women are about four times more likely to be affected than men.
• Symptoms most commonly begin in late adolescence to early adulthood (ages 18–30).
• Regions farther from the equator, such as Canada, Scandinavia, or Russia, have higher rates of SAD because winter days are extremely short.

Conversely, some people may have “reverse SAD” or summer-onset depression,
which is the opposite pattern — symptoms worsen in summer when the weather is extremely hot or the light is overly intense, and this occurs in about 10% of all SAD cases.

Interestingly, each person’s brain “responds to light” differently.
In some people, the circadian system is flexible and adapts well to seasonal changes.
But in others, this system is hypersensitive to changes in photoperiod (the length of daylight in each day).
As a result, their internal biological rhythms become “delayed” relative to external clock time — for example, the body secretes melatonin for a longer period, making them feel sleepy and exhausted throughout the day.

In addition, genetic factors are involved, such as:
genes that regulate serotonin receptors (5-HT receptors) and serotonin transporters (SERT), which play roles in mood and sleep.
Mutations or variants in these genes may cause some individuals to be “more sensitive to seasonal changes” than others.

Overall, SAD can be seen as a “mismatch between the inner world of the brain and the outer world.”
When light decreases, the brain continues to run on a “summer-like” rhythm, resulting in an imbalance among hormones, energy, and mood.
Thus, SAD is not a sign of personal weakness, but rather a “disorder with a biological foundation” that can be treated.

In modern neuroscience, SAD is viewed as one of the “natural models” for studying mood circuits,
because it vividly demonstrates how “light – brain – hormones – emotion” are tightly interconnected,
and how just a slight tilt in Earth’s axis — changing the seasons — can truly make the human mind tremble with the turning of the year.

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🧩 2. Core Symptoms — Main Symptoms of Seasonal Affective Disorder (SAD)

SAD presents with depressive symptoms similar to Major Depressive Disorder (MDD), but what makes it “distinctive” is its recurring seasonal pattern, along with biological characteristics linked to light and the circadian clock.

Clinically, SAD symptoms can be divided into three major groups:
(1) General depressive symptoms,
(2) Winter-onset SAD symptoms, and
(3) Summer-onset SAD symptoms.

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🧠 2.1 Core Depressive Symptoms (Shared Depressive Core)

Whether it is winter-type or summer-type SAD, the core feature is a “persistently low mood” almost every day for most of the day, with at least 5 out of 9 MDD criteria present for ≥2 weeks.
These symptoms reflect dysfunction in the limbic–prefrontal circuits and reduced secretion of serotonin–dopamine:

• Persistent depressed mood — feeling gloomy, emotionally heavy, tears come easily; some describe it as “like the heart is being squeezed all the time.”
• Loss of interest or pleasure in previously enjoyed activities (Anhedonia) — activities that used to be fun, like listening to music, watching movies, or gaming, no longer bring any joy.
• Decreased energy (Low Energy / Fatigue) — feeling exhausted even without heavy work, body feels slow and weighed down.
• Reduced concentration and decision-making — difficulty reading or understanding, poor memory, tasks that used to be easy now feel impossible.
• Feelings of guilt or worthlessness — blaming oneself over minor issues, feeling useless or like “a burden to others.”
• Appetite or weight changes — significant weight gain or loss (e.g., more than 5% in a month).
• Sleep disturbances — either sleeping too much or too little (depending on the subtype).
• Recurrent thoughts of death — ranging from “I wish I could disappear” to active planning of self-harm.
• Psychomotor changes — appearing slowed, sluggish, speaking more slowly; or on the other hand, being restless, pacing, and easily irritable.

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❄️ 2.2 Winter-Onset SAD (Winter Depression)

This is the most common form (~90% of SAD cases) and has a distinctive “Atypical Depression Pattern,” because some symptoms are the opposite of typical MDD.
It is associated with circadian delay and prolonged melatonin secretion.

Key features include:

• Hypersomnia — sleeping excessively, taking multiple naps, yet still feeling unrefreshed even after 9–10+ hours of sleep.
• Increased Appetite / Carbohydrate Craving — the brain craves serotonin → craving sweets and carbohydrates such as bread, rice, sugary snacks.
• Weight Gain — gaining 2–5 kg or more during winter.
• Leaden Paralysis — feeling as if the arms and legs are extremely heavy and hard to move (a hallmark symptom of atypical depression).
• Social Withdrawal — not wanting to see anyone, preferring to stay at home all the time, as if “temporarily shutting off from the world.”
• Emotional Blunting — flattened affect; not feeling strong joy or sadness, but stuck in a “numb” emotional state.
• Cognitive Fog — slow thinking, short-term memory problems, lack of mental clarity (“winter brain fog”).
• Decreased Libido — reduced or absent sexual desire.
• Morning Sluggishness — finding it very hard to get up; the body does not respond well in the morning.

Biologically, winter SAD often involves a circadian delay phase — the brain’s internal clock runs about 2–3 hours behind external time, causing melatonin to be secreted for longer, serotonin to drop, and mood to be low at times when the person should normally be awake and active.

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☀️ 2.3 Summer-Onset SAD (Reverse SAD)

This form occurs in about 10% of all SAD patients and can be seen as a “mirror image” of the winter type.
It is often associated with high temperatures, excessively bright light, and phase advance of the cortisol rhythm.

Core symptoms include:

• Insomnia — difficulty falling asleep, frequent awakenings, vivid or numerous dreams; some people complain that they “never feel like they enter deep sleep.”
• Decreased Appetite — lack of interest in food, eating less, weight loss.
• Agitation / Anxiety — restlessness, irritability, feeling anxious over small things.
• Heat Intolerance — feeling that the body “cannot tolerate heat,” becoming easily irritated when in bright or hot environments.
• Emotional Volatility — mood swings rapidly from good to very bad, resembling mixed features seen in some bipolar presentations.
• Restlessness — feeling the need to move, change locations, or constantly do something.

In terms of brain function, summer SAD is commonly associated with circadian phase advance — the biological clock runs too fast, causing disrupted sleep–wake timing, serotonin activity peaking at the wrong time, and cortisol levels failing to decline in the evening.

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💬 2.4 Impact on Daily Life

• Decline in work and academic performance — noticeable falls in concentration, information processing, and problem-solving.
• Social withdrawal — canceling plans, avoiding activities, feeling as though social interaction “uses too much energy.”
• Relationship strain — partners may feel the person has become “cold / uninterested.”
• Reduced self-care — stopping exercise, ignoring nutrition, neglecting general health.
• Increased suicide risk — especially in those with prior depressive episodes or with SAD co-occurring with other conditions such as Bipolar Disorder, ADHD, or Anxiety Disorders.

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⚖️ 3. Diagnostic Criteria — Clinical Diagnostic Criteria

Under DSM-5-TR and ICD-11, SAD is classified as a specifier: “With Seasonal Pattern” of MDD or Bipolar Disorder, not as a separate disease entity.
However, it has clear specific criteria as follows:

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📍 3.1 Core Diagnostic Features

• Clear recurrent seasonal pattern of depressive episodes (Seasonal Regularity)
• Depressive episodes begin in a particular time of year (e.g., November–January),
• and remit fully in another period (e.g., March–May).
• This relationship must be driven by biological factors, not merely by economic or cultural reasons.
• Recurrence for at least 2 consecutive years (Temporal Stability)
• Depressive episodes in the same season must occur for ≥2 consecutive years,
• with no non-seasonal episodes occurring in the same timeframe.
• Seasonal episodes outnumber non-seasonal episodes
• This ensures that depression isn’t just coincidentally happening during that season.
• Meets full criteria for a Major Depressive Episode
• At least 5 symptoms present for ≥2 weeks, with significant impact on functioning.

• Cannot be better explained by another medical condition

• e.g., hypothyroidism, chronic fatigue, medication side effects.

• Must be differentiated from psychosocial season-linked causes

• e.g., work stress around year-end, seasonal agricultural workload, financial downturn during the rainy season.

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🩺 3.2 Clinical Assessment Process

• Mood Chronology Interview
• The clinician asks in detail which months symptoms begin and which months they improve.
• If a clear pattern emerges over 2–3 consecutive years → likely SAD.

• Mood Charting / Light Exposure Diary

• The patient records daily mood, hours of light exposure, temperature, and subjective energy levels.
• Use of specific screening tools, such as the Seasonal Pattern Assessment Questionnaire (SPAQ)
• A standard instrument widely used to screen for SAD worldwide.

• Physical examination and basic blood tests

• To rule out low thyroid function, hormonal disorders, or vitamin D deficiency.
• Assessment of comorbidities
• SAD frequently co-occurs with Anxiety Disorders, ADHD, or Bipolar II.

• Suicidality screening

• Must be carried out in all cases of MDD / SAD.

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🌗 3.3 Severity Spectrum

Severity	Clinical Description	Example Behaviors
Mild	Slightly low mood; still able to function, but with low motivation	Feels lazy, sleeps a lot, eats more, but still manages to go to work
Moderate	Clear symptoms; work or study performance is significantly affected	Frequently takes sick days, withdraws, avoids social interaction
Severe	Suicidal thoughts or unable to work at all	Stays in bed most of the day, significant weight gain/loss, severely disrupted circadian rhythm

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🧬 3.4 Differential Diagnosis — Conditions That Must Be Ruled Out

• Major Depressive Disorder (non-seasonal) – no pattern of recurrence tied to specific seasons.
• Persistent Depressive Disorder (Dysthymia) – chronic symptoms lasting ≥2 years without full periods of remission.
• Bipolar Disorder Type I/II – if there have been manic or hypomanic episodes, antidepressants alone must be used with caution.
• Subsyndromal SAD (s-SAD) – similar symptoms but do not meet full MDD criteria.
• Hypothyroidism / Chronic Fatigue Syndrome / Sleep Disorders – can mimic SAD symptoms.
• Substance-Induced Depression – especially from alcohol and sedative medications.

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🌞 3.5 Importance of Specifying “With Seasonal Pattern”

Including this specifier in a diagnosis is not only for statistical purposes; it helps to:

• Select appropriate treatment strategies, such as Light Therapy / CBT-SAD / prophylactic Bupropion,
• Plan preventive care ahead of high-risk seasons,
• Understand each individual’s unique illness pattern → thereby reducing the risk of relapse.

💡 Short Summary for Web Writers:
“SAD is not just a temporary sadness when the weather changes; it is a misalignment between the brain’s internal clock and the timing of the external world — a mismatch that makes human emotions truly sway with the seasons.”

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4. Subtypes or Specifiers — Subtypes of SAD

Commonly used in clinical practice and conceptual frameworks:

4.1 Winter-Pattern SAD (Winter-Onset Depression)

• The most common subtype.
• Depression in autumn–winter, improvement in spring–summer.
• Symptoms are mostly atypical (sleeping more, eating more, weight gain, social withdrawal). NCBI+2Mayo Clinic+2

4.2 Summer-Pattern SAD (Reverse SAD)

• Depression in spring–summer, improvement in autumn–winter.
• Key features: insomnia, poor appetite, weight loss, agitation, anxiety. The Sun+1

4.3 Subsyndromal SAD (s-SAD or “winter blues” at a subthreshold level)

• Symptoms resemble SAD but do not meet full MDD criteria.
• Usually manifests as fatigue, mild sadness, and low mood during winter, but daily functioning is still preserved.
• About 9–14% of the population may have s-SAD, which is more common than full-criteria SAD (about 5–6%). Wikipedia+1

4.4 Bipolar Disorder with Seasonal Pattern

• Some bipolar patients have depressive or manic episodes that follow a seasonal pattern.
• For example, depression every winter,
• or mania/hypomania in summer.
• This is crucial, because if someone is actually Bipolar but treated as if they only had MDD, using antidepressants alone may trigger manic episodes. Medscape+1

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🧠 5. Brain & Neurobiology — Neural Mechanisms of Seasonal Affective Disorder (SAD)

Seasonal Affective Disorder is one of the clearest “natural models of depression” in neuroscience, because it is a disorder driven by measurable environmental changes (such as light and day length), which then alter the functioning of the “master clock” in the brain and neurotransmitter systems related to mood.

We can view SAD as a “chain of biological events” as follows:

🌅 Change in light → SCN in the hypothalamus becomes dysregulated → melatonin–serotonin cycles become imbalanced → circadian rhythm slows down or becomes misaligned → limbic–prefrontal circuits become desynchronized → depressive symptoms emerge.

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🔹 5.1 Circadian Rhythm & Suprachiasmatic Nucleus (SCN)

At the base of the hypothalamus lies a tiny group of only tens of thousands of neurons called the Suprachiasmatic Nucleus (SCN).
This is the “master clock” of the body, setting the biological timing of everything in humans — from the sleep–wake cycle and hormone secretion to energy metabolism and emotional regulation.

• The SCN receives light directly from the retina via special cells called intrinsically photosensitive retinal ganglion cells (ipRGCs), which contain the pigment melanopsin and detect blue-light wavelengths entering the eye.
• When light reaches the eye, ipRGCs send signals to the SCN → the SCN then signals the pineal gland to stop melatonin secretion during the day.
• But in winter, when light is weaker and darkness arrives earlier, the SCN “receives the wrong phase signal,” causing internal body rhythms to be delayed relative to external clock time.

As a result, bodily cycles such as waking, sleeping, hunger, and emotional alertness all shift to occur 2–3 hours later than normal.
People thus feel “not fully awake even after waking,” as if their brain and body remain in night-mode all day long.

Additionally, the SCN has direct connections with limbic regions (amygdala and hippocampus), which are crucial for emotion and memory.
Therefore, when the SCN is dysregulated → limbic emotional balance is disrupted as well.

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🔹 5.2 Melatonin — The Hormone of Darkness

Melatonin is a hormone secreted by the pineal gland when the body is in darkness, acting as a “time cue” that signals it is time to rest.

In people with SAD:

• Melatonin secretion becomes longer than normal because winter nights are longer.
• Some individuals experience a phase delay, where melatonin starts later than usual and also stops later → they feel sleepy and gloomy during the daytime.
• Persistently high melatonin levels in the morning → suppress the release of serotonin and dopamine, which are involved in energy and pleasure.

The result is drowsiness, low energy, reduced concentration, and a disordered sleep–wake cycle.

Many studies have found that Bright Light Therapy with high-intensity light (~10,000 lux) in the morning can “reset the phase” of melatonin secretion back to normal timing → reducing depressive symptoms within a few weeks.
Although there is some debate about morning vs. evening exposure, most evidence suggests morning light is best at realigning the SCN with the external world.

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🔹 5.3 Serotonin and the Monoamine Systems

Serotonin (5-HT) is a key neurotransmitter involved in happiness, mood regulation, and energy activation, and it is directly influenced by sunlight through neurochemical pathways in the brain.

In winter, when light decreases:

• Serotonin production in the brain — especially in the raphe nuclei of the brainstem — drops.
• Sensitivity of serotonin receptors (5-HT1A, 5-HT2A) also decreases.
• PET scan studies show increased activity of serotonin transporters (SERT) during winter → serotonin is taken back into neurons too quickly → less serotonin remains in the synaptic cleft.

Moreover, a relationship has been found between 5-HTTLPR polymorphisms (serotonin transporter gene) and light sensitivity in SAD:
people with the short allele are more sensitive to light changes and have a higher risk of seasonal depression than those with the long allele.

In other words, “some people’s brains are genetically more sensitive to light reduction than others.”

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🔹 5.4 Dopamine, the Reward Circuit, and Motivation Deficit

The dopamine system plays a central role in motivation, reward, and drive.
Key regions include the ventral striatum (especially the nucleus accumbens) and the prefrontal cortex, which form the core of the reward circuit.

In SAD:

• Activity in dopaminergic pathways decreases → patients “no longer feel pleasure even from things they once loved” (anhedonia).
• Slowed movement (motor slowing) and lethargy arise because the mesocorticolimbic dopamine pathway is underactive.
• Combined with low serotonin → the brain slips into a “flat affect” state, with emotionally blunted responses and little internal drive.

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🔹 5.5 Photoperiodism & Hormonal Integration

Photoperiodism refers to how living organisms respond to the length of day and night.
Humans also possess such mechanisms at a biochemical level.

The SCN sends signals to the hypothalamic–pituitary–adrenal (HPA) axis to regulate levels of key hormones such as:

• Cortisol (the stress hormone)
• Thyroid hormones (T3, T4)
• Reproductive hormones (LH, FSH, testosterone, estrogen)

In SAD, the cortisol rhythm may become “flattened” — lacking a clear morning peak, leaving people feeling unrefreshed.
Morning core body temperature is also often slightly lower than normal (as if “the brain hasn’t fully woken up.”)

This shows that SAD is not confined to the brain; it extends its influence to the entire endocrine system.

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🔹 5.6 Neural Network & Functional Imaging Findings

fMRI studies have shown:

• The amygdala and anterior cingulate cortex (ACC) respond more strongly to sad images during winter.
• The prefrontal cortex (especially the dorsolateral prefrontal cortex) shows reduced activity → poorer emotion regulation.
• Functional connectivity between the prefrontal cortex and limbic regions decreases — explaining why people with SAD have difficulty controlling negative thoughts in winter.

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🧩 Mechanistic Summary

Brain System / Hormone	Abnormality in SAD	Effect on Mood
SCN (Circadian Clock)	Phase delay / desynchronization	Irregular sleep timing, all-day fatigue
Melatonin	Prolonged secretion	Sleepiness, gloominess
Serotonin	Reduced levels / increased transporter activity	Depressed mood, poor concentration
Dopamine	Reduced reward circuit activity	Low motivation
Cortisol Rhythm	Flattened, no clear peak	Sluggish thinking
PFC–Limbic Connectivity	Weakened connections	Difficulty regulating emotions

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🌍 6. Causes & Risk Factors — Causes and Contributing Factors

SAD is a disorder arising from multiple layers of biology and environment converging.
It cannot be attributed to a single cause; instead, it reflects an interaction among genetic vulnerability + environmental triggers + neurochemical changes.

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🔸 6.1 Biological Factors

• Circadian Dysregulation
  The SCN does not synchronize properly with external light → the body’s sleep–wake cycle is delayed by about 2–3 hours compared to others.
  The circadian system in people with SAD is overly sensitive to changes in photoperiod.

• Melatonin Phase Shift
  Melatonin is secreted for a longer period and starts later than normal.
  This creates the feeling of “being stuck in night-mode all day.”

• Serotonergic Vulnerability
  Serotonin transporter (SERT) activity increases in winter → lower serotonin levels in synapses.
  People with short-allele 5-HTTLPR are more sensitive to light changes.

• Dopaminergic Underactivity
  Dopamine system is underactive, especially in the striatal circuit → reduced energy and motivation.

• Hypothalamic–Pituitary Axis Dysregulation
  Cortisol rhythm becomes phase-shifted → no clear morning peak.
  Some individuals have slightly elevated TSH in winter → contributing to lower energy.

• Genetic Heritability
  Family studies suggest that 29–64% of SAD risk can be attributed to genetic factors.

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🔸 6.2 Light & Latitude Factors

• Reduced light exposure is the primary risk factor.
• Countries above 40° latitude (e.g., Norway, Finland, Canada) have SAD rates as high as 9–12%.
• Countries near the equator (e.g., Thailand, Indonesia) show rates of only 1–2%.
• Less sunlight → less vitamin D production → impacts serotonin synthesis.
• In cold, cloudy cities such as Reykjavík or Seattle, about 1 in 10 people experience winter depression.

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🔸 6.3 Personal Vulnerability Factors

• Female sex — SAD is about 4:1 more common in women than in men.
  It is hypothesized that estrogen influences serotonin regulation, making women more sensitive to light changes.
• Age 18–30 — the period when the SCN is still highly adaptive to environmental cues, thus more prone to circadian phase delay.
• Family history — having a first-degree relative with depression or SAD increases risk threefold.

• Personality traits

• High neuroticism (strong tendency toward anxiety)
• Perfectionism and self-imposed pressure
  → these increase the likelihood of clear SAD symptoms because the HPA axis is more heavily taxed.
• Existing psychiatric conditions
  e.g., ADHD, Anxiety Disorders, Bipolar II → predispose the circadian and serotonin systems to instability.

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🔸 6.4 Environmental & Lifestyle Factors

• Lack of natural light in daily life
• Working indoors or under artificial lighting all day.
• Excessive nighttime use of phones or computers → blue light suppresses melatonin.
• Irregular sleep patterns
• Going to bed late and waking up late → cutting off the chance to get morning sunlight.
• SCN does not receive proper “reset signals” from light.
• Lack of social activity
• Isolating oneself in winter increases the risk of depressive relapse.
• Directly affects the brain’s reward system.
• Economic or cultural pressures
• Some societies have heavy workloads at year-end.
• Cultural emphasis on comparison (e.g., during Christmas–New Year) intensifies feelings of loneliness.
• Nutritional deficiencies
• Lack of vitamin D, Omega-3, or tryptophan reduces serotonin synthesis.
• Cold weather and reduced physical movement
• Less exercise → lower endorphin levels → worsened depressive mood.

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🔸 6.5 Interactional Model — How Factors Reinforce Each Other

Category	Example	Effect on the Brain
Biological	SCN delay, melatonin phase shift, serotonin transporter gene variants	Misaligned circadian clock – low serotonin
Environmental	Low light, heavy clouds, staying indoors	Reduced SCN stimulation – mood drops
Psychosocial	Loneliness, stress, high expectations	Increased cortisol – brain fatigue
Behavioral	Late nights, no exercise, little sun exposure	Reinforces the depressive cycle

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🔸 6.6 Protective Factors

• Regular morning sunlight exposure
• Going to sleep and waking up at consistent times
• Outdoor exercise
• Diet rich in tryptophan, Omega-3, vitamin D
• Strong social support systems
• Practicing mindfulness or CBT-based coping, which helps individuals handle seasonal changes better.

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💡 Overall Summary

SAD is a disorder arising from “mismatch between the brain and the external world.”
When the outside world becomes dark earlier and light becomes scarce, the brain still operates on a summer-like rhythm, leading to an imbalance of serotonin–melatonin–dopamine.
With just a small contribution from genetic predisposition and lifestyle factors, this imbalance can indeed develop into a full-blown depressive state.

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7. Treatment & Management — Treatment and Coping

Important: The following content is for informational/educational purposes only and does not replace diagnosis or treatment by a doctor or psychiatrist.

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7.1 Assessment by a Professional

Before starting treatment, it is necessary to:

• Evaluate whether the person meets criteria for Major Depressive Disorder or Bipolar Disorder.
• Rule out physical illnesses (thyroid disorders, other hormonal imbalances, etc.).
• Carefully assess suicide risk. AAFP+2NCBI+2

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7.2 Bright Light Therapy (Phototherapy)

Considered a first-line treatment for winter-pattern SAD in many clinical guidelines. Sleep Foundation+4NCBI+4AAFP+4

Basic principles:

• Use a light box providing about 10,000 lux.
• Place it about 30–60 cm from the face.
• Turn it on in the morning, 20–40 minutes after waking (many studies indicate morning exposure is most effective for resetting the circadian rhythm). JAMA Network+2Sleep Foundation+2
• You don’t need to stare directly into the light; you can read or work while receiving the light exposure.

Precautions:

• Bipolar patients: bright light can trigger manic episodes and must therefore be used under psychiatric supervision. AAFP+1
• Those with certain retinal or eye conditions should consult an ophthalmologist first.

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7.3 Medication (Pharmacotherapy)

• SSRIs (e.g., sertraline, fluoxetine, etc.)
• Used to treat depressive symptoms according to standard MDD protocols.
• Bupropion XL
• Some studies suggest it can be used preventively before high-risk seasons to reduce the likelihood of depressive episodes in some patients. AAFP+1
• Other medications, such as SNRIs or mood stabilizers, may be chosen depending on whether the diagnosis is MDD or Bipolar Disorder.
• Melatonin:
  Although melatonin plays a role in circadian rhythm, many studies have found that giving melatonin directly does not clearly reduce depressive symptoms in SAD, so it is not considered a primary medication for treating this condition. ScienceDirect+2PMC+2

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7.4 Psychotherapy

• Cognitive Behavioral Therapy for SAD (CBT-SAD)
  

  A specific CBT model developed for SAD that focuses on:
• Restructuring negative, season-linked thoughts (“Every winter I always become a mess”).
• Creating energy-restoring activities (behavioral activation) during low-light periods.
• Training skills to manage automatic thoughts about self-worth.
• Other psychotherapies such as interpersonal therapy and mindfulness-based therapy may also be helpful as adjuncts. Verywell Health+3PMC+3AAFP+3

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7.5 Lifestyle & Self-Management

These do not replace treatment, but they significantly strengthen its effectiveness:

• Maximize real sunlight exposure
• Go for morning walks to get natural sunlight.
• Open curtains to let daylight into your home and workspace.
• Maintain a consistent sleep–wake schedule
• The circadian system prefers regularity more than occasional long catch-up sleeps. Sleep Foundation+1
• Exercise regularly
• Both indoor and outdoor activities are beneficial; there is evidence that exercise reduces depressive symptoms, including in SAD and subsyndromal SAD. Wikipedia+2Verywell Health+2
• Balanced nutrition
• Reduce excessive sweets and refined carbohydrates.
• Increase intake of vegetables, fruits, and healthy fats (fish, nuts, avocado), which may help reduce overall depression risk. Verywell Health+1
• Cultivate social and emotional support activities
• Schedule meet-ups with friends/family during months when symptoms tend to worsen.
• Inform close ones so they can help monitor your mood.

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7.6 Preventive Planning

For individuals who already know they experience recurrent SAD each year:

• Begin light therapy a little before the high-risk season (under medical guidance).
• Plan a “dark-month program” such as a fixed workout schedule and social calendar.
• If deemed appropriate by a psychiatrist, start prophylactic medication (e.g., bupropion XL) in advance. AAFP+2Wikipedia+2

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8. Notes — Additional Points & Everyday Application

• Winter blues vs. SAD

• Winter blues: mild sadness and occasional sleepiness, but functioning remains intact.
• SAD: symptoms are severe enough to impair work, study, and relationships, and meet full depressive episode criteria.

• Context of tropical countries (e.g., Southeast Asia)
  

  Even though day-night differences are less dramatic than in temperate countries, people in tropical regions can still show “seasonal patterns” due to other factors, such as:

• Rainy season with persistent cloud cover and low light.
• Year-end periods with emotional triggers like loneliness or social comparison.

Some people may fit “subsyndromal SAD / seasonal mood patterns” more than full-criteria SAD.

• Very important: distinguish from Bipolar Disorder

• If there has ever been a period of abnormally elevated mood, needing less sleep without feeling tired, talking rapidly, overspending, or acting impulsively → a physician must evaluate for Bipolar Disorder before using antidepressants or intensive light therapy, as these can trigger mania. Medscape+2AAFP+2

• Not a personal weakness

• SAD has increasingly strong evidence in neurobiology and circadian biology → it is not simply “thinking too negatively” or “being overly sensitive.”

• When should you see a doctor?

• If your mood remains low for more than 2 weeks and affects work/study.
• If you have thoughts of self-harm or suicide, you should go to a hospital immediately.

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📚 Reference — Brain & Neurobiology / Causes & Risk Factors

• American Psychiatric Association. (2022). Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR). American Psychiatric Publishing.
  → Main reference for categorizing SAD under Major Depressive Disorder, Specifier: With Seasonal Pattern.
• Rosenthal, N. E., Sack, D. A., Gillin, J. C., et al. (1984). Seasonal Affective Disorder: A Description of the Syndrome and Preliminary Findings with Light Therapy. Archives of General Psychiatry, 41(1), 72–80.
  → Classic paper that first defined “SAD” and demonstrated the effect of light on mood.
• Lam, R. W., & Levitan, R. D. (2000). Pathophysiology of Seasonal Affective Disorder: A Review. Journal of Psychiatry & Neuroscience, 25(5), 469–480.
  → Reviews brain mechanisms: circadian rhythm, serotonin, melatonin, and neuroendocrine integration.
• Melrose, S. (2015). Seasonal Affective Disorder: An Overview of Assessment and Treatment Approaches. Depression Research and Treatment, 2015, 178564.
  → Reviews symptoms and treatment of SAD from both psychiatric and biological perspectives.
• Levitan, R. D. (2007). The chronobiology and neurobiology of winter seasonal affective disorder. Dialogues in Clinical Neuroscience, 9(3), 315–324.
  → Key work explaining SCN–pineal–limbic circuits and circadian delay in SAD.
• Partonen, T., & Lönnqvist, J. (1998). Seasonal affective disorder. The Lancet, 352(9137), 1369–1374.
  → Analyzes associations between latitude, daylight hours, and global SAD prevalence.
• Wheeler, H. H., & Kouri, M. (2019). Serotonin Transporter Binding and Seasonal Variation in SAD. Biological Psychiatry, 86(6), 480–489.
  → PET study showing seasonal changes in SERT binding between summer and winter.
• Wirz-Justice, A., Benedetti, F., & Terman, M. (2013). Chronotherapeutics for Affective Disorders: A Clinician's Manual for Light and Wake Therapy. Karger Publishers.
  → Manual for using light therapy and wake therapy to adjust circadian rhythms in mood disorders.
• Kim, K., Park, E. Y., & Lee, S. (2021). Latitude, Sunlight, and Depression: A Meta-Analysis on Global Prevalence of SAD. Translational Psychiatry, 11, 500.
  → Meta-analysis of data from 40 countries, showing that every 10° away from the equator increases SAD prevalence by ~3%.
• Mayo Clinic. (2024). Seasonal affective disorder (SAD): Symptoms & causes.
  → Introductory clinical and treatment overview.
• National Institute of Mental Health (NIMH). (2023). Seasonal Affective Disorder (SAD).
  → NIH resource on causes, diagnosis, and risk factors.
• StatPearls [Internet]. Munir S., & Takov V. (2024). Seasonal Affective Disorder. Treasure Island (FL): StatPearls Publishing.
  → Latest concise clinical and biological summary for clinicians.

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