Seasonal Affective Disorder: Autumn Onset, Winter Gloom

Ethan A. Singer, RN, MSN



In the United States, 5% to 12% of men and 10% to 25% of women experience a major depressive episode in their lifetime. One major depressive disorder subtype that is characterized by recurrent seasonal patterns is Seasonal Affective Disorder (SAD).

SAD is classified into two discernible types. The more common form, called fall-onset or winter depression, classically begins in late autumn and abates in the spring and summer. In most cases, its symptoms are closely related to those of atypical depression. Patients experience increased sleep, increased appetite, craving for carbohydrates, weight gain, and interpersonal conflict. Other symptoms include irritability and heaviness in the extremities (referred to as leaden paralysis.)

The second type, which is far less common, is called spring-onset SAD. The depressive episode generally begins in late spring or early summer and lasts through early fall. Patients’ symptoms are characteristic of a typical depressive disorder and include insomnia, weight loss, and poor appetite.


Estimated incidence of SAD in the general population in North America is about 6%, ranging latitudinally (south to north) from 2% to 10%. The occurrence of seasonal changes in mood and behavior appears to increase in the northern latitudes. By some estimates, however, the incidence of SAD in North America is double that in Europe — suggesting that climate, culture, and genetics may be more important factors.

In children and adolescents, SAD has not been studied adequately and is not well understood. Children with SAD are reported to have enormous cravings for carbohydrates, to experience severe mood swings, and to be extremely irritable. The condition may be under recognized in younger patients because some signs — tantrums, hyperactivity, and over-tiredness — mimic common childhood behaviors or signs of other disturbances. Labile hormonal changes that occur during puberty may mask symptoms of SAD in adolescents.

In adult patients, possible indicators of SAD include fatigue, depressed affect, and loss of interest in routine activities, especially during the fall. Although it is not clear whether SAD is an inherited disorder, results from one study of adult twins suggest that genetics may account for at least 29% of “seasonality” in men and women.

What Causes It?

The human brain, research shows, has a precise, 24-hour repeating rhythm to regulate daytime and nighttime activities. The biochemical circadian rhythm relies on brain function to manage core body temperature, release hormones, and trigger other processes. At night, circadian rhythm mechanisms lower body temperature and trigger production of melatonin, a hormone secreted by the pineal gland that enhances sleep.

It has been hypothesized that these circadian rhythms in SAD patients are delayed during the winter months when sunlight is diminished. Exposure to bright light in the morning hours often seems to correct these rhythms — although the exact mechanism of action is not clearly understood. Numerous environmental factors may affect circadian rhythms, including sleep, physical activity, and eating.

It was once hypothesized that irregularities in melatonin secretion might explain SAD — that is, until it was shown that winter melatonin rhythms do not differ between SAD patients and other persons. Recent evidence suggests that impaired or altered transmission of the neurotransmitters serotonin, dopamine, norepinephrine, and/or neuropeptide Y may cause a disruption of biological rhythms. Low levels of serotonin, for example, can induce depression — and levels decline in late autumn and throughout the winter months. The association between carbohydrate ingestion and increased serotonin levels may explain SAD patients’ craving for carbohydrates.


Diagnostic Criteria for SAD

The components of SAD are described in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. SAD is a subtype of major depressive disorder. The patient must have experienced a regular seasonal-related pattern of depression during the previous two years, with episodes generally beginning in the fall or winter and remitting in spring. Patients may have had a previous diagnosis of depressive disorder or may give a detailed history of depressive symptoms with fall onset for at least two years.

Treatment of SAD

First-line treatment for the patient with confirmed SAD is bright-light therapy. This modality is defined as exposure to visible light of at least 2,500 lux (units of illumination) at eye level. Apparently it is the eyes, not the skin, that mediate the effects of bright-light therapy. As light passing through the pupil is absorbed by the retina, increased neuromotor activity lessens symptoms of SAD.

Light boxes manufactured for SAD therapy produce 2,500 to 10,000 lux. Acceptable light boxes must filter out potentially harmful ultraviolet rays. Light visors produce lower levels of light than standard light boxes — but they are used closer to the eyes. This apparatus has not yet been shown to be more effective in reducing symptoms of SAD.

Appropriate levels and duration of light therapy vary among patients. Typically, however, therapy is administered for 30 minutes per day at 10,000 lux. Timing can be optimized by estimating each patient’s circadian rhythm phase, perhaps using the Automated Morningness-Eveningness Questionnaire of Terman et al. Morning exposure to bright light, preferably shortly after awakening, appears to offer maximum benefit — perhaps because morning light advances circadian rhythms and fosters an earlier sleep schedule. Patients need not glance directly at the light source; peripheral illumination seems to suffice. It may take three weeks or longer for patients to experience the antidepressant effects of bright-light therapy.

Studies of cumulative exposure to light therapy over six years have shown no ocular damage, although mild to moderate nausea, headache, and nervousness are not uncommon. Additionally, light boxes vary in radiation levels, and patients with unidentified retinal conditions may be at risk. For patients who are taking photosensitizing medications (eg, certain antibiotics, anti-inflammatory agents, diuretics, and hypoglycemics), light therapy is contraindicated.

Pharmaceutical Management

In patients for whom light therapy alone seems insufficient, medication should be considered. Among agents used to treat SAD, the selective serotonin reuptake inhibitors (SSRIs) have demonstrated favorable outcomes. These include fluoxetine, paroxetine, and sertraline. In one placebo-controlled trial, response rates (as defined by at least 50% improvement in combined scores on two depression rating scales) were similar between fluoxetine patients and light therapy patients (65% vs 70%, respectively); however, the remission rate (defined by more exacting criteria) in patients who received bright-light therapy was double that in patients who took fluoxetine (50% vs 25%).

Patients with SAD treated with Hypericum perforatum extract (Saint John’s wort) have reported decreased anxiety and improved libido. However, hypericum has photosensitizing effects.


Seasonal affective disorder, a subtype of the depressive mood disorders, is characterized by recurrent seasonal patterns. Typically, SAD is more prevalent in the fall and winter months. There are many hypotheses regarding the causes of SAD, but the etiology appears to combine a circadian phase delay, inadequate regulation of certain neurotransmitters, and genetics. Light therapy remains the treatment of choice. Although pharmacotherapy with antidepressants has been found somewhat effective in treating patients with SAD, drug treatment should not be used until response to bright-light therapy alone has been tested and found insufficient.

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Dr. Gnap

Dr. Gnap is a family practice physician and behavioral medicine specialist in suburban Chicago.  Dr. Gnap developed the Inner Control™ Program in 1970 and has worked with thousands of people to improve and correct medical, emotional, behavioral and learning problems including performance.  He started the Inner Control program because so many patients asked, “what more can be done along with traditional treatment methods?”

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