Life Extension Final Clerance Sale

Life Extension Magazine

LE Magazine February 2003

image

Preserving Clear Vision

Macular degeneration

The macula is the central and most vital area of the retina. It records images and sends them via the optic nerve from the eye to the brain. The macula is responsible for focusing central vision that is needed for seeing fine detail, reading, driving and recognizing facial features.

image

Age-related macular degeneration is the leading cause of blindness in people over the age of 55, affecting more than 10 million Americans. It is a condition in which the central portion of the retina (the macula) deteriorates. It is equally common in men and women and more common in whites than blacks. The cause is unknown, but the condition tends to run in some families. Macular degeneration affects more Americans than cataracts and glaucoma combined.
There are two forms of macular degeneration: atrophic (dry) and exudative (wet). Approximately 85% to 90% of the cases are the dry type. Both forms of the disease may affect both eyes simultaneously. Vision can become severely impaired, with central vision rather than peripheral vision affected. The ability to see color is generally not affected, and total blindness from the condition is rare, but functional vision is very often lost.

There is little that can be done within conventional medical treatment protocols to restore lost eyesight with either form of the disease. Leading researchers, however, are documenting the benefits of a more holistic approach in the treatment of macular degeneration. Patients are being encouraged to increase physical fitness, improve nutrition (including a reduction in saturated fats), abstain from smoking and protect their eyes from sunlight. Dietary supplementation of trace elements, antioxidants and vitamins is recommended for improving overall metabolic and vascular functioning. Early screening and patient education offer the most hope for reducing the debilitating effects of the disease.

Exposures to sunlight and photochemical damage have been suspected factors in macular degeneration, as well as decreased antioxidant activity responsible for damage control.

An age-dependent drop in glutathione blood status and a significantly lower level of glutathione has been found in older individuals compared to younger ones. Moreover, an increase of oxidized glutathione by-product over time suggests more oxidation and the incumbent higher risk of age-related eye diseases.30 In the early stages of macular degeneration, glutathione has been found to protect retinal pigment epithelial cells from dying.41

Glutathione, which is particularly concentrated in the lens, has been shown to have a hydroxyl radical-scavenging function in lens epithelial cells.19
Lutein and zeaxanthin, the primary carotenoids concentrated in the macula, counter the free-radical forming action of light and oxygen. It's been suggested that macular pigment protects the retina via a dual role that includes scavenging for free radicals and filtering out blue light, which can cause photochemical damage. Some studies have also suggested a link between dietary carotenoid intake and macular pigment density. In fact, eyes with age related maculopathy have revealed significantly lower carotenoid levels in the macula and retina than healthy eyes. Earlier studies had shown that eating dark leafy vegetables was associated with a 43% lower risk of macular degeneration.42

Other studies have been examining how antioxidant status relates to the risk of age-related macular degeneration. The Baltimore Longitudinal Study of Aging, for instance, found that tocopherol, and an antioxidant combination of tocopherol, carotene and ascorbate were protective. Researchers have also been looking at the potentially therapeutic role of individual compounds. For example, a study from Sete, France of 2584 inhabitants showed that higher plasma levels of alpha-tocopherol were inversely related to macular degeneration development and progression.43

The Age-Related Eye Disease Study Research Group43 has shown a protective effect against macular degeneration when higher doses of antioxidants and minerals are taken on a regular basis. The same can be said for cataracts as there is now ample evidence that indicate cataracts have in fact a nutritional connection. It, therefore, appears that prevention is the best solution to postponing or avoiding macular degeneration and cataract surgery. Most eye care professionals to date have told patients affected by these conditions that no treatment exists for macular degeneration and that surgery is the only treatment for cataracts. Emerging research, however, provides new hope for many of these individuals.

Diabetic retinopathy

One of the leading complications associated with diabetes is blindness or other eye diseases stemming from vascular damage to the eyes caused by high blood sugar. Diabetic retinopathy, the most common form of diabetes eye conditions, is caused by damage of the retinal blood vessels. This damage causes the ruptured vessels to leak fluid, restricting oxygen and blurring sight. As the disease progresses, the eye tries to form new vessels on the surface of the retina, which may also bleed or obscure sight by their mere presence. Diligently controlling blood sugar is a major means of preventing or at least slowing the onset and progression of diabetic retinopathy.

In diabetics, the vitreous body of the eye has been found to change more rapidly than with just normal aging. These changes have been implicated in functional disturbances and retinal detachment. The vitreous body is composed of a fine network of hyaluronan gel, collagen, proteoglycans and fibronectin, all of which are susceptible to free radical damage brought on by light and UV damage and glycation.44

A growing body of research shows that oxidation induced by glycation can wreak havoc on the eye. Protein glycation occurs when sugar molecules inappropriately bind to protein molecules, forming crosslinks that distort the proteins and consequently render them useless. Glycation appears to increase oxidative processes, which may explain why both glycation and oxidation simultaneously increase with age. High blood sugar also increases glycation activity, which may also explain the various kinds of tissue damage that characterize advanced diabetes.

Even before an individual is officially diagnosed with Type II diabetes, high serum insulin levels can induce retinopathy. Overweight individuals at risk for Type II diabetes should have their fasting insulin levels checked to guard against a pre-diabetic state (characterized by hyperinsulinemia) that can severely damage the eyes. By following a low glycemic diet, excess serum insulin can be reduced. More on lowering excess insulin will be discussed in an upcoming issue of this publication, but those concerned with diabetic retinopathy can view a new protocol by logging on to www.lef.org and looking under the Health Concerns section for the Retinopathy protocol.

Glaucoma

Glaucoma can result from the build-up of pressure in the aqueous humor, the liquid that fills the area between the cornea and the lens. Pressure build-up sometimes is not the whole story, as optic nerve damage can continue after pressure is returned to normal. It is thus critical to have an ophthalmologist check for optic nerve damage and not just abnormal intraocular pressures.
Glaucoma usually develops after age 40, although congenital glaucoma and physical injury to the eye can account for earlier age of onset. Figures show that one out of every 25 Americans suffers from glaucoma, and over 62,000 are legally blind due to glaucoma.

Useful Supplements for Eye Health

Vitamin E
N-acetyl-cysteine
Vitamin C
Carnosine
Alpha Lipoic Acid
B complex vitamins
Glutathione
Beta carotene
Zeaxanthin
Lutein
Selenium
Zinc
Manganese

Age-related losses of antioxidants increase physical stress on the eye, and oxidative damage are underlying causes. For example, diminished antioxidant activity in lacrimal (tear) fluid and blood plasma seems to coincide with progression of glaucoma. It's also proposed that the rate of nerve damage increases as antioxidant capacity and protease activity declines with age.
In open-angle glaucoma, the common form of the disease, drainage of the aqueous fluid is sluggish. The backup thus causes undue pressure in the eye. The pressure pinches the blood vessels that feed the optic nerve, causing the nerve to die over time, leading to decreased peripheral vision, tunnel vision and finally blindness. A less frequently encountered form of glaucoma is called narrow-angle or congestive glaucoma, whereby the flow of the aqueous liquid is blocked causing pressure to build up.

Evidence is slowly mounting to support the potential effectiveness of antioxidants against glaucoma. A Russian study of 64 patients with primary open-angle glaucoma found that a combined regimen of hyperbaric oxygen and antioxidants over a five-year period stabilized visual function in 80% of patients.45

To read Life Extension's revised Glaucoma protocol, log on to www.lef.org. Click the Health Concerns button and scroll down to Glaucoma.

Preventing degenerative eye disease

Young eyes contain high concentrations of natural antioxidants that protect against cataract, macular degeneration and other ocular disorders. In the aged eye, synthesis of natural antioxidants such as glutathione is reduced, resulting in excessive free radical damage.

According to one published report, "nutritional intervention to enhance the glutathione antioxidant capacity… may provide an effective way to prevent or treat age-related macular degeneration." Even glaucoma has been linked with reduced blood flow and increased levels of damaging free radicals.

Another problem with aging eyes is protein degradation and the formation of advanced glycation end products. Aged eyes fail to break down and remove old proteins, which results in the accumulation of non-functioning protein crosslinks. The resulting accumulation of damaged proteins leads to senile ocular diseases.

The antioxidant supplements consumed by Life Extension Foundation members have been shown to provide considerable protection against senile eye disorders. Unfortunately, aging diminishes circulation to the eye, thereby denying the eyes the full benefits of orally ingested antioxidant and anti-glycating agents.

The good news is that topical eye drop preparations are now available to provide some of the most important nutrients directly into the eye.

Summary

If people live long enough, severe visual impairment or blindness is almost inevitable. Few people know that poor vision from cataracts affects 80% of people 75 years of age and older.

image

The eyes are particularly vulnerable to the effects of aging. Degenerative changes in the eye often begin in middle age. By age 70, a significant percentage of people suffer from macular degeneration, glaucoma and/or cataract. Diabetic retinopathy is also a major cause of visual disability among adults.

A review of the published scientific literature shows that common ocular disorders can be prevented with lifestyle modifications such as following a low glycemic diet, wearing UV blocking sunglasses, avoiding excess saturated fat and not smoking.

A compelling body of evidence indicates that orally ingested antioxidants and anti-glycating agents (such as carnosine) help to prevent and treat eye disease.
Scientific studies indicate that the topical application of certain nutrients may be helpful in the prevention and treatment of common senile eye disorders. In response to these published reports, eye drop solutions have been developed that contain specially designed antioxidants, lubricants and anti-glycating agents. A description of the newest of these topical eye drop preparations appears on the following page.


Purchase Brite Eyes from the Life Extension Foundation


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.

19. Giblin FJ. Glutathione: a vital lens antioxidant. J Ocul Pharmacol Ther 2000 Apr; 16(2):121-35.

20. Kamei A. Glutathione levels of the human crystalline lens in aging and its antioxidant effect against the oxidation of lens proteins. Biol Pharm Bull 1993; 16(9); 170-5.

21. Devamanorharan PS, et al. Oxidative stress to rat lens in vitro: protection by taurine. Free Radic Res 1998 Sep; 29(3): 189-95.

22. Hockwin O. The medical treatment of senile cataract in man: a controlled clinical study on the efficacy of a preparation. Institute for Experimental Ophthalmology, Bonn University, Fed Republic of Germany, Oct 2, 1978 to July 8, 1980.

23. Hockwin O, Ophthalmic Research, 1978, 10 (5-6): 250-8.

24. Oguchi M, et al. Glutathione and eye diseases. Ganka, 1970; 12: 125-32.

25. Fujii S, et al. Effects of an eye drop solution, tathion, on cataract. Nippon Ganka Kiyo 1968; 19:136-42.

26. Kandori F, et al. Clinical use of topical glutathione for cataract. Nippon Ganka Gakkai Zasshi 1967; 71: 689-97.

27. Mitton KP, et al. Modelling cortical cataractogenesis 21: in diabetic rat lenses taurine supplementation partially reduces damage resulting from osmotic compensation leading to osmolyte loss and antioxidant depletion. Exp Eye Res 1999 Sep; 69(3): 279-89.

28. Killic F, et al. Modelling cortical cataractogenesis 22: is in vitro reduction of damage in model diabetic rat cataract by taurine due to its antioxidant activity? Exp Eye Res 1999 Sep; 69(3):291-300.]

29. Devamanoharan PS, et al. Oxidative stress to rat lens in vitro: protection by taurine. Free Radic Res 1998 Sep;29(3):189-95.

30. Brubaker RF, et al. Ascorbic acid content of human corneal epithelium. Invest Ophthalmol Vis Sci 2000 Jun;41(7):1681-3

31. Hankinson SE, et al. Nutrient intake and cataract extraction in women: a prospective study. BMJ 1992 Aug 8;305(6849):335-9

32. Mares-Perlman JA, et al. Vitamin supplement use and incident cataracts in a population-based study. Arch Ophthalmol 2000 Nov;118(11):1556-63.

33. Robertson JMcD. A possible role for vitamins C and E in cataract prevention. Am J Clin Nutr 1991; 53:346S-351S.

34. Taylor A, et al. Long-term intake of vitamins and carotenoids and odds of early age-related cortical and posterior subcapsular lens opacities. Am J Clin Nutr 2002 Mar;75(3):540-9.

35. News from the AAO: New Study Indicates Nutrition May Play Greater Role in Preventing Cataracts. press release from the American Academy of Ophthalmology, March 10, 2000.

36. Kuzniarz M, et al. Use of vitamin supplements and cataract: the Blue Mountains Eye Study. Am J Ophthalmol 2001 Jul;132(1):19-26.

37. Detcho A, et al. Endogenous ascorbate regenerates vitamin E in the retina directly and in combination with exogenous dihydrolipoic acid. Curr Eye Res 1994; 181-9.

38. Robertson JMcD, et al. Vitamin E intake and risk of cataract in humans. Ann NY Acad Sci 1993; 372-82.

39. Olmedilla B, et al. Serum status of carotenoids and tocopherols in patients with age-related cataracts: a case-control study. J Nutr Health Aging 2002;6(1):66-8.

40. Campisi A, et al. Antioxidant systems in rat lens as a function of age: effect of chronic administration of vitamin E and ascorbate. Aging (Milano) 1999 Feb; 11(1):39-43.

41. Ayalasomayajula SP, et al. Induction of vascular endothelial growth factor by 4-hydroxynonenal and its prevention by glutathione precursors in retinal pigment epithelial cells. Eur J Pharmacol 2002 Aug 9;449(3):213-20.

42. Seddon JM, et al. Dietary carotenoids, vitamins A, C and E, and advanced age-related macular degeneration. Eye Disease Case-Control Study Group. JAMA 1994 Nov 9;272(18):1413-20.

43. Delcourt C, et al. Age-related macular degeneration and antioxidant status in the POLA study. POLA Study Group, Pathologies Oculaires Liees a l'Age. Arch Ophthalmol 1999 Oct;117(10):1384-90.

44. Wegener A, et al. Experimental evidence for interactive effects of chronic UV irradiation and nutritional deficiencies in the lens. Dev Ophthalmol 2002; 35:113-24.

45. Popova ZS, et al. Treatment of primary open-angle glaucoma by the method of combimed use of hyperbaric oxygenation and antioxidants. Vestn Oftalmol 1996 Jan-Mar;112(1):4-6.

image


Back to the Magazine Forum