Preserving Clear Vision

When aging individuals are asked what they fear most, one of the most frequently cited concerns is going blind or having a major loss of vision. Elderly people encounter staggeringly high rates of cataract, glaucoma and macular degeneration.

The good news is that degenerative eye disease is not inevitable. Scientific studies conclusively show that the risk can be mitigated via lifestyle and nutritional modifications. While major advances have been made in treating ocular disorders, there are still technological gaps that cause many to lose their precious vision. This article reviews the published literature and reveals new studies showing that common diseases of the eye are largely preventable.

Cataract surgery is virtually a rite of passage in aging Americans. Each year, 1.3 million cataractous lenses are surgically removed and replaced with synthetic lenses.1 The cost of all of these procedures combined has been estimated to be at least 3.5 billion dollars.

With the aging of the American population, it's likely that ophthalmologists who perform these surgeries will find themselves becoming progressively busier as cataract diagnoses climb in number. Cataract surgery has been perfected to the point where it is often viewed as simple surgery because complications are rare and recovery is generally rapid. The facts are that it is actually a complex and delicate surgery wherein things can and do go wrong during and after the surgery. Complication rates can vary significantly from surgeon to surgeon.

Even though complication rates are low, a small fraction of 1.3 million surgeries results in a significant number of people (about 26,000 to 28,000 people in the U.S.) being affected. These unfortunate individuals develop serious complications such as secondary glaucoma, detached retinas, corneal edema, severely compromised corneas requiring corneal transplants and internal eye infections that can cause possible complete loss of the eye.2-9 These complications can mandate hospitalization, and other major surgery to treat the complication.

Twenty to thirty percent of people who have cataracts removed and replaced with artificial lenses develop opacifications (clouding) of the lens capsule. This capsule was originally part of the patient's own lens but was left in the eye to hold the newly implanted lens in the proper position. Laser surgery is required to remove these opacifications and restore clear vision.

Why cataract is so common

In most body tissues, new, healthy cells are constantly replacing worn-out cells. The lens of the eye, however, experiences no turnover of cells at all -which means that the ones you have when you are born are the ones that you have to last you your lifetime.

The lens of the eye is composed mostly of protein and water, which forms a structurally clear tissue allowing light to pass through and focus on the retina. As we age the lens continues to grow and become less transparent to light. Long term photo (light) stress, oxidative stress, glycation and other factors can lead to severe distortions in the lens fiber proteins. The result is that proteins in the eye lens clump (crosslink), become oversaturated with water (water influx), and rupture in the cell fiber wall (bleb formation). All of this structural damage to lens proteins eventually creates opacity (inhibiting light transmission), which by definition is a cataract.

At first, symptoms may be so mild that the visual changes are attributed to a need for new glasses. Patients will often seek help for their visual changes and will be given a new pair of glasses, which will actually help because as the cataract develops it will cause the lens to swell changing the eyeglass prescription. Most doctors will not tell the patient that they have cataracts at this stage. Therefore, you must inform your doctor that you want to know about all lens changes-even small ones.

What causes cataract

Exposure to ultraviolet (UV) radiation is a well-known risk factor for cataract. Excessive UV exposure increases free radical formation in the lens, and can outpace the body's ability to subdue those damaging free radicals with antioxidants. optometrists and ophthalmologists almost universally recommend the use of wide-brimmed hats and sunglasses during sun exposure to minimize the amount of UV radiation that strikes the lens of the eye.

The link between poor nutrition and risk of cataract formation has been illustrated in a large number of clinical studies.10 A fair amount of research has linked shortages of specific nutrients to increased cataract risk, and shown that populations that consume higher levels of those nutrients have reduced risk.11,12 It is widely acknowledged that elevated free radical stress is also at least partially responsible for glaucoma and age-related macular degeneration, two other leading causes of blindness in aging individuals.

Diabetics are at particularly high risk for cataract. The high blood sugar levels found in diabetics have a direct effect on lens health, elevating oxidative stress and a destructive process called glycation.

Glycation is the pathogoical binding of sugars to proteins, which causes the resulting glycated proteins to produce 50 times more free radicals than non-glycated proteins. This heightened oxidative stress works, in turn, to accelerate glycation reactions-a vicious cycle. The end result of uncontrolled glycation is rapid organ aging and increased risk of a number of age-related diseases. Glycated proteins trigger a process called crosslinking, where proteins become bound together, causing them to become inflexible and less able to function in physiological systems.

It is likely that glycation plays a role in aging in non-diabetics as well, especially those who eat diets high in sugars and refined carbohydrates or those who have blood sugars higher than normal but not high enough to merit a diabetes diagnosis.

Diabetes also causes increased activity of an enzyme called aldose reductase, which encourages clouding of the lens. It has been found that nutrients that inhibit the activity of this enzyme-specifically, the flavonoid nutrient quercetin-may slow the progression of diabetes-related cataracts.

Protecting the eye lens

A great deal is known today about the causes of cataract, and significant progress has been made in the search for inexpensive, non-invasive, low-risk methods to halt cataractogenesis and prevent cataracts from forming. Such a preventative therapy could help many aging people avoid surgery altogether and protect the millions who don't have access to surgery against blindness caused by cataract. There could be an added benefit of prevention of other blinding eye diseases, including glaucoma and age-related macular degeneration.

Nutrients that have been shown effective at protecting against cataract include carnosine, glutathione, taurine and cysteine; the antioxidant vitamins C, A and E; and vitamin B2 (riboflavin). The following paragraphs describe how each of these nutrients helps protect against loss of vision.

N-acetyl-carnosine Carnosine

N-acetyl-carnosine is a free radical scavenger that is especially protective against lipid peroxidation.13 Since cell membranes are primarily comprised of fatty acids, carnosine helps maintain membrane function and cellular structure.

N-acetyl-carnosine's best-known effect, however, is its ability to prevent the formation of advanced glycated end products (protein crosslinks). N- acetyl-carnosine competes with proteins for the binding sites they would occupy on sugar molecules, making it the best glycation preventative currently recognized in the world of nutrition research.

N-acetyl-carnosine has been found to significantly extend the life span of cultured cells and fruit flies, inhibit the toxic effects of the protein that accumulates in the brains of Alzheimer's patients, protect against the toxic effects of copper- zinc in the brain and enhance the state of balance (homeostasis) under which physiological systems work best. And, finally, it has been shown to prevent and/or reverse cataract.14,15

When administered topically to the eye in the form of N-acetyl-L-carnosine-(functionally, a time-release form of carnosine), this dipeptide can move easily into both the water-soluble (aqueous) and lipid-containing parts of the eye. Once there, it helps to prevent DNA strand breaks induced by UV radiation and enhances DNA repair.16 Once it has entered the lipid areas of the eye, N-acetyl-L-carnosine partially breaks down and becomes L-carnosine.
Chinese and Russian researchers have studied cataract-preventive nutrients for nearly a decade. A Chinese study done by A.M. Wang in 1999, used 96 patients aged 60 years or older having senile cataracts of various degrees of maturity with the duration of the disease from 2 to 21 years. Patients instilled one to two drops of the carnosine-containing solution in each eye three to four times each day for a period of treatment ranging from three to six months. The level of eyesight improvement and the change of lens transparency were considered as an evaluation index of the curative effect of carnosine. The result showed that carnosine gives a pronounced effect on primary senile cataracts, the effective rate being 100%. For mature senile cataracts, the effect rate was 80%.17

The Russians most recent contribution was published in 2002 in the journal Drugs Research and Development.18 In two separate studies, they applied a one percent solution of N-acetyl-carnosine to the affected eyes of cataract patients twice a day. Only patients with mild cataracts-not anticipated to require surgery within the next two years-in one or both eyes were selected to participate. A matched control group received placebo drops, and another small matched group received no drops at all. The first study lasted six months, while the second continued for a total of 24 months. Tests of visual acuity and glare sensitivity were administered every two months in the first study and every six in the second.

After six months, a full 90% of eyes treated with N-acetyl-carnosine showed improvements in visual acuity ranging from 7% to 100%. Glare sensitivity improved 27% to 100% in 88.9% of carnosine recipients, and image analysis (a measurement of visual clarity) improved in 41.5% of treated eyes. Lens examination revealed fewer areas of lens opacity in the posterior subcapsular region. No worsening of vision was found in the eyes treated with N- acetylcarnosine, and all of these benefits were sustained through the 24 months that treatment continued.

These study results are evidence that N-acetyl-carnosine is one of the most important nutrients for cataract prevention. The entire body of research on carnosine reveals its promise as an anti-aging nutrient that works at several levels to protect multiple organ systems.

References

1. Javitt JC, et al. Cataract and latitude. Doc Ophthalmol 1994-95;88(3-4):307-25.

2. Ariturk N, et al. Secondary glaucoma after congenital cataract surgery. Int Ophthalmol 1998-99;22(3):175-80.

3. Spierer A, et al. Secondary glaucoma after congenital cataract surgery. [Article in Hebrew] Harefuah 1994 Jun 1;126(11):645-7, 691.

4. Svacova H, et al. Retinal detachment in pseudophakia. [Article in Slovak] Cesk Oftalmol 1991 Mar;47(2):98-104.

5. Marty N, et al. Epidemiology of nosocomial infections after cataract surgery and role of the Infection Control Committee in prevention. [Article in French] Bull Acad Natl Med 2002;186(3):635-45; discussion 645-8.

6. Carlson AN, et al. Infectious complications of modern cataract surgery and intraocular lens implantation. Infect Dis Clin North Am 1989 Jun;3(2):339-55.

7. Chercota V. Corneal edema, a complication of cataract surgery. [Article in Romanian] Oftalmologia 1995 Oct-Dec;39(4):343-8.

8. Lumme P, et al. Risk factors for intraoperative and early postoperative complications in extracapsular cataract surgery. Eur J Ophthalmol 1994 Jul-Sep;4(3):151-8.

9. Obuchowska I, et al. The evaluation of incidence of massive suprachoroidal hemorrhage in the material of the Department of Ophthalmology, Medical Academy in Bialystok from 1990 to 2000. [Article in Polish] Klin Oczna 2002;104(2):93-5.

10. Jacques PF, et al. Long-term nutrient intake and early age-related nuclear lens opacities. Arch Ophthalmol 2001 Jul; 119(7):1009- 19.

11. Cumming RG, et al. Diet and cataract: the Blue Mountains Eye Study. Ophthalmology 2000 Mar; 107(3):450-6.

12. Babizhayev MA, et al. Lipid peroxide and reactive oxygen species generating systems of the crystalline lens. Biochim Biophys Acta 1994 Feb 22; 1225(3):326-37.

13. Wang AM, et al. Use of carnosine as a natural anti-senescence drug for human beings. Biochemistry (Mosc) 2000 Jul; 65(7):869- 71.

14. Quinn PJ, et al. Carnosine: its properties, functions and potential therapeutic applications. Mol Aspects Med 1992; 13(5):379- 444.

15. Specht S, et al. Continuing damage to rat retinal DNA during darkness following light exposure. Photochem Photobiol 2000; 71 (5):559-66.

16. Lou MF. Thiol regulation in the lens. J Ocul Pharmacol Ther 2000 Apr; 16(2):137-48.

17. Wang AM, et al. Use of carnosine as a natural anti-senescence drug for human beings. Department of Biochemistry and Department of Neurobiology, Harbin Medical University, China 1999.

18. Babizhayev M, et al. Efficacy of N-acetylcarnosine in the treatment of cataracts. Drugs Research & Development 2002; 3(2):87- 103.