All patients must meet the diagnostic criteria for recurrent major depression or bipolar mood disorder. Seasonal affective disorder (SAD) is then a sub-type specifier used to describe temporal variations of these disorders. As such, SAD is not considered a stand-alone diagnosis or comorbid condition to recurrent major depression or bipolar disorder. Common presentations include the initiation or worsening of depressive symptoms during the autumn or winter months, and full remission during the spring or summer months, or hypo-manic or manic symptoms presenting during spring or summer months.
Circadian and neurotransmitter factors are likely to contribute to the pathophysiology of SAD, although the exact mechanism of action remains ill-understood. The suprachiasmatic nucleus (SCN) of the hypothalamus is being increasingly recognised as the 'master regulator' of several systems implicated in seasonal mood regulation. Diminished light during the autumn and winter may cause a phase shift in various circadian rhythms, including sleep-wake cycle, body temperature, hormone levels, and melatonin secretion.
The age-adjusted incidence of cerebral infarction significantly declined by 37% for men and by 32% for women from the first to the second cohort. It continued to decline by 29% for men, but the decline decelerated for women in the third cohort. The incidence of cerebral hemorrhage steeply declined by 61% from the first to the second cohort in men only, while it was sustained for both sexes in the third cohort. Stroke mortality continuously declined as a result of these incidence changes and significant improvement of survival. In contrast, the incidence and mortality rate of coronary heart disease were unchanged except for the increasing incidence in the elderly. The prevalence of severe hypertension and current smoking significantly decreased, while that of glucose intolerance, hypercholesterolemia, and obesity greatly increased among the cohorts.