Comparing Wavelengths Using LED Light for SAD Treatment

BACKGROUND AND SIGNIFICANCE

Discovery in the late 1970s that bright light affects neuroendocrine rhythms such as melatonin secretion, and can reset the circadian pacemaker in humans, paved the way for the discovery that seasonally recurrent fall/winter depressions--christened Seasonal Affective Disorder (SAD)--can be treated with bright light exposure (Lewy et al., 1980; Rosenthal et al., 1985). It was reasoned that seasonal rhythms of mood in humans, like other seasonal physiological cycles in mammals, could be regulated by the biological "clock." A series of studies has demonstrated that bright light exposure does produce therapeutic effects in SAD patients beyond the level achieved by placebos (Eastman et al., 1998; Lewy et al., 1998; Terman et al., 1998) and that retinal exposure is required for efficacious treatment (Wehr et al., 1987; Koorengevel, 2001).

Attempts to construct an action spectrum for suppression of melatonin secretion and for resetting the circadian pacemaker suggest that 446-477 nm wavelengths are most potent (Brainard et al., 2001; Lockley et al., 2003), which is inconsistent with rod or cone mediation of the responses (Brainard, 2004). Discovery that a melanopsin-containing system of retinal ganglion cells serves as a primary afferent to the hypothalamic circadian pacemaker (Provencio et al., 2000; Gooley et al, 2001; Hattar et al, 2002) suggests a possible basis for the potency of violet/blue light on these neuroendocrine circadian endpoints and raises the possibility that light of this wavelength also might be uniquely potent for treatment of SAD (Brainard, 2004).

Estimates of SAD prevalence range from 0.4 - 9.7% of the general population in the United States, depending on the survey methods and precise criteria used (Rosen et al., 1990; Blazer et al., 1998). In addition to those with recurrent episodes of frank Major Depression, patients with less severe "sub-syndromal" winter depression and those with annual exacerbation of a year-round mood disorder also have been shown to benefit from light treatment in fall/winter months (Kasper et al., 1989). Since the 1990s, cool-white fluorescent sources capable of yielding 10,000 lux polychromatic white light have been the treatment standard (Lewy et al., 1998; Terman et al., 1998; Desan et al., 2001; also see e.g., Lam & Levitt, 1999). Although well-tolerated, some transient adverse effects of the 10,000 lux white light have been reported, such as agitation or feeling "wired," insomnia, headache, eye or vision problems, nausea, sedation, and chest tightness (Labbate et al., 1994; Kogan et al., 1998; Terman & Terman, 1999). The more common of these complaints--headache, eye or vision problems, and insomnia--remit rapidly after discontinuation of light exposure (Oren et al., 1991), however, narrower bandwidth light if more potent in antidepressant effectiveness might be administered at lower intensities and thereby further reduce adverse effects and increase tolerability of the treatment (Brainard, 2004).

A between-subjects double-blind comparison of 3-weeks treatment using narrow-band LED panels at blue (468 nm at 500 mW/cm2) vs red (700 nm at 15 mW/cm2) wavelengths in 24 SAD patients demonstrated both greater reductions in depressive symptoms and also remission rates (54.5% vs 30.8%) in favor of the blue light source (Byrne et al., 2004). Comparisons of this narrow bandwidth blue LED light with white light would be of even greater clinical interest since white fluorescent sources currently are the industry standard.