Light treatment in seasonal and nonseasonal depression : diagnostic, clinical and neurendocrine studies

Abstract

There is a need for evaluation of new treatment modalities in depression. The aims of this thesis were to investigate the effect of 2 hours of daily light treatment for 10 days in patients with a major depression with seasonal or nonseasonal pattern and to study subgroups of depressed patients with respect to clinical, demographic, and neuroendocrine factors, the effect of exposure to bright light, dexamethasone suppression test, CRH stimulation and the hormonal effect of light exposure on healthy controls.

The patients with a seasonal pattern (Seasonal Affective Disorder; SAD, n=99),were less depressed, had higher frequency of carbohydrate craving, increased appetite, and a lower frequency of treatment with drugs, sick leave and hospitalization for depression than those with a nonseasonal pattern (n=28). In a sample of 90 patients those with a seasonal pattern (n=68) improved significantly better to treatment with bright light of 350 cd/m2. No differences were found between light treatment in the morning (6-8 a.m.) or in the evening(6-8 p.m.). The treatment effect was not related to the severity of the depression, sex, age, medication or month when the light treatment was given. In 63 matched depressed patients no differences were seen before or as a result of light treatment between those with a seasonal(n=42) and nonseasonal (n=21) pattern in the area under curve (AUC) and the phase (TC) of serum melatonin, mesor and amplitude of serum cortisol, measured at nine time-points during the night (8 p.m. - 8 a.m.). The melatonin AUC was significantly reduced by light treatment. Serum melatonin TC was advanced by morning light and delayed by evening light. Basal levels or changes of serum melatonin (AUC and TC) were not related to the therapeutic outcome.

The batyphase of serum cortisol was significantly advanced by morning, but not by evening light. The amplitude and the mesor of serum cortisol were not affected by light treatment. A delay in the batyphase of cortisol showed a weak, but significant relation to improvement of the depression. A cosinor analysis of serum melatonin and cortisol showed that the batyphase of cortisol occurred approximately three hours earlier than the acrophase of melatonin and that 43% of the changes in the melatonin acrophase were reflected by a change in the cortisol batyphase.

In a study of 13 healthy volunteers, a 15- minute light exposure in the evening was shown to significantly suppress melatonin, but not cortisol. Light exposure at 10 -11 p.m. in the groups of patients with seasonal and nonseasonal depression suppressed melatonin, but not cortisol. There were no differences between the two groups, and no relationship was found between treatment efficacy and the suppression of melatonin.

In 24 patients with major depression, subgrouped in suppressors and nonsuppressors from their DST response to 1 mg of dexamethasone, nonsuppressors showed a significantly lower ACTH and cortisol responses (AUC) after stimulation with 0.45µg corticotrophin releasing hormone (CRH). These differences were no accounted for in the severity of their depression.

In summary: Depressed patients with a seasonal pattern improved more than those with a nonseasonal pattern to 2 hours of daily light exposure for ten days. The improvement was not related to the severity of their depression, morning or evening light treatment or hormonal changes in the level or phase of serum melatonin or the amplitude ormesor of serum cortisol.