Shorts

briefed by Jule Klotter

Computer Vision Syndrome

Reading text on hand-held computer devices or flat-panel monitors for extended periods is more likely to produce blurred vision and other symptoms of eyestrain than reading hard copy. These symptoms, which also include dry eyes, eye irritation, redness, burning, headache, and neck and shoulder pain, are diagnosed as computer vision syndrome (CVS) by the American Optometric Association. “[S]ome 90% of the 70 million U.S. workers using computers for more than 3 hours a day may experience CVS,” say Jamie Klamm, BSN, RN, and Karen Gahan Tarnow, PhD, RN, in their 2015 CNE article. Good ergonomic positioning of the computer screen and exercises can mitigate neck and shoulder pain. Eye strain, however, requires less time staring at the computer – a difficulty for workers and students who need to finish their tasks.

Reading is an intense workout for the eyes and the orbicularis oculi muscle that controls squinting and blinking, as Jim Reedy and Kevin Larson explain in their 2008 article “Blink: The Stress of Reading.” Glare, small text, and light-colored or gray text make the eye muscle work harder, contributing to eye strain. In addition, we blink less when reading. Less blinking means reduced tear film and less protection from irritants. As a result, symptoms of dry eye – redness, irritation, burning – arise. Although the mean blink rate between reading hard-copy text and computer text does not significantly differ, Christina A. Chu and colleagues observed “a significantly higher percentage of incomplete blinks” when subjects were reading from a computer (7.02% for computer vs. 4.33% for hard copy; p = 0.02) in their 2014 study. “Decreased blink rates and incomplete blinks [also] occur with both fast-paced and slow-paced computer games,” Klamm and Tarnow write.

Klamm and Tarnow offer several recommendations for preventing computer vision syndrome. First, eliminate glare and reflection from the computer screen by adjusting room lighting and using an antiglare cover or coating on the screen. The computer screen should be positioned at least 20 to 24 inches away, as eye muscles have to work harder when text is too close. Klamm and Tarnow also recommend blinking often, closing the lids completely, and taking short breaks by looking about 20 feet away for at least 20 seconds every 20 minutes. Over-the-counter eye drops for the redness and irritation caused by dry eyes are another suggestion. I have also found enlarging the text size and using a darker font, such as Comic Sans MS, to be helpful.

Chu CA, Rosenfield M, Portello JK. Blink patterns: reading from a computer screen vs. hard copy [abstract]. Optom Vis Sci. March 2014;91(3):297–302. Available at http://www.ncbi.nlm.nih.gov/pubmed/24413278. Accessed February 11, 2016.

Klamm J, Tarnow KG. Computer vision syndrome: a review of literature. MEDSURG Nursing. March–April 2015;24(2):89–93. Available at EBSCOhost. Accessed January 20, 2016.

Sheedy J, Larson K. Blink: the stress of reading. Eye Magazine. March 2008;67(17). Available at http://www.eyemagazine.com/opinion/article/eye-strain. Accessed February 11, 2016.

DHA

and Photo-Oxidative Damage

Is it possible that too much docosahexaenoic acid (DHA), an omega-3 fatty acid found in fatty fish and fish oil supplements, increases the risk of photooxidative damage to the retina? It seems counterintuitive, since DHA is known to be essential for vision development. The membranes of light-detecting rods in the retina have a high DHA content. Recent laboratory studies, however, indicate that high DHA levels in the retina exacerbate the damaging effects of intense light. In addition to fish oil, the body can obtain DHA from alpha (α)-linolenic acid, an essential fatty acid found in flaxseed oil (richest source), walnut oil, hemp oil, and totally unrefined canola and soybean oils.

A 2014 in vitro study, led by Y. Liu, looked at the effects of DHA on retinal pigment epithelium (RPE) cells. DHA promoted RPE proliferation under dark conditions. In the presence of high-intensity light, however, DHA “inhibited cellular proliferation, destroyed cell membrane integrity, enhanced cellular senescence, increased vascular endothelial growth factor (VEGF) release, and decreased phagocytic function.”

A 2009 in vivo study, led by Masaki Tanito, also found that the combination of intense light and higher DHA levels leads to increased lipid peroxidation and retinal damage. The researchers gave wild-type mice (controls) and mice genetically-modified to convert omega-6 to omega-3 polyunsaturated fatty acids an omega-3-deficient safflower-oil-rich diet. The researchers found severe functional and morphological damage in the retinas of animals with low omega-6/omega-3 ratios (i.e., more omega-3 DHA than omega-6) that had been exposed to intense light. The authors discuss “the ying and yang roles of [omega-3 polyunsaturated fatty acids] and DHA in retinal physiology and pathology,” pointing out the absolute necessity of DHA for visual acuity and its contradictory role in retinal damage.

Only a few human studies have investigated the effect of omega-3 supplementation on retinal degeneration. The Cochrane Collaboration reviewed two controlled clinical trials involving 2343 people with high risk of developing age-related macular degeneration. Cochrane researchers say, “omega-3 supplementation … for periods up to five years did not reduce the risk of progression to advanced [age-related macular degeneration (AMD)] or the development of moderate to severe visual loss.” The relationship between intense light exposure and omega-3 supplementation was not investigated in these studies.

Both omega-3 supplementation and the increase in intense-light exposure are recent phenomena. The human eye is now exposed to intense light from televisions, smartphones, iPods, and other computers. The light from these sources is bright enough to be used like a flashlight. Would we think of staring into a flashlight for hours on end? Of course, in vitro and animal studies do not necessarily indicate risks for humans, but they do indicate a need for more research.

Enig M G. Know Your Fats. Silver Spring, Maryland; Bethesda Press: 2000:246.

Lawrenson JG, Evans JR. Omega 3 fatty acids for preventing or slowing the progression of age-related macular degeneration [abstract]. Cochrane Database Syst Rev. 2015; Issue 4, Art. Nos: CD010015. Available at http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD010015.pub3/abstract. Accessed February 4, 2016.

Liu Y, Zhang D, Wu Y, Ji B. Docosahexaenoic acid aggravates photooxidative damage in retinal pigment epithelial cells via lipid peroxidation [abstract]. J Photochem Photobiol B. November 2014;140:85–93. Available at www.ncbi.nlm.nih.gov/pubmed/25108204. Accessed January 15, 2016.

Tanito M, Brush RS, Elliott MH, Wicker LD, Henry KR, Anderson RE. High levels of retinal membrane docosahexaenoic acid increase susceptibility to stress-induced degeneration. J Lipid Res. 2009;50(5):807–819. Available at www.jlr.org/content/50/5/807.full. Accessed February 2, 2016.

Light Stress

and

Retinal Damage

High-energy visible light, particularly blue light with a wavelength from 450 to 495 nm, is known to damage the retina and contribute to the development of age-related macular degeneration and retinitis pigmentosa. Blue light energy has a much greater ability to remove electrons from molecules and create reactive oxygen species than other visible light. “The increased risk of mitochondrial damage induced by blue light has been demonstrated in many experimental models,” write Professor Peep V. Algvere, MD, and colleagues. “For example, red light of a certain intensity is insufficient to induce retinal damage, whereas blue light of the same intensity will cause retinal injury. Deep blue light has been described as 50-80 times more efficient at causing photoreceptor damage than green light.” Sources of this high-energy light include sunlight, fluorescent light, and light-emitting diode (LED) light emitted by energy-saving light bulbs and electronic devices. Several natural compounds protect against light-induced oxidative retinal damage.

The American Academy of Ophthalmology recommends a nutrient formula that was tested in the Age-Related Eye Disease Studies (AREDS I & II). The first AREDS clinical trial investigated antioxidant and mineral supplementation (vitamin C 500 mg, vitamin E 400 IU, β-carotene 15 mg, zinc 80 mg and copper 2 mg) in 3640 participants at risk for advanced age-related macular degeneration. “At 5 years, the estimated probability of progression to advanced [age-related maculopathy] (neovascular ARM, geographic atrophy) was 28% for those assigned to placebo, and 20% for those assigned to antioxidants plus zinc,” according to Algvere et al.

Because β-carotene has been linked to an increase in lung cancer in people who smoke, the second AREDS investigated lutein (10 mg) and zeaxanthin (2 mg), two carotenoids found in leafy, green vegetables, as alternatives. Lutein and zeaxanthin are found in the eye lens and retina. A lower level of zinc (25 mg) and omega-3 fatty acids DHA and EPA were also tested. Although the omega-3s showed no effect, the carotenoids did lower the risk of advanced age-related maculopathy, particularly in those who don’t usually eat leafy green vegetables. Also, the lower dose of zinc (25 mg) was as effective as the 80 mg dose.

Other nutrients have also shown protection against blue light damage. Bilberry extract and lingonberry extract and their active components protect the retina against blue LED light-induced retinal photoreceptor cell damage, according to a 2014 in vitro study. The Japanese study used a bilberry ethanol extract containing anthocyanins and a lingonberry ethanol extract containing trans-resveratrol and proanthocyanidins. Kenjirou Ogawa and coauthors report that the extracts “exert not only antioxidant effects but also inhibitory effects against stress response proteins induced by blue LED light exposure.”

Fucoxanthin, found in the marine alga Laminaria japonica, is another compound that protects the retina from blue-light damage, according to in vitro and in vivo research. In their 2016 study, Y. Liu and colleagues report that fucoxanthin provided better retinal protection against light damage than lutein in vivo. In vitro, fucoxanthin “exhibited better bioactivities than lutein, zeaxanthin, and blueberry anthocyanins in inhibiting overexpression of vascular endothelial growth factor, resisting senescence, improving phagocytic function, and clearing intracellular reactive oxygen species in retinal pigment epithelium cells.”

Radiofrequency waves (RFW) emitted by wireless technology also cause oxidative stress and produce eye damage, according to a 2013 study. Gholamali Jelodar and colleagues found that exposing adult male rats to RFW from a base transceiver station antenna used to transmit wireless communication (900 MHz RFW) decreased antioxidant enzymes activity (glutathione peroxidase, superoxide dismutase and catalase) and increased malondialdehyde, an oxidative stress marker, compared with control (p < 0.05). The exposed group that received vitamin C (200 mg/kg of body weight/day by gavage) showed better antioxidant activity and lower malondialdehyde levels, compared with untreated RFW-exposed rats (p < 0.05). The abstract does not say that vitamin C totally negated the effect of RFW exposure.

The widespread use of light-emitting diodes (LEDs), computers, and widescreen mobile phones make it even more urgent to find natural ways to protect vision beginning early in life, particularly if a familial history of macular degeneration is present.

Algvere PV, Marshall J, Seregard S. Age-related maculopathy and the impact of blue light hazard. Acta Ophthalmol Scand. January 23, 2006;84:4–15. Available at http://onlinelibrary.wiley.com/enhanced/doi/10.1111/j.1600-0420.2005.00627.x. Accessed January 20, 2016.

Jelodar G, Akbari A, Nazifi S. The prophylactic effect of vitamin C on oxidative stress indexes in rat eyes following exposure to radiofrequency wave generated by a BTS antenna model (abstract). Int J Radiat Biol. 2013;89(2). Available at www.tandfonline.com/doi/full/10.3109/09553002.2012.721051. Accessed January 20, 2016.

Liu Y, Liu M, Zhang X, et al. Protective effect of fucoxanthin isolated from Laminaria japonica against visible light-induced retinal damage both in vitro and in vivo [abstract]. J Agric Food Chem. January 4, 2016. Available at http://www.ncbi.nlm.nih.gov/pubmed/26708928. Accessed January 20, 2016.

National Eye Institute. For the public: what the AREDS means for you. May 2013. Available at https://nei.nih.gov/areds2/PatientFAQ. Accessed February 9, 2016.

Ogawa K, Kuse Y, Tsuruma K, et al. Protective effects of bilberry and lingonberry extracts against blue light-emitting diode light-induced retinal photoreceptor cell damage in vitro. BMC Complement Altern Med. April 2, 2014;14:120. Available at www.ncbi.nlm.nih.gov/pmc/articles/PMC3992157. Accessed January 20, 2016.

Moisturizing Creams and Skin Cancer

Are moisturizing creams contributing to skin cancer? Yao-Ping Lu and US colleagues performed a study that showed a connection between UVB exposure during early life and topical applications of moisturizing creams and skin cancers in high-risk mice. Initially, they intended to test topical caffeine compounds’ ability to prevent sunlight-induced skin cancers. As a preliminary step, the research team decided to test the skin moisturizer that they wanted to use as a base (Dermabase). To their surprise, mice exposed to the moisturizer developed more skin cancers than the control. They then decided to test other commonly used commercial moisturizers.

In their 2009 study, albino SKH-1 mice, which have a high risk of developing skin cancer, were exposed to UVB twice a week for just 20 weeks early in life. The researchers then randomized the mice into seven groups. One group received no treatment, and the others received daily applications (5 days/week for 17 weeks) of Dermabase, Dermavan, Eucerin, Vanicream, a custom-blend, or water (active control) applied with a Q-tip. The custom-blend cream, prepared at the researchers’ request by Johnson & Johnson (Skillman, NJ), contained purified water, propylene glycol, stearyl alcohol, cetyl alcohol, polysorbate 20, isopropyl myristate, C12-15 alkyl benzoate, benzoic acid, glycerin, and sodium hydroxide. Sodium lauryl sulfate, a known skin irritant, and mineral oil, which stimulates skin tumors in the presence of UVB radiation, were specifically excluded from the custom blend cream. All of the commercial creams except Vanicream contain mineral oil.

All four commercial creams showed increased tumor activity compared with controls. Dermovan-treated mice had the highest tumor volume per mouse (51.3 ±14.0 mm³), and Eucerin was the lowest (40.6 ± 16.1 mm³). The tumor volume per mouse in the custom blend group was 26.2±9.8 mm³. In comparison, tumor volume was 32.0 ± 12.6 mm³ in untreated mice, 23.2 ± 6.6 mm³ in water-treated mice, and 27.3 ±6.9 mm³ in the combined control. Oddly, tumor volume in the water-treated mice was much lower than the untreated group. Also, mice exposed to Vanicream, which contains neither mineral oil nor sodium lauryl sulfate, developed more tumors and greater tumor volume than mice exposed to Eucerin, which contains mineral oil. Did stroking mice with a Q-tip have a stress-relieving effect? Does Vanicream contain a tumorigenic ingredient comparable to mineral oil? Did unconscious bias affect the results since the researchers were not blinded?

The authors caution that their results cannot be generalized to humans. Mice, in general, have thinner and more permeable skin than humans; and the mice in this study have a high genetic risk of developing skin cancer. However, most commercial creams and ointments – with or without UVB exposure – are not tested for carcinogenic activity, according to the authors. Skin care product safety testing usually looks for evidence of irritation and sensitization.

Lu Y-P, Lou Y-R, Xie J-G, et al. Tumorigenic effect of some commonly used moisturizing creams when applied topically to UVB-pretreated high-risk mice. J Invest Dermatol. February 2009;129(2)468-475. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2630214. Accessed January 20, 2016.

Sublingual Immunotherapy and Allergies

Sublingual immunotherapy (SLIT) is a safe and effective alternative to monthly subcutaneous immunotherapy injections for the treatment of allergic rhinitis due to seasonal and house dust mite allergies, according to a 2015 review article by Pascal Demoly and colleagues. In SLIT, specific allergens are delivered in drops or a quick-dissolving tablet placed under the tongue each day. Initial treatment begins with a low dose (e.g., 30 IR) and gradually increases to the maintenance dose of 300 IR. IR (index of reactivity) refers to the wheal size that occurs during skin prick-testing on 30 subjects who are sensitized to the corresponding allergen source. In addition to short-term relief, SLIT provides long-term efficacy (tested up to 2 years posttreatment) when given seasonally for 3 years.

Aging has no effect on SLIT’s efficacy, according to a 2012 placebo-controlled, double-blind Polish study led by A. Bozek. People, aged 60–75 years, with confirmed house dust mite allergy were given SLIT (Staloral 300 IR made by Stallergenes) or a placebo. The total nasal symptom score for the active group (n = 47) decreased by 44% compared to a decrease of 6% for the placebo group (n = 48) after three years. The active group also showed a significant decrease in the use of other symptom-relief medications (e.g. antihistamines). Three patients in the active group experienced local adverse reactions (oral itching and facial flushing), which resolved spontaneously.

SLIT is considered safer than subcutaneous treatment, but adverse events (AEs) do occur. Oral pruritus, burning sensations, lip or tongue swelling, gastrointestinal symptoms, rhinoconjunctivitis, and asthma have all been reported. The more serious AEs are most likely to occur when the maintenance dose is initiated too quickly or when a patient switches to a different SLIT preparation during allergy season. In a letter to Pediatric Allergy and Immunology, Australian allergy specialists Kuang-Chih Hsiao and Joanne Smart report a severe allergic reaction in one of two allergy patients who switched over to a different SLIT preparation when their original preparation became unavailable from the manufacturer. They write: “We believe that manufacturers and suppliers of allergen immunotherapy extracts need to acknowledge the significant clinical impact of treatment interruption and have a responsibility to ensure that allergen immunotherapy extract supply disruptions are minimized.”

Bozek A, Ignasiak B, Filipowska B, Jarzab J. House dust mite sublingual immunotherapy: a double-blind, placebo-controlled study in elderly patients with allergic rhinitis. Clin Exper Allergy. 43:242–248. Available at EBSCOhost. Accessed January 20, 2016.

Demoly P, Passalcqua G, Calderon MA, Yalaoui T. Choosing the optimal dose in sublingual immunotherapy: Rationale for the 300 index of reactivity dose. Transl Allergy. 2015;5:44. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4689001. Accessed January 20, 2016.

Hsiao K-C, Smart J. Comment on ‘Anaphylaxis caused by in-season switchover of sublingual immunotherapy formulation.’ Pediatr Allergy Immunol. 2014; 26:92. Available at http://onlinelibrary.wiley.com/doi/10.1111/pai.12329/full. Accessed January 20, 2016.

Editor’s note: See also “Allergy and Immunotherapy,”by Diego Saporta, MD, FAAOA, on page

xx.

Zinc and Skin

Zinc supplementation improves atopic dermatitis (eczema) in some patients, according to research and empirical clinical evidence. Zinc, an essential trace element, takes part in numerous physical processes including normal cell growth and immune response. Zinc deficiency can lead to dry skin and lesions. It also contributes to chronic inflammation, according to Dr. Ananda S. Prasad, whose studies on zinc deficiency were used to establish an RDA for zinc in 1974.

Korean researcher Jeong Eun Kim and colleagues sought a correlation between hair zinc levels, zinc supplementation, and atopic dermatitis (AD) in 58 children with AD and 43 controls (age range 2–14 years). “At baseline, the mean zinc level was significantly reduced in AD patients (113.1 µg/g vs. 130.9 µg/g, p=0.012),” say the authors. AD patients who received 12 mg/day of zinc for eight weeks showed significant improvement and increased hair zinc levels compared to AD patients who did not receive zinc. In commenting on this study, Dr. Alan Gaby says, “The concentration of zinc in hair does not appear to be a reliable indicator of zinc nutritional status, and it is not clear whether patients with atopic dermatitis need to be zinc-deficient in order to benefit from supplementation.” Gaby reports clinical benefit when using zinc along with essential fatty acids (sunflower oil, safflower oil, flaxseed oil) to treat atopic dermatitis (AD) in children.

Kirk Hamilton, PA-C, founder of Clinical Pearls Publications, says, “That small dose of 12 mg of elemental zinc makes sense in children. In adults it would be in the 25-50 mg/day range.” Dr. Ananda S. Prasad told Hamilton, “If zinc is administered in amounts greater than 50 mg/d, we recommend that 1 mg of copper daily should be also administered to prevent copper deficiency.”

Gaby AR. Zinc for atopic dermatitis (eczema). Townsend Lett. July 2015;32.

Hamilton K. Aging, antioxidants, anti-inflammation and zinc: interview with Dr. Ananda S. Prasad. July 2015. Available at www.vitasearch.com/CP/experts/p2experts.htm. Accessed February 10, 2016.

Hamilton K. Atopic dermatitis, hair zinc and zinc supplementation: interview with Young Suck Ro, MD, PhD. December 2015. Available at www.vitasearch.com/CP/experts/p2experts.htm. Accessed February 10, 2016.

Kim JE, Yoo SR, Jeong MG, Ko JY, Ro YS. Hair zinc levels and the efficacy of oral zinc supplementation in children with atopic dermatitis. Acta Derm Venereol. 2014;94:558–562. Available at EBSCOhost. Accessed January 20, 2016.