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Use nutrition as a tool for managing ocular disease

Patients can participate in their eye care by obtaining vital nutrients in their diet.

by Cheryl Lynn Bergin, OD

This course is jointly sponsored by PCON, the State University of New York State College of Optometry and Vindico Medical Education. It is COPE-approved for 2 continuing education credits.

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Doctors have the technology to detect ocular disorders at their earliest stages when nutritional changes can be powerful defenses against the progression of sight-threatening diseases. Before pharmaceutical or surgical interventions are needed, nutrition can be implemented as a sight-saving tool. Properly focused nutrition could delay the progression of some ocular disorders and for some, even reverse deteriorations in ocular health.

The threat of vision loss terrifies us. Diagnoses involving progressive vision loss often leave patients feeling hopeless and helpless. While we never want to offer false hope, proper nutrition can restore one’s sense of control. Even though we cannot “cure” everything, we are not entirely helpless. Nutrition and exercise are some of the best medicines available to us.

During an era of economic depression, patients too often must choose between purchasing food and medicine. As Hippocrates said, “Let food be your medicine...”

Fat-soluble vitamins

Fat-soluble vitamins (A, D, E and K) – vs. water-soluble vitamins – possess a greater risk of accumulating to toxic levels in the body.

Fat-soluble vitamins

Vitamin A

General signs of vitamin A deficiency include acne; dry, rough, cracked, thickened, scaly and hardened skin (especially on palms of hands and soles of feet); weight loss and dry mouth. Vitamin A deficient hosts are more susceptible to viral, bacterial and parasitic infections.

Vitamin A deficiency is a major cause of worldwide blindness. Night blindness (nyctalopia), impaired vision and dry eyes (progressing to corneal ulceration, descemetocele and perforation) are visual signs of hypovitaminosis A.

Toxicity is characterized by changes in skin (dry, fissured, itching, scaling, peeling) and mucous membranes. Cheilosis (cracking of the corners of the mouth), gingivitis, dry mouth and dry eyes result. Advanced signs include hair loss (alopecia) and brittle nails.

Bone and joint pain and fragility, with an increased incidence of fractures, can result. Brain tumor or hydrocephalus symptoms may arise due to increased pressure in the skull. Headaches, nausea and vomiting accompany hypervitaminosis A.

Anorexia (loss of appetite), irritability, night sweats, sleep difficulties, fatigue, malaise and menstrual irregularities or cessation may occur. Abnormal liver function, hepatomegaly, splenomegaly, ascites, portal hypertension, abdominal pain and GI disturbances are common with hypervitaminosis A.

It is important to note that beta-carotene supplementation is contraindicated in smokers (even 5 years after smoking cessation) due to increased lung cancer risks.

Vitamin D

The signs of hypovitaminosis D include burning of the mouth and throat, nervousness, scalp sweating, diarrhea, insomnia and mineral weakness in bones. Nearsightedness is a visual symptom associated with vitamin D deficiency.

It also causes rickets in children and osteomalacia in adults. Softening of bones, bent and bowed legs, weak muscles and late tooth development characterize rickets.

Hypercalcemia, kidney stones, metastatic calcifications of soft tissues (kidney, heart, lung and tympanic membrane) are associated with hypervitaminosis D. Deafness can result.

Headache, nausea, vomiting, constipation, diarrhea, polyuria and polydipsia are also common symptoms. Irritability, weakness, tiredness and anorexia may be experienced. Kidney failure is the most serious complication of vitamin D toxicity.

Vitamin E

Neurobiological manifestations of hypovitaminosis E include decreased reflexes, difficulty walking, weakened eye muscle movements and a decreased ability to feel vibration. Anemia, arm and leg edema, spinocerebellar degeneration and peroxidation of cellular lipid membranes can also occur.

Vitamin E is generally nontoxic. However, signs of toxicity include stomach upset, nausea, flatulence, diarrhea, dizziness, muscle weakness, fatigue and elevated blood pressure.

Vitamin K

Vitamin K deficiency is rare. In newborn infants, a bleeding tendency is possible. The underlying cause is hypoprothrombinemia. In severe cases, hemorrhaging can result in fatal anemia. Bleeding diathesis is characterized by hematomas, hematuria, melena (passage of black tarry stools containing blood that has been acted on by intestinal juices), ecchymoses and bleeding gums. Vitamin K deficiency occurs in cases of lipid malabsorption, destruction of intestinal flora in those receiving chronic antibiotic therapy and liver disease.

Vitamin K is generally nontoxic. However, jaundice in premature infants is possible.

Water-soluble vitamins

Water-soluble vitamins – B1, B2, B3, B5, B6, B12, biotin, folic acid and vitamin C – excreted via the kidneys, rarely accumulate to toxic levels in the body. See the accompanying table for dietary and natural sources of the water soluble vitamins.

Water-soluble vitamins

Vitamin B1

Early stage deficiency of vitamin B1 (thiamine) involves anorexia, indigestion, constipation, weight loss and malaise. Heaviness and weakness of legs, tender calf muscles, “pins and needles” and numbness in legs, anesthesia of skin (especially tibial) and muscle wasting are possible. Increased pulse rate and palpitations, nausea and vomiting are associated with thiamine deficiency. Psycho-/neurological symptoms include lack of coordination, mental or emotional depression, memory problems and nervousness.

B1 deficiency results in beriberi (which literally translates to, “I can’t! I can’t!”), characterized by high-output cardiac failure, pleural and peritoneal effusions, peripheral neuropathy, decreased pain tolerance, shortness of breath and edema in hands and feet. Seventy percent of those with beriberi have ocular complications.

Wet beriberi involves edema of legs, face, trunk and serous cavities as well as tense calf muscles, fast pulse, distended neck veins, high blood pressure and decreased urine volume. Dry beriberi involves worsening of early-stage polyneuritis, difficulty walking, encephalopathy, loss of immediate memory, disorientation, nystagmus and ataxia. With dry beriberi, Wernicke-Korsakoff syndrome is possible.

Acute infantile beriberi occurs between 2 and 5 months of age and involves decreased urine output, excessive crying, thin and plaintive whining and cardiac failure. Chronic infantile beriberi involves constipation, vomiting, fretfulness, soft toneless muscles and skin pallor with cyanosis.

Wernicke’s syndrome of delirium, stupor, ophthalmoplegia, ptosis and nystagmus results from chronic vitamin B1 deficiency. Wernicke’s mental disturbance includes memory problems, disorientation and confusion. Such signs and symptoms are collectively termed Korsakoff’s psychosis. Wernicke-Korsakoff syndrome is seen as a result of chronic alcohol abuse.

Vitamin B1 is considered nontoxic. As a water-soluble vitamin, it is excreted in the urine and rarely accumulates to toxic levels in the body.

Vitamin B2

Initial B2 (riboflavin) deficiency symptoms include soreness and burning of the lips, mouth and tongue. More advanced symptoms include cheilosis, angular stomatitis, glossitis (smooth, red, painful tongue), purplish or magenta tongue and hypertrophy or atrophy of tongue papillae.

Seborrheic dermatitis of nasolabial folds, vestibule of the nose, ears, eyelids, scrotum and vulva (itchiness and inflammation of the skin of the external genitalia in men and women) and alopecia can occur. Normocytic and normochromic anemia are possible.

Psychological symptoms include depression, deterioration of personality, dizziness and neuropathy.

Ocular pathologic conditions with riboflavin deficiency include inflammation of the conjunctiva, superficial corneal vascularization, corneal ulcerations, redness, itching, tearing, burning, blurred vision, cataract formation and photophobia. Clinicians should examine all patients with a history of malnutrition or alcohol abuse for manifestations of vitamin B1 or B2 deficiency.

Riboflavin is considered nontoxic.

Vitamin B3

Anorexia, fatigue, weakness, heartburn, diarrhea and headache are general symptoms of vitamin B3 (niacin) deficiency. Swollen red tongue and painful swallowing can occur. Red, inflamed, scaling dermatitis – prominent on the face, neck, arms and hands, but present on any sun-exposed areas – are associated with niacin deficiency.

Psychological symptoms include nervousness, irritability, depression, disorientation, delusional thoughts and hallucinations. Classic niacin deficiency state, termed pellagra, includes the four “D”s: dermatitis, diarrhea, dementia/delirium and, if severe enough, death.

“Niacin flush,” or vitamin B3 toxicity, is characterized by burning and itching skin, especially of the face, hands and upper trunk. Severe niacin toxicity involves liver damage, abnormal heart rhythms, gouty arthritis and rash on large areas. GI problems associated with niacin toxicity include upset stomach, cramps, nausea, vomiting and diarrhea.

Vitamin B5

Symptoms of B5 (pantothenic acid) deficiency are exceedingly rare, but can include nausea, numbness in extremities, insomnia, muscle spasms and cramps, headaches, fatigue, stomach pain, gas, diarrhea, nausea, vomiting, alopecia and anorexia. Nerve function impairments include burning foot pain and loss of coordination. Emotional symptoms include depression, irritability and nervousness. Weakness, tachycardia, low blood pressure and eczema are possible with B5 deficiency.

B5 is considered nontoxic.

Vitamin B6

Hypovitaminosis B6 (pyridoxine) symptoms include acne, alopecia, anemia, anorexia, joint pains, growth retardation, cheilosis, painful tongue, mouth ulcers and poor wound healing. Depression, dizziness, pins and needles or electric shock sensations, sleepiness, fatigue and weakness are also possible. Conjunctivitis is an ocular complication of B6 deficiency.

B6 is generally nontoxic. However, high doses (2,000 to 6,000 mg/day) can cause numbness and tingling of the nerves supplying the hands and feet, as well as actual loss of sensation in these areas.

Vitamin B12

Megaloblastic and pernicious anemias are associated with B12 (cobalamin) deficiency. GI problems include constipation and cramping. Fatigue, dizziness, a smooth, red, inflamed tongue and heart rhythm abnormalities are possible.

Neurologic symptoms include numbness and nerve and spinal cord damage. Depression and irritability are psychological symptoms of B12 deficiency.

Even though B12 is considered nontoxic, B12 supplementation may induce an acne-like eruption on the skin or worsening if acne is present.

Biotin

Seborrheic dermatitis, skin rashes and dryness, a waxy, grayish appearance, alopecia and loss of body hair are symptoms of biotin deficiency. Glossitis and a pale, smooth tongue also occur. Anorexia, nausea, hepatic stenosis, hypercholesterolemia and elevated blood sugar are common symptoms. Depression, numbness, muscle pains and weakness, tiredness, anemia, paralysis and sleep disturbances are also characteristic of biotin deficiency.

Biotin is considered nontoxic.

Folic acid

Megaloblastic anemia (folic acid deficiency) is characterized by irritability, weakness, lack of energy, sleeping difficulties and loss of facial color. Headache, faintness, pallor, sore red tongue, diarrhea and weight loss are possible. Psychological symptoms include poor memory, hostility and paranoia.

Folic acid deficiency can cause neural tube defects in the developing fetus. It is critical for women who are pregnant or may become pregnant to have adequate folic acid in their prenatal diets.

In addition to B1 and B2 deficiencies, alcoholism causes folate deficiency.

Folate is considered nontoxic. However, signs of folic acid toxicity include abdominal distention, flatulence, nausea, anorexia, sleep disturbances with vivid dreams and malaise.

Vitamin C

Severe vitamin C (ascorbic acid) deficiency is termed scurvy in adults and Moeller-Barlow disease in children. Signs manifest after 45 to 80 days of vitamin C deprivation and include lesions in mesenchymal tissue, impaired wound healing, increased susceptibility to infection, edema and hemorrhages. Anemia can result. Weakness in bone, cartilage, teeth and connective tissues occur.

Adults with scurvy may have swollen, bleeding gums and eventual tooth loss. Lethargy, rheumatic pains in the legs, muscular atrophy and hemorrhagic lesions of the skin (bruising), mucous membranes (nosebleeds), body cavities and orbits characterize hypovitaminosis C. Alopecia, dry skin, shortness of breath and digestive difficulties also occur. Psychological changes include irritability, hysteria, hypochondria, loss of sense of well-being and depression.

Patients with scurvy are not always substance abusers. Scurvy typically results from accidental malnutrition and poor dietary habits. By consuming large amounts of citrus fruits (limes, lemons and oranges) during extended voyages, British sailors avoided scurvy and earned the nickname, “Limeys.”

Vitamin C is generally nontoxic, but can cause an upset stomach and diarrhea. Megadoses of vitamin C can lead to kidney stones and gout. Large doses above the recommended daily allowance could cause hemolysis in those lacking the enzyme glucose-6-phosphate dehydrogenase.

Although vitamin C may protect against gastric cancer, in 2005, Zhang and Farthing suggested that in conjunction with Helicobacter pylori, vitamin C may increase the risk of gastric carcinogenesis. High levels of vitamin C may increase the general risk of cancer through its pro-oxidant activity.

Minerals

Minerals (calcium, iodine, iron, magnesium, phosphorus and zinc) are vital nutrients, functioning in body metabolism, muscle movement, body growth, water balance and other biological processes. See the accompanying table for the dietary and natural sources of minerals.

Sources of minerals

Calcium

Brittle fingernails, eczema, insomnia, high blood pressure, localized numbness and tingling sensations (arms and legs), muscle cramps and tetany are symptoms of calcium deficiency. Long-term dietary deficiency of calcium contributes to osteoporosis. Low calcium intake may contribute to colon cancer and hypertension. Psychological manifestations of calcium deficiency include agitation, hyperactivity, nervousness and irritability.

Anorexia, muscle weakness, hypercalcemia, calcification in soft tissues (kidneys) and increased bone fractures are associated with calcium toxicity. Neurological symptoms include transient inability to speak and difficulty with balance and walking. In severe cases of calcium toxicity kidney stones may develop.

Iodine

Iodine deficiency in children is associated with poor cognition and is the most common preventable cause of mental retardation in the world. Very low iodine intakes are associated with the development of endemic or simple goiter. Severe iodine deficiency during gestation and early postnatal growth results in cretinism. Cretinism is characterized by mental deficiency, spastic displegia, quadriplegia, deaf mutism, dysarthria, a characteristic shuffling gait, shortened stature and hypothyroidism in infants.

Rash, headaches, metallic taste and iodide goiter characterize iodine toxicity. For those with pathological thyroid conditions, excessive iodine intake may cause hypothyroidism, goiter formation or hyperthyroidism.

Iron

Cheilosis, inflamed tongue, pale skin, anorexia, fragile bones, sensitivity to cold, constipation, dizziness, difficulty swallowing, fatigue, weakness and koilonychias (fingernails with cuplike depressions) are symptoms of iron deficiency. Psychological manifestations of iron deficiency include depression and confusion.

Hypochromic, microcytic anemia is associated with iron deficiency. Iron deficiency, the precursor of iron deficiency anemia, is the most common of all nutritional deficiency diseases.

Headaches, nausea, vomiting, cramps, diarrhea, weak pulse, fatigue, anorexia, weight loss, dizziness, shortness of breath and grayish skin color are symptoms of iron toxicity. Note that loss of appetite, extreme fatigue and dizziness occur with both iron deficiency and toxicity.

Iron overload (hemochromatosis) symptoms include abnormal iron accumulation in the liver, excessive tissue ferritin levels, elevated serum transferrin levels, oxidation of LDL cholesterol and cardiovascular complications. Disorders associated with iron overload include thalassemia, sideroblastic anemia, chronic hemolytic anemia, aplastic anemia (a normochromic-normocytic anemia), ineffective erythropoiesis, transfusional iron overload (secondary to multiple blood transfusions), porphyria cutanea tarda and alcoholic cirrhosis.

Iron toxicity is rare, but may occur in children who eat iron-fortified vitamins or supplements as if they were candy. Iron toxicity involves irritation of the mucosa, ulceration, bleeding, hypoxia, metabolic acidosis, alveolar and hepatic damage and renal failure. Excess dietary iron intake can be fatal in doses of 3 g to 10 g. Death can occur in 12 to 48 hours.

Magnesium

Anemia, caused from red blood cell hemolysis, is possible with magnesium deficiency. Other symptoms include anorexia, nausea, vomiting, tachycardia, hypocalcemia, hypokalemia, impaired responsiveness to parathyroid hormone, sodium retention, tremors, muscle spasm, tetany, myoclonic jerks, athetoid movements, convulsions and coma. Mental changes associated with magnesium deficiency include agitation, anxiety, confusion, depression, disorientation and hallucinations. Because magnesium is required for carbohydrate metabolism, magnesium deficiency has also been linked to insulin resistance and metabolic syndrome.

Bradycardia, fatigue, low blood pressure, flushing, dry mouth, muscular weakness, thirst, nausea and vomiting are symptoms of magnesium toxicity. Magnesium toxicity is seen with impaired kidney function, especially in people taking magnesium supplements.

Phosphorus

Anorexia, weight loss, weakness, fatigue, numbness, tingling sensations and bone pain are symptoms of phosphorus deficiency. Neural, muscular, skeletal, hematologic and renal abnormalities may also occur. Anxiety and apprehension are psychological manifestations of phosphorus deficiency.

Nerve and muscle irritability, muscle spasms and convulsions occur with phosphorus toxicity. Phosphorus toxicity, sometimes referred to as nutritional secondary hyperparathyroidism, results in fragility fractures. The only documented cases involve people with severe kidney disease and renal failure who cannot rid the body of excess phosphorus.

Zinc

Acne, alopecia, brittle nails, white spots on nails, scaly skin rashes and skin lesions are symptomatic of zinc deficiency. High cholesterol, diarrhea, fatigue, mild anemia, low plasma zinc levels, hypogeusia (decreased taste acuity), loss of smell, anorexia and anergy are also possible. Diminished natural killer cell activity (but not with thymic atrophy or lymphopenia), frequent infections and poor wound healing occur.

Poor growth, short stature, delayed puberty, hypogonadism, hypospermia, impotence and male infertility are associated with zinc deficiency. Psychological symptoms of zinc deficiency include behavioral disturbances, irritability, amnesia, memory loss and paranoia.

Ocular complications of zinc deficiency include photophobia and nyctalopia.

Stomach irritation and vomiting accompany zinc sulfate in amounts of 2 g/day or more. Tiredness, kidney failure, anemia, fever, poor coordination and central nervous system disturbances characterize zinc toxicity.

Trace minerals

Trace minerals (chromium, copper, fluoride, manganese, molybdenum, potassium, selenium and sodium) are vital minerals required in dietary amounts less than 100 mg/day. See the accompanying chart for dietary and natural sources of trace minerals.

Sources of trace minerals

Chromium

Symptoms of chromium deficiency include anxiety, fatigue, sugar intolerance and insulin resistance (borderline diabetes), stunted growth and high cholesterol. Disturbances in fat, sugar and protein metabolism can occur.

Skin rashes, stomach ulcers and poor kidney and liver function are attributed to excessive chromium intake.

Copper

Copper deficiency symptoms include alopecia, anemia, rashes, emphysema, fatigue, high cholesterol, frequent infections, neutropenia (low white blood cell count), depression and heart muscle damage. Osteoporosis, skeletal abnormalities (demineralization), subperiosteal hemorrhages, defective elastin formation and hair and skin depigmentation are common symptoms.

Neutropenia and leukopenia are the best early indications of copper deficiency in children. The failure of erythropoiesis, along with cerebral and cerebellar degeneration, may lead to death.

Menkes syndrome (or kinky-hair syndrome) is a sex-linked recessive defect that results in copper malabsorption, increased urinary copper loss and abnormal intracellular copper transport, all of which cause an abnormal distribution of copper among organs and within cells.

Muscle and joint pain, nausea and vomiting, stomach pains and hemolytic anemia are characteristic of copper toxicity.

Psychological symptoms of copper toxicity include irritability and depression. Both occur with excess or deficiency of copper. Although copper toxicity from food is considered impossible, intake of toxic levels can result in liver cirrhosis and abnormalities in red blood cell formation.

Wilson’s disease (hepatolenticular degeneration) is characterized by excessive accumulation of copper in body tissues, such as the eyes, as a result of a genetic deficiency in the liver synthesis of ceruloplasmin.

Fluoride

Weak, brittle bones and teeth and dental caries are associated with fluoride deficiency. However, because of fluoride in water, deficiency is not known in humans.

Excess fluoride intake can result in poor bone health, poor kidney function and nerve and muscle problems. Brown mottling of tooth enamel is possible in children on doses of 2 mg/kg to 8 mg/kg of body weight. Fluorosis can develop from daily doses of 0.1 mg/kg. Higher intakes lead to tooth flaking and more serious dental effects.

Manganese

Data on manganese deficiency is confined to animal studies. Fragile bones, rashes, sugar intolerance, high cholesterol, nausea, weight loss, reproductive tract (ovary and testes) degeneration, sterility, skeletal abnormalities and ataxia characterize the offspring of mothers who are manganese deficient.

Manganese toxicity can result in anorexia, muscle pains, abnormal MRI results and hepatic dysfunction. The psychological and neurological symptoms of manganese toxicity include hallucinations, impaired judgment and memory, sleeplessness, Parkinson-like symptoms, headaches, dizziness, psychiatric and nerve disorders.

Molybdenum

Rapid breathing, tachycardia, mental changes and abnormalities of sulfur and purine metabolism characterize molybdenum deficiency. Increased risk for gout, cancer, cavities and sexual impotence are also possible. Nyctalopia is an ocular manifestation of molybdenum deficiency.

Aside from increases in uric acid and gouty attacks at doses of 10 mg/day to 15 mg/day, molybdenum is considered nontoxic in humans.

Potassium

Acne, constipation, salt and fluid retention, stunted growth, low blood pressure, fatigue, insomnia, muscle weakness and cramping, thirst, sugar intolerance, high cholesterol, heart palpitations and extremely dry skin and mouth characterize potassium deficiency. Those with bulimia nervosa exhibit hypokalemia (excessively low potassium levels). Depression, nervousness and clouded thinking are possible psychological symptoms associated with potassium deficiency.

Difficulty speaking, muscle weakness and pain characterize potassium toxicity. Cardiac complications include abnormal heart rhythms and heart failure. Clouded thinking occurs with too much or too little potassium.

Selenium

Although selenium deficiency is rare and takes years to develop, it can cause high cholesterol, stunted growth, frequent infections, poor liver and pancreas function, sterility in men and heart problems. Two selenium deficiency diseases are Keshan disease, a form of cardiomyopathy, and Kashan-Bek disease, which involves symmetric stiffness and swelling and pain in the interphalangeal joints of the fingers, followed by generalized osteoarthritis.

Selenosis is characterized by alopecia, arthritis, brittle nails, diabetes mellitus, garlic breath odor, metallic taste, muscle pains, irritability, jaundice, rashes, pale complexion, tooth decay and nonspecific gastrointestinal and neurologic abnormalities. Poor immune, kidney and liver function are also associated with selenium toxicity.

Sodium

Anorexia, hypogeusia, weight loss, nausea and vomiting, stomach cramping, gaseousness, difficulty balancing to walk, lethargy, muscle weakness, skin rashes and frequent infections are general symptoms of sodium deficiency. Psychological and neurological symptoms of sodium deficiency include dizziness, confusion, hallucinations, memory problems, mood swings, tearfulness and possibly seizures.

Symptoms of sodium toxicity include cloudy thinking, edema, nerve irritability, muscle tremors, polydipsia, polyuria and anorexia. Sodium toxicity is associated with hypertension and congestive heart failure.

Eye-specific nutrients

Eye-specific nutrients include vitamin C (ascorbic acid), vitamin E (d-alpha tocopherol), zinc (zinc oxide), omega-3, zeaxanthin, mixed tocopherols, lutein and alpha linolenic acid (ALA).

Dietary sources of lutein and zeaxanthin include kale, collard greens, spinach, turnip greens, broccoli, Swiss chard, corn and orange pepper. ALA is found in flax, flaxseed oil, canola oil, soybeans and perilla. The accompanying tables list dietary sources of beneficial carotenoids (lutein, zeaxanthin and beta-carotene) and alpha-linolenic acid.

A diet rich in beneficial carotenoids
Color coding for fruits and vegetables

A colorful plate provides a plethora of vital nutrients. The body best utilizes nutrients when they are consumed in raw foods. Remember water, the forgotten nutrient, which provides the working environment for other vital nutrients.

Rutin, a bioflavinoid with vitamin-like actions, may reduce IOP in people with open-angle glaucoma. Patients at risk for glaucoma should avoid caffeine (coffee, chocolate and soft drinks) and consumption of trans fatty acids. A diet excessive in protein may increase IOP.

Even if cataracts have begun to develop, a combination of the antioxidants, vitamins A and C, may arrest cataract progression and delay the need for cataract surgery.

Those with a family history of cataracts should take vitamin E to potentially reduce their risk of developing cataracts by 50%. Because vitamin E can increase blood pressure, one must monitor blood pressure when increasing vitamin E intake.

A diet high in simple sugars; table sugar and corn syrup (sucrose), honey (glucose), milk sugar (lactose), fruit sugar (fructose) and xylose (sugar-free substance used to sweeten sugar-free diabetic candies, chewing gum and cookies); may promote cataract development. Diabetics tend to develop cataracts well before nondiabetics.

Food sources of alpha-linolenic acid

Vitamin deficiencies and toxicities can cause a wide range of ocular manifestations:

The ocular effects of general malnutrition

Five broad classes of nutrients – proteins, carbohydrates, fats, minerals and vitamins – are recognized as necessary for human survival. A meal plan for the average person should consist of 50% carbohydrates, 30% healthy fats and 20% protein. Clinically, the absence of proteins and vitamins has the most profound effect.

Lack of protein intake results in Kwashiorkor syndrome, characterized by severe weight loss, dermatitis, alopecia and impaired healing. Ocular manifestations include eyelid edema, chemosis and frequent conjunctival infections.

The clinician should record the frequency, onset and duration of infectious conditions and the type of discharge (watery, stringy or mucopurulent). Swollen preauricular nodes could indicate a viral cause. A careful slit-lamp examination should be performed, noting eyelid debris, discharge, palpebral conjunctival papillae, follicles and pseudomembranes.

Chronic alcohol abuse results in protein energy malnutrition, thiamine (B1), riboflavin (B2), pyridoxine (B6), folate and vitamin A deficiencies. Such severe deficiencies are caused by defective gastrointestinal absorption, abnormal nutrient use and storage, increased metabolic needs and increased rate of nutrient depletion. Failure to recognize possible thiamine deficiency in chronic alcoholics may result in irreversible brain damage (Korsakoff psychosis).

It is important to refrain from judgments regarding weight. If a patient is clinically obese (20% over prescribed healthy weight), this must be addressed professionally and politely.

When one’s vision is restricted, dietary restrictions can seem like another major loss. There is no reason to miss out on one of life’s basic pleasures, eating. Variety is the spice of life. Moderation and balance are essential.

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