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Not the last word The Age-Related Eye Disease Study (AREDS) concluded that a formulation of vitamin A, vitamin C, beta carotene, zinc (Zn) and copper (Cu) was effective in slowing the progression of AMD, but was not particularly effective in preventing the disease, even without adding lutein or zeaxanthin. My own research pointed to the importance of the copperand zinc-dependent protective enzyme superoxide dismutase (SOD), which I measured as indexed in red blood cells. The consensus is that the AREDS succeeded mainly because of the supplementation of zinc (40 mg .d.) and copper (1 mg .d.) and 250 mg .d. vitamin C and 200iu .d. of vitamin E. In fact, the lutein and zeaxanthin concentrations in serum decreased in subjects given beta carotene. Studying the effects of lutein Even before the AREDS study, investigators had recognized the value of lutein and zeaxanthin in treating AMD. In fact, the NEI is currently conducting the Dose Ranging Study of Lutein Supplementation in Persons Over Age 60. It's significant because there's already excellent data that lutein and zeaxanthin are factors in preventing the atrophic and geographic species of AMD and are helpful in protecting the retinas of all eyes. But the most effect tive, long-term safe dosage for supplementation is not yet known. Identifying vulnerabilities The AREDS demonstrates that a combination supplement of Zn and Cu along with vitamins C, E and beta carotene as antioxidants effectively slow the progression of AMD - in AMD-susceptible persons who already had signs of the disease. It didn't seem to make a difference in persons who had little or no signs of AMD, suggesting a biochemical vulnerability in patients with various species of AMD. Diet-responsive vulnerabilities differ in different species of AMD. In 1991, I reported the results of studies suggesting special diet-responsive biochemical vulnerabilities, different lifestyle oriented, diet-responsive vulnerabilities for atrophic AMD, different from exudative AMD, and yet with different lifestyle and risk factors for patients with only vitreous-pathology-induced macular pucker. These are best appreciated by examining patients who have only hard drusen compared to patients who have only soft drusen, compared to patients who have exudative AMD without evidence of hard drusen. Oils linked to higher risk One study found that excessive intake of mono- and polyunsaturated fatty acids, especially from linoleic fatty acid (., salad dressings and vegetablebased cooking oils) increased risk for exudative maculopathy. This included even olive oil taken in excessive quantities. There was no apparent risk for AMD attributable to omega-3 fatty acids. Supplement savvy Julie Mares-Perlman notes that it isn't good policy to rely on a multivitamin-mineral to protect the eyes. Excellent quality, minimally processed whole foods have the potential to be superior sources of balanced nutrients as compared with supplements. But supplements make possible a quicker catch up to ideal nutriture levels with minimal lifestyle change. You can apply them radically at a therapeutic dosage level when the urgency is great, or conservatively at a maintenance or insurance level. Don't remain at a high therapeutic administration longer than necessary because it increases the risk for new imbalances. Guiding your patients Most therapeutic formulas guide patients with instructions as to dosage limits that they shouldn't exceed without professional guidance. Still, many supplement takers believe that more is better, so it's important to remind patients that this is not necessarily the case unless they require radical measures. Reviewing what's available The supplements in "Supplements for AMD" (pg. 44) reflect those designed from three different levels of criteria: 1. The results of the AREDS clinical trial, confirmed and with predictable results [level one] 2. Evidence drawn from casecontrol studies not yet verified by clinical trials with dosages that appear to be safe [level two] 3. Thoughtfully conceived combinations of nutrients, probably helpful and individually shown to have value but not yet tested in any large clinical trials as to the effectiveness of the suggested combinations [level three]. * Level #1: Safe, effective prescribing. Three of the 13 supplements listed in the table below (Icaps AREDS formula; Ocuvite PreserVision; and I-Sense Ocushield) follow the AREDS recipe. They represent the best of safe, conservative prescribing. Their efficacy has been demonstrated in a large clinical trial with superior results over a seven-year period. Their best offer is slowed progression. The third formula follows the AREDS recipe, but adds lutein and zeaxanthin. The formulas don't address the lifestyle differences associated with atrophic AMD as compared with exudative AMD or macular pucker. * Level #2: Probably more effective prescribing. The consensus among nutrition scientists is that several of the formulas in the table below prudently use the best part of the AREDS formula with the improvement of lessened beta carotene and less preformed vitamin A and better tol erated reduction in zinc, but wit the addition of lutein and zeaxanthin (Eye-Vite Plus with Lutein, Icaps, Lutein & Zeaxan thin, MaculaRx Plus and Ocuvite Lutein). The consensus is that these formulas are safe and probably more effective than the cloned AREDS formula. But we don't have a carefully designed, large study seven-years-or-longer assessment of the long-term benefits of each or any of the combinations. The formulas don't directly address the lifestyle differences associated with atrophic AMD as compared with exudative AMD or with macular pucker. Combined with good nutrition and lifestyle improvements, they offer hope of preventing further macular degeneration. * Level #3: Promising new combinations. The following formulas include nutrients that have individually been found associated with reduced risk for the atrophic form of AMD: I-Sense, MacuCare, Macula, OcuGuard Plus and Ocuvite Extra. All are worthy of a clinical trial. Assessing patient needs Breakdown in any of the support systems serving the macula putatively can lead to AMD. None of the formulas address all the possibilities. Presumably, they address the more common factors that promote AMD. The likelihood remains that some individuals will respond excellently because the supplement supplies precisely the nutrients they are lacking. Others may require a different menu of supplements. So how is the general optometrist to assess each patient's needs? Get a handle on prescribing I recommend using the following tests as a guide in nutritional prescribing, * Diet assessment. The American Optometric Association supports a dietary assessment tool that it and the Vitamin Nutrition Information Service developed for optometric patients. It's not a perfect tool, but it's good and will hopefully get better. You can access the free tool directly at .org/eyeonnutrition. * Hair-mineral assay. Because hair is an excretion material, hair specimen analysis is usually excellent and cost-effective for estimating body storage adequacy of copper and zinc, as well as other minerals of optometric interest. Patients who have recently swam in copper-sulfate treated pools will obtain too high a reading of Cu because of adsorption of the Cu to the hair. There have been abuses in the commercialization of hair testing, but proper employment of the methodology brings extremely useful information not readily available elsewhere. * Special cellular blood mineral tests. Because blood-mineral concentrations are so well regulated by the body, blood testing has a different meaning than hair-mineral measurements. Extremely low mineral concentrations in hair are usually excellent evidence of low storage values, but high or even normal concentrations need investigating as to the possibility of contamination. For AMD patients, we like also to look at blood test findings for red-blood-cell (Erythrocyte) Cu, Zn and Zn's antagonist/competing trace minerals Cr and Mn, and also Cr's principal antagonist, vanadium (V). * ESOD and EGOT Two red blood cell enzyme tests are of special value in designing supplement programs in AMD. > I reported in 1991 that persons with deficient erythrocyte superoxide dismutase (ESOD) are statistically vulnerable to atrophic AMD. ESOD is the first line of defense in the retina against oxidative insult from excessive light exposure. If below normal, the patient is likely deficient in either Cu or Zn or both. The patient should use a supplemental 2 mg to 3 mg Cu and/or 20 mg to 30 mg Zn as appropriate. Amino acid chelates of Cu and Zn are acceptable and many supplement companies offer them individually. Reduce therapeutic dosing to maintenance doses as appropriate. Those experiencing exudative AMD but with no evidence of hard drusen tend to have normal or elevated levels of ESOD. > Those who have exudative AMD and/or soft drusen also have high concentrations of erythrocyte glutamic oxaloacetic transaminase (EGOT) and other transaminase enzymes. Transaminase enzymes are the class of gut enzymes that enable our digestive systems to convert the amino acids in our diet to the amino acids our bodies may require for making specific proteins. When we eat too much wellcooked protein, the transaminase enzymes can't convert the amino acids; the unused enzymes accumulate. Supplement with 50 mg to 100 mg of pyridoxine (vitamin B6) and restrict protein intake not to exceed 100% of the RDA for protein. Nutrition beyond supplements Several greens have been identified as effective in helping to prevent and even reverse aspects of some eye diseases. They also help with some common species of cataract and glaucoma. The five greens rich in both lutein and zeaxanthin are, in approximate decreasing order of total concentrations, kale, turnip greens, collard greens, spinach and lycium barbarum. The fifth plant-derived food is also known also as Lycium berries, Go-Qi-Zi and, in dried fruit form, as Barbary Wolfberry; other names include Box Thorn and Tea Tree. Nutritional keys Two possible keys in nutritional optometry are the power of alerting patients to dietary and environmental modifications affecting the visual system, and the ability of optometrists to measure the changes over time. References are available from the author upon request. BY BENJAMIN CLARENCE LANE, ., ., . Dr. Lane is a Fellow of the American College of Nutrition and is a certified nutrition specialist. Call him at (973) 335-0111 or fax him at (973) 335-2882.
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