Seasonal Affective Disorder

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Basics

Description

  • Seasonal affective disorder (SAD) describes mood episodes that occur as a part of major depressive disorder, bipolar 1 disorder, or bipolar 2 disorder in a seasonal pattern. Patients may experience depressive, hypomanic or manic episodes, although depression is most common.
  • Depressive episodes typically occur during winter months (fall-winter onset), with full remissions in the spring and summer. Less commonly, patients may experience a spring-summer onset with remission in the fall-winter months.
  • Ranges from a milder form (winter blues) to a seriously disabling illness

Epidemiology

Incidence
  • Affects up to 500,000 people every winter
  • Up to 30% of patients visiting a primary care physician (PCP) during winter may report winter depressive symptoms.
  • Predominant age: occurs at any age; peaks in 20s and 30s
  • Predominant sex: female > male (3:1)

Prevalence
  • Lifetime prevalence of the general population is 0.5 to 3%.
  • Point prevalence in primary care patients is 5–10%, whereas in depressed patients is 15%.

Etiology and Pathophysiology

The major theories currently involve the interplay of phase-shifted circadian rhythms, genetic vulnerability, and serotonin dysregulation.

  • Melatonin is produced by the pineal gland at increased levels in the dark and is linked to depressive symptoms; light therapy on the retina acts to inhibit melatonin secretion.
  • Serotonin dysregulation, which is secreted less during winter months, must be present for light therapy to work, and treatment with central acting serotonergic agents such as SSRIs appear to reverse SAD symptoms.
  • Decreased levels of vitamin D, often occurring during low-light winter months, are associated with depressive episodes in individuals experiencing SAD symptoms.
Genetics
  • Twin studies and a preliminary study on GPR50 melatonin receptor variants suggest a genetic component.
  • Recent studies indicate an association with melanopsin gene (OPN4) variants.
  • Increased incidence of depression, ADHD, and alcoholism in close relatives, or first-degree relatives with SAD increase the chance an individual will develop SAD.

Risk Factors

  • Most common during months of January and February: Patients frequently visit their PCP during winter months complaining of recurrent flu, chronic fatigue, and unexplained weight gain.
  • Working in a building without windows or other environments without significant exposure to sunlight

General Prevention

  • Consider use of light therapy at the start of winter (if prior episodes begin in October), increase time outside during daylight, or move to a more southern location.
  • Bupropion (Wellbutrin) is the only FDA-approved antidepressant for the prevention of SAD.

Commonly Associated Conditions

Patients with SAD often have other comorbid psychiatric disorders including alcohol use disorder, ADHD, and binge eating disorder, among others. Some individuals with SAD have a weakened immune system and may be more vulnerable to infections.

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Basics

Description

  • Seasonal affective disorder (SAD) describes mood episodes that occur as a part of major depressive disorder, bipolar 1 disorder, or bipolar 2 disorder in a seasonal pattern. Patients may experience depressive, hypomanic or manic episodes, although depression is most common.
  • Depressive episodes typically occur during winter months (fall-winter onset), with full remissions in the spring and summer. Less commonly, patients may experience a spring-summer onset with remission in the fall-winter months.
  • Ranges from a milder form (winter blues) to a seriously disabling illness

Epidemiology

Incidence
  • Affects up to 500,000 people every winter
  • Up to 30% of patients visiting a primary care physician (PCP) during winter may report winter depressive symptoms.
  • Predominant age: occurs at any age; peaks in 20s and 30s
  • Predominant sex: female > male (3:1)

Prevalence
  • Lifetime prevalence of the general population is 0.5 to 3%.
  • Point prevalence in primary care patients is 5–10%, whereas in depressed patients is 15%.

Etiology and Pathophysiology

The major theories currently involve the interplay of phase-shifted circadian rhythms, genetic vulnerability, and serotonin dysregulation.

  • Melatonin is produced by the pineal gland at increased levels in the dark and is linked to depressive symptoms; light therapy on the retina acts to inhibit melatonin secretion.
  • Serotonin dysregulation, which is secreted less during winter months, must be present for light therapy to work, and treatment with central acting serotonergic agents such as SSRIs appear to reverse SAD symptoms.
  • Decreased levels of vitamin D, often occurring during low-light winter months, are associated with depressive episodes in individuals experiencing SAD symptoms.
Genetics
  • Twin studies and a preliminary study on GPR50 melatonin receptor variants suggest a genetic component.
  • Recent studies indicate an association with melanopsin gene (OPN4) variants.
  • Increased incidence of depression, ADHD, and alcoholism in close relatives, or first-degree relatives with SAD increase the chance an individual will develop SAD.

Risk Factors

  • Most common during months of January and February: Patients frequently visit their PCP during winter months complaining of recurrent flu, chronic fatigue, and unexplained weight gain.
  • Working in a building without windows or other environments without significant exposure to sunlight

General Prevention

  • Consider use of light therapy at the start of winter (if prior episodes begin in October), increase time outside during daylight, or move to a more southern location.
  • Bupropion (Wellbutrin) is the only FDA-approved antidepressant for the prevention of SAD.

Commonly Associated Conditions

Patients with SAD often have other comorbid psychiatric disorders including alcohol use disorder, ADHD, and binge eating disorder, among others. Some individuals with SAD have a weakened immune system and may be more vulnerable to infections.

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