Search by Keyword
Dr. Bernard Presser D.C.
5696 Magnolia Woods Drive
Memphis, TN 38134
If you have any questions, please contact us at 901-417-7905.
More articles coming soon.
CATARACTS -- MACULAR DEGENERATION -- GLAUCOMA
Leonardo da Vinci marveled at the eyes: "Who would believe that so small a space could contain the images of all the universe?" The eyes gather, guide, and filter light, converting tiny amounts of light into the language of the brain.
To transmit and focus light on the retina, the lens must be transparent and pliable. A cataract (Latin for "waterfall") is a cloudy area (opacity) in the lens that blocks light. Its gradually spreading haziness turns the lens milky yellow-white so incoming light is scattered and vision is blurred - like looking through a waterfall or frosted window. As a cataract develops, vision deteriorates and the lens hardens.
Symptoms can include: cloudy, fuzzy, or foggy vision; the impression of having a film over the eye, changes in the way colors are seen, difficulty driving at night because headlights seem too bright, problems with glare from lamps or sun, double vision, frequent changes in eyeglass or contact lens prescription. Cataract formation occurs in 4.5% of persons aged 52 to 64, 18% of those 65 to 74 and 45.9% of those aged 75 to 85. Every year, 400,000 Americans develop cataracts and over one million cataract surgeries are performed at a cost of about $3.5 billion.
The unique, normally transparent structure of the lens is due to the organ-specific proteins - crystallines. There is no protein turnover, so most crystallins present at birth are present at death. The lens "seems to be programmed to remain transparent, under optimum circumstances, until the age of around 120 years." Yet, the clarity of the lens proteins fails prematurely in some individuals due to alterations in the crystallins. The primary cause is thought to be old age, since almost half of people over age 75 develop cataracts and many age related debilities are associated with the protein clumping that clouds the lens. However, over half of people over 75 do not develop cataracts!
Oxidation - "assault by light and oxygen" - is a presumed cause of cataract formation, "although whether it is an initiating or secondary event is not known with certainty." In other words, free radical damage is blamed, though this process has never been observed in vivo (in live, functioning body tissues) but only in vitro(in petri dishes in laboratories). "Because the half-life of most free radicals is extremely short, they cannot be isolated from human or animal tissue. No one has ‘seen' the free radicals from tissues." Their presence is only inferred. Oxidative free radicals may be the result of damage or breakdown of cells, not the cause. Oxidation (free radical breakdown) occurs in nature after injury, not before (e.g., cellular breakdown of a sliced apple is shown by its turning brown).
Despite the theories, cataract development is "generally acknowledged to be a multifactorial process," and the scientific literature "presents compelling evidence that diet may have as much, if not more, to do with cataracts than does aging." Chronic diseases (e.g., diabetes) plus medications used in these diseases are implicated as causes. Even small doses of cortisone or prednisone, for example, can result in cataract. Sunlight has been accused, though historically, evidentially, and experimentally, artificial lighting is more likely the culprit. Prolonged exposure to artificial light damages the lens and retina of laboratory animals. "Infrared light" from incandescent lighting "is powerfully cataractogenic " (cataract-causing).
Excess glucose (sugar) in the lens causes cataract. Lactose and/or galactose from pasteurized milk - (altered and devoid of natural enzymes) -- can create risk due to enzyme deficiency or a tendency for abnormal galactose or lactose metabolism. Other causes include Wilson's disease, Down's syndrome, Paget's disease, tetany, lens injuries, high doses of radiation, and some toxic chemical substances. Daily alcohol consumption and smoking are strongly implicated. Refined sugars, especially if consumed in large amounts, yields alcohol by-products that are often not metabolized properly and collect in the lens, contributing to gradual deterioration. Obese individuals have over 50% higher risk of developing cataract than those of average weight.
Usual medical advice is to "let the cataract ripen until it bothers you" and then have surgery. Indeed, surgery is inevitable if the cataract does advance so it seriously impairs vision. But some experts think surgery is done too often or sooner than required. All or part of the lens is removed and an artificial lens is implanted (otherwise special glasses or contact lenses, which can cause visual distortions, must be prescribed). About 5% of those undergoing surgery experience a change for the worse, and 30% get relief from one symptom only to find another worsens after the operation. Some need subsequent laser treatment.
Prevention is always to be preferred. Studies show that proper nutrition may slow or prevent cataract formation and perhaps reverse it in the early stages. Because free radical oxidation is theorized as the cause, antioxidants have been the most-studied nutrients.
All sources of vitamin A and carotenes (converted into vitamin A in the body) are excellent for overall eye health. Vitamin A helps maintain the normal structure and function of ocular epithelial cells and mucous membranes, and is involved in the synthesis of light-sensitive cells needed for vision. Women who consumed the most amounts of carotenes and vitamin A in their diets had a 39% lower risk of cataract than women who consumed the least amounts.
Foods rich in the carotenoid lutein appear to be more protective for women and foods rich in beta-carotene appear to help men, although "something else" in carotene loaded foods may be responsible. The cooperative nutritional synergism in whole foods is the likely answer. People aged 40 to 70 who did not develop cataracts had higher blood levels of carotenoids and vitamin C than those who developed cataracts. Plasma levels of beta-carotene, vitamin C, and vitamin E are low in patients with sub-capsular cataracts. Serum levels of vitamin E and beta-carotene (the only carotene measured) were lower in patients requiring cataract surgery than in controls.
Vitamin C complex is concentrated in the lens and inner fluid of the eye. It is 30 times higher in the lens than in the blood. The "highest protective effect" against cataract formation "was seen in people with unusually high blood levels of vitamin C." When lenses of persons with cataracts are removed and analyzed, there are lower concentrations of vitamin C than in normal lenses. Levels of the vitamin in the lenses of nonsmokers of normal weight are consistently higher than in overweight smokers, those at highest risk.
Vitamin C (synthetic ascorbic acid) but NOT multivitamin supplementation seemed to offer some protection. However, the researchers did not conclude that ascorbic acid supplements would protect the lens. This trial "did not show whether or not diet alone or the combination of diet and supplementation caused less lens clouding (cataracts)." Whole foods rich in vitamin C complex can provide needed protection, so diet was emphasized. An editorial pointed to the adverse effects of high doses of ascorbic acid to the eyes and other areas. Obviously, aspects of synthetic vitamin disadvantages and whole food advantages were gleaned from the study.
Animals experimentally induced to develop cataract seem to be protected when given ascorbic acid (so-called "vitamin C," a synthetic isolate), but either the tests were done in vitro (in petri dishes with surgically removed lenses) or are of questionable relevance since there are no animals that develop age-related cataract and require a dietary source of vitamin C.
In a human study, ascorbic acid plus citrus extract (a source of vitamin C complex) was much more effective in reducing cataract risk than ascorbic acid alone. The extract's content of bioflavonoids was mentioned as a possible protective component. High dietary vitamin C intake is associated with reduced cataract risk. Increasing foods high in vitamin C during early-stage cataract development resulted in vision improvement in 60% to 90% of cases. Boosting vitamin C and vitamin A enabled a majority of subjects to avoid surgery.
Low plasma vitamin E levels are associated with increased risk of early cataract progression. Subjects with a high intake of vitamin E showed "a significantly lower risk" for lens opacities compared to those with low intake. Vitamin E complex safeguards fatty cell membranes, supports epithelial and endothelial tissues, aids oxygen conservation, and supports cellular differentiation.
Low levels of calcium are associated with lens opacity. Imbalances in calcium and/or magnesium metabolism are often found. Deficits of vitamin D complex may also contribute due to the effects on calcium metabolism. After cataract formation, elevated lens calcium or magnesium levels may occur, suggesting an attempt to maintain the stability of the lens protein gel.
Deficiencies of vitamin B complex (particularly folic acid, riboflavin, and pantothenic acid), vitamin C complex, vitamin A complex, vitamin D complex, vitamin E complex, carotenoids, zinc, selenium, copper, various amino acids, and numerous combinations of these nutrients are associated with cataract development.
B vitamins are essential to eye health. Thiamin (B1) deficiency symptoms include burning or bloodshot eyes, conjunctivitis, unclear or double vision, eye fatigue, sensitivity to light, dimming of vision, changes in eye pressure, possible paralysis of eye muscles, involuntary oscillation of eyes, and dark spots in the visual field. Similar symptoms appear with deficits of other members of the B complex, emphasizing the cooperative relationship. Riboflavin (B2) works with vitamin A in preventing cataracts and eye fatigue. Riboflavin is part of an enzyme system that maintains the lens' supply of glutathione (a protein found in high levels in the lens). Low levels of glutathione exist in "virtually all forms of cataracts." Glutathione, made of three amino acids (glycine, cysteine, and glutamic acid), is a component of glucose tolerance factor along with chromium, niacinamide (B3) and other nutrients important to eye health.
Enzymes, including glutathione peroxidase, catalase, and superoxide dismutase, all decrease in activity with increased cataract development. Only raw food complexes are rich in enzymes and nutrients naturally associated with them, such as zinc, copper, manganese, vitamin C complex, and many other known and unknown components. Enzymes are the "live principles" - the catalysts - that make biochemical reactions work. Synthetic or isolated nutrients do not contain active enzymes.
When zinc is deficient, supplementation will aid about 50% of early-stage cataract patients avoid surgery by halting opacity development. Zinc plays a vital role in eye nutrition and is involved in vitamin A metabolism, so deficiency of either nutrient can result in similar symptoms. A decrease of selenium has been found in the aqueous humor and serum of cataract patients.
The herb bilberry may guard against cataract development, assist eye ailments associated with high blood pressure, aid nearsightedness, reduce eye strain from pollution, help diabetes-induced glaucoma, and other eye disorders. Bilberry extract used in combination with vitamin E stopped cataract development in almost 97% of patients with senile cortical cataracts. The berries contain rutin, flavonoids, and other nutrients that strengthen capillary walls, reduce permeability of capillary membranes, and improve delivery of blood and oxygen to the eyes. Bilberries seem to aid the regulation of glucose levels in the blood and alcohol sugars in the eye, excesses of which can lead to cataract development. One study found marginal protection in participants taking a multivitamin, but noprotection from synthetic vitamin E or C. Other studies did not find a protective effect from multivitamins or didfind protective effect with synthetic vitamin C and/or E supplements. Why the inconsistencies? Each research group admits that people who take supplements differ in other ways - particularly diet - that relate to the risk of cataract development. So many scientists recommend whole, natural foods as the best source of eye protection.
Cataract development in rats was slowed by changing their diet from commercial rat chow to whole, nutrient-rich, foods. Highly refined and/or processed foods are the human equivalent of commercial rat chow. Switching to natural whole foods and concentrated food complex supplements is always advantageous.
Cataract-free subjects consume more fresh vegetables and fruits -- excellent sources of carotenes, vitamin C complex, most B vitamins, minerals, trace minerals, and, when raw, enzymes. Oils in vegetables, grains, raw nuts and seeds provide vitamin E and essential fatty acids. Natural cheeses, unrefined oils, and other healthful foods have been associated with lowered risk. Those eating only few vegetables and fruits had four to eight times the risk for cataract. The scientists stressed the need to eat more and a variety of fruits and vegetables, and "not just in their later years." It takes decades to develop cataracts. Identifying or isolating nutrients that help, eludes researchers due to the complexity and synergism of food. "As with other degenerative conditions...it looks like fruits and vegetables are the heroes of the day."
When fractionated, manufactured synthetic vitamin, mineral, or multivitamin supplements are used, "studies have been less clear." The cooperative function of elements in whole foods may "be responsible" for the consistent positive findings. "There's no conclusive evidence that [fractionated or synthetic] antioxidant supplements (with or without added minerals) are going to help". So far, the only thing known to help is fresh, natural, whole foods. When people with and without eye problems are studied, "one of the biggest differences" that shows up is "in eating habits."
Every year up to 200,000 Americans are diagnosed with "age-related macular degeneration" (AMD) and many eventually become legally blind. AMD affects about 25% of people aged 65 and older, almost 30% of those over 75. Currently, 1.5 million Americans have seriously impaired vision, and another 10.5 million show early signs of this "most common uncorrectable cause of vision loss in the elderly."
This disease is a deterioration and impairment of the outer layers - retinal pigment epithelium or RPE - of the retina. The RPE coats (protects) the retina and nourishes the underlying photoreceptor cells. Specifically affected is the oxygen rich, central part of the retina, the macula, which contains densely-packed, light sensitive cells and is responsible for acute, central vision (reading words, recognizing faces, discerning other fine details).
"AMD is one of the most complex and poorly understood diseases of the eye." Cells of the RPE gradually accumulate sacs of molecular debris: remnants of normal or damaged (abnormal) molecules within RPE cells or from phagocytized (engulfed and digested) rod and cone membranes. Progressive accumulation of these residues contributes to increased deterioration of the RPE. Loss of vision results from death of visual (retinal nerve) cells due to the degeneration of the RPE cells or the effects of leakage from neovascular (new blood vessel) formation invading the region.
Normally, old disks from the outer segment of rods in the retina slough off, are digested and removed. The inner core of the rods produces new disks, pushing old disks into the RPE for digestion. This "shedding" and digestion of old disks is critical to proper visual function of the rods. In the AMD eye, these old or damaged disks (cellular debris) are not digested; they accumulate and interfere with visual acuity. Some scientists believe that abnormal chemicals (poisons) may damage the retinal cells, causing increased "shedding" and accumulation. Retinal enzymes can break down many chemicals, but with deficiencies of nutrients needed for optimal enzymatic function, or with overwhelming toxic insult, the enzymes may not be able to keep up.
There are two types of AMD, "and the causes of both are unknown."
In the "dry" or atrophic form, the vision may be unchanged at least in the beginning but there are changes in the macula including pigmentary irregularity and the appearance of drusen. The pigmentary alterations are due to damage of the RPE cells. Drusen are small yellow spots appearing on the retinal pigment cells, thought to represent the buildup of waste products (or toxic substances) that can no longer be metabolically processed by the RPE.
In the "wet" or disciform type, there is fluid (serum) and blood leakage from a buildup of tiny abnormal blood vessels and tiny mounds of fibrous (scar) tissue that penetrate the macula, causing a serious and dramatic loss of vision. This type is usually progressive. Within a few years, only coarse peripheral vision remains and, with detailed vision gone, reading, driving, and other activities are no longer possible.
The dry form, though less dangerous, can progress to the more serious wet form. The majority of middle-aged and elderly Americans show signs of the dry form, and 1% of adults already have the wet form. Only 10%-20% of all cases are the wet type, but they account for almost 90% of cases of legal blindness in the U.S.
Blindness may arise from abnormal growth of new blood vessels in the retina, "triggered by oxygen deprivation." The extra blood vessels may be a compensative attempt to get more blood flow, oxygen and nutrients to the area. Causes may include: (1) systemic vascular disease (weakness of vascular walls and placement of plaque "patches") or (2) vasoconstriction (blood vessel narrowing), or (3) cellular damage, or (4) excessive cellular breakdown due to deficiencies or insult (chemical poisons; processed, altered, refined, chemicalized foods; artificial light sources, etc.).
For example, cigarette smokers have nearly a threefold increased risk of AMD than nonsmokers. Smoking depletes the body of nutrients (especially vitamin C complex needed for healthy, strong blood vessels), causes vasoconstriction, adds damaging poisons, and diminishes oxygen.
"Retinal cells do not replicate" so once sufficient degeneration of these cells takes place, regeneration may be impossible.
However, since the scarring occurs in the RPE - an outer layer - doctors think that removal of that injured layer before the underlying membrane and tissue is damaged, could result in regeneration of RPE cells and photoreceptor cells beneath. Experiments on monkeys and humans, using surgery and laser beams, have been encouraging. But lasers burn out nearby photoreceptors. And, persons suffering with AMD longer than a year (excessive damage) probably would not benefit.
Interest has focused on the theory of "free radical production and subsequent lipid peroxidation mediating damage," as well as roles of foods and supplements that may block AMD "by scavenging free radicals and inhibiting these oxidative processes." It is presumed AMD is "just another" aging consequence due to the "destructive" influence of light. However the escalation of AMD is a recent phenomenon and many elderly individuals never develop it. Researchers have "speculated" that some nutrients in foods might protect against the slow march of AMD.
Dozens of studies show that people who eat foods rich in antioxidants (and a multitude of other nutrients not studied) tend to have thicker macular pigments. People who suffer with AMD have low blood levels of antioxidants, the protective agents for the functional parts of a nutrient complex. Presence of the antioxidant components in the blood would indicate the concurrent presence of the rest of the complex (unless the isolated antioxidant was pharmacologically administered).
Individuals increasing their consumption of spinach and corn for 15 weeks experienced increased density of macular pigments. It was assumed the antioxidants zeaxanthin and lutein were responsible. Foods abundant in beta-carotene (one of many needed carotenoids), vitamins C complex and E complex, zinc, selenium, copper, catalase, superoxide dismutase (zinc/manganese and zinc/copper forms), glutathione peroxidase (requiring selenium, zinc, and copper), glutathione reductase (requiring riboflavin), metallothionein (needing zinc), and retinal dehydrogenase (requiring zinc), lycopene, zeaxanthin, lutein, and other nutritives have been found to be supportive to the health and function of the macula, where they are found in abundance. Low levels of carotenoids, vitamins E and C complex, lycopene, and other nutrients are found in persons with AMD. Yet studies testing isolated or synthetic versions of these nutrients have produced conflicting or disappointing results.
Administration of lutein for 140 days produced some increase in macular density in two subjects. A few studies using "broad spectrum vitamin and mineral supplements" have reported vision protective benefits. Vitamin C supplementation was associated with a decreased incidence of early AMD. High plasma levels of vitamin E and vitamin C complex, and carotenes were associated with increased protection. However, a large epidemiologic study found that the use of isolated or synthetic antioxidant supplements was not generally beneficial.
Inverse associations were found between advanced AMD and blood levels of four carotenoids tested. Beta-carotene has been much studied, yet it never occurs by itself in foods. It is always accompanied by other carotenoids, minerals, trace minerals, amino acids, enzymes, vitamin complexes, etc. "And in their naturally occurring state, carotenoids and other plant chemicals probably work together in just the right combinations and just the right proportions to protect against disease."
For example, eating greens such as collard, beet, and mustard greens, significantly lowers the risk of AMD. "There's no way in the foreseeable future that this exquisitely complex chemical structure could ever be reproduced [manufactured] in a laboratory and put into pills that would offer the same health benefits." No fragmented, laboratory fabricated supplement can duplicate nature. A variety of nutrients work together and are integral to the function of their associated nutritives in producing benefits. "We cannot judge which food items or which specific nutrients are important for" the protective and favorable effects.
Eyes need vitamin A complex to produce rhodopsin, the retinal light-sensitive pigment. When exposed to light, rhodopsin "trips a switch" that sends a signal along nerves to the part of the brain responsible for sight. Every time rhodopsin performs its job, a bit of vitamin A is used up.
A study comparing persons with either dry or wet AMD and persons without AMD found that a diet low in vitamin A-rich foods was associated with significantly higher risk. Elderly people who regularly ate at least five servings of vegetables a week - foods high in carotenoids - cut their risk of AMD by almost half. Especially helpful were dark green, leafy vegetables (rich in chlorophyll). The greater the vegetable consumption, the lower the risk. This study also found that supplements of vitamins A, C, E, and retinol - all synthetic fractions - did not decrease the risk. "No one knows why the vegetables appear to decrease the risk of macular degeneration." Could it be that the whole, cooperative complex is greater than the sum of the individual - or human fabricated - parts?
Minerals such as selenium and zinc are important to a normally functioning retina. The RPE contains a high concentration of zinc and copper. RPE zinc content is decreased "remarkably" when there are signs of AMD. Many retinal enzymes require zinc for proper function. Zinc supplementation can increase the activity of these enzymes by as much as 190% "which might affect eye function and visual acuity." Selenium, zinc, vitamin C complex, and vitamin E complex may aid in the absorption of abnormal chemicals in the eye. Significant increase of vision was reported among persons with AMD who increased intake of organic zinc. Zinc supplementation resulted in improved visual acuity and fewer adverse changes in the retina, including far less growth of abnormal blood vessels. Caution should be used if zinc - by itself rather than in food complex form - is taken in large amounts or for long periods of time since it can imbalance other minerals and/or cause harm. People with the greatest intake of zinc from foods had a lower risk for early AMD than those with the lowest intake of zinc from foods. Similarly, odds of getting AMD were lower in those with the highest intake of vitamins C and E complexes from foods.
Ginkgo biloba, an herb rich in bioflavonoids and rutin, is used to treat vascular problems. Ginkgo has been used to assist visual disorders and may be beneficial in AMD; some sufferers find it has helped.
Using any one vitamin, mineral, or other isolated or manufactured ‘nutrient' will not help determine the role of nutrition in the development or progression of AMD. Researchers cannot "sort out the complex interplay between certain nutrients and a given health benefit." In the meantime, many scientists advise people to consume a diet rich in fresh fruits and vegetables.iii
Glaucoma is the third major cause of blindness (almost 12,000 cases a year) in the U.S. There are many forms; the most common is chronic open-angle glaucoma in which fluid pressure within the eye gradually rises and, in time, damages the optic nerve, narrowing the field of vision and eventually leading to blindness. Referred to as the "sneak thief of sight," there are often no symptoms initially and sight is lost gradually. Both eyes are affected. It can begin in middle age but is more common in people over 60.
The normal range of intraocular (inner eye) pressure is 10 to 20 mm Hg. In glaucoma, the pressure can rise as high as 70 mm Hg, though pressures only 25 to 30 mm Hg can cause vision loss when sustained for years. The rise in pressure results from a build up of aqueous humor, a transparent, nutrient-providing liquid produced in the front chamber of the eye (between the cornea and lens). Normally, the fluid passes to the back chamber, circulates over the lens and toward the pupil, then over the rim of the iris and back to the front chamber. At the outer edge of the front chamber is a sieve-like meshwork of tiny fibers and canals (ducts) that constantly drain the aqueous humor at the same rate it is produced.
If this drainage system fails to work properly, fluid buildup creates increased pressure throughout the eye. Tiny capillaries that provide nourishment for the minute nerve fibers within the eye are squeezed. Eventually, some of these nerve fibers - such as those responsible for transmitting peripheral vision - die. Dark spots appear in the visual field. In the final stages, tunnel vision or blindness occurs.
What causes the blockage of aqueous humor? Insult or injury to the eye with unresolved inflammation and repair might be involved, though the cause is usually "unknown." It is known that white blood cells, red blood cells, and tissue debris can obstruct the fluid -- all these are increased during inflammation with attempted repair of injured tissue. Insufficient blood supply, nerve supply, or nutrient reserves, and/or interference with the innate inflammation system can contribute to incomplete repair and residual debris.
Glaucoma is commonly treated with medications which experts agree are not very effective. When medication is no longer effective at all or when an acute attack occurs (severe eye pain and sometimes abdominal pain, nausea, vomiting), surgery or laser treatment is recommended to release fluid pressure. Surgery, too, is often ineffective.
Although glaucoma is associated with a rise in fluid pressure, most people with high eye pressure never develop glaucoma. It is merely a risk factor. Only 1% to 30% of the 20 million people with elevated pressure go on to develop glaucoma each year. In fact, "intraocular pressure above the normal range...is no longer part of the definition of the disease." From 25% to 30% of those who do develop glaucoma have normal eye pressure. The "air puff" or other test used to measure eye pressure is not enough to diagnose glaucoma. Other tests are needed (optic disc inspection, visual field test, and more). High blood pressure, diabetes, African ancestry, myopia, and other risk factors need to be considered.
Regardless, some doctors treat everyone with elevated pressure. The drugs have side effects and "may do more harm than good" especially in people who would not develop the disease. Some studies found no difference in pressure between untreated people and those using eye drops. Some people (10% by one estimate) who take glaucoma medication will lose their vision to glaucoma anyway. Further, intraocular pressure can be increased by some prescription drugs such as glycosteroids, tricyclic antidepressants, nitroglycerin, and the recreational drug, amyl nitrite. All steroid hormone drugs can cause or advance glaucoma, including DHEA or other cortisol-type steroids.
Unfortunately, simply waiting and watching individuals with elevated pressure can be disastrous since, by the time a problem is detected with standard tests, about a third of the optic nerve may be destroyed. The dilemma is how to identify people with high eye pressure and those with normal pressure who will develop glaucoma.
The optic nerve passes through a bed of supportive elastin, stretchable connective tissue through which nerve bundles pass. In glaucoma, the elastin appears as if it had been over-stretched like the elastic waistband of an old pair of underwear, "with wavy lines and curlicues." At the back of the eye, this would squeeze or crush nerve fibers. Ganglion nerve cells connected to rods and cones can be choked off, unable to send or receive nourishing substances through the nerve fibers. Tests on patients, animals, and human eyes donated by glaucoma patients after death, show damaged ganglion cells.
Elastin requires specific amino acids, trace minerals (e.g., manganese), and other nutrients. Blood vessel walls and elastin depend on vitamin C complex (including its rutin and bioflavonoids) and vitamin E complex for strength, integrity, and proper elasticity. The aqueous humor normally contains a significant amount of vitamin C. The isolated, synthetic ascorbic acid has been used to treat glaucoma, but is not considered a "cure." A deficiency of vitamin C complex and lowered tissue chromium are associated with increases in intraocular pressure (IOP). Glaucoma, in fact, "appears strongly associated" with a deficiency of vitamin C intake. Vitamin C complex supports strong ciliary muscle eye focusing activity. Persons with primary glaucoma who used rutin had a 15% or greater reduction in IOP after only four weeks. Use of the whole C complex would no doubt yield much better results. In some cases, glaucoma may be an indication of adrenal gland fatigue and thus hormonal disruption. Vitamin C complex with its tyrosinase (organic copper enzyme) intact is imperative to adrenal health. Vitamin B complex and other nutrients are also essential to the adrenals as well as the nervous system. Anxiety and "stress" are frequently associated with glaucoma.
Thiamin (B1) deficiency may contribute to optic nerve atrophy in glaucoma. Riboflavin (B2) deficiency can produce dark spots in the visual field and is needed for vitamin A utilization. Pyridoxine (vitamin B6) may be involved in eye pressure regulation and may help prevent glaucoma. Other members of the B complex have also been found to be supportive. This complex contains elements that assist proper vasodilation, are antispasmodic (relaxing) and support fat metabolism. Choline and inositol, important in normal nerve transmission, fat metabolism and transport, have been found to be helpful.
The IOP of some patients with vitamin A deficiency dropped after supplementation. Ingestion of fish oils - high in vitamin A complex, fatty acids (including omega-3), vitamin D complex, and more - appear to reduce the pressure of fluids in the eye. Zinc is involved in vitamin A metabolism, so an insufficient supply of one can affect the other. In glaucoma patients the ratio of zinc to copper may be decreased in the aqueous humor due to reduced zinc and/or increased copper.
Calcium and vitamin D complex assist proper dehydration of the sclera. If this fibrous tissue which covers the "white" of the eye (from the optic nerve to the cornea) has excess fluid, the IOP may build up and lead to elongation. A diet high in refined carbohydrates (refined sugars, refined flours, etc.) results in deficiencies of many nutrients and an overabundance of phosphorus can further reduce calcium levels and increase IOP.
Carbamide (urea), produced by the liver, is an osmotic regulator. That is, it regulates the passage of liquid through membrane, separating solutions of different concentrations. It can assist the balance of pressure by which water-soluble toxic substances or excessive products of metabolism can be eliminated. Carbamide may therefore assist in balancing fluid pressure in the eye.
A large case-controlled study demonstrated an association between glaucoma and the intake of trans fatty acids (hydrogenated vegetable oils such as margarine). Caffeine in coffee was found to significantly increase IOP. Alcohol, tobacco, coffee, regular tea, and chocolate all may decrease circulation to the eye. iv
Mounting evidence points to nutrition as a major factor in the prevention and early treatment of eye disorders. Results of supplementation with synthetic, and/or isolated substances have been disappointing whereas whole foods keep appearing as benefactors.
Years ago, Dr. Royal Lee observed that the eye conditions of some patients improved while they were taking food concentrate supplements and eating a whole food diet for another ailment. He reasoned that these responses occurred when imbalances or deficiencies were corrected so that "body tissues assume their normal structure and function." In many cases, "nutritional treatment," if extensive, specific, and begun in the beginning stages, can be a significant aid to recovery. V
i Vander, Sherman, Luciano, Human Physiology, 5th Ed., NY: McGraw-Hill, 1990, pp.230-241.
ii Nutr Aspects Ambul Care, HHN0429, April 1992; W. Douglass, Second Opinion, Vol.V11, No.3, March 1997, p.8; L. Wong, et al., J Epidem & Comm Health, Vol.47, No.1, Feb 1993, pp.46-49; E. Somer, The Nutrition Report, Vol.11, No.7, July 1993, p.50; Science News< Vol.137, No.12, 24 Mar 1990, p.189, Health Letter, Vol.9, No.5, Mar 1993, pp.5-7; Vol.9, No.7, July 1993, pp.1-2; J. DeCava, Real Truth About Vitamins, Columbus: Brentwood, 1996, pp.64-82; Health News, Vol.3, No.9, 15 July 1997, pp.1-2, Vol.3, 7 Oct 1997, p.8; Amer Health, Jan/Feb 1993, p.9; J. Manson, Amer J Preven Medicine, Vol.10, No.3, May/June 1994, pp.156-161; Univ of CA Berkeley Wellness Letter, Vol.12, Is.2, Nov 1995, pp.2-3, Vol.12, Is.12, Sept 1996, pp.1-2; Brit Med J, S. Harkinson, Vol.305, 1992, pp.335-339, & P. Knekt, et al., Vol.305, No.6866, 5 Dec 1992, pp.1392-1394; Am J Clin Nutr, J. Mares, Vol.66, No.4, Oct 1997, pp.739-740, 10 & J. Robertson, Vol.53, 1991, pp.3465-3515, & A. Taylor, Vol.62, No.6(S), Dec 1995, pp.1439-1447; & P. Jacques, Vol.66, No.4, Oct 1997, pp.911-916; V. Courey, Nutr Res, Vol.12, 1992, pp.915-922; R. Rouhiainen, Amer J Epidem, Vol.144, No.5, 1 Sept 1996, pp.496-500; S. Vitale, Inv Ophth V, Vol.32, 1991, p.723; J. Seddon, et al., Amer J of Public Health, Vol.84, No.5, May 1994, pp.788-792; Lancet, E. Blau, Vol.347, No.9001, 2 Mar 1996, p.626, & G. Johnson, Vol.351, No.9107, 28 Mar 1998, pp.925-926; Arch of Ophthal, R. Sperduto, et al., Vol.111, 1993, p.1246 & J. Perlman, et al., Vol.114, 1996, pp.991-997; C. Lowe, Energy Times, Vol.7, No.4, April 1997, pp.42-49; S. Karakucuk, et al. ACTA Ophthal Scand, Vol.73, 1995, pp.323-332; C. Gruning, Health News & Review, Vol.2, No.3, 1992, pp.1-3; J. Scheer, Health Freedom News, Vol.16, No.6, Nov/Dec 1997, p.30; N. Fuchs, Women's Health, Vol.V, No.6, June 1996, pp.1-4; L. Lindner, Amer Health, July/Aug 1990, pp.92-93; A. Tavani, Ann of Epidem, Vol.6, No.1, Jan 1996, pp.41-46; Ann Ophthal Clin Ocul, Vol.115, 1989, p.109; M. Werbach, Nutritional Influences on Illness, Tarzana: Third Line Press, 1993, pp.195- 202.
iii R. Young, Sury Ophthal, Vol.31, No.5, 1987, pp.291-306; Science News, Vol.146, No.20, 12 Nov 1994, p.310, & Vol.152, No.13, 27 Sept 1997, p.198, & Vol.138, No.13, 29 Sept 1990, p.207; Science, Vol.276, No.5319, 13 June 1997, pp.1706-1710, & Vol.254, 22 Nov 1991, p.1109, & Vol.277, No.5333, 19 Sept 1997, pp.1765-1766; JAMA, Vol.271, No.21, 1 June 1994, pp.1695-1696, & Vol.277, No.9, 5 Mar 1997, pp.698-700, & L. Levin, Vol.273, No.21, 7 June 1995, pp.1703-1706, & S. Hankinson, et al., Vol.272, No.18, 9 Nov 1994, pp.1455, & J. Seddon, et al., Vol.272, No.18, 9 Nov 1994, p.1413-1420, & Vol.273, No.23, 21 June, 1995, p.1835; Health News, Vol.3, No.17, 30 Dec 1997, p.7; J. Bishop, Wall St J, 8 May 1992, p.86; C. Northrup, Health Wisdom for Women, Vol.5, No.3, Mar 1998, pp.5-6; D. Newsome, Ophthal Prac, Vol.12, No.4, 1994, pp.169-171; M. Snodderly, Am J Clin Nutr, Vol.62, No.6(S), Dec 1995, pp.1448-1461; Arch of Ophthal, J. Perlman, Vol.113, 1995, pp.1518-1523, & S. West, et al, Vol.112, 1994, pp.222-227; Inv Ophth V, J. Mares-Perlman, et al., Vol.34, 1993, p.1133, & J. Seddon, et al., Vol.34, 1993, p.1134; Eating Well, Vol.6, No.6, July/Aug 1996, p.37, & Vol7, No.9, Nov 1997, p.50, Vol.5, No.4, Mar/April 1995, pp.38-39; G. Liou, et al. FASEB J, Vol.12, No.1, Jan 1998, pp.129-138; Prim Care Med Drug Alerts, Vol.XV, No.5, May 1994, pp.38-39; Health, Vol.10, No.5, Sept 1996, p.128; Health Facts, Vol.XX, No.188, Jan 1995, pp.1,4,6; J. Wright, Health News Naturally, Winter 1996, p.2; D. Newsome, et al. J Trace Elem & Exper Med, Vol.8, 1995, pp.193-199; Compl Med for Phys, Vol.2, Is.3, April 1997, p.19; M. Larkin, Lancet, Vol.351, No.9096, 10 Jan 1998, p.117; N. Fuchs, Women's Health Ltr, Vol.VII, No.4, Apr 1998, p.7; C. Lowe, Energy Times, Vol.7, No.4, Apr 1997, p.46; M. Werbach, Nutr Influences on Illness, pp.416-419.
iv S. Blakelee, NY Times, 6 Oct 1991, p.4B; Amer Health, Vol.XII, No.8, Oct. 1993, p.24, & Vol.XV, No.7, Sept 1996, pp.71-73; Health Facts, Vol.XX, No.193, June 1995, pp.4-5; M. Sator, et al., Lancet, Vol.348, No.9029, 14 Sept 1996, pp.761-762; G. Vogel, Science, Vol.275, No.5300, 31 Jan 1997, p.621; Healthline, Vol.16, No.3, Mar 1997, pp.3-4; True Health, Summer 1997, pp.19-20; M. Passeo, et al., Arch Ophthal, Vol.109, 1991, pp.1096-1098; Doctor's People, Vol.4, No.7, July 1991, p.3; C. Gruning, Health News & Review, Vol.2, No.3, 1992, pp.1-2; J. DeCava, Adj Tips, Vol.4, No.1, pp.3-6; W. Douglass, Second Opinion, Vol.8, No.1, Jan 1998, pp.3-5; M. Werbach, Nutri Influ Illness, pp.297-302; G & J Kirschmann, Nutrition Almanac, NY:McGraw-Hill, 1996, p.283.
v R. Lee, Therapeutic Food Manual, Milwaukee: Lee Fndtn Nutr Res, 1957, p.69.
Originally published as an issue of Nutrition News and Views, reproduced with permission by the author, Judith A. DeCava, CNC, LNC.
Find all the facts about human eye diseases and the facts about glaucoma. We have the best natural remedies for eye diseases including macular degeneration treatment for eye cataracts and more.