Neurological complications, vitamin

Folic acid Men women 400 MQ/d Coenzyme in the metabolism of nucleic acids and amino acids prevents megaloblastic anemia Adverse effects have not been documented, but high doses may mask neurological complications in people with Vitamin B12 deficiency... 

Neurological complications also are associated with vitamin B-12 deficiency and result from a progressive demyelination of nerve cells. The demyelination is thought to result from the increase in methylmalonyl-CoA that result from vitamin B-12 deficiency. Methylmalonyl-CoA is a competitive inhibitor of malonyl-CoA in fatty acid biosynthesis as well as being able to substitute for malonyl-CoA in any fatty acid biosynthesis that may occur. Since the myelin sheath is in continual flux the methylmalonyl-CoA-induced inhibition of fatty acid synthesis results in the eventual destruction of the sheath. The incorporation methylmalonyl-CoA into fatty acid biosynthesis results in branched-chain fatty acids being produced that may severely alter the architecture of the normal membrane structure of nerve cells... 

Because there have been no double-blind, placebo-controlled intervention studies of the effect of folic acid, the question of whether folic acid in patients with vitamin B12 deficiency aggravates the neurological complications cannot be answered definitively. From the data at hand we cannot exclude the possibility that folic acid may exacerbate the effects of vitamin B12 deficiency. For that reason an upper limit of 1 mg/day folic acid... 

Folic acid Megaloblastic anemia, diarrhea, glossitis Serum folate Decreased with increased cellular/tissue turnover (pregnancy, malignancy, hemolytic anemia) masks neurologic complications of vitamin B12 deficiency decreases risks of neural tube defects... 

In view of the discrepancies between studies, it is important to note that a low serum B12 level is not necessarily a cause of neurologic damage. Less than 10% of patients with pernicious anemia have clinical neurologic complications, perhaps because stores in different organs are variably depleted (Reynolds, 1976). Cerebral disease may be related to coexistent deficiencies of other vitamins, such as folate, or to the duration of Bi2 deficiency (Reynolds, 1976). In general, the prognosis for cognitive recovery is related to the duration of illness and not to absolute vitamin levels. No criteria have been established to indicate clearly which patients will improve. 

Early studies indicated that treatment of patients of vitamin B12 deficiency with folic acid led to aggravation of neurological complications or allowed them to progress by masking the anaemia (Reynolds 2006). 

Remission of hematological symptoms (megaloblastosis) can occur within few weeks of parentral vitamin B12 supplementation in small doses. Treatment of patients with vitamin B12 deficiency with folic acid leads to aggravation of neurological complications. 

AU patients with a suspected low vitamin Bn level should be screened. Vitamin Bn values below 150 pg/mL in a patient with macrocytosis, hypersegmented polymorphonuclear leukocytes, peripheral neuropathy, or dementia, is diagnostic of Bn deficiency, even though the Schilling test results may be normal. About one-third of patients with pernicious anemia will not demonstrate macrocytosis if their condition is complicated by iron deficiency, thalassemia, or a predominant neurologic involvement. 

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