Seasonal Affective Disorder

Seasonal affective disorder is recurrent major depression with a seasonal pattern, typically starting in autumn and remitting in spring, and it carries an atypical symptom profile: hypersomnia rather than insomnia, increased appetite with carbohydrate craving, weight gain, and heavy leaden fatigue. That profile distinguishes it from non-seasonal depression, where weight and sleep more often decrease. The mechanism is thought to involve phase delay of circadian rhythm relative to sleep, reduced retinal light input in winter, and altered serotonin transporter binding that rises in winter months. Bright light therapy is the first-line treatment and is genuinely effective, with meta-analyses showing effect sizes similar to antidepressant medication. The details determine whether it works: 10,000 lux at roughly 30-40cm, for 20-30 minutes, within an hour of waking, with eyes open but not looking directly at the light. Timing is the most common error, since evening use can worsen phase delay. Dawn simulation and cognitive behavioural therapy adapted for SAD both have supporting evidence, and CBT-SAD shows lower recurrence in subsequent winters than light therapy alone. Vitamin D is intuitively appealing and empirically disappointing: the large VITAL-DEP trial found no effect on mood outcomes, so treat vitamin D as deficiency correction rather than SAD treatment.

• •Low mood beginning in autumn
• •Oversleeping and difficulty waking
• •Carbohydrate craving and weight gain
• •Leaden heaviness in the limbs
• •Social withdrawal
• •Spring remission

• •Reduced winter daylight and circadian phase delay
• •Altered serotonin transporter activity
• •Melatonin timing shifts
• •High-latitude living
• •Family history of mood disorder
• •Shift work reducing morning light exposure

Circadian phase delay from reduced morning light, seasonal increase in serotonin transporter binding reducing synaptic serotonin, altered melatonin secretion timing, reduced retinal light sensitivity in some individuals, latitude and short winter photoperiod, and genetic vulnerability.