Articles

Ocular Health

Introduction

The visual system provides a supremely efficient means for the rapid assimilation of information from the environment to aid in the guidance of behavior. (1) The importance of eye examinations cannot be over emphasized, as an eye examination often reveals signs of systemic disease and intrinsic ocular disorders, as well as the effects of drugs that are either administered systemically or instilled into the eye itself. The eyes are mounted in a prominent position on the head, and thus are vulnerable to a myriad of disturbances.

Vision can be damaged by trauma, exposure, or infection. Diseases intrinsic to the eye including glaucoma, cataracts, or retinal detachment, may also affect vision. Many systemically acquired diseases may have ocular symptoms, as do some of the neurologic diseases affecting areas of the cortex, thalamus, and brainstem that are devoted to visual perception or to the execution of eye movements. Although it may be determined that a patient requires specialized eye care, the initial examination and assessment of visual acuity, pupils, eye movements, visual fields, and fundi lies within the realm of all physicians. The slit lamp and ophthalmoscope provide the best view of the transparent anatomy of the eye and afford the opportunity to directly inspect blood vessels.

The eye is composed of three anatomical subdivisions: the eyelid, the external eye structures, and the internal eye structures. (2) The eyelids have an external covering of skin and are lined internally by conjunctiva. The purpose of the eyelids is to protect the eye from foreign objects, bright light, and to distribute fluids over the surface of the eye to prevent drying. Eyelids normally cover the upper border of the iris, and contain several anatomical features that provide the protection and lubrication needed for normal vision. The eyelashes help protect the eyes from foreign material; and Mebomian glands secrete sebaceous materials that lubricate the inner eyelids. The eyelids are controlled by the oculomotor nerve (cranial nerve 3), the facial nerve (cranial nerve 7), and the sympathetic nervous system. The conjunctiva, a thin translucent membrane, is richly supplied with blood vessels, covers the anterior eye, and folds into the inner eyelid. The palpebral conjunctiva covers the inner aspect of the eyelids, and the bulbar conjunctiva coats the sclera. It joins the corneal margin at the limbus.

The external eye includes the lacrimal glands and lacrimal sac located in the temporal region of the bony orbits that house the eyeball. Ophthalmic lacrimal, sebaceous, and mucous glands produce tears, which flow over the corneal surface, then collect in the conjunctival cul-de-sac and drain through the puncta. The lacrimal drainage system then directs tears into the nasal cavity. Disruption in any of these systems may cause an abnormality of tear formation, composition, or flow process.

Tears are necessary to provide nutrition for anterior surface cells; aid in metabolism, secretion, waste removal, and maintenance of optical clarity; and exert an antibacterial action. The preocular tear film is actually a three-layer system. Mucin is the innermost layer and adheres to the corneal and congunctival cell microvilli. Mucin, produced by goblet cells, changes the normally hydrophobic surface of the corneal epithelium to hydrophilic by a surfactant action, enabling it to become wet. (3) , (4) The intermediate layer is aqueous and can spread more easily over the conjunctiva as a result of the action of mucin. The aqueous layer composes about 90 percent of the thickness of the tear film, contains chemicals responsible for corneal metabolism (e.g., glucose, inorganic ions) and the antimicrobial agent lysozyme. The outermost layer of tears is a lipid layer, which helps retard evaporation and prevents instability or rupture of tear film. Aging and certain hormonal disorders may alter the composition of this lipid layer, resulting in dry eye.

The internal eye is the area immediately behind the cornea. It is divided into three concentric layers: the sclera, which is the whitish creamy outer layer; the choroid or darkly pigmented middle layer, rich in veins and capillaries that supply nutrients to the inner concentric layer, known as the retina. It is within the retina that rods and cones are housed that transform light into electrical impulses which are transferred over the optic nerve to the visual cortex of the brain. The veins and arteries that supply the retina are seen in the posterior section of the eye at the optic disc. The optic disc is the point of entry of the optic nerve. At the center of the optic disc is a physiologic cuplike depression that is normally less than one-third the diameter of the disc. Another important retinal landmark is the fovea centralis, or point of central vision. The fovea centralis is located in the center of the area known as the macula, which is very dense in rods and cones. Ciliary muscles control the lens to focus light on the retina, particularly on the fovea centralis. The iris lies before the lens and the opening creates the pupil.

The eyeball itself consists of an anterior and posterior chamber. The jelly-like fluid of the vitreous body fills the posterior chamber of the eye and serves to transmit light and supports the retina and lens. The aqueous humor is the clear liquid that fills the anterior and posterior divisions of the anterior eye. The ciliary body produces aqueous humor, and continuously replenishes the supply. Fluid that is secreted into the posterior chamber of the anterior eye flows through the pupil into the anterior chamber. It is reabsorbed through a network of trabiculae into the canal of Schlemm, a venous channel at the junction between the iris and the cornea. Any obstruction in this pattern of flow causes acute or chronic increase in intraocular pressure (e.g., glaucoma).

Intraocular pressure is measured by tanometry, which measures the resistance of the eyeball to an applied force. The risk of visual field loss increases with increased ocular pressure; however, patients react differently, with some patients demonstrating no optic disc damage with high intraocular pressures (IOP), while others may demonstrate considerable damage when IOP is still within a “normal" range. However, reduction of IOP, no matter what the level of pretreatment IOP, slows or prevents progression of visual field and optic disc changes in most patients diagnosed with glaucoma.

Autonomic and cranial nerves control eye movement. The third cranial nerve (oculomotor nerve) constricts pupillary muscles and directs eye movement in the fields of vision, except the lateral and downward vision to the nose. The fourth cranial nerve controls downward, inward eye movement, and the sixth cranial nerve controls lateral eye movement. Six extraocular muscles attach to the sclera and ocular orbit. Muscular imbalances cause various visual disturbances such as strabismus (wandering eye), diplopia (double vision), and ptosis (drooping of the upper eyelid). (5)

Checking a patient’s refractive state, visual acuity, pupils, eye movements and alignment, stereopsis, color vision, and visual fields are components of an assessment of visual function. In emmetropia, parallel rays from infinity are focused perfectly on the retina. In myopia, the globe is too long, and light rays come to a focal point in front of the retina. (6) Correction requires a diverging lens in front of the eye, as near objects can be seen clearly, but distant objects cannot. In hyperopia, the globe is too short and a converging lens must be used to supplement the refractive power of the eye. In patients with astigmatism, the corneal surface is not perfectly spherical, necessitating a cylindrical corrective lens. Often, patients develop presbyopia after the age of 40. The lens of the eye increasingly hardens, resulting in a loss of accommodation that generally makes reading and close work difficult. Accommodation shifts the eye’s focus from distant objects to near ones. In normal binocular accommodation, the eyes converge, the pupils constrict, and the lenses thicken, resulting in a bending of light rays on the retina. It is also a function of compliance of the lens to refraction.

A cataract is a clouding of the lens sufficient to reduce vision. Most cataracts develop slowly as a result of the aging process, and lead to a gradual reduction in vision. The only treatment is surgical extraction of the opacified lens. Remarkable technical innovations have made it possible to aspirate the cataract while leaving the lens capsule intact. A plastic or silicone lens is then placed in the empty lens capsule, replacing the natural lens, and most generally leading to improved sight in approximately 95 percent of patients.

The spatial arrangement of optic nerve fibers in the optic nerve tract divides the eye into visual fields. If a lesion disturbs the flow of impulses along one or more of the optic pathways, visual fields are lost. To use a possibly oversimplified example, if a patient has a stroke that affects the right optic pathway, he/she may develop hemianopsia, or defective vision/blindness in half of the visual field. If the stroke affects the right side, the patient’s left visual field is affected since the image projected by the eye reverses the field. The term used to describe this condition is left homonymous hemianopsis. The patient would only see the right half of his environment, since the right optic tract impairment has affected his ability to see the left side of his visual field. Using visual field defects can help vastly in attempting to localize the point of a lesion.

The FDA has done a review to determine which ophthalmic conditions may occur that are self-treatable. It must be remembered, though, that each of these may potentially be serious enough to seek treatment by a physician or ophthalmologist. If patients experience eye pain, changes in vision, continued redness, or irritation in the eye, or if the condition worsens or persists, patients must discontinue use of nonprescription products and see a physician. Self-treatable conditions include:

    Dry eye Loose foreign material Redness caused by minor eye irritation Discomfort caused by minor eye irritation Corneal edema Ophthalmic allergic conjunctivitis

Dry eye refers to a syndrome resulting from many conditions that produce abnormalities of tear film flow and/or stability rather than denoting a specific disease entity. (7) This condition can result from a number of circumstances, including aqueous tear deficiency, keratoconjunctivitis sicca, primary Sjogren’s syndrome, blepharitis, vitamin A deficiency, allergic conjunctivitis, certain medications, contact lenses, and exposure to dry air. Tear production is also affected by total body hydration. Peripheral aqueous secretions such as tears and saliva may be compromised as the body conserves water to provide water to the cells of more vital organs.

Vitamin A deficiency is a major cause of childhood blindness in underdeveloped countries because vitamin A deficiency results in mucin deficiency. (8) The eye undergoes a loss of mucin-secreting goblet cells, resulting in an unstable tear film that causes dry patches on the conjunctiva. If not corrected, mucin deficiency can cause corneal and conjunctival xerosis. (9) Impaired dark adaptation is a good test for vitamin A deficiency. Dry eye is usually the result of an abnormality in one or more tear-stability dependent factors. (10) There are six to eight different types of possible abnormal tear film conditions, but the most severe form is keratoconjunctivitis sicca (KCS), which causes 80 to 90 percent of diagnosed cases of dry eye. (11) The typical patient afflicted with KCS produces less mucin than normal, so that elements of the corneal epithelium and mucous form on the eye, causing ocular pain. The process can cause keratinization of the cornea, producing burning, pain, discomfort, a feeling of fullness, and/or a gritty foreign body sensation, with possible loss of vision. (12)

Dry eye may also be caused by a long list of medications such as: certain diuretics like hydrochlorothiazide and chlorthalidone; antihistamines such as diphenhydramine, dexbrompheniramine, and chlorpheniramine; and anticholinergics like atropine and scopolamine. Phenothiazines, tricyclic antidepressants, cimetidine, indapamide, clonidine, and isotretinoin are others that may produce dry eye as a side effect.

Red or painful eyes may be the result of minor irritations that may be self-treated, or may be caused by serious conditions such as trauma to the eye, certain infectious diseases, or glaucoma. Eye pain or redness that does not resolve within 72 hours should be referred to an optometrist or ophthalmologist. Frequent causes of redness or pain include corneal abrasions, which require examination and treatment by a physician. Subconjunctival hemorrhage often creates a spectacular red eye, but needs no treatment. The rupture of small vessels bridging the potential space between the conjunctiva and the episclera causes it; however, vision is not affected, and the hemorrhage resolves without treatment. It may spontaneously occur from blunt trauma, eye rubbing, or vigorous coughing.

A pinguecula, or small raised conjunctival nodule at the temporal or nasal limbus, occurs commonly in adults, and is inconsequential unless it becomes inflamed (pingueculitis). A pterygium is similar to a pinguecula; however, it has crossed the limbus to encroach on the corneal surface. These may be removed if blurring of vision or irritation develops.

Blepharitis is the term used to describe inflammation of the eyelids and must be treated by a physician. Usual treatment includes strict eyelid hygiene, warm compresses, and an antibiotic ointment, such as erythromycin.

An external hordeolum (sty) is caused by staphylococcal infection of the superior accessory glands of Zeis or Moll located in the eyelid margins. An internal hordeolum occurs after suppurative infection of the oil-secreting meibomian glands within the tarsal plate of the eyelid. Systemic antibiotics, usually tetracyclines, are sometimes necessary for the treatment of meibomian gland infection, or chronic, severe blepharitis.

Conjunctivitis is the most common cause of red, painful eyes. Most frequently, pain is minimal and visual acuity affected only slightly. The most frequent viral cause is adenovirus infection, causing a watery discharge, photophobia, and a mild foreign body sensation. Bacterial infection tends to produce a more mucopurulent exudate. Mild cases are usually treated with topical, broad-spectrum ocular antibiotics. Allergic conjunctivitis is often mistaken for infectious conjunctivitis; however, allergic conjunctivitis is generally bilateral, seasonal, and accompanied by prominent itching. The eyes are slightly red, tearing, and burning, but with little discharge. (13)

Prolonged contact wearing, corneal inflammation, glaucoma, infection, iritis, or a degeneration of cells lining the back of the cornea may cause corneal edema. Corneal edema occurs as the water content of the cornea increases causing the cornea to swell and lose transparency. Although corneal edema is one of the conditions deemed self-treatable by the FDA, the wise choice is to be treated by a physician since it may be produced by a serious underlying problem.

Statistic

National Center for Health Statistics (NCHS), 1999.

    Glaucoma was the principal diagnosis of 17.5 million doctor visits during 1991 and 1992, an annual estimate of 8.7 million visits. Glaucoma is the leading cause of irreversible blindness among the African American population. About three-quarters of glaucoma visits were made to ophthalmologists. Nine out of 10 glaucoma visits result in a scheduled return visit. Medication therapy was the most frequently mentioned therapeutic service at glaucoma visits.

Health Communications and Public Relations, World Health Organization, Geneva 1999.

    It has been estimated that the global number of blind in the world in 1990 was about 38 million. The number of persons with low vision was estimated to be 110 million. Cataract, trachoma, and glaucoma, together account for more than 70% of the world's blindness and visual disability. Vitamin A deficiency leads to blindness (xerophthalmia) in some 350,000 children annually. Diabetic retinopathy is the leading cause of blindness and visual disability in adults in economically developed societies. After 15 years of diabetes, approximately 2% of people become blind while about 10% develop severe visual disability.

The World Health Organization (WHO) Programme for the Prevention of Blindness, 1999.

    Trachoma is the most common cause of preventable blindness; the disease, in its active inflammatory form, affects close to 150 million people, mainly children and women. 5.8 million cases of trachoma complications and/or blindness, which corresponds to 15.5% of world blindness.

National Eye Institute, Vision Problems in the US, 2000

  • Estimated number of cases of visual impairment including blindness in those over 40 years of age: 3,406,280

  • Estimated number of cases of blindness in those over 40 years of age: 1,046,920

  • Estimated number of cases of Age-related Macular Degeneration in those over 50 years of age: 1,651,335

  • Estimated number of cases of Cataracts in those over 40 years of age: 20,476,040

  • Estimated number of cases of Diabetic Retinopathy in those over 18 years of age: 5,353,233

  • Estimated number of cases of Glaucoma in those over 40 years of age: 2,227,485

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

There are many different conditions, which may cause one, or a combination of the symptoms. Symptoms for which patients should seek medical advice include; changes in vision, prolonged irritations or eye pain, severe redness, infections of the eyelids, eye injuries (trauma), chemical exposure, and foreign bodies that cannot be removed through tears or flushing with water or saline. A red eye with purulent discharge and minor eye discomfort characterizes bacterial conjunctivitis. Which often results in eyelids being stuck together upon awakening. Viral conjunctivitis is also characterized by redness of the eye; however, the discharge is usually copious and watery.

Allergic conjunctivitis also causes redness, however, the hallmark of allergic conjunctivitis is itching. Edema may also be present. Generally there is profuse watery discharge and tearing. Patients may also experience photophobia.

Dry eye is characterized by ocular discomfort, blurred vision, discharge, an awareness of the eyes, feeling of dirt or sand in the eyes, burning and redness. The human cornea has no nerve receptors for dryness or wetness and cannot interpret dry eye in this manner, it is, however, thought to be perceived through stimulation of receptors for warmth, cold, and pain. There may also be some combination of receptors in the eyelids, cornea, or conjunctiva that interact to produce the perception of dryness.

Symptoms of corneal edema include foggy vision and the presence of haloes or star bursts around lights. Blisters may occur (if condition worsens) that cause photophobia and irritation and patients may experience excruciating pain if the blisters rupture.

Dry eyes

    Ocular discomfort Blurred vision Discharge An awareness of the eyes Feeling of dirt or sand in the eyes Burning Redness

Allergic conjunctivitis

    Itching Redness Edema Photophobia Epiphora

Corneal edema

    Foggy vision Haloes around lights Blisters (if condition worsens) that cause photophobia and irritation Excruciating pain if blisters rupture

Conjunctivitis

    Redness Minimal pain Watery discharge Bacterial infection usually leads to more mucopurulent exudates

Treatment Options

Conventional

Mild forms of dry eye may be treated with nonprescription tear substitutes. Ocular emollients may also be used. Occasionally, surgery may be necessary to narrow the puncta or close it off entirely.

Ophthalmic redness due to minor irritations may be treated with ophthalmic vasoconstrictors such as tetrahydrozaline, oxymetazoline, or naphazoline. These products are contraindicated, however, in patients with glaucoma, since they may produce mydriasis.

Corneal edema may be treated with 2 to 5% sterile hypertonic sodium chloride solution or ointment to draw fluid from the cornea. Usually, the dose is 1-2 drops every three or four hours or as directed by a physician. The nonprescription remedies available for allergic conjunctivitis generally contain vasoconstrictors and antihistamines such as pheniramine or antazoline. The usual recommended dose is 1-2 drops in the affected eye(s) up to four times daily.

Bacterial or viral conjunctivitis is treated with broad-spectrum ocular antibiotics, such as sulfacetamide 10%, polymixin-bacitracin-neomycin, or trimethoprim-polymixin combinations.

Glaucoma is treated with cholinergic drugs to cause miosis and constrict the ciliary muscles in order to facilitate aqueous fluid drainage from the anterior chamber. Timolol, a beta-blocker, is often used to reduce aqueous fluid formation. A complete review of glaucoma and its treatment should be reserved for a more in-depth discussion.

The discussion of ocular health is a broad topic, and many ocular manifestations of systemic diseases have been omitted, as well as detailed discussions of optic neuropathies, retinal detachment, and other conditions.

Nutritional Supplementation


Antioxidant Nutrients

Antioxidant nutrients are thought to help protect the eyes against aging damage. When light enters the eye, it activates oxygen, which can initiate free radical reactions that damage the macula. Results from the Baltimore Longitudinal Study of Aging reported that vitamin E, vitamin C, and beta-carotene all provided antioxidant protection against the development of age-related macular degeneration (ARMD). (14) Epidemiological studies have also found that people with cataracts have lower serum levels of vitamins C, E, and carotenoids than control subjects. In one study, individuals who regularly took vitamin C and/or vitamin E as supplements had more than a 50 percent decrease in cataract risk compared to people that did not supplement with vitamins C and E. (15) , (16) Another study showed that long-term supplementation of vitamin E reduced the progression of age-related lens opacification. (17)


Lutein, Zeaxanthin

Lutein and zeaxanthin are two carotenoids that are found in the eyes. They are concentrated in the lens and macula and have been reported to provide important protective benefits for the eyes. These compounds belong to a sub-category of carotenoids called oxycarotenoids. They are yellow pigments that are mainly deposited in an area called the yellow spot in the macula, which is the central part of the retina. One of their functions is to filter out blue light. The lens and cornea filter out ultraviolet light, but blue light passes on through, reaching the retina where it can create photo damage that contributes to the progression of macular degeneration. A review of studies on these pigments states that the concentration of dietary carotenoids in the macula is not accidental. They are antioxidants that protect the eyes by quenching oxygen free radicals and singlet oxygen, which are generated in the retina as a consequence of the simultaneous presence of light and oxygen and they protect the blood vessels that supply the macular region. (18)

Results of a study conducted at the Department of Ophthalmology, Harvard Medical School, indicated that increasing the consumption of carotenoid-containing foods lowered the risk of developing age-related macular degeneration (ARMD). Individuals with the highest quintile (20 percent) of carotenoid intake had a 43 percent lower risk for ARMD compared to the lowest quintile. In this study, lutein and zeaxanthin were the carotenoids most strongly associated with a reduced risk for age-related macular degeneration. (19) Both pigments occur naturally in a wide variety of green leafy vegetables such as spinach, kale, broccoli, and Brussels sprouts.

In a four-week study that had participants consume diets high in lutein and zeaxanthin-containing foods (spinach and corn), most showed increases in their macular pigment density. (20) In another study, two subjects were given 30mg of lutein daily for 140 days. These individuals gained a tenfold increase in their serum lutein concentration and they increased their macular pigment optical density 39 percent and 21 percent respectively, which they maintained for 40 to 50 days after discontinuing the supplement. This resulted in a 30 to 40 percent reduction in the amount of blue light reaching their photoreceptors and other vulnerable areas of the eye, and represents a substantial protection of the eyes against the type of damage that leads to macular degeneration. (21)


Vitamin A

Vitamin A is a nutrient that plays an important role in vision. In the pigment epithelial tissues of the retina, vitamin A compounds bind to opsin proteins in the rods and cones. This produces the highly photosensitive proteins, rhodopsin (in the rods) and three iodopsins (in the cones), which absorb blue, green, and red wavelengths of light. These photopigments are responsible for night vision. Night blindness (nyctalopia) is the classic vision problem resulting from vitamin A deficiency. Another problem known as xerophthalmia can also develop. This condition causes a drying and hardening of the epithelial cellular membranes in the eye, which often results in blindness. Although xerophthalmia is rare in the United States, the World Health Organization estimates that 250,000 to 500,000 preschool children lose their sight every year as a result of vitamin A deficiency, and half of them die within 12 months of becoming blind. (22) Overall, vitamin A deficiency could be the single most common preventable cause of blindness in the world. (23)


Zinc

Zinc is a mineral that regulates the sensory perceptions of taste, smell, and vision. It has been reported that the retina of the eye contains a higher concentration of zinc than any other organ in the human body. (24) One of zinc’s roles in vision is due to the fact that it is required for the synthesis of rhodopsin, which is also known as visual purple. (25) Zinc also regulates serum levels of vitamin A by controlling the release of stored vitamin A from the liver. Since vitamin A is essential to vision, a zinc deficiency could also affect vision by preventing the release of vitamin A. Another zinc attribute is the fact that it is a mineral cofactor for one of the forms of the antioxidant enzyme known as superoxide dismutase.


Selenium

Selenium deficiencies may be associated with an increased risk of cataracts. The antioxidant enzyme glutathione peroxidase, which requires four atoms of selenium per molecule, provides antioxidant protection in the eyes. (26) In one study, it was reported that the lens tissue from individuals with cataracts had significantly less selenium than the lenses of normal controls. (27)

Herbal Supplementation


Bilberry

Bilberry is one of the most popular herbs on the market today. During World War II when British air pilots ate bilberries, they reported an improved ability to adjust to glare and an increase in their visual acuity and nighttime vision. (28) Bilberry extracts show promise in the areas of diabetic retinopathy, macular degeneration, cataracts, glaucoma, and varicose veins. (29) Bilberry is an excellent antioxidant. (30) Bilberry is claimed to exert a collagen stabilizing activity. (31) Collagen is responsible for the integrity of tendons, ligaments, and cartilage. In conditions such as arthritis, where the connective tissue is attacked and vascularized, anthocyanosides may be helpful. Bilberry reportedly strengthens the cross-linking of the collagen matrix and stimulates the production of collagen and mucopolysaccharides. (32) Bilberry compounds reportedly inhibit mediators of inflammation such as histamine, protease, leukotrienes, and prostaglandins. (33) Anthocyanosides may also decrease capillary permeability. (34) This is of particular importance because of the heightened integrity which occurs at the blood/brain barrier. By strengthening collagen, brain capillary integrity can be improved, as well as a reduction in infiltration by potential toxins. Anthocyanosides reportedly inhibit platelet aggregation. (35) Platelet aggregation tendencies relate to atherosclerotic and blood clotting tendencies. Bilberry has the ability to stimulate gastric mucus production which may be of value for those on nonsteroidal anti-inflammatory drugs. (36) Although all of the above effects are exciting, the most exciting is its potential effect on the eyes. With age, oxidative stress due to free radicals increases in some people more than in others. This damage to ocular tissues may lead to various eye pathologies. If it improves the oxygenation of tissue, bilberry may show promise in the areas of prevention for diabetic retinopathy, minimizing the advance of macular degeneration, and arresting cataract progression. (37) , (38)


Ginkgo

Ginkgo is among the oldest living species on earth and has been used extensively as a medicinal agent worldwide for centuries, and is the most frequently prescribed medicinal herb in Europe. The most dramatic benefits are reported in improving circulation in the elderly. (39) , (40) This can lead to enhanced memory, delaying the onset of Alzheimer's (41) and reducing senile dementia, (42) tinnitus, (43) and vertigo. (44) Ginkgo’s memory-enhancing effects are reported in younger populations as well. The main active components of ginkgo are the flavoglycosides. These compounds act as strong free radical scavengers or antioxidants. (45) Ginkgo is also reported to inhibit platelet activating factor (PAF) which could reduce the adhesive nature of platelets possibly through competitive binding. Ginkgo may foster vasodilation by stimulating endothelium releasing factor and prostacyclin. (46) It may also stimulate venous tone and improves the clearance of homotoxins during ischemic episodes. (47) Gingko reportedly acts as a tonic for the circulatory system. It may increase cerebral brain flow and, therefore, improve delivery of nutrients to the brain, enhancing elimination of the byproducts of cell metabolism and oxygenating the tissues. (48) Ginkgo may normalize acetylcholine receptors and, therefore, improve cholinergic function. (49)


Green Tea

Green tea has long been used in much of the world as a popular beverage and a respected medicinal agent. An early Chinese Materia Medica lists green tea as an agent to promote digestion, improve mental faculties, decrease flatulence and regulate body temperature. The earliest known record of consumption is around 2700 B.C. Green tea is an antioxidant that is used in promoting cardiovascular health (50) , (51) reducing serum cholesterol levels in laboratory animals and humans. (52) , (53) Studies suggest that green tea contains dietary factors that help decrease the development of some infectious diseases and dental caries. (54) , (55) , (56) Green tea also has diuretic, stimulant, astringent and antifungal properties. (57) Green tea has also been reported to enhance immunity. (58)

Green tea reportedly has antioxidant properties (59) and the ability to protect against oxidative damage of red blood cells. (60) Antioxidants protect cells and tissues against oxidative damage and injury. (61) Green tea’s antioxidant effects seem to be dependent upon the polyphenol (catechin) fraction. (62) , (63) It is important to note that the addition of milk to any tea may significantly lower the antioxidant potential. (64)


Grape Seed Extract

Proanthocyanidins (PCO's), the active constituent in grape seed, is a flavonoid-rich compound which is being heavily touted as one of the most potent free radical scavengers. It has been reported to enhance the absorption of and work synergistically with vitamin C. (65) PCO's have been reported to inhibit the release of mediators of inflammation, such as histamine and prostaglandins. (66) , (67) Proanthocyanidins are reported to neutralize many free radicals, including hydroxyl, lipid peroxides and iron-induced lipid peroxidation. (68) , (69) , (70) They may inhibit the enzyme xanthine oxidase. (71) PCO's have been used in allergies because of their reported ability to inhibit degradation of mast cells and the subsequent release of histamine and other mediators of inflammation.

Clinical Lab Assessment

Some of the following laboratory testing can provide information necessary for diagnosis and treatment. In addition, the tests listed may also give insight to functional metabolism and functional nutrient status in the body.

Chemistry Profile (Blood)

A multifactorial assessment of chemistry profile values can reveal useful information regarding concurrent disorders and possible nutrient imbalances.

Melatonin

Melatonin is a potent antioxidant that may be especially effective in preventing and treating cataracts. (72) Melatonin production slows down in people over the age of 40, and by age 60 there is virtually no melatonin being naturally produced. Most cataracts develop after age 60.

Mineral Analysis

The evaluation of essential and/or toxic elements can be of use in the evaluation of many clinical conditions. Essential mineral imbalances can affect nearly any tissue and organ resulting in a myriad of disorders. Trace element deficiencies can disproportionately affect enzyme systems that are used in regulatory substrates resulting in amplified disease conditions. A number of researchers have asserted that trace minerals are important in the assessment of eye disorders. (73) Toxic elements can be particularly damaging as a result of toxicity responses and inhibition of essential nutrient-dependent mechanisms.

Glucose

High glucose levels, such as in diabetes, are associated with cataracts. Blood glucose levels vary in response to food intake, stress, physical exertion, and various disorders. Elevations of serum glucose should lead to confirmatory testing such as fasting insulin, serum phosphorus, magnesium, hemoglobin A1c, and/or fructosamine.

Zinc

Subnormal levels of zinc are associated with macular degeneration. (74)

Oxidative Stress

Increased oxidation is a documented dynamic of ocular disorders. Research suggests that oxidative mechanisms may play an important role in the pathogenesis of cataract and age-related macular degeneration. (75) Oxidant levels increase in relationship to the inflammatory process. Abnormal glutathione levels can affect eye health significantly. Glutathione helps maintain fluid balance in the lens.

Magnesium Level

Functional deficiencies do occur in stress syndromes related to chronic disease processes. (76) High extracellular magnesium concentrations significantly alter lens metabolite levels. Excessive intake of magnesium is not likely to result in toxicity except in cases of renal insufficiency. (77) Normal serum levels may occur despite severe intracellular deficit. (78)

References

  1. Horton JC. Disorders of the eye. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine 14th ed. New York: McGraw-Hill; 1998:159-172.
  2. Longe RL, Calvert JC. Eye. In: Young LY ed. Physical Assessment A Guide for Evaluating Drug Therapy. Vancouver, WA: Applied Therapeutics Inc; 1994:5-1—5-26.
  3. View Abstract: Khurana AK. Tear film profile in dry eye. Acta Ophthalmol. 1991;69:79.
  4. View Abstract: Versura P. Mucuc alteration and eye dryness. Acta Ophthalmol. 1989;67:455.
  5. Longe RL, Calvert JC. Eye. In: Young LY ed. Physical Assessment A Guide for Evaluating Drug Therapy. Vancouver, WA: Applied Therapeutics Inc; 1994:5-1—5-26.
  6. Horton JC. Disorders of the eye. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine 14th ed. New York: McGraw-Hill; 1998:159-172.
  7. View Abstract: Khurana AK. Tear film profile in dry eye. Acta Ophthalmol. 1991;69:79.
  8. Kaden I, Mayers M. Systemic associations of the dry-eye syndrome. Int Ophthalmol Clin. 1991;31:69.
  9. Pray WS. Ophthalmic Conditions. In: Nonprescription Product therapeutics. Baltimore MD: Lippincott, Williams & Wilkins; 1999:396-411.
  10. Patel S. A Possible reason for the lack of symptoms in aged eyes with low tear stability. Optom Vis Sci. 1990;67:733.
  11. View Abstract: Fassihi AR, Naidoo NT. Irritation associated with tear-replacement ophthalmic drops. A pharmaceutical and subjective investigation. S Afr Med J. Mar1989;75(5):233-5.
  12. View Abstract: Xu KP, Yagi Y, Tsubota K. Decrease in corneal sensitivity and change in tear function in dry eye. Cornea. 1996;15:235.
  13. View Abstract: Fujishima H, et al. Allergic conjunctivitis and dry eye. Br J Ophthalmol. 1996;80:994.
  14. View Abstract: West S, et al. Are antioxidants or supplements protective for age-related macular degeneration? Arch Ophthalmol. Feb1994;112(2):222-7.
  15. View Abstract: Robertson JM, et al. A possible role for vitamins C and E in cataract prevention. Am J Clin Nutr. Jan1991;53(1 Suppl):346S-351S.
  16. View Abstract: Chylack LT, et al. The Roche European American Cataract Trial (REACT): A randomized clinical trial to investigate the efficacy of an oral antioxidant micronutrient mixture to slow progression of age-related cataract. Ophthalmic Epidemiol. Feb2002;9(1):49-80.
  17. View Abstract: Jacques PF. Long-term nutrient intake and 5-year change in nuclear lens opacities. Arch Ophthalmol. 2005 Apr;123(4):517-26.
  18. View Abstract: Schalch W. Carotenoids in the retina--a review of their possible role in preventing or limiting damage caused by light and oxygen. EXS. 1992;62:280-98.
  19. View Abstract: Seddon JM, et al. Dietary carotenoids, vitamins A, C, and E, and advanced age-related macular degeneration. Eye Disease Case-Control Study Group. JAMA. Nov1994;272(18):1413-20.
  20. View Abstract: Hammond BR Jr, et al. Dietary modification of human macular pigment density. Invest ophthalmol Vis Sci. Aug1997;38(9):1705-1801.
  21. View Abstract: Landrum JT, et al. A one year study of the macular pigment: the effect of 140 days of a lutein supplement. Exp Eye Res. Jul1997;65(1):57-62.
  22. Bender DA, Bender AE. Nutrition: A Reference Handbook. New York: Oxford University Press; 1997:236-242.
  23. Micronutrient deficiencies. Combating vitamin A deficiency. Nutrition: World Health Organization; Jul2002.
  24. Underwood EJ. Trace Elements in Human and Animal Nutrition, 4th Edition. London. Academic Press; 1977:198.
  25. View Abstract: Shuster TA, et al. Zinc causes an apparent increase in rhodopsin phosphorylation. Curr Eye Res. Oct1996;15(10):1019-24.
  26. View Abstract: Cai QY, et al. Biochemical and morphological changes in the lenses of selenium and/or vitamin E deficient rats. Biomed Environ Sci. Jun1994;7(2):109-15.
  27. Swanson AA, et al. Elemental analysis in normal and cataractous human lens tissue. Biochem Biophys Res Commun. Dec1971;45(6):1488-96
  28. Jayle GE, et al. Study Concerning the Action of Anthocyanoside Extracts of Vaccinium myrtillus on Night Vision. Ann Ocul. Paris. 1965;198(6):556-62.
  29. Morazonni P, et al. Vaccinium myrtillus. Fitoterapia vol. LXVII, no. 1; 1996:3-29.
  30. Morazonni P, et al. Vaccinium myrtillus. Fitoterapia vol. LXVII, no. 1; 1996:3-29.
  31. Jonadet M, et al. Anthocyanosides Extracted from Vitis vinifera, Vaccinium myrtillus and Pinus maritimus, I. Elastase-inhibiting Activities in Vitro, II. Compared Angioprotective Activities in Vivo. J Pharm Belg. 1983;38(1):41-46.
  32. Jonadet M, et al. Anthocyanosides Extracted from Vitis vinifera, Vaccinium myrtillus and Pinus maritimus, I. Elastase-inhibiting Activities in Vitro, II. Compared Angioprotective Activities in Vivo. J Pharm Belg. 1983;38(1):41-46.
  33. Morazonni P, et al. Vaccinium myrtillus. Fitoterapia vol. LXVII, no. 1; 1996:3-29.
  34. View Abstract: Detre Z, et al. Studies on Vascular Permeability in Hypertension: Action of Anthocyanoside. Clin Physiol Biochem. 1986;4(2):143-49.
  35. Bottecchia D, et al. Vaccinium myrtillus. Fitoterapia. 1977;48:3-8.
  36. Wichtl M, in Bisset NA, ed. Herbal Drugs and Phytopharmaceuticals. Stuttgart: Scientific Press; 1994:351-52.
  37. Bonanni R, et al. Clinical Study of the Action of Myrtillis Alone or Associated with Betacarotene on Normal Subjects and on Patients with Degenerative Changes of the Fundus Oculi. Atti Accad Fisiocrit Siena. 1968;17(2):1470-88.
  38. View Abstract: Varma SD, et al. Diabetic Cataracts and Flavonoids. Science. 1977;195:205-06.
  39. View Abstract: Kleijnen J, et al. Ginkgo biloba for Cerebral Insufficiency. Br J Clin Pharm. 1992;34:352-58.
  40. Kleijnen J, et al. Ginkgo biloba. Lancet. 1992;340(8828):1136-39.
  41. View Abstract: Maurer K, et al. Clinical Efficacy of Ginkgo biloba Special Extract EGb 761 in Dementia of the Alzheimer Type. J Psychiatr Res. 1997;31(6):645-55.
  42. View Abstract: Kanowski S, et al. Proof of Efficacy of the Ginkgo biloba Special Extract EGb 761 in Outpatients Suffering from Mild to Moderate Primary Degenerative Dementia of the Alzheimer Type or Multi-infarct Dementia. Pharmacopsychiatry. 1996;29:47-56.
  43. View Abstract: Meyer B. Multicenter Randomized Double-blind Drug versus Placebo Study of Ginkgo biloba Extract in the Treatment of Tinnitus. Presse Med. 1986;15:1562-64.
  44. Odawara M, et al. Ginkgo biloba. Neurology. 1997;48(3):789-90.
  45. View Abstract: Kose L, et al. Lipoperoxidation Induced by Hydrogen Peroxide in Human Erythrocyte Membranes. 2. Comparison of the Antioxidant Effect of Ginkgo biloba Extract (EGb 761) with Those of Water-soluble and Lipid-soluble Antioxidants. J Intern Med Res. 1995;23:9-18.
  46. View Abstract: Auguet M, et al. Effects of Ginkgo biloba on Arterial Smooth Muscle Responses to Vasoactive Stimuli. Gen Pharmacol. 1982;13(2):169-71.
  47. View Abstract: Bauer U. 6-Month Double-blind Randomised Clinical Trial of Ginkgo biloba Extract Versus Placebo in Two Parallel Groups in Patients Suffering from Peripheral Arterial Insufficiency. Arzneim-Forsch/Drug Res. 1984;34(6):716-20.
  48. Kleijnen J, et al. Ginkgo biloba. Lancet. 1992;340(8828):1136-39.
  49. View Abstract: Ramassamy C, et al. The Ginkgo biloba Extract, EGb761, Increases Synaptosomal Uptake of 5-hydroxytryptamine: In-vitro and Ex-vivo Studies. J Pharm Pharmacology. 1992;44(11):943-45.
  50. View Abstract: Imai K, et al. Cross Sectional Study of Effects of Drinking Green Tea on Cardiovascular and Liver Diseases. BMJ. Mar1995;310(6981):693-96.
  51. View Abstract: Weisburger JH. Tea and Health: A Historical Perspective. Cancer Lett. Mar1997;114(1-2):315-17.
  52. View Abstract: Miura S, et al. Effects of Various Natural Antioxidants on the Cu(2+)-mediated Oxidative Modification of Low Density Lipoprotein. Biol Pharm Bull. Jan1995;18(1):1-4.
  53. View Abstract: Yokozawa T, et al. Influence of Green Tea and Its Three Major Components upon Low-density Lipoprotein Oxidation. Exp Toxicol Pathol. Dec1997;49(5):329-35.
  54. View Abstract: Tagashira M, et al. Inhibition by Hop Bract Polyphenols of Cellular Adherence and Water-insoluble Glucan Synthesis of Mutans Streptococci. Biosci Biotechnol Biochem. Feb1997;61(2):332-35.
  55. View Abstract: Yu H, et al. Anticariogenic Effects of Green Tea. Fukuoka Igaku Zasshi. Apr1992;83(4):174-80.
  56. View Abstract: Stoner GD, et al. Polyphenols as Cancer Chemopreventive Agents. J Cell Biochem Supp. 1995;22:169-80.
  57. Snow JM. Camellia sinensis (L.) Kuntze (Theaceae). Protocol Journal of Botanical Medicine. 1995;1(2):47-51.
  58. View Abstract: Yan YS. Effect of Chinese Tea Extract on the Immune Function of Mice Bearing Tumor and Their Antitumor Activity. Chung Hua Yu Fang I Hsueh Tsa Chih. Jan1992;26(1):5-7.
  59. Cheng TO. Antioxidants in Chinese Green Tea. J Am Coll Cardiol. Apr1998;31(5):1214.
  60. View Abstract: Grinberg LN, et al. Protective Effects of Tea Polyphenols against Oxidative Damage to Red Blood Cells. Biochem Pharmacol. Nov1997;54(9):973-78.
  61. View Abstract: Halliwell B. How to Characterize an Antioxidant: An Update. Biochem Soc Symp. 1995;61:73-101.
  62. View Abstract: Kumamoto M, et al. Evaluation of the Antioxidative Activity of Tea by an Oxygen Electrode Method. Biosci Biotechnol Biochem. Jan1998;62(1):175-77.
  63. View Abstract: Hirayama O, et al. Evaluation of Antioxidant Activity by Chemiluminescence. Anal Biochem. May1997;247(2):237-41.
  64. View Abstract: Hertog MG, et al. Antioxidant Flavonols and Ischemic Heart Disease in a Welsh Population of Men: The Caerphilly Study. Am J Clin Nutr. May1997;65(5):1489-94.
  65. Maffei Facino R, et al. Regeneration of Endogenous Antioxidants, Ascorbic Acid, Alpha Tocopherol, by the Oligomeric Procyanide Fraction of Vitus vinifera L:ESR Study. Boll Chim Farm. 1997;136(4):340-44.
  66. View Abstract: Maffei Facino R, et al. Procyanidines from Vitis vinifera Seeds Protect Rabbit Heart from Ischemia/Reperfusion Injury: Antioxidant Intervention and/or Iron and Copper Sequestering Ability. Planta Med. 1996;62(6):495-502.
  67. View Abstract: Maffei Facino R, et al. Free Radicals Scavenging Action and Anti-enzyme Activities of Procyanidines from Vitis vinifera. A Mechanism for Their Capillary Protective Action. Arzneim-Forsch/Drug Res. 1994;44(5):592-601.
  68. View Abstract: Lagrue G, et al. A Study of the Effects of Procyanidol Oligomers on Capillary Resistance in Hypertension and in Certain Nephropathies. Sem Hop. 1981;57(33-36):1399-1401.
  69. View Abstract: Fitzpatrick DF, et al. Endothelium-dependent Vasorelaxing Activity of Wine and Other Grape Products. Am J Physiol. 1993;265(2 Pt 2):H774-H778.
  70. Uchida S, et al. Active Oxygen Free Radicals Are Scavenged by Condensed Tannins. Prog Clin Biol Res. 1988;280:135-38.
  71. View Abstract: Hatano T, et al. Effects of Interaction of Tannins with Co-existing Substances. VII. Inhibitory Effects of Tannins and Related Polyphenols on Xanthine Oxidase. Chem Pharm Bull. Tokyo. 1990;38(5):1224-29.
  72. View Abstract: Abe M, Reiter RJ, Orhii PB, Hara M, Poeggeler B. Inhibitory effect of melatonin on cataract formation in newborn rats: evidence for an antioxidative role for melatonin. J Pineal Res. Sep1994;17(2):94-100.
  73. View Abstract: Teichmann KD. Treatment of macular degeneration, according to Bangerter. Eur J Med Res. Germany. Oct1997;2(10):445-54.
  74. View Abstract: Ishihara N, Yuzawa M, Tamakoshi A. [Antioxidants and angiogenetic factor associated with age-related macular degeneration (exudative type)] Nippon Ganka Gakkai Zasshi. Japan. Mar1997;101(3):248-51.
  75. View Abstract: Christen WG. Antioxidant vitamins and age-related eye disease. Proc Assoc Am Physicians. Jan1999;111(1):16-21.
  76. View Abstract: Kopp SJ, Glonek T, Greiner JV. Dynamic changes in intact crystalline lens metabolism modulated by alkaline earth metals: I. Effects of magnesium. Exp Eye Res. Mar1983;36(3):327-35.
  77. Gibson RS. Principles of nutritional assessment. New York: Oxford University Press; 1990:487-510.
  78. Wester PO. Magnesium. Am J Clin Nutr. 1987;45(suppl):1305-1312.