Why working with the right kind of blue light is important.

Posted in Eye Health

The Lowdown on Blue Light:
Good vs. Bad, and Its Connection to AMD

Release Date: February 2014

Expiration Date: January 31, 2015

Goal Statement:

This educational activity will explore the role of light, including how it can damage the eye and its link to age-related macular degeneration (AMD). The expert faculty will also cover other relevant topics, such as ways to prevent or reduce the risk of AMD as it strives to increase awareness of this general topic.

Faculty/Editorial Board:

Mark Dunbar, OD, and Ronald Melton, OD

Credit Statement:

This course is COPE approved for 2 hours of CE credit. COPE ID is 40549-PS. Please check your state licensing board to see if this approval counts toward your CE requirement for relicensure.

Joint-Sponsorship Statement:

This continuing education course is jointly sponsored by the University of Alabama School of Optometry.

Disclosure Statement:

Dr. Dunbar has disclosed the following relationships: Allergan Optometric Advisory Panel, Carl Zeiss Meditec Optometric Advisory Board, ArticDx Optometry Advisory Board, Sucampo Pharmaceutical Optometry Advisory Board, Vision Expo Continuing Education Advisory Board East and West: 2005–Present. Dr. Melton disclosed having direct fi nancial and/or proprietary interests in Alcon Laboratories, Bausch + Lomb, ICARE-USA, Jobson Publishing and Nicox.

Ultraviolet and Blue Light

By Ronald Melton, OD

We all know that light can be both harmful and beneficial for our vision as well as our overall health. Here, I’ll provide a background on ultraviolet (UV) light and blue light.

Light: The Good and the Bad

Sunlight contains UV and blue light. UV light is part of the non-visible light spectrum and we are exposed to it every day when we’re out in the sun. It can cause damage to our eyes, particularly the cornea and the lens. The cumulative effect of UV exposure can con tribute to cataracts as well as the potential for pinguecula and pterygium.

Blue light, which is part of the visible light spectrum, reaches deeper into the eye and its cumulative effect can cause damage to the retina. Furthermore, in certain wavelengths, blue light is implicated in the develop ment of age-related macular degeneration (AMD).1–3 The amount of exposure to blue light varies, depending on the time of day, the location and the season. The average proportion of blue light that’s found in sunlight during the day is between 25% to 30%. Even on a cloudy day, up to 80% of the sun’s UV rays can pass through the clouds.

Light is also essential for various functions. It helps us to see better, it helps us with our visual acuity and con trast acuity, it helps us perceive colors, and it helps with various non-visual functions of the body. For example, light helps to regulate our sleep/wake cycle, which in turn helps to maintain and regulate memory, mood and hormonal balance.4,5

The Nitty Gritty on UV Light

Visible light covers the range from 380 nm to 780 nm and UV light falls just beyond the shorter end of the visible spectrum, so it’s invisible to the human eye. It is divided into three zones: UVA, UVB and UVC.

UVA is between 315 nm to 380 nm, and is the least damaging of the UV light. Tanning is the most popular effective UV exposure.

UVB is between 280 nm and 315 nm, and has more energy. It is more energetic and fairly damaging if we’re exposed to it on a day-to-day basis. Acutely, it can cause sunburn and destruction of vitamin A. In more chronic forms, it can lead to skin thickening, wrinkling and possibly damage to DNA, which can lead to mela nomas and other skin disease. So exposure to UVB is cumulative to both the body and the eyes.

UVC is in the range of 100 nm to 280 nm, and is the most biologically active of the UV light. Brief exposure can create permanent damage to human tissue. Fortu nately, UVC is absorbed mainly by the ozone layer in the upper atmosphere.

To review, UV light can have an additive effect to damage the eye and can be a major risk factor for the formation of cataract cell life. It’s important to remember and to keep emphasizing the fact that not all blue light is bad. Furthermore, blue light also helps to regulate our pupil size around the wavelength of 480 nm.

The Danger Zone

Many environmental factors such as location, season, time and lifestyle can affect UV risk. Contrary to what many people believe, the time when maximum amounts of UV reaches the eye is not consistent throughout the year. Specifically, in the summer between 10 a.m. and 2 p.m. is the highest level of UV exposure, but in the winter, this maximum exposure is going to be between 8 a.m. and 10 a.m. and between 2 p.m. and 4 p.m.

Just as UV light is dangerous to our skin, it’s also dangerous to our eyes. So it’s important that we protect them from UV damage. UV light affects the front of the eye (cataract formation), while blue light causes damage to the back of the eye (risk of AMD).

Nowadays, there’s an increase in the use of digital devices and modern lighting—such as LED lights and compact fluorescent lamps (CFLs)—most of which emit a high level of blue light. CFLs contain about 25% of harmful blue light and LEDs contain about 35% of harmful blue light. Interestingly, the cooler the white LED, the higher the blue proportion. And by 2020, 90% of all of our light sources are estimated to be LED lighting. So, our exposure to blue light is everywhere and only increasing.

As baby boomers age, there’s an increasing incidence of cataract and macular degeneration cases in the United States. In 2012, there were approximately 24 million cases of cataracts in people aged 40+ the United States,6 which is a 19% increase from 2000 numbers. For macular degeneration, two million people aged 50+ had late AMD in 2012,6 which is a 25% increase from 2000. By the year 2050, the cataract population is going to hit 50 million, whereas AMD tops off at around 5 million, it’s estimated.7 So the bottom line is that cataract and AMD cases are expected to double over the next 30 years, in part because of the aging of the population.

Ninety percent of the vision loss associated with AMD is secondary to the wet form.8 When we look at the AMD population, 10% of those with the disease have the wet form, and 90% have the dry form.8 However, 80% to 90% of AMD patients whose acuity is <20/200 have the wet form, while 10% to 20% have the dry form. The number of legally blind patients from macular degeneration in 2003 was 1.2 million with 200,000 new cases annually at that date.9 And by the year 2030, the number of legally blind is projected to be 6.3 million with 500,000 cases annually.9

Research on Blue-Violet Light

Essilor had a partnership with Paris Vision Institute in 2008 and their directive was to find the bands of visible light that were the most harmful to the eyes.10 They split the visible light into multiple bands of 10 nm and each band was then focused on porcine retinal pigment epithelial (RPE) cells for several hours. So using this method, the specific band of blue light most harmful to the retina and to the RPE cells was identifi ed to be at 415 nm to 455 nm.

The blue-violet light that was discovered as part of this study is a 40 nm band of visible light that causes the maximum retinal cell death. Over time, our eyes are exposed to various sources that emit this blue-violet light (e.g., the sun, LED lighting, CFLs). Combine that with the use of tablets, TVs, computer screens and smart phones, and there’s no doubt our exposure to blue-violet light is on the increase. This cumulative and constant exposure to the blue-violet light is going to accumulate over time and has the potential to cause damage to the retinal cells, which is going to slowly lead to retinal cell death and can in turn lead to AMD.

The level of light emitted by newer energy-saving lighting techniques (e.g., LED, CFLs) is very high. For example, CFLs, white LED light and even sunlight emit high levels of blue-violet light compared to the rest of the blue light spectrum. This underscores the need for us to protect our eyes from the harmful bands of blue-violet light.

The Good Side of Blue Light

Not all blue light is bad. The labeled blue-turquoise light range, which is from 465 nm to 495 nm, is essential to our vision, the function of our pupillary reflex, and in general to human health. It also helps to regulate our Circadian sleep/wake cycle.11 So blue light in general can have healthy affects on vision as well as the body, and it is this blue-turquoise light that tends to have these beneficial effects. Inadequate light exposure means inadequate blue-turquoise light, which can throw off our Circadian biological clock and our sleep/wake cycle. So this blue-turquoise light really plays a vital role in the general health of the individual.

Protection from UV and Blue-Violet Light

How can we block the harmful blue rays of light but allow the helpful blue rays of light to penetrate through and get into the eye? Essilor and the Paris Vision Institute established a goal of finding a selective light filter or a lens to block out UV as well as the harmful blue-violet light and yet allow the blue-turquoise light and the longer wavelengths of light to continue to penetrate through it. They did this with Light Scan, a patented, selective, noglare technology with three key features: 1) it selectively filters out harmful blue-violet and UV light, 2) it allows the beneficial visible light, including the blue-turquoise light, to pass through and 3) it maintains an excellent transparency of the lens, so there’s no color distortion and you get excellent clarity with the lens.

They ended up providing a lens with front-side as well as back-side protection. The front side of the lens defl ects UV light as well as about 20% of the blue-violet light to then defl ect away the harmful rays. And the back side protects the patient from the refl ective glare that comes off the back surface of the lens, mainly from UV light. Traditional blue blockers give you pretty sunsets, but that’s not what you want. You don’t want color distortion; you want your colors to be natural. The traditional blue blockers do not discriminate in the blue light spectrum. They just block all the blue light. This new lens technology is based on laboratory studies over a four-year period of time by a high-class group of scientists as well as clinicians who came up with some very important data that allowed them to zoom in on the light that needed to be blocked and the light that needed to get through. So this new lens design really is very specific for more selective light.

Who’s going to need the most protection? Those who have high exposure to white LED or fluorescent light bulbs in offi ces and homes, frequent users of LED computer monitors, tablets, or smart phones, and those at risk for AMD, particularly those at high risk, (those with family history, smokers, etc.). Many companies are working on technology to look at harmful blue light and ways to block that and still allow healthy blue light to remain.

Reason to Be Inquisitive

We know that patients at risk for AMD need to protect their eyes from harmful blue-violet light, so we need to get up to speed educationally on what’s going on there so we can properly educate our patients. Not only do we look at our AMD patients and determine whether to recommend nutritional supplements to them, but we also have to work at giving these patients protection against both the UV invisible light as well as the blueviolet light spectrum. Optical companies that currently offer blue-blocking technology include Nikon (SeeCoat Blue), Essilor (Crizal Prevencia), PFO Global (iBlu coat), HOYA (Recharge), VSP (UNITY BluTech) and Spy Optic Inc. (Happy Lens). We need to be asking patients if they currently protect their eyes on a daily basis, if there is a family history of macular degeneration, and how much time they spend in front a digital device or computer. We also need to find out if our patients are currently protecting their eyes against UV damage, so there’s a lot of homework out there for us. These are all questions that are going to come to the forefront as this new technology continues to evolve.

Dr. Melton practices at Charlotte Eye Ear Nose & Throat Associates, P.A. and is an adjunct faculty member at Indiana University School of Optometry and Salus University College of Optometry. He has authored and co-authored more than 100 articles on eye diseases and eye care for peer-reviewed journals and magazines and has served as an investigator or co-investigator on more than 50 clinical research activities.


Beatty S, Koh HH, Henson D, Boulton M. The role of oxidative stress in the pathogenesis of age-related macular degeneration. Surv Ophthalmol. 2000;45(2)115–134.

Algvere PV, Marshall J, Seregard S. Age-related maculopathy and the impact of blue light hazard. Acta Ophthalmol Scand. 2006;84(1)4–15.

Dillon J, Zheng L, Merriam JC, Gaillard ER. Transmission of light to the aging human retina: possible implications for age related macular degeneration. Exp Eye Res. 2004;79(6)753–759.

Wooten V. Sunlight and sleep. Discovery Fit and Health. Available at: http:// health.howstuffworks.com/mental-health/sleep/basics/how-to-fall-asleep2.htm. Accessed: January 2014.

How your internal “body clock” affects sleep. Helpguide.org. Available at: http://www.helpguide.org/harvard/sleep_cycles_body_clock.htm. Accessed: January 2014.

Vision Problems in the U.S.: Prevalence of Adult Vision Impairment and Age-Related Eye Disease in America, Fifth Edition. Prevent Blindness America, 2012. Available at: www.preventblindness.org/visionproblems. Accessed: December 2013.

National Eye Institute. Available at: http://www.nei.nih.gov/eyedata/cataract.asp. Accessed: December 26, 2013.

AMD Alliance International. Available at: http://www.amdalliance.org/information_overview_basic_facts.html. Accessed: December 26, 2013.

Singerman LJ, Miller DG. Pharmacological Treatments for AMD. Review of Ophthalmology. Oct. 2003.

Smick K et al. Blue light hazard: New knowledge, new approaches to maintaining ocular health. Report of a roundtable sponsored by Essilor of America. March 16, 2013, NYC, NY.

Researchers use blue light to treat sleep disturbances in the elderly. Lighting Research Center. 2005; April 14. Available at: http://www.lrc.rpi.edu/resources/ news/enews/Apr05/general245.html. Accessed: January 2014.

What We Now Know About AMD

Mark T. Dunbar, OD

We have an aging population that will result in a growing demand for eye care. With that, we can expect to see more patients with agerelated macular degeneration (AMD). And even though 90% of our patients have dry AMD, a large percentage of those patients could develop the wet form of the disease. I look at this as an incredible opportunity for optometry to monitor these patients, take

care of them, and really be their primary eye-care provider. This comes with the responsibility of knowing when to refer, in addition to making the appropriate recommendations for our patients. All of this is a critical role for optometry, and thanks to the latest technology, there’s so much we can do to help change the outcome of AMD.

A Recipe for AMD

We now understand that genetics play a critical role in AMD, and that environment and lifestyle factors also play a role. We know that those who smoke have up to a 16 to 20 times higher risk of developing AMD and that those with higher body mass indexes, poor diets and greater ultraviolet (UV) light exposure are at an increased risk.1So it’s really that interaction between genetics and those external factors that predispose a person to go on to develop macular degeneration. But there’s a lot that we can do to make sure that the genetics don’t take over, and we’ll talk about that a bit later. We’ve evolved to the point that we can do genetic testing and identify patients who have the highest risk of going on to not only develop AMD with a high degree of certainty, but those who are going to progress to the wet form of the disease.

I think it’s an exciting time for our patients now that we have sight-saving treatments, as well as a great opportunity for optometry, because with advances in technology, we can closely monitor and take better care of these patients. As our understanding of AMD has evolved, we recognize that it’s almost this “two-hit theory.” You may have “bad” genetics or a series of genes that predispose you to AMD, but that doesn’t necessarily mean you’ll go on to develop macular degeneration. There are other factors that I view as being the second hit. Maybe it’s smoking, poor diet as well as other lifestyle factors that trigger various genes to interact and ultimately predispose you to develop macular degeneration. Perhaps it’s even as simple as living in an area where there’s a lot of sun exposure or working outside a lot and not taking the necessary precautions to protect yourself from the sun.

Photoreceptor cells are triggered by light to set off a series of electrical and chemical reactions, and this process begins at birth. In the retina, the retinal pigment epithelium (RPE) aids the photoreceptors by providing enzymatic re-isomerization of the daily turnovers of photoreceptor disc membranes. A marker for dysfunction in the RPE is seen clinically as drusen, altered RPE pigmentation and accumulation of lipofuscin. Lipofuscin in particular is a highly autofluorescent retinoid that accumulates when the aging RPE is unable to completely digest the outer segment disc membranes. Simply put, it is a marker for disease activity. Lipofuscin is most easily seen with fundus autofluorescence (FAF) imaging.

Drusen and AMD

Drusen are the earliest clinically detectable feature of dry AMD. They lie between the basement membrane of the RPE and Bruch’s membrane. Hard drusen tend to be smaller and can also have a calcified appearance, whereas soft drusen are larger and more ill-defined. Sometimes they coalesce and resemble small serous detachments. These are the ones that worry me most. When I look at these patients clinically, I always try to ask myself if I see any fluid, subretinal hemorrhages, exudates or elevation of the retina, as these are red flags that the patient may have progressed from dry AMD to the wet form of the disease.

Sometimes in these patients, it is difficult to determine whether they have converted to wet AMD based solely on the clinical exam. This illustrates, in part, the importance of looking at the macula three-dimensionally, as some of the retinal changes can be very subtle, especially with a patient who still has excellent visual acuity. Viewing the macula stereoscopically can help detect some of these subtle changes that are indicative of a patient who has progressed. Fortunately, in the era of OCT imaging, detecting these early changes is much easier. As a clinician, you don’t have to rely as much on your clinical skills and ability, which, in some patients, isn’t enough. There are times when OCT imaging is an absolute necessity to pick up some of the early changes to which we have already alluded. The OCT allows you to make earlier diagnoses, which in turn leads to better and more appropriate referrals.

Geographic atrophy (GA) is a less common form of dry AMD. Once again, we’ve been helpless in monitoring these patients because we haven’t had a treatment. However, now with a better understanding of genetics and other factors that affect this disease, a number of new treatments are in the pipeline that will hopefully not only stop progression, but also possibly result in a cure for AMD.

Managing AMD

The treatments currently available have revolutionized how we manage and treat AMD. In fact, any more, some argue that macular degeneration isn’t the leading cause of blindness. Thanks to today’s treatments, many of our patients are actually enjoying better acuity and consequently, better quality of life because they are able to read, drive a car, and other important tasks.

The downside is that sometimes a patient’s condition requires a monthly injection. However, if you’ve seen a patient who has received injections of any of these drugs, you know that they typically tolerate them well and that the outcomes are very good. Keep in mind that we are looking at the secondary effects of a lifetime of exposure to light, a lifetime of faulty genes, a lifetime of diet and other factors that can ultimately be detrimental.

Conventional treatments aside, what about other approaches to managing AMD? Does making lifestyle change make a difference? Can it prevent the development of macular degeneration? We know that it can in other diseases such as diabetes and hypertension, so it’s a fair question to ask in the setting of AMD. Certainly we can talk about quitting smoking with our patients, but what about making dietary and nutritional recommendations?

Nutritional Supplementation

The National Eye Institute studied the effects of nutritional supplements in the Age-Related Eye Disease Study (AREDS) in the 1990s.2 AREDS assessed the clinical course, prognosis and risk factors of AMD and cataract and evaluated (in the randomized, clinical trial) the effects of pharmacologic doses of antioxidants and zinc on the progression of AMD and of antioxidants on the development and progression of lens opacities. It was determined that eyes at moderate and high risk of developing advanced AMD lowered their risk by 25% when treated with high dose combination vitamin C, vitamin E, beta-carotene and zinc.3

At the time of the first AREDS study, we didn’t have available to us the carotenoids lutein and zeaxanthin, but we did have beta-carotene, and so that was the one that was studied. Now, however, lutein and zeaxanthin are available—so would substituting these carotenoids for beat-carotene make a difference? One would think so, considering that the macula contains larger amounts of both of those carotenoids as well as meso-zeaxanthin. This was one of the initiatives of the AREDS2 study, which evaluated the effects of lutein and zeaxanthin in place of beta-carotene on the progression of AMD.4 It also looked at the effects of omega-3 fatty acids, which was also believed in other studies to play a role in the progression of AMD. The point of the study was to answer in a randomized, controlled clinical trial, whether there is a benefit to lutein and zeaxanthin, as well as the omega-3s, alone or in combination with other nutrients, on slowing the progression to macular degeneration.

AREDS2 randomized 4,000 patients aged 50 to 85 who are at high risk of having advanced AMD to one of four groups: placebo (original AREDS supplement); lutein and zeaxanthin only; fatty acids only; and lutein and zeaxanthin plus fatty acids.4 Unlike other studies, AREDS2 looked at patients who had intermediate and advanced macular degeneration, rather than those who didn’t have AMD or who had early macular degeneration.

The placebo group in AREDS2 consisted of patients from the original AREDS trial, with the beta-carotene, zinc, vitamin A, C and so on. Everybody else was randomized to these other forms of nutritional supplements (see figure above). 

AREDS2 sought to find out if adding lutein and zeaxanthin, adding omega-3 or a combination of the two to the original AREDS formulation reduced the risk lower or beyond the original 25%. The data did not demonstrate a signifi cant reduction in the progression, which was surprising.

The secondary analysis revealed a 10% reduction in progression to advanced AMD when compared to no lutein + zeaxanthin (not in addition to the original 25%). There was also an 18% reduction in progression to advanced AMD in subjects who received the AREDS supplement with lutein + zeaxanthin in place of betacarotene compared to the original AREDS supplement. Furthermore, a 26% reduction in progression to advanced AMD was noted in the lowest quintile of dietary lutein and zeaxanthin intake.

The study concluded that lutein and zeaxanthin did not add any more benefit than what beta-carotene did. However, because there is a higher risk of lung cancer in smokers (or previous smokers) who were on beta-carotene, lutein and zeaxanthin would be a safer substitute. Finally, it was also determined that the omega-3s didn’t have any beneficial effect.

Preventing and Protecting Against AMD

When we look in particular at treatments for the dry form of AMD, nutritional therapy is really the only treatment that has been shown to reduce the risk. Certainly, lifestyle changes have a benefit, so I think it’s our role as primary and secondary care eye-care providers to recognize the potential of environmental and lifestyle changes, to talk about nutrition and diet and quitting smoking, but more particular perhaps, recommending specific lens types that will block the harmful effects of UV radiation and high-energy visible light before these changes ever develop.

Dr. Dunbar serves as the director of Optometric Services and the optometric residency supervisor at the University of Miami’s Bascom Palmer Eye Institute. He has authored numerous papers and is the writer for Review of Optometry’s monthly column “Retina Quiz.”


Coleman HR. Modifi able risk factors of age-related macular degeneration. Pages 15-22. In: A.C. Ho and C.D. Regillo (eds.), Age-related Macular Degeneration Diagnosis and Treatment, 15 DOI 10.1007/978-1-4614-0125-4_2, © Springer Science+Business Media, LLC 2011. Available at: http://www.springer. com/978-1-4614-0124-7. Accessed: January 2014.

Age-Related Eye Disease Study Research Group. The Age-Related Eye Dis ease Study Group: design implications. Control Clin Trials. 1999:20(6):573-600.

A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss. AREDS Report No. 8. Arch Ophthalmol. 2001;119:1417-1436.

Age-Related Eye Disease Study 2 Research Group. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. JAMA. 2013; 209(19):2005–15.