http://www.altcancer.com/candida_dysbiosis.htm


Dr Orian Truss

In 1953 Dr Orian Truss discovered the devastating effects of antibiotics in an Alabama (USA) hospital. During a hospital round Truss was intrigued by a gaunt, apparently elderly man who was obviously dying. However, he was only in his forties and in hospital for four months. No specialist had been able to make a diagnosis. Out of curiosity Truss asked the patient when be was last completely well.

The man answered that he was well until six months before when he had cut his finger He had received antibiotics for this. Shortly afterwards he developed diarrhoea and his health deteriorated. Truss had seen before how antibiotics cause diarrhoea. It was known that Candida was opportunistic and thrived in debilitated patients, but now Truss wondered if it might not be the other way round, that Candida actually caused the debilitated condition.

He had read that potassium iodide solution could be used to treat Candida infestation of the blood. So he put the patient on six to eight drops of Lugol's solution four times a day and soon the patient was again completely well.

Soon afterwards he had a female patient with a stuffy nose, a throbbing headache, vaginitis and severe depression. To his amazement all her problems immediately cleared with Candida treatment. Some time later he saw a female patient who had been schizophrenic for six years with hundreds of electroshock treatments and massive drug dosages. He started treating the woman for sinus allergies with a Candida vaccine. Soon she had recovered mentally and physically, and remained well.

From then on he treated his patients against Candida at the slightest indication of its presence. Many of his patients made remarkable recoveries from most unusual conditions including menstrual problems, hyperactivity, learning disabilities, autism, multiple sclerosis and auto-immune diseases such as Crohn's disease and lupus erythematosus.

Every experienced naturopath can relate similar success stories. Ironically, antibiotics are usually not necessary in the first place. In a few per cent of the cases in which they are necessary their serious after effects could easily be avoided using fungicides and lactobacilli.

Many people doubt the effectiveness of natural therapies against apparently serious infections, but my experience leads me to believe that frequently natural therapies are more effective, without causing the repeated and chronic infections seen after antibiotics. I have seen patients who have been unsuccessful on long-term antibiotic treatment recover within days or weeks with natural therapies.

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http://www.springboard4health.com/notebook/health_candida_albicans.html



1. Iodine deficiency causing defective free radical generation.

Most people who do not regularly eat seafood (either fish or kelp) or use iodized salt have some degree of iodine deficiency; this can also occur as a result of a low-salt diet. These individuals may become hypothyroid and hypometabolic, because iodine is an essential ingredient in thyroid hormone. At the same time they may become more sensitive to yeast infections, due to inactivity of the myeloperoxidase enzyme, which uses iodine in cell mediated immune function. The iodine is used by this enzyme to product iodine-free radicals which are part of the cellular anti-yeast “free radical artillery”. (3) Previous to the use of nystatin as an antifungal drug, iodine therapy was successfully used to treat yeast infections; however, one must be very careful with the dosage. People who are sensitive to various foods and chemicals are frequently intolerant to iodine and should only use it in very low dosages.

2. Selenium deficiencies limit cellular immunity against yeast.

Phagocytes (cells active in cell-mediated immunity) require selenium for the enzyme glutathione peroxidase function. Peroxidase activity in phagocytes is higher than in most other tissues (approximately twice that in red blood cells), and this is reflected in a higher need for selenium. The glutathione peroxidase system is an antioxidant enzyme system and is especially critical for phagocytic cell function. It has been experimentally demonstrated that selenium deficiency selectively causes a predisposition to yeast infection

(4). Food and chemically sensitive patients should start with very low doses of selenium - according to a “selenium titration program” developed by Dr. Alfred Zamm, M.D. and myself.

3. Other varied antioxidant deficiencies.

Antioxidant nutrients include: ascorbic acid, vitamin E, riboflavin, pantothenate, glutathione, taurine, cysteine and minerals such as copper, selenium, zinc and manganese, which function as coenzymes such as superoxide dismutase and glutathione peroxidase. Antioxidant nutrients and enzyme defenses are fundamental protectors against all forms of stress. They are critical during infection. Cysteine is a sulphur containing amino acid, which acts to internally bind together antibody molecules. Other antioxidants, including those above mentioned, are especially important with regard to cell-mediated immune function which requires that cells become activated in what is called a respiratory burst in which large amounts of iodine radicals, superoxide and other oxidizing species are directed out from the cell membrane as artillery to kill invading organisms. Simultaneously the cell generates antioxidant protection intracellularly to protect itself against the back diffusion of hydrogen peroxide (protected by the glutathione peroxidase system) formed from the primary radicals it produced. The primary killing of yeast is accomplished by these radicals an hydrogen peroxide, and the immune capacity of the host cells is limited by its ability to produce intracellular antioxidant defenses to protect itself from the oxidants. This amount to a very simple but effective method of waging war against pathogens. This phagocytic activity appears to be the major factor in limiting the spread of infection by opportunistic fungi. (5) The simple attachment of the hyphae of the yeast activates the oxidative metabolism of the phagocytes which sets the respiratory burst in action.