Preventing Vision Loss Through Diet

Noted Tufts nutritionist, Allen Taylor, Ph.D., explains how diet impacts age-related eye disorders.

Cataract is the major cause of treatable vision loss worldwide, while AMD is the leading cause of non-treatable blindness among the elderly. The costs associated with both conditions are enormous and will continue to rise. Over the next few decades, the number of those affected by cataracts and AMD here in the United States is expected to increase by 50% and 69%, respectively.

Results from the National Eye Institute's Age-Related Eye Diseases Study (AREDS) have already shown that antioxidants can delay vision loss in moderate to advanced AMD for at-risk individuals. It's been estimated that delaying cataract by only 10 years would reduce the number of extractions by 50%. Modifying dietary patterns and increasing intakes of specific nutrients may very well be factors that can impact the onset or progression of these age-related eye disorders. For insight into the current state of nutrition, cataract and AMD research, we turned to Allen Taylor, Ph.D., director of the Laboratory for Nutrition and Vision Research and senior scientist at the Jean Mayer USDA Human Nutrition Research Center on Aging. Dr. Taylor is also a professor at the Friedman School of Nutrition Science and Policy at Tufts University and in the biochemistry department and Department of Ophthalmology of Tufts University Medical School. He is the 2007 recipient of the Osborne and Mendel awards for outstanding basic research in nutrition and the 2007 Denham Harmon Award for Excellence in Aging Research.

Allen Taylor (AT) is interviewed by nutritionist Penelope Edwards (PE), MPH, CNS, Nutrition & Science Advisor to Science Based Health.

PE: Dr. Taylor, you and your collaborators, including epidemiologist Dr. Chung-Jung Chiu, have led the field in investigating the effects of carbohydrate intake on AMD and cataract. Several studies indicate that high glycemic index diets (dGI) raise the risk for early AMD and that low dGI patterns might be protective for nuclear cataracts. The glycemic index — a weighted measure of how quickly carbohydrates raise blood-glucose levels — speaks to carbohydrate quality. Could you please tell us more about your research in this area, and can you elaborate on how carbohydrates may be harmful to eye tissues?

AT: We were the first to show that people who consume diets richer in more readily available sugar from carbohydrates are at a higher risk for all grades of AMD and prevalent types of cataract. We believe carbohydrates damage proteins that are directly needed for the visual function of the lens and retina. Carbohydrates also cause indirect damage by compromising the function of pathways that usually serve to identify and remove the damaged proteins. This leaves the cells with accumulations of dysfunctional and cytotoxic proteins. Thus, the carbohydrates cause "double trouble."

PE: The data also suggest that carbohydrate quantity rather quality is important for cortical cataracts. Does that imply that nuclear and cortical cataracts form in different ways?

AT: We are not sure why there are different relationships with cortical cataract, or cataract in general, from the relationships that are observed for AMD and dGI. It might be that there is far lower blood supply and slower migration of sugars into the cortical or nuclear areas of the lens as compared with the retina. We are currently investigating this.

PE: Do you think it would it be appropriate to begin labeling foods with dGI information to help consumers plan a healthy diet?

AT: In my opinion, yes. I base my opinion on practical considerations that include: (1) Eating a lot of simple carbohydrates is unnecessary and leads to many adverse health effects, including obesity, metabolic syndrome and all of their complications, as well as vision problems, (2) Diminishing sugar intake is not difficult, (3) Having excess sugars does damage the protein workhorses of the cells of the body and (4) Consumption of simple sugars has increased dramatically during the last 30 years or so.

PE: You've also investigated the relationship between cataract and dietary fats that can affect the composition and function of cellular membranes in the lens. What have you found?

AT: Higher intake of alpha-linolenic acid was associated with slightly higher risk for, and more rapid progress of, early nuclear cataracts. Because nuclear cataracts are often right in the visual axis, they disturb vision more than some cortical cataracts, and it is important to diminish risk for such cataract. In comparison, higher intake of long-chain omega-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid) and consumption of fish may modestly reduce the risk of cataract. Higher intake of omega-3 fatty acids is associated with several health benefits.

PE: Realizing that people eat groups of foods rather than single nutrients, you've analyzed the effects of eating according to the food guide pyramid and by looking at food groupings. Tell us what your findings indicate about eating according to those patterns and the risk for eye diseases?

AT: Generally we found that people who consume lower glycemic index diets and who consume larger proportions of fruits and vegetables, as well as meals containing dark-meat fish, enjoy better eye health, as measured by lower risk for AMD and cataract.

PE: You designed and directed the Nutrition and Vision Project (NVP) — a longtime collaboration between your group, the Brigham and Women's Hospital, and the Nurses' Health Study at Harvard. Please tell us a little about the NVP and some of the project's key findings.

AT: The NVP was an outgrowth of the larger Nurses' Health Study (NHS). Because the NHS was already obtaining state-of-the-art nutritional information and we were generously given access to the cohort in the Boston area by Drs. Frank Speizer and Walter Willett, we asked those nurses who live locally if they would undergo a thorough eye examination at approximately 5-year intervals. We also were able to collaborate with ophthalmologists such as Dr. Lahav at Tufts Medical Center and Dr. Chylack at Harvard, who generously provided the eye examinations. Using a "reading" center at Wisconsin and photo grading at Harvard, we obtained numerically graded images of the retinas and lenses at both visits. Thus, we obtained photographs of different aspects of the lenses and retinas of each nurse and we were also able to monitor the change over 5 or so years by comparing images from the "baseline" and the 5-year follow-up. By collaborating we saved millions of dollars in setup costs and we were able to complete analysis at a fraction of the cost. Because we were also given access to a wealth of additional data about the participants, we were able to associate our new findings with prior information to get added value to the work and to provide a more mature perspective to prior NVP investigations, such as relations between risk for cataract extraction and fat intake or post-menopausal hormone use.

Since we now invest over $57 billion in eye care in the United States, if we can save a small proportion of the population from vision loss this would enhance their life quality immeasurably, and the small cost of these studies is an excellent investment of public dollars. Our studies regarding carbohydrates indicate that we can diminish risk significantly. In fact, we predict that we can save about 200,000 people from advanced AMD in only 5 years just by limiting simple carbohydrate intake. Thus, we are already repaying the small investment.

PE: One finding from the NVP is the observed link between vitamin C supplement use for a decade or more and a decreased risk of cortical or nuclear cataract in women. Will you fill us in on how long-term antioxidant intake dovetails with the process of catarogenesis?

AT: Many tissues of the body replace their constituents often. For example, every few days you get new cells in your intestine. Every 10 days, you get new receptors for light in your retina. In comparison, lens proteins last for decades and are damaged by the light, oxygen and sugars to which they are exposed. The accumulation of such damage is causally related to onset and progress of cataract. Stated a different way, if we are to protect the lens, the protection should begin early and last a long time. Thus, we rationalize our observations that prolonged intake of adequate levels of antioxidants, such as vitamin C, confers protection to lens proteins, as compared to lens proteins in persons who are poorly nourished.

PE: A large-scale prospective study of women health professionals who were followed for 10 years just reported in January that higher intakes of lutein, zeaxanthin and vitamin E are associated with a reduced risk of cataract. A month before that, the same research group found that giving women 600 IU natural-source vitamin E every other day for nearly 10 years provides no benefit for age-related cataract or subtypes. Your thoughts?

AT: Measuring and quantifying cataract is a highly specialized field. My guess is that in the former case, photograding of the opacities was not possible, and this may have compromised their ability to execute the study properly. But certainly there are different opinions. There are several studies that failed to find associations between vitamin E intake and cataract, although we did find such a relationship. One might hypothesize that the lens is primarily an aqueous environment and thus rationalize stronger roles for vitamin C, which is also water-soluble. Vitamin E is lipid-soluble. But the confusion is unsatisfactory. Given the huge rewards and returns on maintaining sight among the elderly, the returns are certainly worth the investment and more studies should be done.

PE: You've said that daily dietary intake of about 250 mg vitamin C, 90 mg vitamin E and 3 mg/day lutein — begun early in life — should provide sufficient reserves to provide lens and macular health benefits. These levels are considerably higher than the current recommended daily intakes for vitamins C and E and higher than the average amount of lutein we consume. How "early in life" should a higher level of intake begin, in your estimation?

AT: I think that healthy eating should begin at birth and be inculcated early and reinforced regularly. Our health would be certainly be improved if by young adulthood we were already consuming diets that are rich in fruits and vegetables and not high in fats or simple carbohydrates.

PE: For older individuals participating in the cataract portion of AREDS, high-dose C, E and beta-carotene had no apparent benefit. Yet a subsequent AREDS analysis found a reduced risk of nuclear cataract — and any cataract — in those who elected to take a simple multi-nutrient supplement throughout the trial. Can you comment on these findings?

AT: I have several responses to this question. First, it is important to remember that a large proportion of the AREDS subjects were already taking a multivitamin. Additional analyses of the AREDS cohort implied some benefit to consuming multivitamins with respect to risk for cataract. The benefit of taking the high-dose supplement with respect to nuclear cataract is consistent with several other studies. It should be pointed out, however, that only high-dose supplements were used. It is also possible that the benefit could be gained using lower levels. Clearly, more study is required.

PE: Can you tell us more about why cataract and AMD form or occur?

AT: The lens and retina both have the job of "processing" light. The lens receives it and transmits it to the retina, where it is received and converted to chemical and electrical impulses. Just as a newspaper in the back of a car window gets brown from the light of day and the oxidation that the light energy causes to the paper, so do our retinas and lenses get oxidized. The oxidation of the proteins and sugars in these cells cause the proteins to clump and precipitate. Such precipitation in the lens results in opacification of the normally clear milieu.

In the retina, the oxidation has many repercussions, including accumulation of deposits, called drusen, which push cells away from their blood supply, thus resulting in their dysfunction and loss. Such loss results in AMD-associated vision loss. Moreover, cells usually have protein quality control machinery that can identify and destroy damaged proteins before they become cytotoxic. This "machinery" is also damaged by oxidative or glycoxidative stress. Thus, in the aged tissue, the cells are subject to multiple insults and an inability to recover from those insults. For example, one system for identifying damaged proteins involves the "ubiquitin pathway." Discovery of this ubiquitous protein digesting pathway was awarded the Nobel Prize in 2004 because it has so many uses. Among them is the tagging of the damaged protein prior to its degradation. We find that the function of the ubiquitous pathway is itself compromised upon aging: hence the multiple jeopardy of aged tissues. We hypothesize that similar compromises occur in many tissues upon aging.

PE: Dr. Taylor, in your opinion what are the biggest challenges to reducing the prevalence of cataract and AMD in our aging population?

AT: I think that identifying the optimal ways to protect the eye and when protection needs to be started are crucial. Also, it is important to instill in children and youths the value of good sight and good health in general. As it is said, "You do not even think about it when you have sight, but when it is gone it is invaluable." When we compare the expenditures on health care or less rewarding investments vs. the costs of research, given the repeating returns of the research, it is clearly well worth the investment. But the time required for that research may exceed political memories of a few months or a few years. Thus, the public must demand that this research be given high priority.

Given that we will all eventually have compromised vision, it is essential to understand how the lens and retina are originally assembled and maintained and to harness such capabilities to prolong their function over time and in the face of stress. OM

Suggested Further Reading

Chiu CJ, Taylor A. Nutritional antioxidants and age-related cataract and maculopathy. Exp Eye Res. 2007;84:229-245.

Chiu CJ, Morris MS, Rogers G, et al. Carbohydrate intake and glycemic index in relation to the odds of early cortical and nuclear lens opacities. Am J Clin Nutr. 2005;81:1411-1416.

Taylor A, ed. Nutritional and Environmental Influences on the Eye. Boca Raton, FL: CRC Press; 1999.

Lu M, Taylor A, Chylack LT Jr, et al. Dietary linolenic acid intake is positively associated with five-year change in eye lens nuclear density. J Am Coll Nutr. 2007;26:133-140.

Chiu CJ, Milton RC, Gensler G, Taylor A. Association between dietary glycemic index and age-related macular degeneration in nondiabetic participants in the Age-Related Eye Disease Study. Am J Clin Nutr. A2007;86:180-188.

Chiu CJ, Milton RC, Gensler G, Taylor A. Dietary carbohydrate and the progression of age-related macular degeneration: a prospective study from the Age-Related Eye Disease Study. Am J Clin Nutr. 2007;86:1210-1218.

Chiu CJ et al. Diet, supplement and risk of age-related macular degeneration in the Age-Related Eye Disease Study. Manuscript submitted.