Living in biological darkness III: Effects of low-level pre-midday lighting on markers of depression in healthy subjects

Abstract

Affective disorders are associated with dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and changes in sleep architecture. Both HPA and sleep are circadian modulated, thus influenced by light and darkness. Surprisingly, the impact of low-level daytime lighting – we call “Living in Biological Darkness” – remain largely unexplored. Recently we reported extremely low habitual light levels healthy urbans were exposed to, accompanied by depression-like sleep patterns. This study aimed to examine how exposure to low light levels affects depression-related markers in healthy individuals.In a between-subjects design, twenty healthy subjects (mean ± SD:24.5 ± 2.8yrs; 10f) were randomized into two groups of ten and exposed to low-intensity incandescent (2700K, 55lx, 12mlux) or higher-intensity fluorescent lighting (3500K, 800lx, 481mlux) during five mornings (8:00–12:00) over a seven-day period. Assessments conducted prior to and after interventions included: two-night polysomnography, 32-h fractionated urine cortisol, salivary cortisol and melatonin levels, reaction time, daytime sleepiness and sadness.Low-level pre-midday lighting led significantly to: 1. increased urine cortisol levels in the evening (19:00–23:00;p = .021), 2. increased salivary cortisol in the afternoon (16:00;p = .026), 3. reduced Total-Sleep-Time (about 25min;p = .016), 4. shifted slow-wave activity from second to third NREM-REM cycle (p = .018), 5. increased subjective sleepiness (p = .023) and sadness (p = .016). In contrast, higher-intensity fluorescent lighting resulted in an increase in REM sleep towards end of the sleep period. Circadian phase remained unchanged across both groups.In healthy subjects repetitive exposure to low-intensity lighting during pre-midday hours was associated with increased cortisol levels over the day and delayed slow-wave-activity within nighttime sleep, changes known to occur in patients with depressive illnesses. Insomnia-like changes in sleep architecture shown here may pave the avenue to more vulnerability to depression and contribute to the understanding of pathophysiology in depressive illnesses.