Adequate Intake folic acid

No specific dietary restrictions are recommended for patients with IBD, but avoidance of high-residue foods in patients with strictures may help to prevent obstruction. Nutritional strategies in patients with long-standing IBD may include use of vitamin and mineral supplementation. Administration of vitamin B12, folic acid, fat-soluble vitamins, and iron may be needed to prevent or treat deficiencies. In severe cases, enteral or parenteral nutrition maybe needed to achieve adequate caloric intake. 

Furthermore, the two pathways that normally degrade homocysteine are absent from the neurone and glial cells and so homocysteine can accumulate in the brain (Chapter 8, Appendix 8.2). Consequently, the maintenance of adequate intake of folic acid and vitamin over many years, to ensure low levels of homocysteine, may help to protect neurones and reduce the risk of development Alzheimer s disease. 

Because the potential benefits outweigh the possibilities of harm, many experts recommend a daily multivitamin that does not exceed the RDA of it component vitamins. Multivitamins ensure an adequate intake for those vitamins—folic acid, vitamin B6, vitamin B12, and vitamin D—that are most likely to be deficient. However, the the evidence is insufficient to recommend for or against the use of supplements of vitamins A, C, or E multivitamins with folic acid or antioxidant combinations for the pre vention of cancer or cardiovascular disease. Most experts recommend against the use of p-carotene supplements, either alone or in combina Don, for the prevention of cancer or cardiovascular disease. 

When present in excess methionine is toxic and must be removed. Transamination to the corresponding 2-oxoacid (Fig. 24-16, step c) occurs in both animals and plants. Oxidative decarboxylation of this oxoacid initiates a major catabolic pathway,305 which probably involves (3 oxidation of the resulting acyl-CoA. In bacteria another catabolic reaction of methionine is y-elimination of methanethiol and deamination to 2-oxobutyrate (reaction d, Fig. 24-16 Fig. 14-7).306 Conversion to homocysteine, via the transmethylation pathway, is also a major catabolic route which is especially important because of the toxicity of excess homocysteine. A hereditary deficiency of cystathionine (3-synthase is associated with greatly elevated homocysteine concentrations in blood and urine and often disastrous early cardiovascular disease.299,307 309b About 5-7% of the general population has an increased level of homocysteine and is also at increased risk of artery disease. An adequate intake of vitamin B6 and especially of folic acid, which is needed for recycling of homocysteine to methionine, is helpful. However, if methionine is in excess it must be removed via the previously discussed transsulfuration pathway (Fig. 24-16, steps h and z ).310 The products are cysteine and 2-oxobutyrate. The latter can be oxidatively decarboxylated to propionyl-CoA and further metabolized, or it can be converted into leucine (Fig. 24-17) and cysteine may be converted to glutathione.2993... 

Recommended daily requirement [RDA) or adequate intake CAQ for men and nonpregnant women over 20 years old. Recommended values for certain vitamins Ce.g., folic acid) may be higher in women who are pregnant. Values for children are typically lower, and are adjusted according to the child s age. 

The identification of hyperhomocysteinemia as an independent risk factor in atherosclerosis and coronary heart disease (Section 10.3.4.2) has led to suggestions that intakes of vitamin Be higher than are currently considered adequate to meet requirements may be desirable. Homocysteine is an intermediate in methionine metabolism and may undergo one of two metabolic fates, as shown in Figure 9.5 remethylation to methionine (a reaction that is dependent on vitamin B12 and folic acid) or onward metabolism leading to the synthesis of cysteine (trans-sulfuration). Therefore, intakes of folate, vitamin B12, and/or vitamin Be may affect homocysteine metabolism. 

Folic acid deficiency, a macrocytic anemia, results from in- adequate intake, decreased absorption, hyperutilization, or inadequate utilization. Treatment consists of the oral administration of folic acid, even in patients with absorption problems. Adequate folic acid intake is essential in women of childbearing years to decrease the risk of neural tube defects in their children. 

It is of paramount importance to rule out vitamin B12 deficiency when folate deficiency is detected, as symptoms are similar. Laboratory changes associated with folate deficiency are similar to those seen in vitamin Bn deficiency, except vitamin Bn levels are normal. Decreases occur in the serum folate level (<3 ng/mL) within a few days of dietary folate limitations. The RBC folate level (<150 ng/mL) also declines and may be a better indicator of deficiency, as levels remain constant throughout the life span of the erythrocyte. Serum folate levels are sensitive to short-term changes such as dietary restrictions or alcohol intake, which may result in a short-term decline in serum levels with adequate tissue stores. It should be noted that an estimated 60% of patients with pernicious anemia have falsely low RBC folate levels, in all probability due to the requirement of cobal-amin for the normal transfer of methyltetrahydrofolate from plasma to cells. Additionally, if serum or erythrocyte folate levels are borderline, serum homocysteine is usually increased with a folic acid deficiency. If serum MMA levels are also elevated, vitamin B12 deficiency needs to be ruled out. 

Ensure adequate intake of vitamins and minerals to meet DRI, except where noted below Folic acid (5-10 mg/d) or FoUnic acid (1-5 mg/d) [5,8]... 

CAUTIONS (1) Boiling destroys folacin in cow s milk, so infants receiving boiled formulas prepared from pasteurized, sterilized, or powdered cow s milk should receive additional folacin to assure an adequate intake and (2) if the diet consists of goat s milk, folic acid supplementation should be given because of the low content and poor availability of folacin in goat s milk. 

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