www.balancedhealthtoday.com www.balancedhealthtoday.com * Thyroid disease. Both an overactive and underactive thyroid can cause hair loss. The hair loss associated with thyroid disease can be reversed with proper treatment. * Inadequate protein in diet. Some vegetarians, people who go on crash diets that exclude protein, and those with severely abnormal eating habits, may develop protein malnutrition. When this happens, a person’s body will help to save protein by shifting growing hairs into the resting phase. Massive hair shedding can occur two to three months later. Hair can then be pulled out by the roots. This condition can be reversed by eating the proper amount of protein. * Medications. Prescription drugs can cause temporary hair shedding in a small percentage of people. Examples of such drugs are blood thinners, some drugs used to treat gout and arthritis, acne, or psoriasis, and some medications for heart problems. * Cancer treatment drugs. Most drugs used in chemotherapy will cause hair cells to stop dividing. Hair shafts become thin and break off as they exit the scalp. This can occur one to three weeks after beginning chemotherapy. The patient may lose all of his hair, but this will usually re-grow after treatment ends. Syria, Damascus Croatia, Zagreb Sale, Victoria Wichita Falls, Texas Greece, Athens Chesapeake, Virginia Holland, Amsterdam Kansas City, Kansas Dubai, United Arab Emirates, Dubai, UAE Hungary, Budapest www.balancedhealthtoday.com www …
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curegoutpainnow.com Gout occurs when uric acid in the blood stream becomes too concentrated.
curegoutpainnow.com – Uric acid crystals cause gout pain and inflammation.
curegoutpainnow.com – Gout usually occurs in one foot but it is possible to have both feet afflicted at the same time.
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www.swamiramdevmedicines.com Cherries are very much useful in Gout. Cherries are rich in vitamin C, which can help in eliminating the gouty deposits.
One biochemical cause of gout is decreased levels of functional HGPRT, the enzyme shown here. Gout can also result from episodes of massive necrosis, renal insufficiency and other biochemical defects. Gouty arthritis results when uric acid crystallizes in the joint synovial fluid where it may be phagocytized by macrophages leading to cell lysis and inflammation. In the presence of HGPRT, guanine and hypoxanthine are salvaged by the transfer of a phosphate from PRPP to form GMP and IMP respectively. Decreased levels of functional HGPRT thus results in poor “salvage” of Guanine and Hypoxanthine. If this enzyme is defective, levels of PRPP may also be elevated. Both of these factors can cause increased flux through the de novo purine synthesis pathway and thus more uric acid formation. In the absence of HGPRT, unphosphorylated guanine and hypoxanthine are degraded by guanase and xanthine oxidase respectively; this results in the formation of xanthine, which is converted to uric acid via the enzyme xanthine oxidase. Excess conversion of xanthine to uric acid can lead to gout. The hereditary basis of gout is attributable to the location of the HGPRT gene on the X-chromosome. As one might expect, this is more common in males. Complete deficiency of HGPRT results in the tragic Lesch-Nyhan syndrome. Gout is treated with allopurinol, an inhibitor of the enzyme xanthine oxidase, which prevents the conversion of xanthine to uric acid.
