Dry Eye
Dry Eye Prevention and Reversal
Dry eye syndrome is one of the most common eye conditions. In 1990, about 33 million Americans experienced varying degrees of dry eye symptoms. By 1997 that figure increased to an alarming 59 million. The symptoms may include dryness, grittiness, irritation, burning, and even excessive tearing or watering. While many people find temporary relief with artificial tear preparations, this only palliates the symptoms, and preservatives found in many of these products can even aggravate the condition itself. In fact, these preservatives can kill corneal cells. Recovery of corneal health after exposure to preservatives takes a full week, while the conjunctiva takes up to 2 months to heal. The common eye drop preservative benzalkonium chloride causes worsening of dry eyes, making one more and more dependent on the use of such drops. This preservative, along with thimerosal and Tween, occurs in toxic concentrations in eye drops. Other pharmaceutical ingredients in eye drops contribute to dry eyes, too. Vasoconstrictors that ‘get the red out’ reduce circulation in the eye, decrease the production of the tear film, and worsen dry eye symptoms.
Research shows that unpreserved eye drops enhance corneal healing and improve dry eye problems in comparison to preserved products. Fortunately, several unpreserved tear substitutes are available, including VIVA drops (which contain 19 I.U. of vitamin A per drop) and several single-dose tubes. Concern has been expressed however about the risk of corneal abrasion by the sharp ends of single-dose tubes. Among the other problems with eye drops is that 80% of people have difficulty getting them in the eyes, and even with practice 49% continue to have poor aim. Less than a third have even been shown how to do it right! The best method is to pull down the lower lid so the drop can be instilled onto the lower cul de sac (blind pouch) of the conjunctiva rather than directly onto the cornea. For those who have difficulty, eye drop guides are available to assist. For those who are unable to open the eyes while drops are instilled, drop them into the inner corner of the closed lids, and the drops will enter the eyes on opening. Keep drops refrigerated if you experience stinging on instillation. Be sure to keep your eye drops separate from any similar-looking bottles, and to prevent contamination, be very careful not to touch the dropper with anything including fingers or the eye itself. Look for a ring of dirt between the cap and lid as a sign that contamination has probably occurred. Be sure to wash your hands before using eye drops and keep the bottle in a clean place. Nearly one out of three bottles become contaminated and should be replaced with a clean, fresh supply.
Blinking and tearing following the use of an eye drop can dilute the remedy to less than 1% of its original concentration in just a few minutes. To optimize therapeutic effectiveness after instillation, donÕt blink, but rather close the eyes for up to 2 minutes. You can even pinch gently at the root of the nose to prevent drainage through the tear ducts, increasing effectiveness by 65%. This is also a perfect time to help the eyes relax and improve circulation to the eyes with techniques like palming, the 'eye stretch,' and acupressure or shiatsu eye massage. Between applications, it is important to blink frequently and fully, as this spreads the tears over the front of the eye, moistening any dry areas. The normal tear breakup time (BUT) is over 10 seconds, permitting that length of staring before the cornea begins to show dry spots. With dry eye syndrome, this often shortens to just a few seconds. Staring also contributes to visual stress and is related to increases in myopia. Related eye muscle tension may further reduce circulation in the eye area.
Many doctors recommend treatments that can include placing silicone plugs to block the eyes tear ducts and even cauterizing the ducts closed to retain moisture in the eye. While such treatments do reduce the quantity of artificial tears needed for many with severely dry eyes, it may merely mean applying drops every 4 hours or more rather than every 3 hours or less. Humidifiers may be helpful in dry or air-conditioned environments, and special moisture chamber goggles can also be worn to minimize tear evaporation. Even neutral gray wrap-around sun goggles may offer some relief, especially from aggravation by sun, wind, and dust. Side shields reduce evaporation by up to 40%. Perhaps if we look a little deeper at the pathophysiology and biochemistry of the tears and tear production, we will find healthier solutions for many dry eye sufferers.
There are three common hypotheses for the cause of dry eye:
Dry spots on the ocular surface
Inflammation of the eye surface
Elevated tear film osmolarity with loss of water from the tear film
Dry spots are associated with but don’t cause dry eye, as half of dry eye patients have enough tear film stability to prevent dry spots between blinks.
Lemp MA, Hamill JR: Factors affecting tear film breakup in normal eyes. Arch Opthalmol 89:103-105, 1973.
Dry eye surface disease is most severe within the palpebral aperture, but there are also changes on the superior and inferior bulbar conjunctiva, where dry spots do not occur. Rabbit studies show that loss of the corneal cell surface proteins that make the cornea wettable is a late change in dry eye disease.
In the 1800s, Hass theorized that dry eye was caused by a direct immune or inflammatory assault on the eye surface and that the changes on the eye surface are unrelated to the decrease in tear production. This hypothesis was intriguing until researchers started looking at ocular surface pathology in dry eyes. Surface pathology in patients who develop dry eye after having their lacrimal glands removed for epiphora (which is why this operation went out of favor) and in patients with Sjogren’s syndrome. The group with the iatrogenic disease had exactly the same ocular surface changes as the Sjögren’s group.
Scherz W, Dohlman CH: Is the lacrimal gland dispensable? Keratoconjunctivitis sicca after lacrimal gland removal. Arch Opthalmol 93:281-283, 1975.
In rabbits, every ocular surface change in Sjögren’s syndrome is manifest in normal rabbits by raising tear film osmolarity, whether by blocking tear secretion, decreasing corneal sensation, or inducing meibomian gland dysfunction. Research shows an expression of inflammatory mediators (cytokines) on the eye surface in dry eyes, but inflammation is a non-specific response to any tissue damage. Inflammation helps clean up the damage. Increases in tear film osmolarity cause the increase of pro-inflammatory cytokines on the eye surface. There is no primary immune-inflammatory attack on the eye surface in dry eye.
Dursun D, Wang M, Monroy D, Li D, Lokeshwar BL, Stern M, Pflugfelder SC: Experimentally induced dry eye produces ocular surface inflammation and epithelial disease. Adv Exp Med Biol 506(PtA):647-55, 2002.
When Sjögren’s first described the ocular surface pathology in dry eye, he concluded that it looked as if some “force” was pulling water across the ocular surface epithelium. It turns out that force was the osmotic force created by the osmotic gradient created by an elevation of tear film osmolarity. The ocular surface disease in dry eye is dependent on and proportional to elevations in tear film osmolarity.
Elevated tear film osmolarity causes the ocular surface changes in dry eye. Farris finds that tear film osmolarity in dry eye patients increases through the course of each day.
Farris RL, Stuchell RN, Mandel ID. Tear osmolarity variation in the dry eye. Trans Am Ophthalmol Soc (United States) 84: p250-68, 1986.
The Tear Film
There are three layers to the normal tear film that keep the front surface of the eye comfortably lubricated and optically clear. The first is a lipid (oil) layer which prevents tears from evaporating. This is secreted by the meibomian glands. The middle, and thickest layer, is the aqueous or watery layer, secreted by the lachrymal gland. The third layer, which binds the tears to the surface of the eye by making the eye tissue wettable, is a protein layer called mucin. This is secreted directly from the conjunctival surface on the white of the eye by goblet cells.
Dry eye syndrome is often related to other health conditions in the body. It is commonly associated with dryness of other mucus membranes (see Sjogren’s syndrome, below) and even interior body surfaces like joints (arthritis). Many dry eye patients also complain of connective tissue problems like brittle nails and many experience skin sensitivity to detergents. Digestive imbalances and autoimmune processes like Sjogren’s syndrome and lupus are frequently discovered underlying dry eye symptoms. When dry eye symptoms improve, there is also frequently noted an improvement in sinus and post-nasal drip conditions.
Sjogren’s syndrome is considered the most commonly misdiagnosed of all health conditions in women over the age of 40, affecting 4 million Americans. In Sjogren’s syndrome, dry eye symptoms are accompanied by dryness in other parts of the body. This cluster of symptoms is produced by an autoimmune process in which antibodies attack fluid-secreting cells. These glandular cells can ultimately be destroyed, and occasionally even become cancerous. Dry eye may be accompanied by fatigue, dry mouth (perhaps with a sore throat and swelling of the parotid gland), dry joints (arthritis), dry skin, dry cracked lips, dry scalp (dandruff), and dry, brittle nails. Lack of saliva can lead to dental caries. Doctors may prescribe anti-inflammatory and immunosuppressive steroids. In advanced cases, cyclosporin may be prescribed as well. Allergy to drugs, especially penicillin, may be linked to Sjogren’s syndrome.
Risk Factors
The aging process, which involves free radical damage to body tissues, increases the prevalence of dry eye symptoms. As we get older, on average our eyes produce 40% less lubrication. Pregnancy can also trigger dry eyes. Environmental allergens, toxins, and other irritants, like exposure to air conditioning, wind, excessive sunlight, dust, contact lenses, dry airplane air, smog, and smoke contribute as well. For example, in one study 40% of dry eye patients were smokers. Second-hand cigarette smoke also reduces the breakup time of the tears by 40%. Even a single cigarette can produce a level of carbon monoxide of 400 ppm (parts per million). Carbon monoxide, along with smog and chemical fumes inactivate lysozyme, the natural antibiotic secreted in the tears. Eye makeup, typically made of synthetic chemicals, depletes the lipid layer of the tears. Eye makeup is also frequently contaminated with bacteria.
Many synthetic medications also trigger dry eyes. These include oral contraceptives and other estrogens, sympathomimetic agents, anticholinergic drugs like atropine and scopolamine, synthetic vitamin A analogs (isotretinoin or Accutane), diuretics (especially those that deplete potassium), codeine, morphine, antihistamines, decongestants (including eye drops like Visine, murine, prefrin and clear eyes), marijuana, cancer drugs, and radiation treatments, phenothiazines, tranquilizers and antidepressants (like valium and Elavil), glaucoma medications (including Timoptic or timolol, betoptic, Betagan and ocupress) and other beta-blockers like practolol. Pesticides and other petrochemical xeno-estrogens may also be a problem, so avoidance of commercial produce is recommended as much as possible. When organic produce is unavailable, peeling grapes and strawberries, in particular, is recommended due to the common use of persistent fungicides such as captan.
Mechanical problems with the eyelids such as scars, drooping lids (sometimes even due to pressure from eyeglass nose pads), sleeping with the eyelids partially open, and incomplete closure on blink can cause dry eyes. Neurological problems like BellÕs palsy (paralysis of the facial nerve) can interfere with lid function, too. Ergonomic factors like the height of computer screens can affect dry eye symptoms, due to effects on eyelid positioning and resultant tear evaporation. Computers also double visual stress compared to conventional desk work, which can involve increased staring. Electromagnetic fields from computers contribute to the overall stress pattern, and the resulting stress can be alleviated with a variety of new technologies including ultralow radiation computer monitors and even special computer software. Even vitamin A, important for mucin production, is used up more rapidly in the eye during computer work due to the invisible flickering of the screen. A number of nutritional factors play a role and will be discussed next.
Diet and Nutrition
Digestion
Digestive function is impaired in Sjogren's syndrome patients, including deficiencies in hydrochloric acid and pepsin. Resultant hypochlorhydria symptoms include bloating, gas, and nausea as well as allergies and depression associated with Sjogren's syndrome. Herbal bitters and homeopathic remedies like Digestzymes help stimulate the secretion of digestive juices. Digestive enzyme supplementation (substitution therapy) has even been suggested except when stomach ulcers or pain are present. In some cases, the underlying cause may be a bacterial parasite in the stomach, called helicobacter pylori. Correction of such an infestation may involve anti-parasitic remedies, like Silver & Clove, or antibiotics along with steps to correct the terrain, so that it is not so susceptible to reinfestation. Acidophilus, Bifidus, and other friendly bacterial flora supplements are recommended in general to improve the function and terrain of the gastrointestinal tract. Three capsules a day of Friendly Flora are recommended.
Sugar & Artificial Sweeteners
Sugar (sucrose) intake increases the risk of dry eye by decreasing the tear break-up time, especially when the diet also includes less folic acid. Consumption of more than 11 teaspoons/day of sucrose (most of which is hidden in prepared foods) is the second most significant factor (after folic acid) linked to reduced tissue potassium levels in dry eye patients (see mineral section). Note that a single can of soda contains about 9 teaspoons of sugar! Thus avoidance of sweet processed foods while eating more leafy green vegetables can help improve dry eyes.
Avoidance of aspartame (Nutrasweet) also improves dry eye symptoms and contact lens tolerance in many patients. This can also alleviate a commonly associated symptom of intense thirst. Is it possible that aspartame makes diet soda addictive due to this side-effect of thirst? This may boost sales, but the FDA receives more letters complaining of side effects from aspartame than any other drug on the market!
Photosensitizing Foods
Certain foods may also exacerbate light sensitivity in Sjogren's syndrome patients. These particular foods, including limes, celery, and parsley contain furocoumarins, which are natural compounds that can increase photosensitivity.
Diet
In one study, only 18% of dry eye patients ate leafy green vegetables and only 6% ate fruits. At the same time, 75% were exposed to direct sunlight for over six hours a day. In addition, 72% were strictly vegetarian, lacking a full complement of essential amino acids as well as certain beneficial oils in their diet. These essential nutrients are crucial to the proper function of the mucin and lipid layers of the tear film. In general, a broad spectrum, optimum potency nutritional supplement should be taken as the basis of building an effective supplementation program.
Oils
Essential fatty acids are needed to produce both the lipid layer and the aqueous layer of the tear film. The omega-6 fatty acid gamma-linolenic acid (GLA), found in evening primrose oil and human breast milk, is also a precursor for the prostaglandin PGE-1. The deficiency of pancreatin and bile secretion reduces the absorption of these essential nutrients, as well as vitamin E, from the diet. Studies have found that about half or more of all dry eye sufferers achieve improvement in symptoms like reduced tear production, dry eye, visual acuity, brittle nails, and skin sensitivity to detergents as early as 10 days after beginning supplementation with omega-6 essential fatty acids from evening primrose oil (EPO) together with vitamin C and vitamin B6. In another study, tear production almost doubled in the first month among dry eye patients taking 3,000 mg/day of EPO together with vitamin C and vitamin B6. Symptoms tend to relapse eventually among patients who discontinue supplementation. Eating more small, cold-water fish, flax seeds, and walnuts, as well as supplementation with products like EPA fish oil, flaxseed oil, borage oil, and EPO, is recommended. One author suggests a dosage of 500 to 1000 mg/day of fish oil, EPO, or flaxseed oil for those with Sjogren’s syndrome. Another recommends 6 capsules a day of EPO in divided doses for between 1 and 12 weeks if needed in addition to increased intake of organic raw, fresh foods.
Oxidized, rancid, and toxic fats from commercial red meat and dairy products, fried foods, and hydrogenated oils like margarine compete and interfere with the proper function of the essential fatty acids. They should be eliminated from the diet as much as possible.
Vitamins
A
Vitamin A is normally found in the tear film. In parts of the world where vitamin A deficiency is widespread, severe dry eye syndrome is a leading cause of blindness. Vitamin A is needed for the health of all epithelial (surface) tissues, as well as for good night vision. Sjogren’s syndrome is often associated with decreased night vision performance, and this may be due to low levels of vitamin A and B vitamins as well, resulting from liver dysfunction. Vitamin A is especially needed to produce the mucin layer of the tears. Beta carotene (pro-vitamin A) has been reported to be helpful in dry eyes as well. Eye drops containing vitamin A together with vitamin C have also been reported to improve dry eye syndrome. Vitamin A metabolism is dependent on Zinc.
B complex
B vitamin deficiency is linked to Sjogren’s syndrome due to associated liver dysfunction.
B1
Vitamin B1 (thiamine) is needed for the metabolism of sugars but is deficient in refined foods loaded with refined sugar. Whole foods that contain high sugar levels, such as sweet fruits, also contain the needed vitamin B1 for the body to metabolize those sugars without depleting the vitamin in the process.
B2
Supplemental vitamin B2 has been recommended.
B3
Vitamin B3 (niacin) taken in excess can exacerbate dry eye symptoms. It is generally best to take any B vitamins with a full B complex supplement so that deficiencies of other B vitamins are not induced.
B6
Vitamin B6 (pyridoxine) is needed for the proper absorption of magnesium, which is required in the maintenance of potassium levels in the cells. Both vitamin B6 and magnesium are needed in the body's production of prostaglandin E-1. B6 is also required for sugar metabolism, so refined foods containing sugar deplete this vitamin. Dietary intake of less than 2 mg/day of vitamin B6 is the fourth most significant food factor linked to low potassium in dry eye (see mineral section). If dietary intake is less than 4 mg/day, increasing high protein foods rich in vitamin B6 are suggested including raw walnuts, hazelnuts, spinach, or rare grass-fed beef steak. Medium to well-done proteins results in increased demand for vitamin B6. In 1978, Ned Paige first reported improvement of dry eye syndrome with high doses of vitamin B6 in many patients. Vitamin B6 together with vitamin C and essential fatty acids has been found to improve dry eye symptoms and tear production. In one study, tear production almost doubled in the first month among dry eye patients taking up to 50 mg/day of vitamin B6 together with EPO and vitamin C.
B12
Vitamin B12 deficiency caused by malabsorption associated with digestive dysfunction in Sjogren's syndrome may help to explain the associated fatigue and depression symptoms. A dosage of 1,000 to 1,500 mcg/day is recommended.
Folic Acid
Folic acid is needed for cell mitosis (reproduction, such as for tissue repair) as well as sugar metabolism. Dietary intake of less than 310 mcg/day of food folate is the number one food factor associated with reduced potassium levels (see mineral section). If intake is less than 500 mcg/day, it is recommended to increase consumption of raw fresh fruits and vegetables. Leafy greens, sprouts, and raw fruit are especially high in this commonly deficient and heat-sensitive vitamin.
C
Vitamin C is concentrated in the tear film to a higher level than that found in the blood. It protects the eye from oxidative stresses including toxins, irritants, allergens, and inflammation. Vitamin C is a necessary cofactor for the final phase of the production of prostaglandin E-1. Vitamin C is also needed for proper sugar metabolism. Hypochlorhydria, linked to Sjogren’s syndrome, reduces the absorption of vitamin C. In one study, exposure to ammonia fumes reduced the vitamin C concentration in the tears by 50%. Dietary intake of vitamin C below 175 mg/day is the third greatest food factor (after folic acid deficiency and sugar toxicity) linked to reduced potassium levels in dry eye patients. Increased vitamin C intake is definitely suggested if the diet contains less than 400 mg/day. Dr. Ben C. Lane recommends eating more raw, fresh fruits and vegetables. Oral supplementation at optimum levels helps the eye heal its surface and connective tissues. For example, one study found that while 50 mg/day had no effect, 1500 mg/day greatly increased the healing of corneal ulcerations. Vitamin C together with vitamin B6 and essential fatty acids has been found to improve dry eye symptoms and tear production. In one study, tear production almost doubled in the first month among dry eye patients taking up to 7,500 mg/day of vitamin C together with EPO and vitamin B6. Eye drops containing vitamin C together with vitamin A have also been reported to improve dry eye syndrome.
E
Absorption of vitamin E may be reduced by deficient secretion of pancreatin and bile. Oil-based vitamin E supplements can go rancid if not refrigerated, counteracting the desired effects of the vitamin. Dry vitamin E (succinate form) is also more easily absorbed and utilized. Natural vitamin E (d form) is preferred over synthetic (dl) because half of the synthetic vitamin E molecules have the opposite shape of normal vitamin E, reducing effectiveness, and perhaps producing other forms of metabolic or energetic interference in the body. Topical vitamin E has been recommended for dry skin in Sjogren’s syndrome and has been used successfully in combination with other nutrients in eye drop form for dry eye patients.
Minerals
Hypochlorhydria, linked to Sjogren’s syndrome, reduces the ability to absorb many minerals including calcium, magnesium, and zinc. In 1983, Graeme Wilson and his associates found that the minerals calcium, magnesium, potassium, and sodium were each essential and together provide sufficient mineral content in the tear film to promote the integrity of the corneal epithelium.
Calcium
Calcium stores are depleted by eating refined sugar, as well as excess sodium from junk foods. Magnesium is also essential in regulating calcium metabolism, as is modest exposure to ultraviolet light as in full-spectrum lighting, or a 15-minute daily walk. Calcium is needed to maintain strong connective tissues, such as the cornea and conjunctiva, as well as for sugar regulation, balancing of pH, and proper nerve and muscle function. It is also present in the tear film itself.
Chromium
Glucose-tolerance-factor (GTF) chromium is critical for the metabolism and regulation of sugars, yet it is one of the first nutrients lost in the refining of foods such as grains. Refined sugar also increases the loss of chromium in the urine, leading to increased risks for reduced life span, cardiovascular disease, and diabetes.
Magnesium
Magnesium is required for the regulation of intracellular potassium supplies, for sugar metabolism, for the activation of vitamin B6 into its active form, pyridoxal-5-phosphate (P5P), and for the production of prostaglandin E-1. The most absorbable form of magnesium supplement is magnesium glycinate.
Potassium
Potassium is a critical intracellular mineral, needed for many functions including sugar metabolism and maintenance of the cellÕs electrical membrane potential. Potassium levels measured in hair tissue average 9 ppm for dry eye patients compared to a level of 65 ppm average for controls. This is linked to a low intake of folic acid, ascorbic acid, and vitamin B6, along with high sugar consumption. If dietary potassium intake is less than 4,000 mg/day, it is recommended to increase consumption of fresh fruit and vegetables. One banana contains about 400 mg of potassium, and all fruits and vegetables are high in this important mineral.
Conventional diuretic medications, as well as aspirin, deplete potassium. Supplementation with vitamin C and vitamin B6 can produce diuresis when desired clinically, while improving dry eye.
Sodium
Sodium is a major constituent of the aqueous layer of the tear film.
Zinc
Zinc and Vitamin A are synergistic. An animal study assesses the interaction between zinc and vitamin A on the ocular surface:
Zinc, Vitamin A and the Ocular Surface
Group Diet Microscopy
1 vitamin A and zinc normal
2 zinc decrease epithelial microvilli; corneal keratinization
3 zinc decrease epithelial microvilli
4 vitamin A decrease epithelial microvilli
5 vitamin A decrease epithelial microvilli
(Kanazawa S, Kitaoka T, Ueda Y, et. al. Interaction of zinc and vitamin A on the ocular surface. Graefes Arch Clin Exp Ophthalmol 2002;240(12):1011-21)
Herbs
Eyebright (Euphrasia) is used topically in the eye as an eyewash to relieve the soreness accompanying dry eye.
Homeopathy
Excessive watering of the eyes is sometimes related to dry eye syndrome. This paradox is due to lack of mucin, leading to dry spots which stimulate nerve reflexes to produce more tears in an attempt to rewet the cornea, which contains more nerve endings per square millimeter than any other part of the body. If the excessive tearing, also called epiphora, is due to a blocked tear duct, however, the homeopathic remedy to try is Silicea 6C, taken 4 times a day for up to a week.
Swelling or discomfort around the lacrimal gland, which is superior and temporal to each eye, and lies just posterior to the boney orbital rim, can be treated with the Mumps nosode. Other homeopathic remedies for dacryoadenitis include Acontum napellus (monk's hood), Apis mellifica (honey bee), Hepar sulphuris calcareum (impure calcium sulfide, CaS), Iodum (iodine, I), Rhus toxicodendron (poison ivy), and Silicea (silica, SiO2).
Dry eyes may be a contributing factor to the growth of tissue from the conjunctiva onto the cornea. This growth is called a pterygium. Try homeopathic Zinc 6C 3 times a day for 2 weeks, shifting to Ratanhia 6C if no improvement is noticed.
Similisan #1 from Switzerland is available over the counter as a homeopathic complex for dry, red eyes. It contains Belladonna 6X, Euphrasia 6X, and Mercurius sublimatus 6X.
Diagnostic Tests:
History:
A good way to diagnose dry eye is by the history. Patients with dry eye complain of sandy/gritty irritation, burning or a foreign body sensation worse later in the day. If a patient has these symptoms, they have dry eye until proven otherwise. This is because eye closure at night blocks evaporation, giving the eyes a chance to recover. Upon eye-opening evaporation begins, and symptoms become worse as the day goes on.
There are two main ways that tear film can lose water, increasing tear film osmolarity and causing dry eye:
decreased tear production
increased tear evaporation
Tear production decreases with lacrimal gland disease (e.g. Sjögren’s syndrome), and anything that decreases corneal sensation:
long-term contact lens wear (hard > soft, extended-wear > daily wear)
diabetes
LASIK
PRK (< LASIK)
herpes zoster
herpes simplex
Tear evaporation increases with:
large palpebral apertures, whether anatomical or due to thyroid eye disease
meibomian gland dysfunction due to chronic meibomianitis
Ask about:
contact lens wear
diabetes
past history of refractive surgery
past history of herpes infections
central facial flushing
Look at facial skin for telangiectases. Have the patient look directly ahead at your ipsilateral eye, and measure palpebral fissure width with a millimeter rule. Examine the lid margin, especially the meibomian gland orifices. If you can see them, they are “patent.” If you can’t see them, but when you press on the lid you see oil come out, they are “stenosed.” If you can’t see them, and when you press on the lid nothing comes out, they are “closed.” The more stenosed and closed meibomian gland orifices, the more meibomian gland dysfunction. Based on palpebral fissure width and assessment of the meibomian gland orifices, you can assess evaporative stress.
Take a fluorescein strip, wet with some sterile saline, shake off the excess, pull the lower lid down, and paint the strip across the inferior tarsal conjunctiva. Turn the cobalt blue light on, have the patient blink a few times, and then observe the tear film. In early dry eye, the nasal inferior marginal tear strip won’t fluoresce. As the tear volume decreases, increasing areas of the tear film won’t fluoresce. If the tears are not fluorescing, add a drop or two of sterile saline to the tear film to make the tears fluoresce, improving your view. As the upper lid rises after a blink, the tear film, rather than snapping up with the upper lid, will move more slowly, taking on a more viscous appearance. In drier eyes, debris is visible floating in the tear film. Any of these signs indicates decreased tear production.
With fluorescein in the eye, look at the staining pattern. In mild dry eye there is no staining. The first place that stains is the exposed nasal conjunctiva, followed by the exposed temporal conjunctiva. The inferior cornea stains last. Even in the late stages of dry eye, the conjunctiva stains more than the cornea. Rose Bengal or lissamine green makes staining more prominent.
Test corneal sensitivity if the history includes risk factors for decreased reflex tearing such as ocular surgery or herpes.
In contrast, meibomianitis patients have symptoms worse on waking, because the inflamed eyelids are up against the cornea all night. With meibomian gland dysfunction, the tear film appears more watery. The oil layer, in addition to preventing tear film evaporation, also lowers the surface tension of the tear film, helping to keep it close to the eye. Without the oil layer, tears act more watery and splash out of the eye. (Without the oil layer the Schirmer strip can wet more, giving false negative readings in dry eye.)
Tear film osmolarity in dry eye patients versus normal controls has a sensitivity (positivity in the presence of disease) in the high 90’s and a specificity (negativity in the absence of disease) in the high 90’s. Measure late in the day.
Specific Risk Factors
Sucrose/folic acid (high dietary ratio over 6 x 10-2 tsp/mcg) increases risk of low tear film BUT (break-up time) of less than 10 seconds by a factor of 40.
Potassium (dietary intake less than 2500 mg/day) increases risk of low tear film BUT (<10 seconds) by a factor of 15.
Hair K and/or Na extrememly low (K = potassium <8 ppm; Na = sodium <12 ppm for nape of neck hair) in dry eye syndrome
Tear Na extremely low in dry eye.
Tear K extremely low in dry eye.
Other Tests:
Fatty-Acid Profile of the blood can help to show if there is a need for GLA (e.g. EPO) supplementation.
References:
Memmert, R., ‘Americans fall short of eyecare goals,’ 20/20 September 1990, p.44. ‘In the News,’ Review of Optometry, October 15, 1997, p. 8. (reporting on a study by EagleVision)
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.118-9.
Simmons P.A., et al, ‘Toxic effects f ophthalmic preservatives on cultured rabbit corneal epithelium,’ American Journal of Optometry & Physiological Optics 65:867-73, 1988.
Simmons P.A., Clough S.R., Teagle R.H., Jaanus S.D., ‘Toxic effects of ophthalmic preservatives on cultured corneal epithelium,’ American Journal of Optometry & Physiological Optics 65:867-73, 1988.
Gobbels M., Lemp M., ‘Artificial tears: preservative’s role evaluated,’ Opthalmology Times, p.1 and 28, February 15, 1992.
Gobbels M., Spitznas M., ‘Corneal epithelial permeability of dry eyes before and after treatment with artificial tears,’ Opthalmology 99:873-78m 1992.
Salonen E.M., Tervo T., Beuerman R., ‘Toxicity of ingredients in artificial tears and ophthalmic drugs in a cell attachment and spreading test,’ Journal of Toxicology and Ocular Toxicology 10:157-66, 1991.
Gobbels M.J., Achten C., Spitznas M., ‘Effect of topically applied oxymetazoline on tear volume and tear flow in humans,’ Graefe’s Archive Opthalmology 229:147-49, 1991.
Laflamme M.y., Swieca R., ‘A comparative study of two preservative-free tear substitutes in the management of severe dry eye,’ Canadian Journal of Opthalmology 23:174-76, 1988.
VIVA drops are manufactured by Vision Pharmaceuticals (call 800-325-6789 for a free sample) and are available from Remission Foundation at 800-788-2442, as are individualized non-preserved eye drops in multidose dropper bottles.
Unpreserved eye drops include Refresh, Refresh Plus, and Relief from Allergan, BION and Tears Naturale preservative-free from Alcon, Aquasite from CIBA Vision Care, and Hypotears preservative-free from Iolab.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.119.
Winfield A.J., Jessiman D., Williams A., Esakowitz L., ‘A study of the causes of non-compliance by patients prescribed eyedrops,’ British Journal of Opthalmology 74:238-42, 1990.
Burns E., Mulley G.P., ‘Practical problems with eye drops among elderly Opthalmology outpatients,’ Age and Ageing 21:168-70, 1992. Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.120.
Smith S.E., ‘Eyedrop instillation for reluctant children,’ British Journal of Ophthalmology, 73: 48-81, 1991.
Mansour, A.M., ‘Tolerance of topical preparations: cold or warm?’ Annals of Opthalmology 23:21-22, 1991.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.121.
Waltz K.L., ‘Contamination of dropper bottles in a glaucoma clinic,’ Scientific Poster 141, American Academy of Opthalmology Meeting, October 1990.
Waltz K., Sherwood M.B., ‘Ring around the bottle,’ release from the American Academy of Opthalmology, October 28, 1990.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.122.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.123.
White, W.L., ‘Eye drops work better with two minutes of shuteye,’ American Academy of Opthalmology News Release, October 28, 1990.
Zimmerman T.J., ‘Getting a drop on the eye,’ Research to Prevent Blindness Science Writers Seminar.
Programs for NeuroFitness Training including these and other eye relaxation techniques are available from Remission Foundation at 800-788-2442.
Tuberville A., et al, ‘Punctal occlusion in tear deficiency syndrome,’ Opthalmology 89:1170-72, 1982.
Willis R.M., et al, ‘The treatment of aqueous deficient dry eye with removable punctal plugs,’ Opthalmology 94:514-18, 1987.
Tusbota K., ‘The effect of wearing spectacles on the humidity of the eye,’ Opthalmology 108:92, 1989.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.125.
Talal N., ‘How to recognize and treat Sjogren’s Syndrome,’ Drug Therapy, June 1984, pp. 80-87.
Leuenberger P.M., ‘Cyclosporin, steroids may avert destruction of lacrimal gland,’ Opthalmology Times, September 15, 1991, p.35.
Polorny G., et al, ‘Primary Sjogren's syndrome from the viewpoint of an internal physician,’ International Opthalmology, 15: 401-06, 1991.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.118.
Khurana A.K., et al, ‘Hospital epidemiology of dry eye,’ Indian Journal of Opthalmology 39:55-58, 1991.
Basu P.K., et al, ‘The effect of cigarette smoke on the human tear film,’ Canadian Journal of Opthalmology 13:22-26, 1978.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.126.
Frank C., ‘Fatty layer of the precorneal film in the office eye syndrome,’ Acta Opthalmologica 69: 737-43, 1991.
Bartlett JD. Medications and contact lens wear. In: Silbert JA, ed. Anterior segment complications of contact lens wear. New York: Churchill Livingstone, 1994; 482.
Fraunfelder FT, LaBraico JM, Meyer SM. Adverse ocular reactions possibly associated with isotretinoin. Am J Ophthalmol 1985; 100(4):534-7.
Bergmann MT, Newman BL, Johnson NC Jr. The effect of a diuretic (hydrochlorothiazide) on tear production in humans. Am J Ophthalmol 1985; 99(4):473-5.
Koeffler BH, Lemp MA. The effect of an antihistamine (chlorpheniramine maleate) on tear production in humans. Ann Ophthalmol 1980;12(2):217-9.
Seedor JA, Lamberts D, Bermann RB, Perry HD. Filamentary keratitis associated with diphenhydramine hydrochloride (Benadryl). Am J Ophthalmol 1986; 101(3):376-7.
Fraunfelder FT, Meyer SM. Drug-induced ocular side effects and drug interactions, 2nd Ed. Philadelphia: Lea & Febiger, 1982.
Nielsen NV, Ericksen JS. Timolol transitory manifestations of dry eyes in long-term treatment. Acta Ophthalmol 1979; 57(3):418-24.
Strempel I. The influence of topical beta-blockers on the breakup time. Ophthalmologica 1984; 189(3):110-5.
Van Buskirk EM. Adverse reactions from timolol administration. Ophthalmology 1980; 87(5):447-50.
Almog Y, Monselise M, Amog CH, Barishek YR. The effect of oral treatment with beta-blockers on tear secretion. Metab Ped Syst Ophthalmol 1983; 6(3-4):343-5.
Gold D.H., “Systemic Associations of Ocular Disorders," International Opthalmology Clinics, 31:83, 1991.
Silbert JA. A review of therapeutic agents and contact lens wear. Journal of the American Optometric Association, 67(3):165-72
Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Tsubota K., Nakamora K., ‘Dry eyes and video display terminals,’ The New England Journal of Medicine, February 25, 1993, p.584. for more information on electromagnetic pollution solutions, contact Remission Foundation at 800-788-2442.
Maury C.P.J., Tornroth T., Teppo A.M., ‘Atrophic gastritis in Sjogren's Syndrome,’ Arthritis and Rheumatism, 28:388-94, 1985.
Boyle J., ‘The digestive system and Sjogren's syndrome,’ Sjogren's Digest, 4:5, 1993.
Cater R.E., ‘The clinical importance of hypochlorhydria,’ Medical Hypotheses, 39:375-83, 1992.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.136.
Testing is available from Great Smokies Medical Lab.
Sherwood L., Gorbach M.D., Goldin B.R., ‘Nutrition and the gastrointestinal microflora,’ Nutrition Reviews, 50:378-81, 1992.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.138.
Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Roberts H.J., ‘Aspartame-associated dry mouth,’ Townsend Letter for Doctors, March 1993, p. 201-02.
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Khurana A.K., et al, ‘Hospital epidemiology of dry eye,’ Indian Journal of Opthalmology 39:55-58, 1991
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.138.
Horrobin DF and Campbell AC, 1980. Manthorpe R., et al, ‘Primary Sjogren's syndrome treated with Efamol,’ Danish Rheumatology Society, June 1983.
Horrobin D.F., Clinical Uses of Essential Fatty Acids, Eden Press, 1982, pp. 129-37.
Schafer D.L., ‘Vitamin supplements found to help raise Schirmer value tear volume,’ Ocular Surgery News, November 1986
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Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.137.
McLenachan J., ‘New aspects of the etiology of Sjogren's Syndrome,’ Transactions of the Ophthalmological Society, 76:413-26, 1956.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.130.
Holly F.J., ‘Vitamins and polymers in the treatment of ocular surface disease,’ American Academy of Optometry, New Orleans, LA, December 11, 1989.
McLenachan J., ‘New aspects of the etiology of Sjogren's Syndrome,’ Transactions of the Ophthalmological Society, 76:413-26, 1956.
Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Lockie A. The Family Guide to Homeopathy; Symptoms and Natural Solutions. New York: Simon & Schuster, 1989; p. 160.
Gold D.H., ‘Systemic Associations of Ocular Disorders,’ International Opthalmology Clinics, 31:83, 1991.
Horrobin and Campbell, 1980. Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Horrobin D.F., Clinical Uses of Essential Fatty Acids, Eden Press, 1982, pp. 129-37.
Manthorpe R., et al, ‘Primary Sjogren's syndrome treated with Efamol,’ Danish Rheumatology Society, June 1983
Schafer D.L., ‘Vitamin supplements found to help raise Schirmer value tear volume,’ Ocular Surgery News, November 1986.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.135.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.136-8.
Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Horrobin and Campbell, 1980. Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.136.
Paterson C.A., et al, ‘Vitamin C levels in human tears,’ Archives of Opthalmology 105:376-77, 1987.
Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Boyd T.A.S., Campbell F.W., ‘Influence of ascorbic acid on the healing of corneal ulcers in man,’ British Medical Journal, November 18, 1950, pp.1145-48.
Horrobin D.F., Clinical Uses of Essential Fatty Acids, Eden Press, 1982, pp. 129-37.
Manthorpe R., et al, ‘Primary Sjogren's syndrome treated with Efamol,’ Danish Rheumatology Society, June 1983
Schafer D.L., ‘Vitamin supplements found to help raise Schirmer value tear volume,’ Ocular Surgery News, November 1986.
Holly F.J., ‘Vitamins and polymers in the treatment of ocular surface disease,’ American Academy of Optometry, New Orleans, LA, December 11, 1989.
Sardi B. Nutrition and the Eyes, Vol. 1. Montclair, California: Health Spectrum Publishers, 1994, p.137.
Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Horrobin and Campbell, 1980. Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Cotlier, 1983. Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Lockie A. The Family Guide to Homeopathy; Symptoms and Natural Solutions. New York: Simon & Schuster, 1989; p. 160.
Lockie A. The Family Guide to Homeopathy; Symptoms and Natural Solutions. New York: Simon & Schuster, 1989; p. 166.
Nosode Therapy in Practice. Baden-Baden, Germany: Biologische Heilmittel Heel GmbH, 1985; p. 63.
Moffat JL. Homeopathic Therapeutics in Ophthalmology. New Delhi, India: B. Jain Publishers, 1982; p. 128.
Lockie A. The Family Guide to Homeopathy; Symptoms and Natural Solutions. New York: Simon & Schuster, 1989; p. 164.
Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Lane BC. Fed Proc 1984; 43(March): 1052. Lane BC. Poster at NYAO lecture, 1983.
Gorn RA. 1981 lecture. reported by Lane BC. The Tear Film: Nutriture Considerations. Presented at the College of Syntonic Optometry annual conference, 1995.
Available from Monroe Medical Laboratory, Southfield, NY 10975. Levels often improve within 2 months.