Putting Vitamin and Nutritional Therapy into Practice

Evidence-based recommendations provide the basis of an effective approach.

By David Boyer, MD

Helping patients reduce their risk of developing advanced AMD requires us to use updated preventive therapies and counseling on diet and lifestyle. Here is how I approach these tasks, mindful of continual changes streaming into my computer from the latest research.

WORKING HYPOTHESIS

I accept the hypothesis that the breakdown of antioxidant systems¹ through aerobic metabolism, light exposure and free radicals² contribute to the activation of the complement system and the development of AMD.³ This antioxidant deficiency may predispose patients to disease, underscoring the importance of antioxidant supplements. In addition, lifestyle modifications may slow progression. Consider the following:

■ Smoking cessation: Smoking is a strong risk factor for all types of AMD.^4,5
■ Exercise: Regular exercise can reduce the rate of progression of AMD by as much as 25%.^6,7
■ Weight control: A high body mass index (>25) equals an approximate 2.3-fold increase in relative risk of AMD progression.^8,9
■ Control of hypertension: High blood pressure is more common in patients with large drusen or extensive intermediate drusen and neovascular AMD.¹⁰
■ Good nutrition: In one observational study, the risk of AMD was reduced by 46% in patients receiving a diet rich in dark green leafy vegetables and by 35% among patients consuming more than four servings of fish per week.¹¹ High intake of unhealthy fats increases the risk of AMD.¹²

Meanwhile, as we all know, nutritional supplements based on the AREDS findings have been shown to decrease risk of progression and reduce visual loss.

WHY LUTEIN AND ZEAXANTHIN?

Lutein and zeaxanthin are xanthophylls that are found in the macula at concentrations that are 100 to 1,000 greater than anywhere else in the body.¹³ Studies suggest that they play a protective role through light screening and antioxidant activity in the retina.¹⁴ As patients age, their levels of lutein, zeaxanthin and macular pigment decline, potentially increasing the risk of developing AMD.^15,16

We now know enough to confidently encourage our patients to consume foods that are rich in lutein and zeaxanthin. These foods include spinach, kale, turnip greens, collard greens, corn, lettuce, mustard greens, squash, green peas, broccoli, pumpkin and tangerines. Other items are specific to either of these xanthophylls, including:

■ For lutein only: Broccoli, eggs, orange juice and papayas
■ For zeaxanthin only: Pepper, persimmons (Japanese) and turnip greens.

MODIFYING WEIGHT AND FAT INTAKE

Advise patients to avoid saturated, monounsaturated, polyunsaturated and transunsaturated fats. High levels of these undesirable fats are found in processed baked goods (risk ratio of 2.42). Note that consumption of nuts is protective (risk ratio of 0.6).⁹

Omega-3 fatty acids, including docosahexonoic acid (DHA) and eicosapentaenoic acid (EPA), contribute to an important structural component of phospholipid membranes, adding to membrane fluidity and creating a protective local effect. DHA constitutes 35% of lipid in photoreceptor membranes.^17-19 Good sources of DHA include tuna, mackerel, herring, spinach and soybeans.

MOVING FORWARD

Recent research has shown that the complement membrane attack complex (MAC) might have a significant role in generating a pro-inflammatory microenvironment, contributing to the development of AMD.²⁰ In the not too distant future, we may benefit from convenient genetic testing to help identify patients at risk. Knowing this information, we might recommend specific nutrition and vitamin therapy to a 30-year-old with healthy eyes—and follow the patient closely for 30 or more years.

We are only at the doorstep of better preventive care.

REFERENCES

1. Wiktorowska-Owczarek A, Nowak JZ. [Pathogenesis and prophylaxis of AMD: focus on oxidative stress and antioxidants]. Postepy Hig Med Dosw (Online). 2010;64:333-343.
2. Nowak M, Gnitecki W, Jurowski P. The role of retinal oxygen metabolism in origin of age-related macular degeneration (AMD). Klin Oczna. 2005;107(10-12):715-718.
3. Anderson DH, Radeke MJ, Gallo NB, Chapin EA, Johnson PT, Curletti CR, Hancox LS, Hu J, Ebright JN, Malek G, Hauser MA, Rickman CB, Bok D, Hageman GS, Johnson LV. The pivotal role of the complement system in aging and age-related macular degeneration: hypothesis re-visited. Prog Retin Eye Res. 2010;29(2):95-112.
4. Seddon JM, Willett WC, Speizer FE, Hankinson SE. A prospective study of cigarette smoking and age-related macular degeneration in women. JAMA. 1996;276(14):1141-1136.
5. Kirby ML, Beatty S, Loane E, et al. A central dip in the macular pigment spatial profile is associated with age and smoking. Invest Ophthalmol Vis Sci. 2010;51(12):6722-6728.
6. Clemons TE, Milton RC, Klein R, Seddon JM, Ferris FL 3rd; Age-Related Eye Disease Study Research Group. Risk factors for the incidence of Advanced Age-Related Macular Degeneration in the Age-Related Eye Disease Study (AREDS) AREDS report no. 19. Ophthalmology. 2005;112(4):533-539.
7. Williams PT. Prospective study of incident age-related macular degeneration in relation to vigorous physical activity during a 7-year follow-up. Invest Ophthalmol Vis Sci. 2009;50(1):101-106.
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9. Seddon JM, Cote J, Rosner B. Progression of age-related macular degeneration: association with dietary fat, transunsaturated fat, nuts, and fish intake. Arch Ophthalmol. 2003;121(12):1728-1737.
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13. Bone RA, Landrum JT, Guerra LH, Ruiz CA. Lutein and zeaxanthin dietary supplements raise macular pigment density and serum concentrations of these carotenoids in humans. J Nutr. 2003;133(4):992-998.
14. Gale CR, Hall NF, Phillips DI, Martyn CN. Lutein and zeaxanthin status and risk of age-related macular degeneration. Invest Ophthalmol Vis Sci. 2003;44(6):2461-2465.
15. Bernstein PS, Zhao DY, Wintch SW, et al. Resonance Raman measurement of macular carotenoids in normal subjects and in age-related macular degeneration patients. Ophthalmology. 2002;109(10):1780-1787.
16. Bone RA, Landrum JT, Mayne ST, Gomez CM, Tibor SE, Twaroska EE. Macular pigment in donor eyes with and without AMD: a case-control study. Invest Ophthalmol Vis Sci. 2001;42(1):235-240.
17. Boesze-Battaglia K, Hennessey T, Albert Ad. Cholesterol heterogeneity in bovine rod outer segment disk membranes. J Biol Chem. 1989;264:8151-5.
18. Fliesler SJ, Anderson RE. Chemistry and metabolism of lipids in vertebraeretina. Prog Lipid Res. 1983;22:79-131.
19. Boesze-battaglia k, Fliesler SJ, Albert AD. Relationship of cholesterol content to spatial distribution and age of disc membranes in retinal rod outer segments. J Biol Chem.199;265:18867-18870.
20. Lueck K, Wasmuth S, Williams J, et al. Sub-lytic C5b-9 induces functional changes in retinal pigment epithelial cells consistent with age-related macular degeneration. Eye (Lond). Epub ahead of print: May 20, 2011.