Participants randomized to the treatment arm received lamps that emit bright light (10,000 lux). Based on the previous literature, we elected to use 10,000 lux (the maximum lux used in previous trials) for a shorter duration (30 minutes) rather than lower lux for a longer duration (e.g., 2,500 lux for 2 hours); the longer duration of use would be more difficult for patients to adhere to and both have comparable response rates [21]. Participants in the placebo arm received lamps that emit dim light (500 lux). Although 500 lux is below therapeutic levels [21], both lamps appeared bright to participants and study staff. Participants scheduled for cardiac surgery consented to the study prior to surgery but received their lamps following surgery. Participants hospitalized for ACS received their lamps immediately following consent. All participants began lamp use while in hospital and were asked to take the lamps home once discharged.
A total of 15 participants were enrolled in the pilot trial (Table 1). Eight (53.3%) of the enrolled participants were randomized to the bright light treatment arm, whereas 7 (46.7%) were randomized to the dim light control arm. The sample was composed of 11 men (73.3%) and 4 women (26.6%). The mean age was 60 years (standard deviation: 11). Ten participants were admitted to the hospital for an ACS, while 4 participants were admitted for coronary artery bypass grafting and one for aortic valve replacement.
Several trials have investigated the potential of bright light therapy as a treatment modality for non-seasonal depression. In 2005, Golden et al. [21] conducted a systematic review and meta-analysis of the efficacy of bright light therapy in the treatment of mood disorders. Twenty randomized controlled trials were included in the analysis. The meta-analysis demonstrated significant effects of bright light therapy for the treatment of seasonal affective disorder and non-seasonal depression. Another review conducted in 2004 [24] of 49 studies found that, in high-quality studies, the response to bright light was significantly better than the response to control interventions.
Large-scale studies could consider a less conservative approach to eligibility. As a preventative measure, experts recommend that patients with retinal diseases avoid bright lights [25]. Therefore, we excluded patients with diabetes based on their elevated risk for diabetic retinopathy and cataracts, (47.1% of ineligible patients had diabetes, cataracts, or both). However, it is not clear whether diabetes, in the absence of retinopathy, constitutes a contraindication for bright light therapy. In addition, the literature about the potential adverse effects of light therapy on the eye is inconclusive. A study by Gallin et al. examined the effects of 30 minutes of daily exposure to 10,000 lux in 50 patients with seasonal depressive disorder for a period of up to 6 years of use and detected no ocular changes in the patients [26]. Even with regards to patients with retinopathy, outdoor exposure to sunlight is considered more hazardous than short-term exposure to bright light therapy [27]. It seems likely that a larger trial could safely enroll patients with diabetes who do not have diabetic retinopathy.
A. Clusters with increased functional connectivity to the left frontal pole that correlated with degree of bright light therapy use. B. Clusters with increased functional connectivity to the right frontal pole that correlated with degree of bright light therapy use. Height threshold p < .001 uncorrected, cluster size p < .05 FDR corrected.
A. Percent bright light therapy use and enhanced functional connectivity between left frontal pole and two clusters: one containing the precuneus and posterior cingulate cortex and the other the cerebellum crus2. B. Percent bright light therapy use and enhanced functional connectivity between right frontal pole and five clusters. The largest included cerebellum crus1, cerebellum 6, occipital pole, lingula gyrus, fusiform gyrus and intracalcarine cortex. The other clusters contained the inferior frontal gyrus (IFG) operculum, anterior and posterior middle temporal gyri (MTG) and right and left frontal poles.
A third limitation is that actigraphs cannot estimate sleep stages [102]. Hence, we do not know if use of the device increased proportion of time spent in REM or slow wave sleep. This may be key to understanding the possible influence of bright light on cognition as well as dentate gyrus volume. A statistically significant effect of use may have emerged because sleep deprivation (particularly REM) suppresses neurogenesis in rats [103] through elevations in glucocorticoid levels [34]. Further, reduced sleep efficiency is associated with smaller dentate gyrus volumes in humans [33]. Restoring sleep after a period of deprivation produces a rebound overshoot in dentate gyrus neurogenesis [34]. Hence, the possible effect of BLT on dentate gyrus volume may have been mediated by unmeasured effects on sleep architecture.
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