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Questions? Please call us atCataract 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.
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.
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.
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 sections describe how each of these nutrients help protect against loss of vision.
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.
Carnosine's best-known effect, however, is its ability to prevent the formation of advanced glycated end products (protein crosslinks). 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.
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 topical 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.
The concentration of glutathione in the lens of the eye is higher than in most other tissues. It functions to protect the structural proteins and enzymes necessary for the maintenance of lens flexibility and clarity against free radical assault. Aging lenses or lenses that are under oxidative stress lose glutathione, and this shrinkage of the glutathione pool has been found to lead directly to reactions that cause crosslinking of proteins and lens opacification.19-26 L-carnosine and vitamin E have been shown to protect and restore these levels of glutathione. Oral supplements of NAC (n-acetyl-cysteine) and alpha lipoic acid help increase tissue levels of glutathione in the eye.
Vitamin C protects the eye against damaging ultraviolet radiation and has been found to reduce the risk of cataracts.30 One study found that the higher the vitamin C intake, the less likely cataract was to develop. Women who used a vitamin C supplement for 10 years or more enjoyed the most protection.31
Vitamin C naturally exists in high concentrations in the aqueous humor (the fluid that fills the eyeball and filters light as it passes through to the retina) and the corneal epithelium (the outer layer of the front of the eyeball). Published studies indicate that consuming high doses of vitamin C orally provides substantial protection to your eyes.32-34
Also known as vitamin B2, riboflavin is responsible for removing oxidized glutathione-glutathione that has been "used up" in the process of buffering free radicals and has become a free radical-bearing molecule itself-from the lens of the eye. Research published in the March 2000 issue of the journal Ophthalmology posited a role for the B family of vitamins as protectors against cataract,35 and a more recent epidemiological study found a link between riboflavin supplementation and decreased cataract risk.36 These new findings indicate that the oral consumption of riboflavin, along with other B-complex vitamins provides a considerable degree of protection against common degenerative ocular disorders.
Long known to be essential for proper eye development, vitamin A continues to be important for the health of the eyes throughout the human life span, particularly the retina. Higher dietary intake of vitamin A has been found to decrease cataract risk.36 It-along with vitamin C and vitamin E-is also needed to regenerate oxidized glutathione. Antioxidants work cooperatively, regenerating one another as they are oxidized themselves in the process of buffering free radicals.37 Vitamin A has been used as a topical agent to treat contact lens problems and external eye disorders for some years now.
Several epidemiological studies have found that higher intakes of vitamin E have a protective effect against cataract.38 Low serum levels of vitamin E correlate strongly with increased cataract risk.39 Researchers at the Institute of Biological Chemistry at the University of Catania in Italy found that chronic administration of vitamin E restored glutathione levels in aging rat lenses to those found in young rats.40 A study by a German research team found that vitamin E deficiency in the lenses of rats worsened the damage done by exposure to ultraviolet radiation.40
Scientific findings continue to establish the benefits of antioxidants and anti-glycating agents in the prevention and treatment of cataract. For instance, research from the USDA Human Nutrition Research Center on Aging has demonstrated that antioxidants such as ascorbate, carotenoids and tocopherol, may protect against cataract formation. A five-year study of over 3000 Wisconsin residents, aged 43 to 86, showed that the risk for cataract was 60% lower among people who reported taking multivitamins or any supplement containing vitamin C or E on a long-term basis (more than 10 years) compared to non-users.32
While the evidence is compelling that individual nutrients reduce cataract risk, a more comprehensive approach would involve the oral ingestion of vitamins A, C, and E, alpha lipoic acid, cysteine and riboflavin along with the topical application of carnosine, vitamin A and vitamin E directly into the eye.
Full references are here.
Adapted with permission from an article in Life Extension, Feb 2003
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