There is good reason to be concerned about retinal damage from the use of bright and blue light therapy lamps. Retinal experts have determined that the development of Age-related Macular Degeneration (AMD) is directly related to retinal stress resulting from exposure of the eye to visible blue light. As Dr. Beatty, director of the Macular 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 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
A study by Harvard University's Department of Sleep Medicine confirmed that increasing
the level of blue light wavelengths does not improve the effectiveness of a light therapy lamp to
influence human physiological functioning.3 Experts in the spectral sensitivity of human
circadian physiology have recommended that all light therapy devices screen out potentially hazardous
blue light wavelengths, and that light therapy devices emitting blue wavelengths of light should not be
used. An 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".5a
MORE about blue light, light therapy, and eye damage
While previous studies suggested that blue light wavelengths would be highly effective for light therapy, it has now been determined that hazardous blue light wavelengths do not contribute to the effectiveness of light therapy. Studies now show that monochromatic blue (479 nm) light is no more effective for light therapy than regular fluorescent white (polychromatic) light2. These studies were unable to demonstrate there is any benefit or increase in efficiency from increasing the proportion of blue light wavelengths, i.e. visible light wavelengths shorter than 480 nm, from a light therapy lamp. It has been known for many years that the inclusion of blue light is not necessary for effective light therapy.
Subsequent studies have also expressed strong concerns regarding the potential for retinal damage from the use of light therapy for the treatment of sleep and mood disorders or for the regulation of circadian physiology. 5b,5c
In contrast, Sunnex Biotechnologies Lo-LIGHT lamps using low intensity GreenLIGHT technology emit no blue light but have been shown to be more effective at inducing physiological responses than a blue-enhanced (465 nm) light therapy device that emits 10 times as much light;4 and without any risk of damage to the eye.
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 causes the formation of indigestible debris which accumulates in the outer retina. The cummulative effect of chronic, sub-lethal oxidative retinal stress and the resulting accumulation of oxidative debris in the outer retina contributes to chronic inflamation of RPE cells, which has been directly linked to the development of AMD. We believe it can now be established that cummulative exposure to blue light over a lifetime contributes to the development of Age-related Macular Degeneration (AMD)6. Therefore, the long term use of blue or blue-enhanced light therapy lamps substantially the increases the risk of vision loss at a younger age, and has no offsetting benefit.
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, because the accumulating oxidative debris is phototoxic to blue light, and because defense mechanisms that protect the retina from oxidative damage progressively deteriorate after age 40.
The largest American epidemiological study indicates that a moderate daily increase in exposure to blue light of young adults, in their teens and thirties, advances the onset of macular degeneration later in life by 10 years. This would double the likelihood of becoming blind in one? lifetime7a, 7b. Several specialists involved in macular degeneration research now recommend 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) 8a. 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 858b. As retinal oxidative stress is a causative factor for the development of AMD, increasing levels of exposure to blue light wavelengths from light therapy lamps can only increase the likelihood of developing AMD.
The consequences of macular degeneration for people who find light therapy beneficial 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
The known pathogenesis of Age-Related Macular Degeneration (AMD) involves chronic elevated levels of oxidative stress, chronic inflamation, and the accumulation of oxidative debris in the outer retina. The outer retina includes the photoreceptor cells, an adjacent monolayer of retinal pigment epithelium (RPE) cells, and Bruch's membrane - a complex that acts as a retinal-blood barrier through which the nutrients and oxygen needed to sustain photoreceptor cells and RPE cells must pass. AMD occurs within a small area of the retina called the macula and is associated with malfunctioning of RPE cells adjacent to the macula and with the accumulation of oxidative debris within these cells (lipofuscin). When RPE cells, which are responsible for providing oxygen and nutients to the photoreceptor cells as well as for removing the metabolic waste and oxidative debris generated from photoreceptor cells, are not functioning properly, adjacent photoreceptor cells cannot function or survive.
Blue light wavelengths penetrating to the outer retinal region is absorbed by elements within RPE cells that induces the formation of radical oxygen species (ROS) and can result in oxidative stress. Oxidative stress occurs within a cell when the level of radical oxygen species (ROS) exceeds the capacity of the protective anti-oxidative mechanisms within the cell to negate the harmful effects of ROS, and an inflamatory response is induced. Chronic, low-grade inflamation of RPE cells has been directly linked to the development of AMD.
Malfunctioning mitochondria, the power plant organelle within the cell, generate high levels of ROS. Blue light absorption by RPE mitochondria can cause their malfunctionings, as can retinal stress within the RPE cell. Lipofuscin accumulates in RPE cells over a lifetime and generates radical oxygen species when it absorbs blue visible light. Damage resulting from blue light absorption by the DNA of RPE cells can also cause them to malfunction, though it is generally accepted that the damage to mitochondrial DNA induced by blue light absorption and the resulting ROS generation by these damaged organelles is generally a more significant contributor to heightened oxidative stress levels within RPE cells.
Retinal melanin is one of the protective elements regarding blue light damage within the outer retina. However,absorption of blue light by retinal melanin causes its degradation and retinal melanin is not regenerated. The reduction in levels of functional retinal melanin by blue light absorption over a lifetime attenuates the capacity of this protective mechanism from blue light exposure.
Within the macular region of the retina is, the fovea, the retinal structure primarily responsible for vison. Light entering the eye is focused towards the macula, so this is the retinal region where the highest level of oxidative damage takes place. Damage to this region of the retina also has the greatest effect on vision. When RPE cells malfunction, an accumulation of oxidative debris on the basal side of the RPE occurs, where this material can become cross-linked to the Bruch's membrane complex, and form drusen. The formation of drusen is considered to be the initiation of the process of AMD. Much of the indigestible material generated from oxidative damage to lipids and lipoproteins within photoreceptors and adjacent RPE cells that accumulates within RPE cells is associated generates ROS upon exposure to blue light wavelengths.
An accumulation of material between the RPE cells, which nourish and remove waste materials from photoreceptor cells, and the Bruch's membrane complex limits the access of RPE cells to the blood supply for absorbing nutrients and disposing of metabolic waste. Impairment of all of these processes are associated with the slow deterioration of vision called "dry macular degeneration".
The generation of the large amounts of radical oxygen species and the resulting oxidative stress can induce damage to the Bruch's membrane complex 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 lamps are a safe, low intensity alternative to bright light therapy. Lo-LIGHT lamps are the only light therapy devices that filter out dangerous higher energy blue light rays, with wavelengths shorter than 485 nm. 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 used in the Lo-LIGHT (peak near 500 nm) 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.
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
Current research continues to validate and confirm the propositions outlined on these pages regarding the cumulative
exposure of light on the retina and vision over a lifetime, and the role of blue light as a major contributing factor
in the development of age-related blindness from macular degeneration.
View a few of these more recent references here.
A recent review, Effects of Blue Light on the Circadian System and Eye Physiology. Molecular Vison:(2016) summarizes current understanding of the role of blue light in the development of AMD.
"Experimental evidence indicates that wavelengths in the blue part of the spectrum (400-490 nm) can induce damage in the retina, and although the initial damage following exposure to blue light may be confined to the RPE, a damaged RPE eventually leads to photoreceptor death. Although most studies on the effects of blue light have focused on the mechanisms responsible for the damage to the photoreceptors following an acute exposure to high intensity light, some studies have reported that sub-threshold exposure to blue light can also induce damage in photoreceptors. In addition, several authors have proposed that the amount of blue light received during an individual's entire lifespan can be an important factor in the development of age-related macular degeneration (AMD)."
The paper concludes:
"Because light has a cumulative effect and many different characteristics (e.g., wavelength, intensity, duration of the exposure, time of day), it is important to consider the spectral output of the light source to minimize the danger that may be associated with blue light exposure....Although we are convinced that exposure to blue light from LEDs in the range 470-480 nm for a short to medium period (days to a few weeks) should not significantly increase the risk of development of ocular pathologies, this conclusion cannot be generalized to a long-term exposure (months to years)."
The concern these authors express relates to blue light wavelengths from indirect ambient lighting emitted by LEDs providing white light. As the authors explain
"The white-light LED (i.e., the most common type of LED) is essentially a bichromatic source that couples the emission from a blue LED (peak of emission around 450-470 nm with a full width at half max of 30-40 nm) with a yellow phosphor (peak of emission around 580 nm with a full width at half max of 160 nm) that appears white to the eye when viewed directly. ...
The specific pump wavelength of the phosphor in the range 450-470 nm depends critically on the absorption properties of the phosphor. ... white-light LEDs degrade over time primarily through bleaching of phosphors so that they no longer efficiently absorb blue light. This shifts the color temperature of the device over time, with a corresponding change in the color-rendering index but, more importantly, an increasing blue emission from the device with time."
Several papers in the February 2016 issue of the journal Eye discussed the hazardous effect of blue light exposure on the retina. These papers related to studies on the effect of blue light wavelengths from indoor and outdoor lighting on people with artificial lenses implanted due to cataracts, or concerns about blue light exposure from the increased use of LEDs in general indoor lighting. These concerns relate to exposure to the relatively low intensities of indirect indoor ambient lighting. These intensities are much, much lower than the high intensities of light emitted by white or blue light therapy lamps, which provide direct light exposure of the eye from the therapy lamp.
With regard to blue light exposure of people undergoing cataract surgery, one paper, Ultraviolet or Blue-Filtering Intraocular Lenses: What is the Evidence?, stated:
"With the arrival of blue-filtering intraocular lenses (BFIOLs) in 1990's, a further debate was ignited as to their safety and potential disadvantages. ... The potential disadvantages raised in the literature over the last 25 years since their introduction, regarding compromise of visual function and disruption of the circadian system, have been largely dispelled. The clear benefits of protecting the retina from short-wavelength light make [blue-filtering intraocular lenses] BFIOLs a sensible choice"
With respect to ambient lighting, another paper Light in Man's Environment by a different research group, stated:
"Many studies have demonstrated the spectral dependence of eye health, with the retinal hazard zone associated with wavelengths in the blue, peaking at 441 nm - many of today's low-energy sources peak in this region. Given the increased longevity and artificial light sources emitting at biologically unfriendly wavelengths, attention has to be directed towards light in man's environment as a risk factor in age-related ocular diseases."
Some studies that discuss the state of retinal damage from blue light exposure examine the protective proprties of the carotinoids lutein, zeaxanthin, and meso-zeaxanthin that make up the layer of blue light filtering macular pigment that forms in the inner retina, and through which light must pass to reach the photoreceptors adn RPE cels in the outer retina. These carotinoids are not produced by the body and are obtained though diet or supplements. Several studies have shown that the lower the density of this pigment, that is, the more blue light that is able to pass throgh this layer to reach the outer retina the greater the likelihood of developing AMD.
A few comments from one of these studies, The Photobiology of Lutein and Zeaxanthin in the Eye. Journal of Ophthalmology, Dec 2015, are:
"In adults, the lens absorbs UV-B and all the UV-A (295-400 nm); therefore only visible light ([wavelengths] >400 nm) reaches the retina".
"short-wavelength blue visible light damages the retinas of those over 50 years of age through a photooxidation reaction with an accumulated chromophore, lipofuscin. Lipofuscin...is mainly derived from the chemically modified residues of incompletely digested photoreceptor outer segments. Photoreceptor cells (rods and cones) shed their outer segments (disc shedding) daily to be finally phagocytosed (digested) by RPE cells." ... "In response to [Upon the absorption of] short blue visible light, lipofuscin efficiently produces singlet oxygen and lipid peroxy radicals; there is also some production of superoxide and hydroxyl radicals."
"short-wavelength blue visible light damages the retinas of those over 50 years of age through a photooxidation reaction with an accumulated chromophore, lipofuscin ... a blue light singlet oxygen photosensitizer, leading to damage to RPE cells. Because the rods and cones survival is dependent on healthy RPE, these primary vision cells will eventually die, resulting in a loss of (central) vision (macular degeneration) and other retinopathies"
"Ocular exposure to sunlight, UV, and short blue light-emitting lamps directed at the human eye can lead to the induction of cataracts and retinal degeneration. This process is particularly hazardous after the age of 40 because there is a decrease in naturally protective antioxidant systems and an increase in UV and visible light-absorbing endogenous phototoxic chromophores that efficiently produce singlet oxygen and other reactive oxygen species."
Current studies, including History of Sunlight Exposure is a Risk Factor for Age-Related Macular Degeneration. Retina, 2016 Apr;36(4):787-90. continue to find that increased exposure to sunlight over a lifetime increases the likelihood of developing AMD. Since only the visible light wavelengths from sunlight reach the retina, see previous reference, these studies support the premise that cumulative exposure to visible blue light wavelengths contributes to the development of AMD.
PURPOSE: To evaluate effects of current and past sunlight exposure and iris color on early and late age-related macular degeneration (AMD)
CONCLUSION: Sunlight exposure during working life is an important risk factor for AMD, ... Therefore, preventive measures, for example, wearing sunglasses to minimize sunlight exposure, should start early to prevent development of AMD later in life.
1a. The Irish Medical News. July 2007.
1b. Sunlight Exposure, Antioxidants, and Age-Related Macular Degeneration. Arch Ophthalmol. 2008; 126:1396-1403.
2. Light-Induced Melatonin Suppression in Humans With Polychromatic and Monochromatic Light. Chronobiology International, Nov 2007; 24(6): 1125?137 Revell VL and Skene DJ.
3. Spectral Responses of the Human Circadian System Depend on the Irradiance and Duration of Exposure to Light. Science Translational Medicine 2010 May 12; 2, 31ra33. J.J. Gooley, S. M. W. Rajaratnam, G. C. Brainard, R. E. Kronauer, C. A. Czeisler, S. W. Lockley
Read more on confirmation that increasing the proportion of blue light provides no benefit for light therapy.
4. 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.
5a. Clinical Management of Delayed Sleep Phase Disorder. Behavioral Sleep Medicine 2007, Vol. 5, No. 1, Pages 57-76. Leon C. Lack
5b. Impact of blue vs red light on retinal response of patients with seasonal affective disorder and healthy controls. Progress in Neuropsychopharmacological and Biological Psychiatry 2011; 35(1):227-31. Gagne et al.
5c. Retinal Photodamage by Endogenous and Xenobiotic Agents. Photochemistry and Photobiology. (In Press May 14, 2012). Wielgus AR,and Roberts JE.
6. Read more on demonstrating cummulative blue light exposure contributes substantially to the development of AMD
7a. 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
7b. 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
8a. Opening New Fronts in the Battle Against AMD. Review of Ophthalmology May 2007, 14(5). TA. Ciulla
8b. Age-related Macular Degeneration in Very Old Individuals with Family History Asbjorg et al. American Journal of Ophthalmology May 2007. 143(5):889-890
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
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