Cortisol and Seasonal Changes in Mood and Behavior

The degree to which season changes affect mood, energy, sleep, appetite, food preference, or desire to socialize with others has been called "seasonality."^1,16 Seasonality can manifest in different degrees in different individuals. It can be viewed as a dimension ranging from the absence of seasonal changes to the occurrence of extreme seasonal changes (eg, some people experience only very mild seasonal changes while others are severely affected).

Children with SAD usually present with fatigue, irritability, difficulty in getting out of bed in the morning, and problems in school.¹⁷ Sadness and changes in appetite have also been observed in children with SAD. Children with winter SAD tend to blame the external world (parents, teachers, etc) for treating them poorly.

Seasonality of mood and behavior is common throughout the US population.^16,18-20 Surveys suggest that the prevalence of SAD in the United States increases with increasing latitude--ranging from 1.4% in Florida to 9.7% in New Hampshire.¹⁹ A survey in the Washington, DC, area found that about 4% of the population have winter SAD and over 10% more have subsyndromal features of SAD.¹⁷ Twenty-seven percent of respondents reported that changes in the seasons were a problem for them, 66% reported seasonal changes in energy level, 64% reported some seasonal changes in mood, and 49% reported seasonal changes in weight. Another survey, in New York City, indicated that about 6% of the population had seasonal impairment equivalent to that of patients with SAD, 18% reported milder symptoms that were bothersome, and 35% noted symptoms but did not complain.²⁰

Many clinical studies report that winter SAD mainly affects women.^3,15 However, the high proportion of women seen in research clinics may be a result of selection bias. Blazer and colleagues²¹ suggested that SAD with major depressive episodes is more frequent among men, whereas women more commonly experience minor depression with a seasonal pattern.

Identification of a seasonal pattern can only be made if both the patient and physician actively look for it.^1,3 Clinicians should ask the following questions when SAD is suspected. When the seasons change, do you:

• Feel down or depressed?
• Have less energy than usual?
• Feel less productive or creative?
• Need more sleep?
• Have less control over your appetite?

If physicians fail to ask these questions, many patients with SAD may be labeled as having a nonseasonal depressive disorder.

Various hypotheses related to the pathophysiology of SAD have been proposed.^1,3,22,23 One of these hypotheses suggests that abnormalities of hypothalamic-pituitary-adrenal (HPA)-axis function may contribute to the pathogenesis of SAD. The HPA axis controls the secretion of corticotropin-releasing hormone (CRH), corticotropin (adrenocorticotropic hormone), and cortisol.^24,25 CRH is secreted from the paraventricular nucleus of the hypothalamus as well as from extrahypothalamic sites. It acts on the anterior pituitary gland to cause the release of corticotropin into the bloodstream, where it acts on the adrenal cortex to cause the production and release of cortisol into the bloodstream.

Cortisol has diverse and widespread actions throughout the body and brain. It secondarily inhibits corticotropin and CRH release via negative feedback, although it may augment CRH release in the amygdala. Feedback inhibition is mediated via low-affinity glucocorticoid receptors (GRs) and high-affinity mineralocorticoid receptors (MRs). In the brain, MRs are located primarily in the hippocampus; GRs are more widely distributed in the hypothalamus, pituitary, cortex, and elsewhere. Species from humans to the most ancient organisms share components of the HPA axis.