Sorry to hear you have this Marty. I'll be praying it doesn't get worse. Here's one excerpt about it:
From:
http://www.oralchelation.com/faq/coumadin6.htm
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A branch retinal vein occlusion is essentially a blockage of the portion of the circulation that drains the retina of blood. The arteries deliver blood to the retina. The red blood cells and plasma then course through the capillaries and eventually into the venous system, beginning with small veins and ending with larger ones, and eventually reaching the central retinal vein. With blockage of any vein, there is back-up pressure in the capillaries, which leads to hemorrhages and also to leakage of fluid and other constituents of blood. Usually, the occlusion occurs at a site where an artery and vein cross. The occlusion site determines the extent or distribution of the hemorrhage, ranging from a small vein branch to a quadrantic occlusion involving one fourth of the retina to a hemispheric (hemi-retinal) occlusion involving one half of the retina to an occlusion of the central retinal vein, which involves the entire retina (when the central vein is involved, this is called a central retinal vein occlusion which is discussed below).
Branch retinal vein occlusions are by far the most common cause of retinal vascular occlusive disease. Males and females are affected equally. Most occlusions occur after age 50, although younger patients are sometimes seen with this disorder (in this age group it is often called papillophlebitis). The highest rate of occurrence is in individuals in their 60Â?s and 70Â?s. The risk factors for this disorder are similar to those for vascular occlusive disease elsewhere in the body such as stroke and coronary artery disease. Specifically, aging, high blood pressure, diabetes, and smoking are all risk factors. Glaucoma has also been identified as a risk factor in some studies. There are less common conditions which may put a patient at risk for developing a vein occlusion including blood clotting abnormalities such as hyperhomocysteinemia, activated protein C resistance (Factor V Leiden), protein C and S deficiency, anti-phospholipid antibodies and diseases which cause sludging of the circulation or so-called hyperviscosity. Inflammatory and infectious conditions which cause vasculitis such as sarcoidosis and tuberculosis are also risk factors for vein occlusion.
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Did they check your homocysteine level? Here's an article that says high levels of homocysteine may play a role in BRVO
From:
http://www.lef.org/magazine/mag2001/june2001_report_homocysteine.html
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Eye problems
Just as blood vessels leading to and from the heart and brain can be adverstely affected by homocysteine, so can other blood vessels in the body. Central retinal vein occlusion (CRVO), central retinal artery occlusion (CRAO), and nonarteritic anterior ischemic optic neuropathy (NAION) are three eye conditions associated with elevated homocysteine. All are serious conditions that can lead to vision loss. Ischemic CRVO, which usually occurs in one eye only, leads to all sorts of complications including neovascular glaucoma and macular degeneration. There is no good treatment, and in fact, some researchers believe that treatment will make the condition worse.
In a new study from the University of Michigan, the average homocysteine level was 11.58 micromoles per liter for people with CRVO versus 9.49 for people without. Elevated homocysteine was present in half of all eyes with severe loss of vision caused by CRVO. Because these eye conditions are frequently associated with diabetes, hypertension, cardiovascular and other systemic diseases, a complete physical is highly recommended for anyone diagnosed with any of these eye problems.
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What you can do
There are three principle vitamins involved in the conversion of homocysteine: folate, vitamins B6 and B12. Vitamin B2 (riboflavin) is required for the B6 pathway of homocysteine reduction.
Folate adequately lowers homocysteine in some people. Published studies show that folate supplements (0.5-5 mg/day) reduce homocysteine anywhere from 12% to 30%. In a recent study on cervical dysplasia, women were given 10 mg of folic acid a day, whether they were deficient or not. Homocysteine was significantly reduced at eight weeks, with a continuing trend downwards at six months.
Folate is one answer to homocysteine, but itâ??s not the only answer. Other vitamins help too. Vitamin B12 must be available for folate to work, and vitamin B6 must be present for homocysteine to be converted to cysteine and other beneficial sulfur-type molecules.
Another pathway for the detoxification of homocysteine utilizes betaine (TMG) and requires no vitamin cofactors. Betaine can be taken in conjunction with folate if folate doesnâ??t reduce homocysteine to a satisfactory level. (Relying on betaine alone, however, is not advisable since folate has numerous important functions in addition to reducing homocysteine.
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Age is another factor that elevates homocysteine. Unfortunately, age-related hyperhomocysteinemia hasnâ??t been adequately investigated. However, the data on the dangers of homocysteine is already so compelling that researchers are now urging doctors to do routine testing.
Note: For additional information on what can be done to lower homocysteine levels when folic acid supplements fail, refer to the March 1999 issue of Life Extension (â??A Lethal Misconceptionâ?�) or refer to the Internet magazine archives section at
www.lef.org.
References
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Pianka P, et al. 2000. Hyperhomocystinemia in patients with nonarteritic anterior ischemic optic neuropathy, central retinal artery occlusion, and central retinal vein occlusion. Ophthalmology 107:1588-92.
Vine AK. 2000. Hyperhomocysteinemia: a risk factor for central retinal vein occlusion. Am J Ophthalmol 129:640-4.
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