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Cell replication Folate transfers single carbon atoms in reactions essential to the synthesis of purines and pyrimidines and hence to the production of deoxyribonucleic acid (DNA). Unlike the methylation cycle, the DNA cycle does not depend on vitamin B12. Folic acid can thus maintain the supply of intracellular folate required for DNA synthesis. DNA synthesis, and hence cell replication, can therefore take place in people with vitamin B12 deficiency, provided that folic acid is available as a source of folate. 42 Rossana Salerno-Kennedy A number of drugs interfere with the biosynthesis of folic acid and tetrahydrofolate. Among these are the dihydrofolate reductase inhibitors (such as trimethoprim and pyrimethamine), the sulfonamides (competitive inhibitors of para-aminobenzoic acid in the reactions of dihydropteroate synthetase), and the anticancer drug methotrexate (inhibits both folate reductase and dihydrofolate reductase). DIETARY SOURCES Naturally occurring folate is found in a w

  considered only modest changes, Kaufman noted that improvement among his patients started after four to 12 weeks - the time at which Jonas' study stopped. He also found that people might continue to improve for up to a year before they plateaued. Jonas' recent study identified no significant side effects, but to be safe, those who opt for long-term niacinamide therapy should have their liver enzymes periodically assessed. CONCLUSIONS The preceding discussion establishes that niacin deficiency is very common. It may occur, for example, because of a polymorphism that causes an abnormal need for vitamin B-3 in some alcoholics and schizophrenics. Alternatively, poor quality diets, often maize dominated, can result in pellagra and the extreme longterm deficiencies seen in former prisoners-of-war. Addictions to alcohol, tobacco or LSD also increase the need for vitamin B3. Beyond this, natural methyl acceptors, such as niacin, appear to have a major, high dose role to play in the t

 The relationship between oxidative stress and the catecholamines, seen, for example, in Parkinson's disease and multiple sclerosis, is now apparent. This is largely because of the research conducted in Winnipeg by Behonick and colleagues [29] who first developed a method for measuring adrenolutin in blood. This is very significant because adrenochrome rapidly is converted to adrenolutin in the body. Beyond this, Rouleau and colleagues [30] have demonstrated that high levels of adrenolutin in patients with severe heart failure is associated with a poor prognosis. Macarthur and colleagues [31] also have shown that, in septic shock, excess oxidation occurs and adrenalin is very rapidly oxidized to adrenochrome and noradrenalin to noradrenochrome. This process results in septic shock, in which blood pressure no longer responds to injections of catecholamines. Inhibiting the oxidation helps to restore the vasopressor properties of these catecholamines. Interestingly, vitamin B-12, in l