Information Page for Therapists:
Risks of Eye Damage from Bright and Blue Light Therapy
There is good reason to be concerned about retinal damage from the use of bright and blue light therapy lamps. Experts have now determined that the development of Age-related Macular Degeneration (AMD) is directly related to the retinal stress that results from exposure of the eye to visible blue light. As Dr. Beatty, director of the Macular Pigment Pigment Research Group (MPRG) stated "It is photo-oxidative stress, or the cumulative exposure to free radicals from blue light over a lifetime that causes AMD".1a Recently the European Eye (EUREYE) Study "found that the combination of blue light exposure and low plasma concentrations of antioxidants was also associated with the early stages of AMD, which are common in the population, and that blue light exposure in middle age might be more damaging than at younger ages."1b
It is primarily the blue wavelengths of light (400 - 480 nm) emitted by light therapy lamps that are of concern. Blue light contributes about 90% of the risk of photochemical retinal damage from fluorescent lamps and sunlight, which is why the term "blue light hazard" is used to describe this risk. When blue light is absorbed by retinal tissue it induces oxidative stress and the resulting indigestible debris that is formed accumulates in the retina over a lifetime. The accumulation of this oxidative debris has been shown to contribute to the development of AMD.
The risk of damage to the retina from blue light is increased in people with pre-existing retinal damage, those who use photosensitizing medications or supplements, and older people. The retina becomes increasingly susceptible to damage with age, as a result of the accumulating oxidative debris and because the defense mechanisms that protect the retina from oxidative damage progressively deteriorate after age 40.
However, epidemiological evidence has found that even for young adults, in their teens and thirties, a moderate increase in blue light exposure will advance the onset of macular degeneration later in life by 10 years, which would double the likelihood of becoming blind in one’s lifetime2a,2b. Several specialists involved in macular degeneration now recommend that sunglasses that block blue visible light be used by people of all ages to limit the amount of blue light reaching the retina over a lifetime.
AMD is a severe problem that is approaching epidemic proportions. 25% of people in the developed world will have vision problems caused by AMD by age 75, (10% of people aged 65-74 and 25% over 75 have severe vision loss) 3a. For people with a family history of macular degeneration, the prevalence of severe vision loss increases to 54% at age 75, and 64% at age 853b. As AMD is caused by cumulative retinal stress, increased levels of exposure to blue light wavelengths by users of light therapy can only advance their likelihood of developing AMD.
Hazardous blue light wavelengths do not contribute to the effectiveness of light therapy. While early studies indicated that the eye was more sensitive to blue light wavelengths, recent studies found that monochromatic blue (479 nm) light is not more effective for light therapy than regular fluorescent white (polychromatic) light4. Other studies found that hazardous blue light, with wavelengths shorter than 480 nm, is no more effective for light therapy than non-hazardous green light in the region of 500 nm5a,5b,6. In fact, the low intensities of Sunnex Biotechnologies GreenLIGHT has been found to be much more effective at inducing physiological responses than a light therapy device that emits primarily blue light (465 nm) wavelengths.7
Because blue light is not necessary for effective light therapy, it has been recommended that light therapy devices screen out the potentially hazardous blue light wavelengths, and that light therapy devices emitting blue wavelengths of light should not be used until the potential hazard from blue light from light therapy devices is resolved. As one expert in light therapy stated, "It should be noted that broad-spectrum white light, traditionally used for bright light therapy, also contains blue light of potential concern particularly for very high intensity, long-duration exposure. Clearly, the safety of bright light therapy for people needs investigating. In the meantime it would be suggested that light in the 500 to 530 nm wavelength range (blue–green) should still be effective while avoiding the putative blue hazard".8
The consequences of macular degeneration for people using light therapy are severe. Herbert Kern was the first recipient of light therapy for the treatment of a mood disorder(SAD). In an article in recognition of the 25th anniversary of the use of light therapy to treat mood disorders in the journal Science (Sept, 2007), after decribing how [bright] light therapy became less and less effective for him over the years as his eyesight faded from AMD, he stated, "Now I can hardly see, and all hell has broken loose...I have had periods of depression lasting over a year".9 See ENDNOTE below
There are a number of factors inherent in the manner of use of light therapy that increase the risk of retinal damage and the resulting loss of vision by users of bright or blue light therapy. For a more complete, annotated discussion of this risk please see Risk Factors of Bright and Blue Therapy
A Short Synopsis of the Pathogenesis of Macular Degeneration Induced by Blue Visible Light
The known pathogenesis of Age- Related Macular Degeneration is related to oxidative stress and the accumulation of
oxidative debris within the retinal cells and intercellular spaces adjacent to the macula. The macula is a small region
of the retina that contains the fovea, which is primarily responsible for vison. Retinal oxidative debris, known as
lipofuscin when within cells, and drusen in the intercellular spaces adjacent to the retina, substantially consists of indigestible
material which is generated from oxidative damage to lipids and lipoproteins associated with the absorption of light
by photoreceptor cells. Both lipofuscin and drusen accumulate over a lifetime, and generate large amounts of radical
oxygen species when they absorb blue visible light. These radical oxygen species are capable of directly inducing cell death,
of causing chronic inflammatory responses within the cells adjacent to the retina, and of generating additional oxidative
debris. This accumulation of material between the cells which nourish and remove waste materials from photoreceptor cells
and the structure, Bruch's membrane, limits the ability through which these cells access the blood supply in order to absorb
nutrients and dispose of metabolic waste. Impairment of All of these processes are associated the development of slow
deterioration of vision called "dry macular degeneration".
The generation of the large amounts of radical oxygen species and the resulting oxidative stress can damage the
structure separating the retina from the blood supply and promote its permeation by small weak capillaries.
When these small capillaries invade the macular region of the retina they are susceptible to leakage. This leakage into the
retinal space results in a rapid deterioration of vision that is known as the “wet” form of macular degeneration.
For a more complete annotated discussion of the role of visible blue light in the pathogenesis of AMD. Please see
A technical discussion on the contribution of exposure to blue light (400-480nm) to the pathogenesis of AMD.
Sunnex Biotechnologies' Lo-LIGHT technology is a safe, low intensity alternative to bright light therapy. It is the only light therapy device that filters out the dangerous high-energy blue light rays. While some "blue light" therapy devices emit wavelength in the 460 - 465 nm range, which is 70-80 % of the maximum blue hazard, the blue-green light ( peak 500 nm) used in the Lo-LIGHT is less than one-tenth as hazardous to the eye as blue light with a wavelength of 440, where the blue hazard peaks according to the International Commission on Non-Ionizing Radiation Protection.
1a. The Irish Medical News. July 2007.
1b. Sunlight Exposure, Antioxidants, and Age-Related Macular Degeneration. Arch Ophthalmol. 2008; 126:1396-1403.
2a. Sunlight and the 10-Year Incidence of Age-Related Maculopathy: The Beaver Dam Eye Study, Correction.
Arch Ophthalmol. 2005 Mar;123(3):362} Tomany SC, Cruickshanks KJ, Klein R, Klein BE, Knudtson MD
2b. Sunlight and the 10-Year Incidence of Age-Related Maculopathy: The Beaver Dam Eye Study.
Arch Ophthalmol. 2004 May; 122(5): 750-7} Tomany SC, Cruickshanks KJ, Klein R, Klein BE, Knudtson MD
3a. Opening New Fronts in the Battle Against AMD. Review of Ophthalmology May 2007, 14(5). TA. Ciulla
3b. Age-related Macular Degeneration in Very Old Individuals with Family History
Asbjorg et al. American Journal of Ophthalmology May 2007. 143(5):889-890
4.Light-Induced Melatonin Suppression in Humans With Polychromatic and Monochromatic Light.
Chronobiology International, Nov 2007; 24(6): 1125–1137 Revell VL and Skene DJ.
5a. Differential effects of light wavelength in phase advancing the melatonin rhythm. J Pineal Res. 2004 Mar;36(2):140-4.Wright HR et al
5b. Effect of light wavelength on suppression and phase delay of the melatonin rhythm. Chronobiol Int. 2001 Sep;18(5):801-8.Wright HR, Lack LC.
6. Immunohistochemical evidence of a melanopsin cone in human retina.Invest Ophthalmol Vis Sci. 2006 Apr;47(4):1636-41.
Dkhissi-Benyahya O, Rieux C, Hut RA, Cooper HM.
7. Circadian Phase Delay Induced by Phototherapeutic Devices. Aviation, Space, and Environmental Medicine. July 2007; 78(7):645-52
Paul MA, MillerJC,. Gray G, Buick F, Blazeski S, Arendt J.
8. Clinical Management of Delayed Sleep Phase Disorder. Behavioral Sleep Medicine 2007, Vol. 5, No. 1, Pages 57-76. Leon C. Lack
9. Psychiatric research. Is internal timing key to mental health? Science. 2007 Sep 14;317(5844):1488-90. Bhattacharjee Y.
10. Do blue light filters confer protection against age-related macular degeneration? Prog Retin Eye Res. 2004 Sep;23(5):523-31.
Margrain TH, Boulton M, Marshall J, Sliney DH.
11. Light-Induced Damage to the Retina: Role of Rhodopsin Chromophore Revisited. Photochem Photobiol. 2005 Nov-Dec;81(6):1305-30. Review.
Rozanowska M. Sarna T
ENDNOTE
Some manufacturers of light therapy units that emit high proportions of blue light wavelengths claim that an authoritative
source has determined their products are safe. An examination of these claims show that the rationale for the safety of
these products is based on the intensity of blue light needed to induce a retinal lesion in an animal retina, 50% of the time.
This manner of analysis for acute retinal damage, whether flawed or not, is not logically applicable to a determination of
the hazard to vision from AMD, the pathogenesis of which appears to be related to cumulative sub-threshold retinal stress
over a lifetime.
The same authoritative source cited by these light therapy device manufacturers to support the claim their devices are safe is an author of a paper that states "we believe that there is support for the long-held belief that light has a role in the pathogenesis of ARMD. That is, the recent findings that antioxidant therapy has a protective effect confirms that oxidative stress has a role in the pathogenesis of AMD and laboratory studies have demonstrated that light, and in particular blue light, is a source of oxidative stress via its interaction with retinal chromophores. Therefore a reduction in blue light exposure might reasonably be expected to reduce progression in ARMD"10 This is consistent with other investigators who have explained that "avoiding exposures to bright short-wavelength [blue] light is the simplest preventative measure against light damage".11
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