Lazy Eye - amblyopia
2007-05-05 12:50:30
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“Vision and other sensory functions began to improve within 2 months of vitamin therapy, and normal vision was eventually restored.” 1995.  Department of Ophtalmology, Harvard Medical School.

 

Amid all the medical news spin regarding the patch-versus-drops studies, a curious silence persisted as to the fact that ‘lazy eye (amblyopia, optic nerve neuropathy),’ may be a manifestation of nutritional deficiency, drugs (such as antibiotics, steroids and antihistamins) as well as environmental toxicity .  Even in a case when amblyopia was associated with a DNA mutation known to cause “hereditary Optic neuropathy,” vitamin B12 was found lacking, and the patient’s vision was restored following vitamin supplementation. 

 

Lazy eye,  or amblyopia, widespread among children, describes a situation in which one eye has less vision than the other.  It is a neurological condition and it results in faulty focusing such as myopia,  hyperopia  or astigmatism (short-, long-, of uneven- sightedness, respectively). Another condition, strabismus, or crossed eyes, is manifested in one eye looking in a different direction than the other, usually inwardly, as, in early childhood, one may develops the ability to ignore the eye. 

 

If this occurred with alcoholic intoxication, the individual would have double vision. Strabism may also lead to amblyopia if the wondering eye is always the same eye, as in such case, the eye is not being used and simply atrophies.  The lazy eye, if not treated, may lead to blurred vision, or even blindness, in the affected eye. Usually the treatment at young age (before 7-8 years of age) is aimed at manipulating the central vision in the brain (with eye patches or atropine drops), or the eye muscles, when muscles are involved,  into exercising the weak eye, on the theory that if you don’t use it, you loose it.  If done early, it usually works, by recovering  some vision and aligning the eye, at least to a certain degree where glasses are possible.

 

The Greens and the Liver


It is widely recognized that children and adults in poor countries around the globe develop various Vision problems due to nutritional deficiencies.


 

Reported clinical studies will reveal that, when adults develop amblyopia, they are usually treated with vitamins.  Amblyopia’s ‘synonyms and related keywords’ are alcohol -and tobacco-amblyopianutritional-amblyopia, malabsorption neuropathy, vitamin deficiency,  deficiency amblyopia or subacute combined degeneration, and Peripheral Neuropathy.  The first treatment of choice in these cases is dispensing of vitamins, particularly vitamin B12 and folic acid.  Other vitamins are also used.  In a German clinical report,  25 out of  33 patients diagnosed with what researchers called tobacco-alcohol-amblyopia,  the visual acuity improved with the vitamins (Vitamin B1, B2, B6, B12, folic acid)  in spite of the fact that some of the patients were still drinking alcohol. A clinical study reported by two ophtalmologists in South Carolina treated six tobacco and alcohol consumers with bilateral, progressive visual loss “of unknown origin” with folic acid  which treatment resulted in “significant improvement in visual function.”
According to a study at the Medical College of Georgia in Atlanta, “Folic acid is essential for DNA and RNA, and protein synthesis, and deficiencies in folates  can lead to nutritional amblyopia and optic nerve neuropathy.”

 

In another published clinical case, a 47-year old woman who was found sufficient in Vitamin B12 but deficient in folic acid presented amblyopia (as bilateral retrobular optic nerve neuropathy). After changing her diet and supplementing with folic acid, her “visual function returned to normal.”  The conclusion of the report was that “ The case supports the role of folic acid deficiency as an important cause of some causes of nutritional Optic neuropathy.” In another clinical case, an individual who had a “mithocondrial DNA mutation associated with Leber’s hereditary Optic neuropathy,” was found to have subnormal levels of vitamin B12. The authors report that “complete recovery of vision following vitamin replacement therapy suggest that the subnormal level of vitamin B12 precipitated visual loss.”


When between 1991 and 1993, numerous cases (an estimated of 50,000)  of Optic neuropathy of “unknown origin” appeared among a group of individuals in Cuba, that country’s government dispatched vitamins to its citizens.  Malnutrition was epidemic in Cuba at the time of U.S. Embargo, and when the country had lost its ties with Eastern Europe, following the fall of the Iron Curtain. A 1993 article in Nutritional Review points out to the political situation that lead to food shortages and to a “compromised nutritional status, especially B vitamin sufficiency, which appear to be related to the neuropathic illnesses.”  A study by Cabrera-Gomez and his colleagues  revealed that  42% percent of a sample of the epidemic patients had the same type of nerve damage which occurs in amblyopia (retrobulbar nerve damage), while the rest manifested various other types of nerve damage. On the other hand, following a review of cases of nutritional amblyopia,  S. Lessel from Harvard Medical School, concluded that “Protein  deficiency, antioxidant deficiency, physical labor, and tobacco smoking are likely to contribute to the occurrence of amblyopia.”

 

While tobacco amblyopia is a result of a more complex situation in which the lack of vitamin B12 prevents cyanide detoxification, and alcohol amblyopia is probably a multiple-cause nerve damage,  amblyopia also occurs in Chron’s disease, as a result of   intestinal inflammation.  In Chrons, intestinal lining may become damaged to the degree that the individual cannot absorb nutrients from food propertly. Such a condition is treated with intravenous nutrients and vitamins. Vitamin  B12 is also available in sublingual form, to be melted under the tongue.

 

According to R. Andres Sewell, M.D., member of American Academy of Neuropathy, and  Lawrence D. Recht M.D., from Stanford University Medical School, insufficient  Vitamin B12 may result in neural damage, including optic  (retrobulbar) neuropathy, amblyopia.  However, the authors write, amblyopia,  may also be caused not by solely vitamin B12 deficiency but by a “complex deficiency.”  Folate deficiency manifests the same symptoms as Vitamin B12 deficiency.

 

For small children, at a time when the central nervous system is developing, vitamin B12 is paramount.  A diet sparse in animal  protein or exposure to toxins may lead to deficiency of this vitamin.  Small children do not smoke tobacco, however, they may suffer from mild carbon monoxide intoxication, or other types of chronic, insidious exposures. Also a number of drugs such as  including antibiotics, may cause damage to the optic nerve.  Among these drugs, aspirin, corticosteroids, diuretics and antihistamines, indomethacin, streptomycin, sulfa drugs, and tetracycline may be prescribed to children for infections, inflammations and allergies. Other drugs that may cause malabsorption and subsequent nerve damage are  isoniazid, hydralazine, cycloserine, penicillamine, desoxypyridoxine and oral contraceptives.

 

Vitamin B12 is important in proper maintenance of the myelin sheathes over the nerves, responsible for the basic nerve function of electrical conductivity.  According to Elson M. Haas, M.D., vitamin B12  “is one of the most difficult vitamins to acquire through diet and to metabolize.”.  Soreness and weakness in arms and legs, limb jerking, physical and mental fatigue and mood changes may be overt symptoms of insufficiency of this vitamin. Vitamin B12 is needed in small amounts and it is stored in the liver.

 

It is very possible that children who do not eat sufficient meat protein and who, additionally, have intestinal disturbances, perhaps due to antibiotics or food allergies, may have vitamin B12 deficiency.   The lack of B12 may be masked for a long time by the presence of folic acid which is more common in the diet.  Folic acid can take over some of the B12 functions, however, Haas points out, this is a dangerous situation, as B12 deficiency will not show for a long time, and by then, the nerve damage (neuropathy) may be irreversible.   During psychological stress or stress caused by disease, the requirements are higher and the reserves may be depleted.. Any kind of allergy causes extreme stress on a child’s system, similar in some ways, to taking steroids or ingesting huge amounts of salt.

 

Refined grains, common in children’s diets, do not contain the vitamins and minerals needed for proper development. According to Haas, refined grain contains only half of the nutrients of its unrefined counterpart.  Other aspects of grain refinement are equally  worrisome. For example, Haas points out, Zinc, an indispensable mineral in dozen of metabolic paths, is lost in the outer layer of the grain, while the toxic mineral cadmium, seated in the kernel,  is preserved.  Neuropathies can also be caused by other nutrients.  Either a  deficiency or an excess of   pyridoxine (B-6) for example, may cause sensory polyneuropathy (multiple nerve damage such as those in the eyes and ears) .  Thiamin deficiency can also manifest itself as polyneuropathy.  With this condition,  numbing and tingling appear in the feet,  occasionally in the fingers and hands.

 

In many advanced European countries with public health systems, a course of vitamin injections for children manifesting multiple allergies or repeated bouts of cold is common. In the United States, repeated courses of antibiotics is usually the preferred choice.  Antibiotics are likely to lead to nutrient malabsorption as they create an environment in the intestines in which proper food digestion is not possible. Humans live in symbiotic relationship with  millions of Bacteria.

 

Gluten-sensitivity neuropathy (celiac disease) and Other Conditions.


In children with gluten-sensitivity,according to Sewell and Recht, antibodies to gluten in wheat, Barley, and Oats attack the nerves leading to serious neurological diseases, including Peripheral Neuropathy.
Other conditions leading to nutritional deficiencies are chronic Pancreatitis, pernicious Anemia, gastric mucosa atrophy,  inflammatory bowel syndrome, and infections. 

 

Altered Fats and Deficiency of Essential Fatty Acids and Antioxidants


The nerve cell membranes (myelin sheath) contain 80 percent phospholipids (fats) and 20 percent protein.  Ophtalmologists explain that amblyopia is not an eye condition, but a  mysterious abnormality of the brain ( the white matter of the brain).  “Amblyopia arises because the part of the brain that deals with the vision for that eye has failed to develop normally,” explains an eye surgeon on his web site.  This often gets even deeper, into the mitochondria and the DNA.  The medical establishment often finds that chronic diseases are ‘genetic’ and many understand this as ‘inherited.’ 

 

These terms are not interchangeable, as many environmental substances produce genetic mutations and many inherited mutations common in some diseases are not the diseases themselves, as previously seen in the case of the vitamin B12 -deficient patient with a  mutated ‘neuropathy gene’  The ‘white matter’ in the brain is made of fats and many children today eat fats which are not recognized by the body.  Altered fats such as rancid fats, hydrogenated oils, shortenings, and fried and deep-fried oils, are ubiquitous in processed foods, and staples in the diet of many children. According to Udo Erasmus, author of Fats that Heal, Fats that Kill the consumption of altered fats lead to “degeneration of all cells,  tissues and organs.” In addition to these fats, many children’s diets are deficient in antioxidants, phytonutrients, minerals, and  Essential Fatty Acids (EFAs) (present in fish, flax, hemp, and evening Primrose oils), to counteract the effect of toxicity and inflammation caused by faulty diets, food additives, allergies,  toxic metals and the carbon monoxide in the environment. 

 

The Patch Versus Atropine – Is This the Real Dilemma?


 A campaign for awareness of ‘lazy eye ’ in children took place recently.  The condition which traditionally has been treated with eye patches is now said to be equally effectively treated by atropine drops.  Both treatments consist in temporarily blinding the good eye (with a patch or muscle-paralyzing eye drops) in order to force the child to use the weak eye. To put it simple, at the end of the treatment, the weak eye gets two or three degrees better, and the good eye gets a degree weaker, perhaps temporarily. 

 

An interesting ‘community-based study,’ was done using 200 ophtalmologists in three countries (United States, Canada and Mexico) who volunteered to gather data on the benefits of eye patch versus eye drops.  The conclusion was that eye drops work as well. The study took place under the aegis of the Johns Hopkins Institutes and the National Eye Institute of the NIH.  Although, children on patches fared better visually, the spin of the story appeared to favor the atropine drops.  After six months of treatment, the children on patches showed an improvement average of 3.16 lines while the atropine group showed 2.84 lines.   Fifteen percent of  the children in the atropine group lost 1 line of vision in their good eye, twice as many as the patch children, perhaps temporarily.  While the atropine scored just a little worse in vision, it apparently scored much better in compliance, the commentators point out, and the scores are equal.  Logically, if the visual benefits of the patch was higher in spite of lower compliance, the conclusion should have been that the patch is a better option medically and its use should be reinforced.

 

The general belief in the medical community was that once past the age of 10 amblyopia treatment has no effect, however, a study by Charles Vega, earlier this year that included older children, concluded that they too may benefit from the treatment with both patches and atropine drops, or at least some of them (children and patches), some of the times, in certain conditions and with certain doubts, due to the limitations of the study.   Although the title of the published news was that ”Older Children May Benefit from Amblyopia Treatment”  the figures reveal a 2 % benefit from atropine/patch treatment compared to optical correction alone (25% and 23% respectively benefited). In addition, as in the ‘community’ study, most patients ended the treatment courses with a visual impairment in their good eye,  perhaps temporary.  Anyway, since most older children will not wear eye-patches several hours a day, their choice is perfectly visible to anyone.  

 

As a commentary, David G. Hunter, M.D., Ph.D. from Harvard Medical School in Boston was quoted in the media that it was important to identify and treat the condition earlier in life by increasing parent awareness, screening preschool children, and offering access to treatment. 
No mention was ever made that widely accepted aspects of nutrition and drug toxicity may constitute a cause, a means of prevention, a supporting aspect, a complementary treatment, or a treatment in themselves.

 

Missing Factors in the Patch-Drops Dilemma

In discussing the advantages and disadvantages between eye patches and atropine drops, effectiveness, compliance and cost were factored in (with the atropine scoring as negligibly less effective, but ‘better in compliance’).  Picking up from the Archives of Ophtalmology journal, the media spin was that “Drops are a Good Option for Amblyopia Treatment.”  “Moms and Dads no longer need to face a daily battle…,” where the possible side effects of atropine was literally shoved under the rug.  Atropine is a potent drug and among its side effects are:  irregular or Fast heart rate, hallucinations or unusual behavior (especially in children), swollen or distended stomach (especially in infants), blurred vision, sensitivity to sunlight, stinging and burning, swelling of the eyelids. An allergic reaction may include difficulty breathing, closing of the throat, swelling of lips, tongue or face, or Hives

 

The benzalkonium chloride (BAK) that comes as a preservative together with the atropine may also be toxic. While one week-long study in albino rabbits found the preservative non-toxic and able to improve ocular penetration by the drug, two other studies in normal rabbits found that BAK is seriously toxic.  From a study in normal and albino rabbits published in a Japanese ophtalmology journal, the scientists reported effects in normal rabbits such as “retinal detachment, visual cell loss, and atrophy of the retinal pigment, epithelium and choroid,” effects attributed by them to benzalkonium chloride preservative which, they believe, “accumulates in ocular pigments.” Another study in vitro found that benzalkonium chloride causes “severe cell damage,” “cell dysfunction,” cytoplasmic damage” at various concentration and durations of use.  The authors noted that corneal epithelial dysfunction was “more pronounced when BAK is used frequently or for periods longer than 30 minutes, even when the BAK concentration was low.  Benzalkonium chloride is frequently used as a preservative in eye drops, including some over the counter eye washes. 

 

References:

Elson N. Haas, M.D. ,  1992. Staying Healthy with Nutrition, Celestial Arts, Berkeley, California.

Udo Erasmus, 1993. Fats that Heal, Fats that Kill, Alive Books, Burnaby BC Canada.

R. Andrew Sewell, M.D. Lawrence D. Recht M.D. Nutritional Neuropathy, www.emedicine.com September, 2005.

Lessell S. Nutritional Amblyopia. J. Neuroophtalmology. 1998 Jun; 18(2):106-11.

Gary Price Todd Eyes and Nutrition. www.innvista.com/health/ailments.

Rizzo JF 3rd. Adenosine triphosphate deficiency: a genre of Optic neuropathy. Neurology, 1995. Jan;45(1):11-6

National Eye Institute. www.nei.nigh.gov

Moon Dragon’s Health and Wellness. www.moondragon.org/health/disorders/healthyeyes.html

Sadun A. Acquired mitochondrial impairment as a cause of optic never disease. Trans. Am Ophtalmol S0c. 1998;96:881-923.

Golnik KC, Schaible ER. Folate Response Optic neuropathy.  J. Neuroophtalomology 1994 Sept.: 14(3):163-9.

Smith SB, Kekuda R, Gu X, Chancy C, Conway SJ, Ganapathy V. Expression of folate receptor alpha in the mammalian retinol pigmented epithelium and retina. Invest. Ophtalmol Via Sci. 1999. Apr; 40(5);840-8

Older Children May Benefit From Amblyopia Treatment  CME
News Author: Laurie Barclay, MD
CME Author: Charles Vega, MD, FAAFP

Www.drugs.com

Komei Okabe,1 Hideya Kimura,2 Junko Okabe,1 Aki Kato,1 Hideo Shimizu,3 Takashi Ueda,4 Shouichi Shimada,4 and Yuichiro Ogura1
Effect of Benzalkonium Chloride on Transscleral Drug Delivery . Nagoya City University Medical School, Nagoya, Japan.

Chou A, Hori S, Takase M. Ocular toxicity of beta-blockers and benzalkonium chloride in pigmented rabbits: electrophysiological and morphological studies.
Jpn J Ophthalmol. 1985;29(1):13-23.

Cha SH, Lee JS, Oum BS, Kim CD. Corneal epithelial cellular dysfunction from benzalkonium chloride (BAC) in vitro. Clin Experiment Ophthalmol 2004;32(2):180-4.

 

 

 

 

 

 

 

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