Deficiencies, nutritional folic acid

Megaloblastic anem/a.- Treatment of megaloblastic anemias due to a deficiency of folic acid as seen in tropical or nontropical sprue, anemias of nutritional origin, pregnancy, infancy, or childhood. 

Deficiency of folic acid is a common nutritional problem of worldwide importance.13 A recommended daily intake is 0.2 mg, but because of the association between low folic acid intake and neural tube defects in infants, women of child-bearing age should have 0.4 mg / day.c e... 

Folic acid - [FOOD TOXICANTS, NATURALLY OCCURRING] (Volll) - [FINECHEMICALS - PRODUCTION] (Vol 10) -m animal nutrition [VITAMINS - FOLIC ACID] (Vol 25) -biosynthesis [VITAMINS - FOLIC ACID] (Vol 25) -m dairy substitutes [DAIRY SUBSTITUTES] (Vol 7) -deficiency [VITAMINS - FOLIC ACID] (Vol 25) -metabolism of [VITAMINS - FOLIC ACID] (Vol 25) -metabolites [VITAMINS - FOLIC ACID] (Vol 25) -mmilk [MILKANDMILKPRODUCTS] (Vol 16) -one-pot synthesis [VITAMINS - FOLIC ACID] (Vol 25) -properties [VITAMINS - FOLIC ACID] (Vol 25) -role m veterinary medicine [VETERINARY DRUGS] (Vol 24)... 

Although requirements for vitamins and trace elements are known in health (Table 30-1), the effects of illness on these requirements are poorly understood and quantified. However, it is now apparent that as an individual develops progressively more severe depletion in vitamin or trace element status, the person passes through a series of stages with biochemical or physiological consequences. The metabolic or physiological penalty of such suboptimal nutritional status is usually not clear, but the assumption remains that the suboptimal metabolism is likely to have detrimental effects (e.g., subclinical deficiency of folic acid is associated with an increase in serum homocysteine concentration, which is an independent risk factor for coronary artery disease—see Chapter 26). Similarly, subclinical deficiency of chromium may be associated with impaired glucose tolerance in certain types of diabetes. 

There are two major types of nutritional megaloblastic anemia one is due to a deficiency of folic acid, and the other is due to a deficiency of vitamin B-12. 

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. 

In a totally different field, studies were being carried out on children who had a deficiency of methionine synthase and an impaired ability to convert homocysteine to methionine, so that they had increased blood levels of homocysteine. It was noted that these children had an increased incidence of thrombosis in cerebral and coronary arteries. This led to a study which eventually showed that an increased level of homocysteine was a risk factor for coronary artery disease in adults. Since methionine synthase requires the vitamins, folic acid and B12, for its catalytic activity, it has been suggested that an increased intake of these vitamins could encourage the conversion of homocysteine to methionine and hence decrease the plasma level of homocysteine. This is particularly the case for the elderly who are undernourished (see Chapter 15 for a discussion of nutrition in the elderly). 

Alcohol indirectly affects hematopoiesis through metabolic and nutritional effects and may also directly inhibit the proliferation of all cellular elements in bone marrow. The most common hematologic disorder seen in chronic drinkers is mild anemia resulting from alcohol-related folic acid deficiency. Iron deficiency anemia may result from gastrointestinal bleeding. Alcohol has also been implicated as a cause of several hemolytic syndromes, some of which are associated with hyperlipidemia and severe liver disease. 

Studies on growth factors required by certain microorganisms, for example Streptococcus faecalis and Lactobacillus casei, and of their relevance in animal nutrition, led to the isolation and characterization of folic acid, pteroylglutamic acid (104), the structure of which was determined in 1946. It is an essential vitamin for man and together with vitamin B12 it is involved in the development of blood cells. Deficiency causes macrocytic anaemia. Many microorganisms do not use exogenous folic acid, but synthesize their own, and some... 

In many animals, dietary deprivation of choline leads to liver dysfunction and growth retardation, and some patients maintained on choline-free total parenteral nutrition develop liver damage that resolves when choline is provided, suggesting that endogenous synthesis may be inadequate to meet requirements (Zeisel, 2000). There is inadequate information to permit the setting of reference intakes, but the Acceptable Intake for adults is 550 mg (for men) or 425 mg (for women) per day (Institute of Medicine, 1998). In experimental animals choline deficiency is exacerbated by deficiency of methionine, folic acid, or vitamin B12, which impairs the capacity for de novo synthesis. 

Folic acid deficiency may result in neural tube defects in newborns. Folic acid is one of the few nutritional supplements shown in clinical trials to be effective in preventing disease. Maternal prenatal supplementation with 400 mg/day folic acid reduced significantly the incidence of neural tube defects in newborns, which indicates that low maternal folate concentrations were associated with these defects. 

It is estimated that the minimum daily requirement of folate is 5 micrograms/kg. Liver stores are about 160 micrograms in premature children, and 220 micrograms in full-term infants. Infants who require parenteral nutrition will rapidly become folate deficient unless fohc acid is included in the regimen. Since many multivitamin supplements do not contain folic acid, its inclusion should be ensured by the addition of folic or folinic acid. 

Folic acid is a nutritional supplement frequently used during periods of deficiency. Folic acid needs increase during chronic diseases, such as malabsorption liver disease, alcoholism, and anticonvulsant or oral contraceptive use. Folic acid supplementation during pregnancy is strongly recommended to prevent neural tube defects to the unborn child. The active form of folic acid, folinic acid, is used in the management of certain medical diseases (e.g., patients taking methotrexate, and 5-fluorouracil). 

There are many causes of folic acid deficiencies. Inadequate nutrition during periods of increased requirements is one of the main causes of megaloblastie anemia of pregnaney and neural tube defects. Alcoholism is considered the leading cause of folic acid deficiency... 

One often-overlooked major factor that may contribute to anemia in the older population is nutritional status. Cross-sectional studies demonstrate a higher prevalence of anemia in low socioeconomic populations, as well as a high prevalence of other nutritional deficiencies. Thus nutritional deficiencies not usually severe enough to affect the hematopoietic system in the younger population may account for anemia in the aged. Edentulous or infirm elderly who may be too ill to prepare their meals are at risk for nutritional folate deficiency. However, unlike cobalamin levels, it has been demonstrated that folate levels increase rather than decline with age. This may be due to the dramatic increase in folate supplements used by the elderly, especially in white women, as well as the fortification of the American diet with folic acid. ... 

Many patients in intensive care units receive intravenous nutrition, which is a mixture of various amino acids, sorbitol, and ethanol. In a study of 30 patients with normal preoperative folate levels who were operated on for gastrointestinal disease, the serum folate fell within 48 hours by 60-95% in 20 patients receiving intravenous nutrition (W24). Seven patients had a megaloblastic bone marrow. Daily treatment with 0.5 mg of folic acid given intravenously prevented any clinical signs of folate deficiency. These patients received between 100 and 150 g of ethanol daily as part of their parenteral nutrition, and this may have played a significant role in the development of folate deficiency. However, Tennant (T12) examined this possibility and found that acute depression of the serum folate concentration occurred with both alcohol-firee and alcohol-containing preparations used for parenteral nutrition. It was also noted that only one particular brand of... 

E., Acute folate deficiency associated with intravenous nutrition with aminoacid-sorbi-tol-ethanol Prophylaxis with intravenous folic acid. Br. J. Haematol. 37, 521-526... 

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