by Janet R Simpson
Treatments of Eczema - If you follow the advice of only one of my many articles let this be the one.
Read carefully as this information is like gold dust as a Treatments of Eczema. This is the key to success with regard to sprouts and curing eczema.
Every day without fail I prepare at least one large biogenic salad. This is not your everyday limp, lifeless salad. This is a salad that is dense with nutrition.
I start with the everyday salad vegetables, such as cucumber, carrots, spring onions, etc.
Then the important bit; a three cupful mixture of at least four sprouts. Try aduki bean, lentil, alfalfa and chickpea sprouts. Add a handful of soaked hemp seed and a sprinkling of pumpkin, sesame and sunflower seeds.
Now add some protein such as chicken or fish. And that's it.
If you're looking at various Treatments of Eczema, eat a biogenic salad like this every day for at least one month and watch as your health tremendously improves and your eczema magically disappears.
Here are some of the benefits of eating in this manner:
#1 - Sprouts increase the micro-electrical potential of cells, improving the body's use of oxygen so that cells, skin and body are energised and rejuvenated for healing.
#2 - The body will receive the maximum vitality from all the nutrients contained in the sprouts. Nutrients that will heal every cell in the body.
#3 - Sprouts contain a large quantity of lecithin which will dramatically increase the quality of every cell in your body.
#4 - Sprouts will improve your blood profile, keep blood glucose levels balanced and energise you.
#5 - Mung beans are rich in pentose which helps fight against free radicals and will cleanse your body.
You can create smooth, clear, beautiful complexion and eliminate your Eczema by changing your diet. Include a mixture of sprouts in your daily salad, add some seeds with some fish and watch your skin improve over a short period of time.
Here's to healthy skin.
Wednesday, July 11, 2007
What is Vitamin C
by Vitamins Guide
The structure of vitamin C, designated as a hex uronic acid, was established in 1933 at the University of Birmingham in England by Walter Haworth and his associates, who also accomplished its synthesis. Szent-Györgyi and Haworth renamed hexuronic acid 'L-ascorbic acid' to convey its antiscorbutic properties; the new name was offi cially accepted in 1965. Both Szent-Györgyi and Haworth were to be awarded the Nobel Prize in 1937, the former for Physiology and Medicine and the latter for Chemistry. Synthetic ascorbic acid proved to have identical physicochemical and biological properties to the vitamin C isolated from plant or animal tissues, and there was no difference in biological potency between the synthetic and natural products. In 1934, Reichstein and Grüssner in Switzerland worked out a chemical route for synthesizing ascorbic acid commercially, starting from glucose.
The term 'vitamin C' refers to both ascorbic acid and dehydroascorbic acid, since the latter oxidation product is reduced back to ascorbic acid in the body. The principal natural compound with vitamin C activity is L-ascorbic acid. There are two enantiomeric pairs (mirror images) of the 2-hexenono-1,4-lactone structure; namely, L- and D-ascorbic acid and L- and D-isoascorbic acid. D-Ascorbic acid and L-isoascorbic acid are devoid of vitamin C activ- ity and do not occur in nature. D-Isoascorbic acid (commonly known as erythorbic acid) is an epimer of L-ascorbic acid, the structural difference being the orientation of the hydrogen and hydroxyl group at the fi fth carbon atom. D-Isoascorbic acid is also not found in natural products, apart from its occurrence in certain microorganisms. It possesses similar reductive properties to L-ascorbic acid, but exhibits only 5% of the antiscorbutic activity of L-ascorbic acid in guinea pigs (Pelletier & Godin, 1969). At around neutral pH, ascorbic acid exists as the ascorbate anion due to facile ionization of the hydroxyl group on C-3. Ascorbate is easily and reversibly oxidized to dehydro-L-ascorbic acid, forming the ascorbyl radical (also known as semidehydroascorbate) as an intermediate. The delocalized nature of the unpaired electron in the ascorbyl radical makes it a relatively unreactive free radical and two ascorbyl radicals can react together non-enzymatically to produce ascorbate and dehydroascorbic acid. In the body, enzymes are available to reduce the ascorbyl radical and dehydroascorbic acid back to ascorbate. Dehydroascorbic acid is not a true organic acid as it contains no readily ionizable protons. In aqueous solution, dehydroascorbic acid exists not as the 2,3-diketo compound, but as the bicyclic hemiketal hydrate. In buffered solution at neutral or alkaline pH, dehydroascorbic acid undergoes a non-reversible oxidation in which the two rings open to give 2,3- diketogulonic acid in a straight-chain structure.
Dietary sources of Vitamin C Fresh fruits (especially citrus fruits and blackcurrants) and green vegetables constitute rich sources of vitamin C. Potatoes contain moderate amounts but, because of their high consumption, represent the most important source of the vitamin in the British diet. Liver (containing 10-40 mg per 100 g), kidney and heart are good sources, but muscle meats and cereal grains do not contain the vitamin in measurable amounts. Human milk provides enough ascorbic acid to prevent scurvy in breast-fed infants, but preparations of cow's milk are a poor source owing to oxidative losses incurred during processing.
Source: http://important-vitamins.blogspot.com/2007/07/vitamin-c.html
To find out about Beri Beri disease visit - http://important-vitamins.blogspot.com/2007/07/beriberi.html
For more information visit http://important-vitamins.blogspot.com
The structure of vitamin C, designated as a hex uronic acid, was established in 1933 at the University of Birmingham in England by Walter Haworth and his associates, who also accomplished its synthesis. Szent-Györgyi and Haworth renamed hexuronic acid 'L-ascorbic acid' to convey its antiscorbutic properties; the new name was offi cially accepted in 1965. Both Szent-Györgyi and Haworth were to be awarded the Nobel Prize in 1937, the former for Physiology and Medicine and the latter for Chemistry. Synthetic ascorbic acid proved to have identical physicochemical and biological properties to the vitamin C isolated from plant or animal tissues, and there was no difference in biological potency between the synthetic and natural products. In 1934, Reichstein and Grüssner in Switzerland worked out a chemical route for synthesizing ascorbic acid commercially, starting from glucose.
The term 'vitamin C' refers to both ascorbic acid and dehydroascorbic acid, since the latter oxidation product is reduced back to ascorbic acid in the body. The principal natural compound with vitamin C activity is L-ascorbic acid. There are two enantiomeric pairs (mirror images) of the 2-hexenono-1,4-lactone structure; namely, L- and D-ascorbic acid and L- and D-isoascorbic acid. D-Ascorbic acid and L-isoascorbic acid are devoid of vitamin C activ- ity and do not occur in nature. D-Isoascorbic acid (commonly known as erythorbic acid) is an epimer of L-ascorbic acid, the structural difference being the orientation of the hydrogen and hydroxyl group at the fi fth carbon atom. D-Isoascorbic acid is also not found in natural products, apart from its occurrence in certain microorganisms. It possesses similar reductive properties to L-ascorbic acid, but exhibits only 5% of the antiscorbutic activity of L-ascorbic acid in guinea pigs (Pelletier & Godin, 1969). At around neutral pH, ascorbic acid exists as the ascorbate anion due to facile ionization of the hydroxyl group on C-3. Ascorbate is easily and reversibly oxidized to dehydro-L-ascorbic acid, forming the ascorbyl radical (also known as semidehydroascorbate) as an intermediate. The delocalized nature of the unpaired electron in the ascorbyl radical makes it a relatively unreactive free radical and two ascorbyl radicals can react together non-enzymatically to produce ascorbate and dehydroascorbic acid. In the body, enzymes are available to reduce the ascorbyl radical and dehydroascorbic acid back to ascorbate. Dehydroascorbic acid is not a true organic acid as it contains no readily ionizable protons. In aqueous solution, dehydroascorbic acid exists not as the 2,3-diketo compound, but as the bicyclic hemiketal hydrate. In buffered solution at neutral or alkaline pH, dehydroascorbic acid undergoes a non-reversible oxidation in which the two rings open to give 2,3- diketogulonic acid in a straight-chain structure.
Dietary sources of Vitamin C Fresh fruits (especially citrus fruits and blackcurrants) and green vegetables constitute rich sources of vitamin C. Potatoes contain moderate amounts but, because of their high consumption, represent the most important source of the vitamin in the British diet. Liver (containing 10-40 mg per 100 g), kidney and heart are good sources, but muscle meats and cereal grains do not contain the vitamin in measurable amounts. Human milk provides enough ascorbic acid to prevent scurvy in breast-fed infants, but preparations of cow's milk are a poor source owing to oxidative losses incurred during processing.
Source: http://important-vitamins.blogspot.com/2007/07/vitamin-c.html
To find out about Beri Beri disease visit - http://important-vitamins.blogspot.com/2007/07/beriberi.html
For more information visit http://important-vitamins.blogspot.com
Treating Alzheimer's Disease
by Juliet Cohen
Alzheimer's disease is a progressive, irreversible brain disorder. Alzheimer's disease (AD) is the most common form of dementia among older people. Alzheimer' destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Genetic factors are suspected, and dominant mutations in three different genes have been identified that account for a much smaller number of cases of familial, early-onset AD. People with dementia often have trouble thinking and speaking clearly, remembering recent events, and learning new things. Over time, it becomes hard for them to handle everyday activities and take care of themselves. Age is the most important risk factor for AD; the number of people with the disease doubles every 5 years beyond age 65. Three genes have been discovered that cause early onset (familial) AD. Other genetic mutations that cause excessive accumulation of amyloid protein are associated with age-related (sporadic) AD. AD is part of an immune response that is attempting to contain the disease. The former may be more likely, since research indicates that anti-inflammatory drugs can prevent or retard AD development.
Alzheimer's disease advances at widely different rates. Family history is another risk factor of Alzheimer's. Several risk factor genes may interact with each other and with non-genetic factors to cause the disease. Cardiovascular Risk Factors The same factors that increase the risk for heart disease and stroke, such as high blood pressure, may also increase the risk for late-onset AD. Most people with mild forgetfulness do not have AD. In the early stage of AD, people may have trouble remembering recent events, activities, or the names of familiar people or things. Oxidative damage refers to cell damage caused by excess free radicals, which are highly reactive chemicals. Free radicals are often formed as a by-product of metabolism, or chemical processes within the cell. Excess free radicals may cause substantial neuronal damage, contributing to AD development. Type 2 Diabetes. A link between AD and type 2 diabetes, the form of diabetes in which insulin levels are high. One theory is that too much insulin in the blood promotes inflammation and oxidative damage in the brain, both of which contribute to AD development.
Symptoms of AD include memory loss, language deterioration, impaired ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings. Alzheimer's disease may also include behavioral changes, such as outbursts of violence or excessive passivity in people who have no previous history of such behavior. In the later stages, deterioration of musculature and mobility, leading to bedfastness, inability to feed oneself, and incontinence, will be seen if death from some external cause (e.g. heart attack or pneumonia) does not intervene. Moderate -As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities. Severe -- As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need constant supervision. They may even lose the ability to walk or eat without assistance. They might forget to eat and starve.
Treatment Alzheimer's Disease Tips
1. Acetylcholinesterase (AChE)-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons).
2. Ginkgo for the treatment of "cognitive impairment and dementia," a Cochrane Review concludes that "there is promising evidence of improvement in cognition and function associated with Ginkgo According to this review the two randomized controlled studies that focused on Alzheimer's patients both showed significant improvement in these areas.
3. Tramiprosate (3APS or Alzhemed) is a GAG-mimetic molecule that is believed to act by binding to soluble amyloid beta to prevent the accumulation of the toxic plaques.
4. R-flurbiprofen (MPC-7869) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide.
5. Leuprolide has also been studied for Alzheimer's. It is hypothesized to work by reducing leutenizing hormone levels which may be causing damage in the brain as one ages.
6. Antihistamine drug Dimebon has also recently been found to show beneficial effects against Alzheimer's disease in preliminary trials
7. Vaccines or immunotherapy for Alzheimer's, unlike typical vaccines, would be used to treat diagnosed patients rather than for disease prevention.
8. Proposed alternative treatments for Alzheimer's include a range of herbal compounds and dietary supplements.
9. Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacologic treatment, especially in the early to moderately advanced stages of disease.
10. DNA-based therapy is also Treating Alzheimer's Disease.
Alzheimer's disease is a progressive, irreversible brain disorder. Alzheimer's disease (AD) is the most common form of dementia among older people. Alzheimer' destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Genetic factors are suspected, and dominant mutations in three different genes have been identified that account for a much smaller number of cases of familial, early-onset AD. People with dementia often have trouble thinking and speaking clearly, remembering recent events, and learning new things. Over time, it becomes hard for them to handle everyday activities and take care of themselves. Age is the most important risk factor for AD; the number of people with the disease doubles every 5 years beyond age 65. Three genes have been discovered that cause early onset (familial) AD. Other genetic mutations that cause excessive accumulation of amyloid protein are associated with age-related (sporadic) AD. AD is part of an immune response that is attempting to contain the disease. The former may be more likely, since research indicates that anti-inflammatory drugs can prevent or retard AD development.
Alzheimer's disease advances at widely different rates. Family history is another risk factor of Alzheimer's. Several risk factor genes may interact with each other and with non-genetic factors to cause the disease. Cardiovascular Risk Factors The same factors that increase the risk for heart disease and stroke, such as high blood pressure, may also increase the risk for late-onset AD. Most people with mild forgetfulness do not have AD. In the early stage of AD, people may have trouble remembering recent events, activities, or the names of familiar people or things. Oxidative damage refers to cell damage caused by excess free radicals, which are highly reactive chemicals. Free radicals are often formed as a by-product of metabolism, or chemical processes within the cell. Excess free radicals may cause substantial neuronal damage, contributing to AD development. Type 2 Diabetes. A link between AD and type 2 diabetes, the form of diabetes in which insulin levels are high. One theory is that too much insulin in the blood promotes inflammation and oxidative damage in the brain, both of which contribute to AD development.
Symptoms of AD include memory loss, language deterioration, impaired ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings. Alzheimer's disease may also include behavioral changes, such as outbursts of violence or excessive passivity in people who have no previous history of such behavior. In the later stages, deterioration of musculature and mobility, leading to bedfastness, inability to feed oneself, and incontinence, will be seen if death from some external cause (e.g. heart attack or pneumonia) does not intervene. Moderate -As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities. Severe -- As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need constant supervision. They may even lose the ability to walk or eat without assistance. They might forget to eat and starve.
Treatment Alzheimer's Disease Tips
1. Acetylcholinesterase (AChE)-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons).
2. Ginkgo for the treatment of "cognitive impairment and dementia," a Cochrane Review concludes that "there is promising evidence of improvement in cognition and function associated with Ginkgo According to this review the two randomized controlled studies that focused on Alzheimer's patients both showed significant improvement in these areas.
3. Tramiprosate (3APS or Alzhemed) is a GAG-mimetic molecule that is believed to act by binding to soluble amyloid beta to prevent the accumulation of the toxic plaques.
4. R-flurbiprofen (MPC-7869) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide.
5. Leuprolide has also been studied for Alzheimer's. It is hypothesized to work by reducing leutenizing hormone levels which may be causing damage in the brain as one ages.
6. Antihistamine drug Dimebon has also recently been found to show beneficial effects against Alzheimer's disease in preliminary trials
7. Vaccines or immunotherapy for Alzheimer's, unlike typical vaccines, would be used to treat diagnosed patients rather than for disease prevention.
8. Proposed alternative treatments for Alzheimer's include a range of herbal compounds and dietary supplements.
9. Cognitive and behavioral interventions and rehabilitation strategies may be used as an adjunct to pharmacologic treatment, especially in the early to moderately advanced stages of disease.
10. DNA-based therapy is also Treating Alzheimer's Disease.
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