The Aging Eye
...And What Can be Done to Protect it.February 2002
If people live long enough, severe visual impairment or blindness is almost inevitable. 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 changes. A compelling body of evidence indicates that orally ingested antioxidants and anti-glycating agents (such as carnosine) help to prevent and treat eye disease. Unfortunately, the aging process causes reduced blood flow to the eye, thereby inhibiting the delivery of orally ingested supplements into the eye.
This month, we discuss a new way of administering topical agents directly into the eye to help protect against multiple pathologies related to senile eye disorders.
Few people know that poor vision from cataracts affects 80% of people 75 years of age and older. Cataract surgery costs Medicare more money than any other medical procedure, with 60% of those who initially qualify for Medicare already having cataracts. Taking steps to prevent the disease early in life may mean you are one of those 20% of people who enjoy good eye health and never suffer from cataracts.
A cataract is the clouding of the lens of the eye, which reduces the amount of incoming light and results in deteriorating vision. Often described as similar to looking through a waterfall or a piece of waxed paper, the condition makes daily functions such as reading or driving a car increasingly difficult or impossible. Sufferers may need to change eyeglass prescriptions frequently. It is estimated that 20 million people worldwide suffer from cataracts. More than 350,000 cataract operations are performed in the United States yearly.
Many people are born with minor lens opacities that never progress, while others progress to the point of blindness or surgery. Many factors influence vision and cataract development such as age, nutrition, medications and sunlight exposure. High blood pressure, kidney disease, diabetes or direct trauma to the eye can also cause cataracts.
The aging process itself lends to certain metabolic changes that may predispose the lens to cataract development. Some of this occurs due to low supply of oxygen and nutrients, which leave the eye open to free radical damage. According to a 1983 report from the National Academy of Science, cataracts are initiated by free-radical hydrogen peroxide found in the aqueous humor. Free radicals such as hydrogen peroxide oxidize glutathione (GSH), destroy the energy-producing system of the eye, and allow leakage of sodium into the lens. Water follows the sodium, and the edema phase of the cataract begins. Then, body heat in the lens of the eye oxidizes (cooks) lens protein, and it becomes opaque and insoluble (similar to egg protein).
The good news is that a lot of published research exists showing that the cataract progression can be slowed or prevented by the use of natural therapies and minor lifestyle changes. Researchers at Brigham and Women’s Hospital, Harvard Medical School, stated in a scientific research report published in the January/February 1999 issue of Journal of Association American Physicians that, “Basic research studies suggest that oxidative mechanisms may play an important role in the pathogenesis of cataract and age-related macular degeneration, the two most important causes of visual impairment in older adults.” The researchers recommended that additional research be conducted in the promising area of preventive therapy and treatment. Preserving lens function through adequate antioxidant levels and delaying cataract formation by 10 years would result in saving at least half of the $3.2 billion spent annually in cataract surgeries and physician visits.1
Prevention and treatment of cataracts are probably one of the more scientifically documented and beneficial uses of dietary supplements. Free-radical action has been directly linked to and accepted as one of the major causes of cataracts and damage to the healthy eye. Numerous well conceived, scientific studies have been conducted to test and document the possible effect of supplements due to their capability to reduce free-radical damage, and in some cases allow the body to reverse the damage done by free radicals.
Although it is difficult to treat cataracts with oral antioxidants since there is only minimal blood circulation within the eye compared to other parts of the body, nutritional supplements have been shown to reduce the risks of cataracts as well as slow or reverse their progression.
A UK study recently reported that plasma antioxidant levels influenced cataract development, independently of age, gender and other risk factors. The study, published in Ophthalmology [(2001) 108: 1992-1998], looked at 372 men and women, aged 66 to 75 years, born and still living in Sheffield, England. Results showed that the risk of nuclear, cortical and posterior subcapsular cataracts was lowest in individuals with the highest blood concentrations of carotene and beta-carotene, lycopene and lutein, respectively. A decreased risk was not found in relation to vitamin C, vitamin E or carotenoids (zeaxanthin and ß-cryptoxanthin) status. Like other studies that have examined possible preventive links between various antioxidants and age-related eye diseases, such as glaucoma and age-related macular degeneration (AMD), this study helps to pinpoint which nutrients are most helpful for halting specific sight problems. Results also support the argument for supplemental and dietary intake of antioxidants in prevention, and for blood levels being relevant markers for eye disease risk.
Age-related macular degeneration (AMD)
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.
Age-related macular degeneration (AMD) 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.
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 AMD. Patients are being encouraged to increase physical fitness, improve nutrition (including a reduction in saturated fats), abstain from smoking and protect their eyes from excessive light. 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.
Exposure to light and photochemical damage have been suspected factors in AMD,2 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.3 In the early stages of AMD, glutathione has been found to protect retinal pigment epithelial cells from dying.4 Glutathione, which is particularly concentrated in the lens, has been shown to have a hydroxyl radical-scavenging function in lens epithelial cells.5
form of the disease, drainage of the
aqueous fluid is sluggish, so the backup
causes the undue pressure in the eye.
The pressure pinches the blood vessels
that feed the optic nerve, causing the
nerve to die over time.
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, happens due to damage of the retinal blood vessels. The 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.
As it is, in diabetics, the vitreous body has been found to change more rapidly than with just normal aging, changes which 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.6
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.
Glaucoma, usually an inherited disease, results from the build-up of pressure in the aqueous humor, the liquid that fills the area between the cornea and the lens. Generally, the condition develops after age 40, although congenital glaucoma and physical injury to the eye can account for earlier age of onset. Figures show that 1 out of every 25 Americans suffers from glaucoma, and over 62,000 are legally blind due to glaucoma.
Age-related losses of antioxidants increase physical stress on the eye, and oxidative damage ensues.7 For example, diminished antioxidant activity in lacrimal (tear) fluid and blood plasma seems to coincide with progression of glaucoma.8 It’s also proposed that the rate of crystalline damage increases as antioxidant capacity and protease activity declines with age.9
In open-angle glaucoma, the common form of the disease, drainage of the aqueous fluid is sluggish, so the backup causes the undue pressure in the eye. The pressure pinches the blood vessels that feed the optic nerve, causing the nerve to die over time, and leading to decreased peripheral vision, tunnel vision and finally blindness. A rarer form of glaucoma is called narrow-angle or congestive glaucoma, whereby the flow of the aqueous liquid is blocked causing pressure to build up.