Management Strategies for AION

Both AAION and NAION can cause devastating, irreparable visual field loss. Proper patient diagnosis and management are essential to maintain visual function.

By Joseph A. Pruitt, O.D.

6/16/2011

Anterior ischemic optic neuropathy (AION) is commonly referred to as a stroke of the optic nerve. There are two types of AION: arteritic (AAION) and non-arteritic (NAION). Vision impairment secondary to AION often includes both visual field and visual acuity loss, and the damage can range from minimal (e.g., 20/20) to severe levels (e.g., no light perception). 

NAION is the most common form of AION and is more likely to occur in younger individuals than AAION. No matter the clinical presentation––whether arteritic or non-arteritic––the visual prognosis usually is poor and the visual acuity and/or visual field loss is permanent. 

Here, we present a case of non-arteritic anterior ischemic optic neuropathy. Additionally, we discuss the etiology of AAION and NAION as well as routine work-up and treatment strategies for both conditions. 

History 
A 48-year-old white male presented to my low vision clinic on March 19, 2009 following referral by his primary care provider (PCP) for an evaluation of his “field cuts,” as well as to learn more information about “adaptive measures and resources.”

With a bit of uncertainty, the patient reported that he had been diagnosed with AION in his right eye three years ago and then in his left eye approximately one year later. Further, the patient indicated that he was diagnosed with hypertension five months earlier and was being medicated with 25mg hydrochlorothiazide (HCTZ) every morning. The patient had no other visual and/or ocular complaints and denied any flashes, floaters, redness, discharge and/or ocular/peri-orbital pain. 

In addition to hypertension, his medical history was remarkable for hearing loss, tinnitus, nasal polyps and hyperlipidemia. The patient’s current medications include HCTZ, mometasone furoate, sertraline and 81mg aspirin q.d.

On February 12, 2009, his PCP performed an extensive blood work-up, which yielded normal findings (including a Westergren sedimentation rate of 9mm/h). The patient also underwent a bilateral carotid ultrasound, which indicated the presence of non-significant hemodynamic plaques. Finally, a functional vision and visual prognosis comprehension assessment was performed.

The patient indicated that he, for all intents and purposes, understood the etiology of his vision loss to be the result of “low-blood flow to the optic nerves.” His hobbies included reading and hunting, and he said that he did not experience any difficulties with mobility, near vision and/or lighting. The patient said that he wore sunglasses regularly. Lastly, he indicated that he had never worn corrective glasses or used any low vision devices.

Diagnostic Data 
The patient’s entering uncorrected distance visual acuity on an Early Treatment of Diabetic Retinopathy Study (ETDRS) chart was 20/50 O.D. and 20/32 O.S. His entering uncorrected near visual acuity on a continuous text near acuity card was 0.4/1.6M O.U. 

Retinoscopy revealed -0.50D +0.75D x 180 O.D. and -1.50D +0.75D x 070 O.S. Subjective trial-frame distance refraction yielded a result of +0.25D +0.25D x 015 with a visual acuity of 20/40 O.D., plano +0.75D x 085 with a visual acuity of 20/20 O.S. and a combined visual acuity of 20/25 O.U. Subjective trial-frame near refraction was +1.75D +0.25D x 015 O.D. and +1.50D +0.75D x 085 O.S. and yielded a near visual acuity of 0.4/0.5M O.U. and 20/20 O.U. on a reduced Snellen near card. 

Color vision was assessed using Ishihara pseudoisochromatic plates; the patient correctly identified 10/10 plates O.D., O.S. and O.U. Extraocular muscles (EOMs) exhibited a full range of motion, with no pain and/or diplopia. Pupils were equal, round and reactive to light, with no afferent pupillary defect. 

Slit-lamp biomicroscopy revealed clear lids and lashes O.U.; a fully functional and unremarkable lacrimal system O.U.; clear conjunctiva and corneas O.U.; deep and quiet anterior chambers O.U.; clear and flat irises O.U.; grade 1+ nuclear sclerotic cataracts O.U.; and a vitreal syneresis O.U.

We then instilled 1gtt of Fluress (fluorescein and benoxinate, Akorn) O.U. and measured his IOP at 15mm Hg O.D. and 16mm HG O.S. Next, we dilated the patient with 1gtt of tropicamide 1% and phenylephrine 2.5% O.U. 

While waiting for dilation, we performed a Humphrey 24-2 SITA Fast visual field test. The results were reliable in the right eye, with 2/13 fixation losses, 1% false positives, 0% false negatives, an outside-normal-limits glaucoma hemifield test, a mean deviation of -20.56dB and a pattern standard deviation of 14.23dB. 

Likewise, the results were reliable in the left eye, with 0/13 fixation losses, 0% false positives, 0% false negatives, an outside-normal-limit glaucoma hemifield test, a mean deviation of -12.68dB and a pattern standard deviation of 15.24dB. In the right eye, the field was interpreted as a dense, inferior, altitudinal defect that extended nasally above the horizontal midline—which was perceived as a sign of NAION (Figure 1). In the left eye, we also noted a dense, inferior, altitudinal defect (Figure 2). Accordingly, we determined that the patient wasn’t legally blind.

1, 2. Here are the visual fields test results of our patient (O.D. left, O.S. right). The right eye exhibited a dense, inferior, altitudinal defect that extended nasally above the horizontal midline, which was perceived as a sign of NAION. We also noted a dense, inferior, altitudinal defect in the left eye. The results were highly reliable in both eyes.

Dilated binocular indirect ophthalmoscopy and indirect biomicroscopy revealed clear media O.U.; cup-to-disc ratios of 0.1 x 0.1 O.U.; distinct margins O.U.; 2+ superior segmental pallor O.U.; attenuated vasculature O.U.; homogenous background O.U.; clear and flat maculae O.U.; and peripheral retinas that were negative for holes, tear, breaks and/or detachments 360° O.U. 

Following fundoscopy, we ruled out superior segmental hypoplasia after noting the normal limit size of both optic nerves (1.7mm to 1.8mm). We also ruled out disc-at-risk/crowed discs due to the bilateral presentation and no evidence of occlusive events (e.g., diffuse retinal hemorrhages in all four quadrants, dilated and tortuous vasculature, cotton-wool spots and/or cherry-red spot of the macula that would indicate central retinal vein occlusion, afferent pupillary defect and markedly reduced visual acuities that would indicate central retinal artery occlusion). 

After ruling out the aforementioned conditions, and given the patient’s history of hypertension, we diagnosed him with NAION. We then referred him to my colleague in visual rehabilitation, specifically to address the inferior field cuts’ impact on his mobility. 

Additionally, we notified his PCP of the exam findings and recommended yearly comprehensive eye examinations. We encouraged the PCP to consider referring the patient to a cardiologist to rule out any cardiac turbulence that could have produced the small emboli that caused the ischemia. 

Finally, we issued an updated, reading-only spectacle prescription, as well as a pair of yellow 54% NoIR fit-over goggles for full-time wear.

Discussion 
Anterior ischemic optic neuropathy typically manifests suddenly and unilaterally, but often progresses to the contralateral eye over time. It is the result of ischemia of the posterior ciliary circulation just posterior to the lamina cribrosa. The posterior ciliary artery (PCA) travels along the optic nerve from the ophthalmic artery to the choroid, supplying the optic nerve with tiny penetrating branches. 

A surrounding pial plexus derived from these small branches supplies the posterior part of the optic nerve. The optic nerve head receives its arterial blood supply from an anastomotic arterial circle (the circle of Zinn-Haller) that is formed by anastomoses between side branches from the nearby pial arterial network and choroidal vessels.¹

AAION and GCA 
Giant cell arteritis (GCA) almost exclusively causes AAION. GCA is a systemic vasculitis which preferentially involves medium- to large-sized arteries.² (However, other conditions, such as periarteritis nodosa, should be considered as a causative etiology as well.³) GCA has a special predilection to involve the PCA, thus resulting in thrombotic occlusion.² 

GCA most commonly affects individuals over the age of 55 with a higher incidence in white females.^1,4-6 Symptoms of GCA may include general fatigue, weight loss, fever, temple pain, neck pain, pain on chewing, scalp tenderness when combing their hair, headache, anemia, joint pain and tender temporal artery.^4-6 However, it has been noted that approximately 21.2% of patients with visual loss due to GCA have occult GCA.² This means that, contrary to universal beliefs, one in five patients with GCA is at risk for vision loss without showing any of the classic GCA symptoms.² 

Visual Rehabilitation for AION Patients with Field Loss

With respect to AION patients, low vision rehabilitation is focused upon increasing contrast and glare control, maximizing magnification and improving management of visual field loss.4Therefore, rehabilitation can include special magnification reading eyewear (e.g., bioptics), magnifiers (e.g., hand-held magnifiers, stand magnifiers and pocket magnifiers) and yellow or amber sun filters (e.g., NoIR filters) for glare control and increased contrast. In cases where patients exhibit severe vision loss, closed circuit television magnification systems are very helpful because they provide both magnification and increased contrast.4  Management of visual field loss includes orientation and mobility training as well as prisms (both yoked and un-yoked), mirrors and visual field awareness systems. The purpose of orientation and mobility training is to improve scanning techniques while teaching and reinforcing sound and safe navigational techniques and skills. Prisms, mirrors and visual awareness systems function to expand the patient’s visual field. Mirrors reflect the field that the patient does not see and prisms shift/superimpose this field into another field that he or she can still see. Furthermore, visual awareness systems utilize prisms. For example, the Gottlieb Visual Field Awareness system orients a small circular prism that is situated outside the visual axis of the spectacle lens that allows the patient to scan into the prism to gain awareness of the field they are missing.

Ocular signs and symptoms of GCA may include sudden, unilateral, painless decreased visual acuity and color vision (dyschromatopsia); positive afferent pupillary defect; altitudinal visual field defects (usually inferior); swollen optic disc (chalky-white pallor or atrophy after six to eight weeks); cotton-wool spots; and in the event of anterior chamber ischemia, ocular hypotony and/or marked exudation in the anterior chamber (most often misdiagnosed as anterior uveitis).^2,6

Approximately 30% of individuals who experience permanent vision loss secondary to AAION will first experience episodes of transcient visual loss (e.g., amaurosis fugax).¹ Another 5% to 10% of AAION patients will experience transient diplopia secondary to ischemia of the optic nerve head, extraocular muscles or cranial nerves.1 Furthermore, peripapillary, retinal and/or choroidal ischemia in the presence of AAION is highly suggestive of GCA.⁷ 

• Work-up. The diagnostic work-up for GCA includes erythrocyte sedimentation rate (ESR), complete blood count (CBC), fasting blood glucose, C-reactive protein, venereal disease research laboratory test (VDRL), fluorescent treponemal antibody absorption test (FTA-ABS), antinuclear antibody test (ANA), fibrinogen, platelets and temporal artery biopsy.^5,6 Classically, a diagnosis of GCA has hinged upon these five criteria advocated by the American College of Rheumatologists:² 

1. Fifty years of age or older at onset. 
2. New onset of localized headache. 
3. Temporal artery pulse. 
4. Elevated ESR. 
5. Positive temporal artery biopsy.

Keep in mind that a patient is classified as having GCA if at least three out of the five criteria are met. However, it must be noted that this diagnostic criteria is highly controversial, because there is a significant risk for vision loss––especially with regards to occult GCA (few or no accompanying systemic symptoms). As a result, there is a movement amongst clinicians to signify temporal artery biopsy as the gold standard diagnostic test for GCA. 

• Treatment. Treatment of AAION requires immediate and aggressive therapeutic intervention to prevent permanent visual loss. Visual compromise caused by AAION tends to be more severe than that caused by NAION. More specifically, initial vision loss can progress to hand motion or no light perception in up to 54% of AAION patients.⁷And, when left untreated, vision loss may become bilateral within days to weeks in at least 50% of cases.⁷ 

Systemic corticosteroids should be initiated upon diagnosis of GCA. If the patient experiences accompanying vision loss, steroids may need to be administered intravenously.⁸ Typically, patients with GCA on systemic steroid therapy will experience a rapid and dramatic relief of headache and malaise within 24 hours; however, just 4% to 15% of patients with arteritic AION experience an improvement in vision loss.¹ But, if vision improvement does occur, the patient will usually experience improved visual acuity with persistent and lasting visual field defects.⁹

NAION 
NAION is the most common form of AION and is usually seen in younger patients. However, several researchers have suggested that NAION can affect a patient at any age, with about 10% of incidences occurring in individuals less than 45 years of age.^4,7 Additionally, while NAION affects both males and females equally, up to 95% of all cases occur in whites.^4,7 

From an etiological and pathogenic perspective, NAION presents in one of two forms:

––Transient non-perfusion or hypoperfusion of the optic nerve head. 
––Embolic lesion of the arteries/arterioles that feed the optic nerve head.

Transient non-perfusion or hypoperfusion is the most common cause of NAION. The majority of NAION cases are due to transient reductions in blood pressure during sleep.² This explains why approximately 75% of patients with NAION report a sudden loss of vision upon awakening.⁴ Less common causes of hypoperfusion include transient reductions in blood pressure secondary to shock and/or a sharp increase in IOP. Embolic causes of NAION are less likely, but when compared to NAION as a result of hypotensive events, the extent of optic nerve head damage is much more extensive and severe.² 

Common diseases and/or conditions that could potentially lead to NAION include hypertension, diabetes mellitus, hyperlipidemia, rheumatoid arthritis, herpes zoster, anemia, sickle cell trait, syphilis, Behçet’s disease, antiphospholipid antibody syndrome, carotid occlusive disease, polyarteritis nodosa and nocturnal hypotension.^2,4-6,10 

• Work-up. Typically, NAION is diagnosed on ocular examination. Examination usually reveals the presence of sudden and painless vision loss, optic neuropathy, a relative afferent pupillary defect, visual field loss, optic disc edema and possibly peripapillary hemorrhages.1 Further, progressive worsening of vision over a few days or weeks is not uncommon.¹ 

It must be noted that a small or absent cup is not truly a risk factor or predisposing consideration for NAION, but merely a secondary, contributory feature.² The sequence of events for NAION begins as subclinical ischemia of the optic nerve; then axoplasmic flow stasis in the optic nerve fibers; then axonal swelling; then asymptomatic optic disc edema; and finally, compression of the intervening capillaries by swollen axons in a crowded disc. Therefore, a crowed disc is a secondary contributing factor because its impact occurs only after the process of NAION has started.²

Additionally, when disc edema is present, it may be diffuse or segmental and will involve only the superior or inferior portion of the optic disc. Findings of inferior or superior segmental edema may correspond to a division of the circle of Zinn-Haller into distinct upper and lower halves.⁷ One to two months after the onset of visual loss, disc edema often resolves and optic disc pallor manifests.¹ 

Significant optic disc edema, as seen here, is a hallmark symptom of NAION.

Regarding long-term visual prognosis, researchers in the Ischemic Optic Neuropathy Decompression Trial found that up to 43% of patients who presented with visual acuities worse than 20/64 spontaneously regained three lines at six-month follow-up, with 31% sustaining that benefit at 24-month follow-up.³ Therefore, in acute AION, initial visual loss may resolve spontaneously but never to the acuity level prior to the event. Therefore, despite the prospect of spontaneous improvement, the initial visual acuity loss will remain permanent to some extent. Given that spontaneous visual field improvement is rare, permanent acuity loss is very common when the patient experiences associated visual field defects.²

Because our patient’s visual symptoms began three years ago in his right eye and two years ago in his left eye, the visual loss likely is permanent. Therefore, we did not initiate treatment, but rather strongly urged that his primary care provider address and rule out all possible systemic etiologies. 

The process of diagnosing NAION is very similar to that of AAION. This is due to the necessity of ruling out AAION, not due to the necessity of confirming the diagnosis of NAION. In fact, NAION is widely a diagnosis of exclusion when GCA is effectively ruled out as the cause of a presenting AION. Nevertheless, when considering a diagnosis of NAION, the universal symptom is a visual field defect.² Therefore, perimetry is one of the most critical diagnostic tests. Common perimetry findings in NAION patients are an absolute inferior nasal sector defect followed by a central scotoma, relative inferior altitudinal defect and absolute inferior altitudinal defect.² 

Upon further analysis of his visual field results, our patient demonstrated what could be described as an absolute nasal sector defect and relative inferior altitudinal defect O.D. and a relative inferior altitudinal defect O.S. 

• Treatment. Treatments for NAION are minimal and unsubstantiated at best.^2,4-6 These include optic nerve sheath decompressions, subtenon injections of vasodilators, intravitreal bevacizumab injections, intravenous or topical intraocular pressure-lowering agents, vasopressors, stellate ganglion block, levodopa, carbidopa, diphenylhydantoin, anticoagulants, oral corticosteroids and, more recently, intravitreal triamcinolone acetonide.^1,2,10 

Triamcinolone acetonide injections have been shown to decrease the duration of disc edema while increasing the prospect of a recovery in visual acuity, but not in visual field loss.¹⁰ Despite this success, the use of triamcinolone acetonide is not without controversy because, with such a high spontaneous recovery rate in non-treated patients, it is thought that the benefit of such an injection might be exaggerated.² Further, intravitreal triamicinolone injection in an eye with NAION can be harmful because of the potential for associated IOP increase.² 

The primary treatment modality for NAION consists of 80mg to 325mg of aspirin q.d.^5,6 This treatment modality is controversial, however, because although aspirin has well documented effects on thromboembolic conditions, NAION is more often a hypotensive condition.² Furthermore, a few studies have shown that aspirin neither benefits eyes with NAION nor prevents the development of NAION in an unaffected eyes.² 

Consequently, due to a lack of viable and effective treatments for clinicians who manage these patients, the primary goal is to rule out an AAION, detect and preemptively control vascular risk factors in the hope of thwarting disease progression and/or occurrence in the contralateral eye (e.g., avoid steps to reduce the likelihood of nocturnal hypotension via consultation with primary care provider to eliminate q.h.s. anti-hypertensive medications).^4,10

Because the incidence of AION increases with age, vision rehabilitation clinics should be prepared to treat an increasing number of baby boomers. During the next decade, eye care professionals should be prepared to appropriately handle these patients because a sudden, painless and unilateral loss of vision is often the presenting symptom. 

And perhaps, within a few more years, increasingly effective treatments for AAION and NAION will be developed to help reduce the incidence of permanent vision loss. 

Dr. Pruitt is the staff optometrist at the Minneapolis Veteran Affairs Medical Center in Minnesota. He is responsible for the outpatient polytrauma/traumatic brain injury and low vision care clinics. 

1. Luneau K, Newman N, Biousse V. Ischemic optic neuropathies. Neurologist. 2008 Nov;14(6):341-54. 
2. Hayreh S. Ischemic optic neuropathy. Prog Retin Eye Res. 2009 Jan;28(1):34-62. 
3. Newman NJ, Scherer R, Langenberg P, et al. The fellow eye in NAION: report from the ischemic optic neuropathy decompression trial follow-up study. Am J Ophthalmol. 2002 Sep;134(3):317-28. 
4. Windsor L, Windsor R. Understanding stroke of the optic nerve: Anterior ischemic optic neuropathy. Vision Enhancement. 2002 Spring;7(2):24. 
5. Kunimoto DY, Kanitkar KD, Makar MS (eds.). The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. Philadelphia: Lippincott Williams & Wilkins; 2004. 
6. Kaiser PK, Friedman NJ, Pinead R. The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology. Philadelphia: Saunders; 2004. 
7. Arnold AC. Ischemic Optic Neuropathy. In: Miller NR, Newman NJ, Biousse V, et al. (eds.). Clinical Neuro-Ophthalmology. 6th ed. Vol. 1. Philadelphia: Williams & Wilkins; 2005:349-84. 
8. Chan CC, Paine M, O’Day J. Steroid management in giant cell arteritis. Br J Ophthalmol. 2001 Sep;85(9):1061-4. 
9. Foroozan R, Deramo VA, Buono LM, et al. Recovery of visual function in patients with biopsy-proven giant cell arteritis. Ophthalmology. 2003 Mar;110(3):539-42. 
10. Sohn BJ, Chun BY, Kwon JY. The effect of an intravitreal triamcinolone acetonide injection for acute nonarteritic anterior ischemic optic neuropathy. Korean J Ophthalmol. 2009 Mar;23(1):59-61.

Here’s how to protect your vision as you age

Original writer :By Christina Ianzito  but i hv done preci and editing as thought needed. ..Alok

Our eyes provide us with a window on the world, but that window gets a little foggy and fragile as we age. or gets damaged due an accident or nowadays commonly gets affected due to serious side effects of many modern medicines. 

Close-up vision blurs, and cataracts lie ahead for many. Tear ducts function less well, and eyes can get dry and inflamed.

Worse, glaucoma and macular degeneration, NAION  can pose serious threats to vision, making reading difficult and jeopardizing independent living.Blindness is among the public’s top health fears. 

As baby boomers age, more people will be confronted with vision problems. Among Americans older than 40, there are an estimated 41 million cases of blindness, low vision or age-related eye disease, according to the patient advocacy organization Prevent Blindness, which predicts that this number will grow to 64 million by 2032. 

So what can you do to keep your eyes working? 

Glaucoma

Would that there were such a happy-ending fix for glaucoma, a condition involving damage to the optic nerve, whose early stages can be detected only through an eye exam. It is diagnosed by evaluating the optic nerve and measuring the pressure of the fluid in the eye; high pressure can harm the optic nerve.

Prevent Blindness estimates that more than 2.7 million Americans age 40 and older have glaucoma. Most at risk are African Americans, Mexican Americans, smokers, diabetics and people who are severely nearsighted or have a family history of glaucoma.

There is no way to prevent glaucoma — or to restore the vision loss it causes — but its progression can be halted with early intervention. That requiresregular eye exams. The American Academy of Ophthalmology recommends that adults without the risk factors mentioned above have a baseline exam at age 40, then evaluations every two to four years until 55. From that point on, they should be checked every one to three years, and one to two years once they’re 65. Those at risk for glaucoma and other eye diseases should be seen more frequently. Ignore the guidelines at your peril. “Unfortunately about once a year I have a patient who walks in the door and has lost significant vision, and has no idea he or she has glaucoma,” Pluznik says. Since it’s irreversible, he adds, “the whole idea is to pick it up early so we can treat it.”

And treatment can be extremely effective. Daily eye drops help lower the pressure in the eye, though sometimes ophthalmologists will use lasers or surgery. Once your pressure is stabilized, you should have your eyes checked every four to six months, Buttross says; “otherwise, if the pressure creeps up, you won’t know it.”

Age-related macular degeneration

AMD is a disease where the cells in the central part of the retina — the part most important for central vision, called the macula — deteriorate. Though eyesight can be preserved when the disease is caught at an early stage, theCenters for Disease Control and Prevention calls it “the leading cause of permanent impairment of reading and fine or close-up vision among people aged 65 years and older,” and says 1.8 million Americans older than 40 have the condition and another 7.3 million are at risk of developing it. Unlike glaucoma, AMD, which runs in families, is a greater risk for whites than for African Americans.

There are two kinds of AMD, dry and wet. More common is the dry, which can cause loss of central vision — essential for reading and driving — but so gradually that many people have it for decades with no obvious effect. Wet, or neovascular, is more dangerous. Abnormal blood vessels grow into the retina, in some cases leading to bleeding or leaking of fluid. Wet AMD is frightening, Pluznik says, because it may alter vision suddenly: “Patients can wake up one day and just see a central black spot.”

Don Albrecht, 85, of Great Falls, Va., was recently diagnosed with dry AMD in his left eye and wet AMD in his right eye. The warning sign came last fall, when he was watching a baseball game on TV and couldn’t see certain details on the players’ uniforms. He became alarmed and eventually was referred to a retina specialist, who treated his wet AMD with injections that eliminated the intruding blood vessels, a relatively new procedure. “If it had been 10 years ago,” he says, “I may have lost my sight.”

The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that people with AMD who take certain vitamins and minerals can slow the disease’s progression. Those antioxidants include vitamins A and E, beta carotene, lutein, zinc and copper; they are sold over-the-counter in pill form as the AREDS formula. The researchers recently altered the mix by adding lutein and zeaxanthine and eliminating beta carotene. Called AREDS2, this formula is what ophthalmologists often suggest now.

Because these treatments can cause side effects, Buttross recommends checking with a doctor before taking them.

Along with the AREDS2 pills, ophthalmologists suggest a low-fat diet that includes fruits and vegetables, especially leafy greens such as spinach, kale and collard greens, and eating omega-3 fatty acids, which are found in salmon and tuna.

Albrecht says he eats lots of salad and takes AREDS2 supplements. “I feel very lucky,” he adds. “I have an eye problem, but it’s under control.”

Seven tips for healthy eyes:

●Be alert to the early signs of vision problems.

●Protect eyes from ultraviolet light with sunglasses. (Make sure yours offer full UV protection.)

●Get regular comprehensive eye exams.

●Don’t smoke.

●Keep weight normal to avoid diabetes.

●Control your blood pressure.

●Eat a diet rich in dark leafy greens and omega-3 fatty acids (found in foods such as salmon, flaxseed and walnuts).

Ianzito is a freelance health writer.

New! PreserVision AREDS 2 Formula for ur eyes

New! PreserVision AREDS 2 Formula

ONLY PreserVision AREDS 2 contains the exact levels of all six clinically proven nutrients now recommended by the National Eye Institute (NEI) to help reduce the risk of progression in people with moderate to advanced age-related macular degeneration (AMD)*. This advanced formula builds on the original, clinically proven PreserVision AREDS formula, with lutein and zeaxanthin replacing beta-carotene based on the NEI’s recent Age Related Eye Disease Study 2 (AREDS2).

Ask your doctor if PreserVision AREDS 2 Formula is right for you.

Completed in 2013, AREDS2 was a 5-year study including thousands of patients, conducted by the National Eye Institute of the National Institutes of Health. For more information from the NEI on the Age-Related Eye Disease Study and AREDS2, click here.

Key Features & Benefits

• Contains the exact same levels of all six clinically proven nutrients now recommended by the NEI based on the clinical evidence from the AREDS2 Study
• Beta-carotene free
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Ingredients:

Directions:

Take 2 Soft Gels daily; 1 in the morning, 1 in the evening with food.

Is this product right for you? Age Group(s) 40s and 50s Eyes 60+ Eyes Condition(s) Age-Related Macular Degeneration

New! PreserVision AREDS 2 Formula : Additional information NEI: Age-Related Eye Disease Study 2 (AREDS2) NEI: Age-Related Eye Disease Study (AREDS) Free Joy of Sight program for PreserVision users. Coupons and more - join today!

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 May 15;309(19):2005-15. National Eye Institute website: http://www.nei.nih.gov/areds2/ Accessed October 2013. AREDS2 is a registered trademark of the United States Department of Health and Human Services (HHS).  

Age-Related Eye Disease Study (AREDS) and well researched formulation for saving eye from AMD

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For the Public:What the Age-Related Eye Disease Studies Mean for You

Researchers with the Age-Related Eye Disease Study (AREDS) reported in 2001 that a nutritional supplement called the AREDS formulation can reduce the risk of developing advanced age-related macular degeneration (AMD). The original AREDS formulation contains vitamin C, vitamin E, beta-carotene, zinc and copper.

In 2006, the same research group, which is based at NIH's National Eye Institute, began a second study called AREDS2 to determine if they could improve the AREDS formulation. They tested...

• Adding the antioxidants lutein and zeaxanthin
• Adding omega-3 fatty acids
• Removing beta-carotene
• Lowering the dose of zinc

This page provides information about the results and implications of AREDS2. If you are at risk for advanced AMD or have a family member who is at risk, the questions and answers below may help you discuss using AREDS and related nutritional supplements with a health care professional.

What is the original AREDS formulation?

• 500 milligrams (mg) of vitamin C
• 400 international units of vitamin E
• 15 mg beta-carotene
• 80 mg zinc as zinc oxide
• 2 mg copper as cupric oxide

What modifications were tested in AREDS2?

• 10 mg lutein and 2 mg zeaxanthin
• 1000 mg of omega-3 fatty acids (350 mg DHA and 650 mg EPA)
• No beta-carotene
• 25 mg zinc

Why change the formulation?

Why add lutein/zeaxanthin and omega-3 fatty acids? Previous studies had found that dietary intake of lutein/zeaxanthin and omega-3 fatty acids is associated with a lower risk of developing advanced AMD.

Why eliminate beta-carotene? During the AREDS trial, two large trials funded by the National Cancer Institute found that beta-carotene may increase lung cancer risk among people who smoke. Lutein and zeaxanthin are in the same family of nutrients as beta-carotene and are believed to have important functions in the retina. Therefore, the researchers theorized that lutein/zeaxanthin might be a safer and possibly more effective alternative than beta-carotene.

Why reduce zinc? Although zinc was found to be an essential component of the AREDS formulation in the original trial, some nutritional experts recommended a lower dose.

What are lutein, zeaxanthin and beta-carotene?

Lutein, zeaxanthin, and beta-carotene belong to a family of nutrients known as carotenoids. Carotenoids are made by plants and are especially enriched in green leafy vegetables. They can be stored in animal tissues and are found at relatively low levels in animal food products. In the body, beta-carotene is used to make Vitamin A, which is required by the retina to detect light and convert it into electrical signals. Beta-carotene itself is not found in the eye. In contrast, lutein and zeaxanthin are found in the retina and lens, where they may act as natural antioxidants and help absorb damaging, high-energy blue and ultraviolet light.

What are omega-3 fatty acids?

Omega-3 fatty acids are made by marine algae and enriched in fish oils; they are believed to be responsible for the health benefits associated with regularly eating fish, including lower rates of cardiovascular disease. The AREDS2 study focused on the omega-3 fatty acids DHA and its precursor EPA. DHA is needed for the integrity of the retinal cells, and has been shown to promote retinal development and repair in prior studies.

What were the effects of changing the original AREDS formulation?

In the first AREDS trial, taking the original formulation reduced the risk of advanced AMD by about 25 percent over a five-year period. In the AREDS2 trial, adding DHA/EPA or lutein/zeaxanthin to the original formulation (containing beta-carotene) had no additional overall effect on the risk of advanced AMD. However, trial participants who took AREDS containing lutein/zeaxanthin and no beta-carotene had a slight reduction in risk of advanced AMD, compared with those who took AREDS with beta-carotene. Also, for participants with very low levels of lutein/zeaxanthin in their diet, adding these supplements to the AREDS formulation helped lower their risk of advanced AMD. Finally, former smokers who took AREDS with beta-carotene had a higher incidence of lung cancer. (Please see below for more details on the effects of lutein/zeaxanthin vs. beta-carotene.) The investigators found no significant changes in the effectiveness of the formulation when they removed beta-carotene or lowered zinc.

Who should consider taking a combination of antioxidants and zinc like those examined in AREDS and AREDS2?

People at high risk for developing advanced AMD should consider taking the antioxidant-zinc combinations examined in AREDS and AREDS2. These people are defined as having either:

1. Intermediate AMD in one or both eyes. Intermediate AMD can be detected by an eye care professional, but usually involves little or no vision loss.
2. Advanced AMD in one eye, but not the other eye. Advanced AMD involves either a breakdown of cells in the retina (called geographic atrophy or dry AMD), or the growth of abnormal blood vessels under the retina (called neovascular or wet AMD). Either of these forms of advanced AMD can cause vision loss.

Will taking an AREDS formulation prevent AMD?

There is no known treatment that can prevent the early stages of AMD. However, the AREDS formulations may delay progression of advanced AMD and help you keep your vision longer if you have intermediate AMD, or advanced AMD in one eye. The participants in the first AREDS trial have now been followed for 10 years, and the benefits of the AREDS formulation have persisted over this time.

Can I take a daily multivitamin if I am taking one of the AREDS formulations?

Yes. The AREDS formulation is not a substitute for a multivitamin. In the AREDS trial, two-thirds of the study participants took multivitamins along with the AREDS formulation. In AREDS2, almost nine of ten participants took multivitamins.

Can a daily multivitamin alone provide the same vision benefits as an AREDS formulation?

No. The vitamins and minerals tested in the AREDS and AREDS2 trials were provided in much higher doses than what is found in multivitamins. Also, it is important to remember that most of the trial participants took multivitamins. Taking an AREDS formulation clearly provided a benefit over and above multivitamins.

Can diet alone provide the same high levels of antioxidants and zinc as the AREDS formulations?

No. The high levels of vitamins and minerals are difficult to achieve from diet alone. However, previous studies have suggested that people who have diets rich in green, leafy vegetables—a good source of lutein/zeaxanthin—have a lower risk of developing AMD. In the AREDS2 trial, the people who seemed to benefit most from taking lutein/zeaxanthin were those who did not get much of these nutrients in their diet. Within this group, those who received lutein/zeaxanthin supplements had a 26 percent reduced risk of developing advanced AMD compared with those who did not receive the supplements.

What is the risk of lung cancer from taking beta-carotene?

In the AREDS2 trial, current smokers or those who had quit smoking less than a year before enrollment were excluded from receiving beta-carotene. Despite this precaution, lung cancers were observed in 2 percent of participants who took an AREDS formulation with beta-carotene, compared with 0.9 percent of participants who took AREDS without beta-carotene. Across both groups, about 91 percent of participants who developed lung cancer were former smokers.

How does lutein/zeaxanthin compare to beta-carotene?

Lutein/zeaxanthin has not been associated with increased cancer risk. Moreover, analysis from the AREDS2 trial suggests that it offers similar or better protective benefits against advanced AMD, compared with beta-carotene. In the trial, participants who took an AREDS formulation containing lutein/zeaxanthin (no beta-carotene) had an 18 percent lower risk of progressing to advanced AMD compared with those who took AREDS containing beta-carotene (no lutein/zeaxanthin).

Does the high-dose vitamin E in the AREDS formulations affect the risk of prostate cancer?

There have been conflicting data on the relationship between vitamin E and prostate cancer.

• In 1994, the Alpha-Tocopherol, Beta Carotene (ATBC) trial found a 35 percent reduced risk of prostate cancer in men taking 50 mg of vitamin E daily for a follow-up of six years.
• In 2009, the Physicians Health Study II (PHS II) found that 400 IU of vitamin E every other day for a follow-up of eight years had no effect on the incidence of prostate cancer.
• In 2011, the Selenium and Vitamin E Cancer Prevention Trial (SELECT) found a 17 percent increase in the risk of prostate cancer among men taking 400 IU of vitamin E daily for a follow-up of seven years. That risk equates to 1-2 more prostate cancers per 1000 patients who took high-dose vitamin E for one year. For reasons that are unclear, men who took both vitamin E and selenium did not have an increased rate of prostate cancer.

In the AREDS trial, high-dose vitamin E had no effect on the risk of prostate cancer among male participants. The AREDS2 trial began in 2006 (before the SELECT trial was reported) and all study participants were offered an AREDS formulation containing vitamin E. A group of independent researchers monitoring the AREDS2 trial for safety noted no concerns about an increased risk prostate cancer. The final data from the study do not suggest a higher rate of prostate cancer among male participants than expected in an aging male population.

If you have concerns about vitamin E and prostate cancer, it is important to understand that many factors influence the risk of prostate cancer, including age, family history and race. Visit the National Cancer Institute web site for more information about prostate cancer risk factors, and talk to your health care provider about the possible risks and benefits from taking vitamin E supplements.

Are there any other side effects or risks from taking the AREDS formulations?

Many older Americans take prescription medications, and a considerable number use over-the-counter drugs, dietary supplements, and herbal medicines. High-dose supplemental nutrients can sometimes interfere with medications and compete with other vital nutrients for absorption into the body. Individuals who are considering taking an AREDS formulation should discuss this with their primary care doctors and/or eye care professionals.