The vitamin E is an antioxidant which prevents the neurodegenerative disease of the brain called ataxia. Ataxia is a term for a group of disorders that affect co-ordination, balance and speech. Any part of the body can be affected, but people with ataxia often have difficulties with balance and walking, speaking, swallowing and tasks that require a high degree of control, such as writing and eating. The exact symptoms and their severity vary depending on the type of ataxia a person has. Vitamin E is not good for all kinds of disease. One other disease vitamin E cures is called nonalcoholic steatohepatitis, which is an accumulation of fat in the liver, not due to excess alcohol consumption.
Vitamin E is the collective name for a group of fat-soluble compounds with distinctive antioxidant activities. Antioxidants protect cells from the damaging effects of free radicals, which are molecules that contain an unshared electron. Unshared electrons are highly energetic and react rapidly with oxygen to form reactive oxygen species. Antioxidants protect cells from the damaging effects of reactive oxygen species formed in the body endogenously when it converts food to energy. Health risks from excessive vitamin E can cause hemorrhage and interrupt blood coagulation by inhibiting platelet aggregation.
Vitamin E supplements have the potential to interact with several types of medications. Vitamin E can inhibit platelet aggregation and antagonize vitamin K-dependent clotting factors. Some take vitamin E supplements with other antioxidants, such as vitamin C, selenium, and beta-carotene. These collections of antioxidant ingredients blunt the rise in high-density lipoprotein cholesterol levels, which is the most cardioprotective high-density lipoprotein. There are potential risks of concurrent antioxidant supplementation with conventional therapies treating cancer.
So essentially, we are left with a vitamin which is not good for all kinds of disease, but only where two situations are cured. One is called nonalcoholic steatohepatitis and the other one is a neurodegenerative disease due to an absence of vitamin E called ataxia.
Age-Related Macular Degeneration: Age-related macular degeneration affects the macula, resulting in a loss of central vision. Two forms of age-related macular degeneration exist: the most common, dry (non-exudative) type, and the wet (exudative) type of age-related macular degeneration. Dry age-related macular degeneration typically progresses from an early, mostly asymptomatic phase—observed only by an ophthalmologist as pigment irregularities of the retinal pigment epithelium and the presence of small deposits comprised of lipids and proteins called drusen—through intermediate and then the later stages of geographical atrophy and neovascularization. Drusen are a precursor to geographical atrophy. As the disease progresses, small drusen converge into large confluent drusen with hyperpigmentation. This is usually followed by hypopigmentation. In some cases, drusen regress in size as refractile deposits appear. Progression from large confluent drusen to geographical atrophy takes approximately 6.5 years, during which time the patient experiences gradual visual loss, dark adaptation abnormalities, difficulty reading, and problems with face recognition. Alternatively, the neovascular form of age-related macular degeneration may develop, probably in response to pro-angiogenic factors. Another characteristic often seen in the eyes of age-related macular degeneration patients are reticular pseudodrusen, a yellowish-white material that appears as material under the retina organized in ill-defined networks of broad interlacing ribbons. Retinal pseudodrusen are a sign of retinal dysfunction and appear to be a risk factor for late age-related macular degeneration, although they may also occur in individuals who do not have age-related macular degeneration.
The etiology of age-related macular degeneration appears to be strongly influenced by both genetic and environmental factors. The non-genetic factors that play important roles include cigarette smoking, diet, and obesity. The interaction of lifestyle and genetic factors likely contributes to the development and progression of age-related macular degeneration through a variety of genetic pathways that are only beginning to be understood. Cardiovascular, immune, and inflammatory biomarkers associated with age-related macular degeneration point to mechanisms that may explain the influence of environmental factors on age-related macular degeneration progression. These biomarkers include C-reactive protein, a marker of inflammation, and homocysteine, an amino acid that adversely affects the vascular endothelium. Other genetic factors have been linked to age-related macular degeneration through Genome Wide Association Studies. Several studies indicate that genes involved in complement regulation, lipid metabolism, extracellular matrix remodeling, and angiogenesis are associated with advanced age-related macular degeneration. Further studies with next generation sequencing methods have identified rare variants of genes in the complement pathway that might have an even stronger effect on age-related macular degeneration progression. Predictive modeling of disease progression indicates that a combination of rare and common variants might improve the accuracy of risk assessment.
Genetic studies have yielded a number of biological pathways that could be targeted for drug development, yet the pathobiology of the disease remains poorly understood and is likely multifactorial. Treatment may require engagement of multiple targets.
Assessing the presence and progression of geographical atrophy from an anatomical perspective requires quantifying the total area affected as well as the location of atrophy, particularly relative to the foveal center. Various complementary in vivo imaging methods are used, including color photography using multi-spectral visual or infrared or wide field imaging, flurorescein angiography, fundus autofluorescence, and optical coherence tomography. Each of these methods has strengths and weaknesses; the challenge lies in extracting qualitative and quantitative data and mapping these data to a patient’s genotype and disease history.
Color fundus photography is the classical endpoint used in many trials and natural history studies but suffers from poor reproducibility and interference from cataracts. Fluorescein angiography requires intravenous injection, making it useful for examining leakage but impractical for large studies. Fundus Autofluorescence imaging allows for automated measurements; however, blue light Fundus Autofluorescence may be affected by natural darkening at the foveal center. In addition, blue Fundus Autofluorescence is uncomfortable for some subjects because of bright illumination of the retina. Wide field autofluorescence is a newer method not yet fully tested to determine its usefulness for clinical studies. Optical coherence tomography is an established medical imaging that has shown promise in evaluating both retinal and choroidal morphology in geographical atrophy. It allows examination and quantification of changes in the retinal layers, including the loss of photoreceptors and retinal pigment epithelium. It will be important to further define the relationship between Fundus Autofluorescence and optical coherence tomography regarding the extent of retinal atrophy. In addition, there is a need to better define anatomic descriptors of retinal changes in eyes with geographical atrophy that are reproducible across larger populations.
The gold standard functional measure for assessing age-related macular degeneration progression has been best corrected visual acuity. An electronic version of the Early Treatment for Diabetic Retinopathy has made it quicker and easier to assess best corrected visual acuity and has been widely used. However, visual acuity lacks sensitivity for assessing age-related macular degeneration in early stages. Noting that people with geographical atrophy have increased visual impairment in dim light, a low luminance visual acuity test was developed simply by placing a neutral density filter in front of the eye. Low luminance deficit has been shown to predict subsequent visual loss, and low luminance visual acuity captures foveal functional deficits better than best corrected visual acuity in intermediate and advanced age-related macular degeneration. Another technique, microperimetry, performs even better in assessing central retinal sensitivity in early stages of age-related macular degeneration. However, microperimetry tests may be redundant (particularly mesopic microperimetry) and burdensome for some patients. Scotopic microperimetry, a technique used to measure rod sensitivity, which is shown to be anatomically affected early in age-related macular degeneration. Dark adaptometry represents another approach with high diagnostic potential.
A multimodal approach including both anatomical and functional measures may be necessary to evaluate progression of disease; however, further phenotype/genotype studies will be needed to determine the best options. In addition, different types of assessments serve different purposes. For example, functional endpoints may lack sufficient precision for short studies but correlate better with quality of life and thus may be useful.
Treatments Available for Dry Macular Degeneration:
1. Eating antioxidant-rich foods, such as fresh fruits and dark green leafy vegetables delay the onset or reduce the severity of dry age-related macular degeneration. Eating at least one serving of fatty fish per week may also delay the onset or reduce the severity of dry age-related macular degeneration. These types of fish are high in omega-3 fatty acids, which help decrease inflammation and promote eye health. It is important to keep a balance between omega-6 fatty acids and omega-3 fatty acids in our diets. Virtually every food in a package contains omega-6 fatty acids in the form of vegetable oil. We need to increase our intake of omega-3 and decrease our intake of omega-6. Low-fat foods are good options if they have achieved their low-fat status through a process that physically removes the fat. Skim milk and low fat cottage cheese are examples of these types of good low-fat foods. A low-fat cookie or a no-fat cake, however, is a nutritional contradiction. Usually a low-fat or no-fat label on baked goods does not mean less fat was used in the production of the food, but that an artificial fat was used, usually partially hydrogenated vegetable oil. These types of fats are artificial ingredients made in a laboratory and our bodies can’t metabolize them. So it’s best to eat real cookies – just do not eat the whole dozen! Incorporate exercise into your everyday life. Obesity increases the risk for progression to advanced age-related macular degeneration.
2. Age-Related Eye Disease Study Formulation includes:
A. 500 milligrams of vitamin C.
B. 400 international units of vitamin E.
C. 80 milligrams of zinc as zinc oxide.
D. 2 milligrams copper as cupric oxide (to avoid anemia with high zinc intake).
E. 10 milligrams of lutein.
F. 2 milligrams of zeaxanthin.
Be sure to talk with your doctor before adding any nutritional or vitamin supplements to your diet.
3. Mesoxanthin and MacuHealth supplement: A cousin of lutein and zeaxanthin named “mesoxanthin” is actually the most active of the three specifically in the macula and that the combination of lutein, zeaxanthin, and mesoxanthin is what is needed. That is what the MacuHealth supplement contains.
4. Avoid ultraviolet and blue light (light waves that make the sky, or any object, appear blue) as much as possible and wear sunglasses that block blue light. In commercial sunglasses, this is usually in the yellow-orange-amber tints.
5. Control Blood Pressure. Individuals with hypertension are 1.5 times more likely to have wet AMD than persons without hypertension.
6. Avoid smoking: If you do smoke, stop – and avoid secondhand smoke as well.
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