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What Causes Folic Acid Deficiency?
Last reviewed: 19.10.2021
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Causes of deficiency of folic acid.
Inadequate receipts due to:
- predilections in nutrition, low economic level;
- ways of cooking (prolonged boiling leads to the loss of 40% of folates);
- feeding with goat's milk (1 liter contains 6 micrograms of folate);
- eating disorders (kwashiorkor, marasmus);
- Special diets (with phenylketonuria, maple syrup disease);
- prematurity;
- state after bone marrow transplantation (special food processing).
Absorption disorders:
- congenital isolated folate malabsorption;
- acquired:
- idiopathic steatorrhoea;
- tropical sprue;
- full or partial gastrectomy;
- multiple diverticula of the small intestine;
- resection of jejunum;
- inflammation of the ileum;
- Whipple's disease;
- lymphoma of the intestine;
- medicines: broad-spectrum antibiotics, diphenylhydantoin (Dilantin), primidone, barbiturates, oral contraceptives, cycloserine, metformin, ethanol, food amino acids (glycine, methionine);
- condition after bone marrow transplantation (total irradiation, drugs, intestinal lesion).
Increased demand:
- increased growth (prematurity, pregnancy);
- chronic hemolysis, especially in combination with ineffective erythropoiesis;
- dyseritropoietic anemia;
- malignant diseases (lymphoma, leukemia);
- hypermetabolic conditions (eg, infections, hyperthyroidism);
- extensive skin lesions (lichen-like dermatitis, exfoliative dermatitis);
- cirrhosis of the liver;
- state after bone marrow transplantation (bone marrow and epithelial cell regeneration).
Abnormalities in the metabolism of folic acid:
- congenital:
- deficiency of methylene-tetrahydrofolate reductase;
- deficiency of glutamate formiminotransferase;
- functional insufficiency of 5-methyltetrahydrofolate-homocysteine-methyltransferase due to pathology of CblE and CblG;
- insufficiency of dihydrofolate reductase;
- deficiency of methyl-tetrahydrofolate-cyclohydrolase;
- primary failure of 5-methyltetrahydrofolate-homocysteine-methyltransferase;
- purchased:
- medicines: folate antagonists (dihydrofolate reductase inhibitors): methotrexate, pyrimethamine, trimethoprim, pentamidine;
- deficiency of vitamin B 12;
- alcoholism;
- pathology of the liver.
Increased excretion:
- regular dialysis;
- vitamin B deficiency ; 12;
- liver disease;
- heart disease.
Alimentary folate deficiency ranks second in the world in terms of prevalence among deficient conditions (after iron deficiency of iron) and develops as a result of malnutrition and starvation. The incidence of disease in women is higher than that of men. Folate stores are depleted for 3 months with increased demand for them (during pregnancy, during lactation). With insufficient folate content in the fetal body, its nervous system develops incorrectly. That is why before conception and during pregnancy, women are prescribed folic acid for preventive purposes. Inadequate intake of folic acid during pregnancy leads to premature birth and birth of children with low body weight. At birth, clinical manifestations of folate deficiency are rare. Rapid growth in the first few weeks of a child's life is accompanied by an increased need for folic acid, so during this period, with a prophylactic goal, it is recommended to prescribe the drug at 0.05-0.2 mg per day.
Discussing the causes of the development of folic acid deficiency anemia, it is especially necessary to consider the increased need for folate in premature infants and children of the first year of life. The concentration of folates in the blood serum and erythrocytes in newborns is 2-3 times higher than in adults. However, in the first weeks of life, it decreases to the level observed in older children and adults. The average daily loss of folate per unit surface area of the body is greatest in children of the first days of life, so it is not possible to cover the needs of folate at the expense of the diet. Especially easy folate deficiency and megaloblastic anemia develop in preterm infants 6-10 weeks of age, born with a small depot of folates. This is due to the rapid depletion of the depot of folic acid due to intensive growth, eating habits and intercurrent diseases.
During pregnancy, the increase in the requirements for folic acid is due to the fetal needs, which is 100-300 mcg / day.
In hemolytic anemia, the emerging folate deficiency is associated with increased folate utilization by the young cells of the erythroid germ. Especially low levels of folic acid are noted in patients with sickle cell anemia, large thalassemia.