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Folic acid deficient diet reduces the duration and severity of intravenous megimide seizures in the rat after 6 months of diet. Plasma and serum folate levels are strongly reduced after that period. The difference between Lactobacillus casei and Streptococcus faecalis activity in brain show a slight, but not significant, decrease after 12 months of diet.
Folic acid deficiency was produced by injecting aminopterin into adult male albino rats, resulting in inhibition of spermatogenesis. Bone marrow smears were studied to serve as an index of folic acid deficiency; however, changes in spermatogenesis were noticed earlier than the bone marrow changes. Meiotic division was affected more than mitotic division. The nuclei of spermatogenic cells showed degenerative changes. Chromosomal abnormalities, chiefly sticky chromosomes, were noticed in squashed preparations of seminiferous tubules.
The effect of a vitamin B12 and folic acid deficient diet on juvenile and adolescent baboons (Papio cynocephalus anubis) was studied. The baboons developed clinical and hematological signs characteristics of folacin deficiency, although they were less severe in juvenile baboons. The signs disappeared when folic acid was replaced in the diet. The serum vitamin B12 levels increased in all baboons fed the vitamin B12 and folic acid deficient diet. When folic acid was added to the diet, the levels gradually decreased in adolescent baboons, liver vitamin B12 levels decreased to a lesser extent when fed a vitamin B12 and folic acid deficient diet than when fed a vitamin B12 deficient diet. In juvenile baboons fed a vitamin B12 and folic acid deficient diet, for 7 months and a vitamin B12 deficient diet for a further 11 months, liver vitamin B12 levels did not decrease at any time but were similar to those in baboons fed a vitamin B12 and folic acid supplemented diet.
Folic acid deficiency is very common in elderly patients who have a mean red cell volume greater than 94 fl. Eighteen out of 40 elderly patients with red cell macrocytosis who initially had normal red cell folate and serum B12 levels subsequently developed folic acid deficiency.
The serum folate level of 100 aged persons (after 70) was decreased (less than 4 ng/ml) in 41% of the cases (manifest deficiency of folic acid). In the group of aged persons having normal folate values, in 41% of the cases the clearance method proved a latent folic acid deficiency, being the 15 minute value after 15 gamma/kg folic acid i.v., less than 25 ng/ml.
The influence of chronic alcohol ingestion and artificially induced folic acid deficiency on iron absorption has been measured in rabbits by whole body counter. Results show that chronic alcohol ingestion does not modify iron absorption. Folic acid deficiency increases iron absorption by two probable mechanisms: first by increased plasma iron turnover (PIT), which parallels ineffective erythropoiesis, and second by a probable direct effect on the intestinal mucous membranes. This second mechanism appears to be independent of PIT: concomitant deficiency of folic acid and alcohol ingestion produces an increase in iron absorption without modification of PIT. Experience with drugs inhibiting protein synthesis suggests that this increase may be mediated by decreased protein synthesis.
Two groups of patients with folic acid responsive neurological and psychiatric disorders are reported. The first group (7 patients) had well-established acquired folate deficiency due either to defective absorption (4 cases with atrophy of jejunal mucosa) or to a deficient diet (3 cases). One patient had a subacute combined degeneration of the spinal cord while others were depressed and had weight loss, permanent muscular and intellectual fatigue, restless legs syndrome, depressed ankle jerks, diminution of the sense of vibration in the knees and a stocking-type tactile hypoesthesia. The second group (9 patients) comprised idiopathic cases of folic acid deficiency. Their main subjective complaints were chronic fatigability and familial restless legs syndrome. The neurological findings were similar to those of the patients with acquired disorders. Neuropsychological testing procedures revealed an abnormal intellectual functioning in all 16 patients. Abnormal patterns of radionuclide cisternograms and computerized transaxial tomography (CTT) were found in 11 patients. After 6-12 months of folic acid therapy a striking improvement regarding their intellectual functioning was noticed: the IQ, Kohs Block Design and Category tests were significantly improved. The correlation of neuropsychological findings with CTT and radionuclide cisternograms led to the conclusion that chronic folate deficiency could induce cerebral atrophy.
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The authors report 12 cases of neurological syndromes due to folic acid deficiency, due in 8 cases to chronic alcoholism. In 5 cases there was polyneuritis, 3 cases had cerebellar atrophy, whilst 4 patients had subacute combined degeneration of the cord. Folic acid deficiency occurred alone in five cases out of twelve, as in 3 cases vitamin B1 deficiency was associated, and in four cases there was malabsorption of vitamin B12. A neuropathological study of these cases showed: 1) moderate involvement of the mamillary tubercles as observed in deficiency encephalopathies. 2) severe peripheral nerve involvement especially of axonal type. 3) involvement of the anterior horns of the spinal cord with appearances of central chromatolysis and a few atrophic neurones.
An ionization chamber method was used in vivo to demonstrate a delayed oxidation of [14C] formaldehyde and [14C] formate to 14CO2 in folic acid-deficient rats as compared to control rats or folic-acid-deficient rats treated by folic acid. Results obtained showed that oxidation of these two molecules required the presence of folic acid.
One case each of pernicious anemia and folic acid deficiency with chronic malabsorption with disease of the cord and histologically demonstrated concomitant disease of the peripheral nerve system in the sense of a polyneuropathy are described. The histological findings of nerve obtained by biopsy show, in both cases, the loss of individual nerve fibers as an expression of a chronic axonal degeneration. The pathogenetic basis to be considered in these cases is presented.
Two groups of 63-day-old female Wistar rats were fed a folic acid deficient diet, based on 20% of vitamin-free casein and containing 1% of succinylsulfathiazole, for 5 weeks (group A) and 9 weeks (group B) before being bred, and the same diet was continued through pregnancy and lactation. Three out of eleven (21.3%) and three out of seven (42.9%) rats in groups A and B, respectively, resorbed completely, while no control rat resorbed. No pups from group B survived to weaning. Both groups (A and B) showed depressed feed consumption (although the effect in group A rats was small) and weight gains and increased formiminoglutamic acid excretion in the urine during gestation, and low serum folic acid by the end of lactation. A study of blood components in group A rats revealed leucopenia, granulocytopenia, and increased reticulocyte count. While no congenital deformities were observed in pups from deficient dams, group A and group B dams in contrast to controls produced smaller sized litters with lower birth weights and poor survival rate. Surviving pups from group A dams had decreased weaning weights with significantly lower brain weights and brain DNA per gram of tissue.
Three different kinds of anaemia are seen in hypothyroidism: (1) normocytic, normochromic anaemia; (2) microcytic, hypochromic anaemia; (3) macrocytic normochromic anaemia. The latter is either a true pernicious anemia, which occurs fairly frequently in Hashimoto's thyroiditis, or maturation disorder of erythropoiesis as a result of folic acid deficiency. In three patients with primary hypothyroidism and macrocytic anaemia there were decreased levels of serum folic acid. After short-term administration of folic acid and 1-year of thyroxine the blood picture became normal in two of the patients.
Structural abnormalities and disaccharidase deficiency were demonstrated in biopsies of duodenal mucosa from four infants who had symptoms of failure to thrive and chronic diarrhea associated with a megaloblastic anemia. Goat's milk was the main dietary constituent for each infant for six to eight months prior to presentation. The structural abnormalities consisted of villous blunting, crypt hypertrophy, megaloblastic changes in epithelial cells, and nuclear enlargement. All changes reverted to normal with the addition of folic acid to the diet. This study provides evidence that nutritional folic acid deficiency can cause structural and functional alterations of the small intestine in infants.
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Thirteen patients with significant hemorrhage, severe thrombocytopenia, and megaloblastic bone marrows are described. Unusual features of this problem included its acute onset, frequent absence of the typical peripheral blood changes of megaloblastic anemia, normal serum B12 levels, and serum folates which were often not clearly abnormal. Most patients were critically ill and common clinical features included reduced dietary intake, renal failure, renal dialysis, the postoperative state, and sepsis. These clinical features, the laboratory findings, and a platelet increase in most patients after folate therapy lead to the conclusion that this problem is probably due to acute folic acid deficiency. Possible explanations for the atypical laboratory findings include the acuteness of onset, recent blood transfusion therapy, and impaired folate utilization. This problem may be relatively common. Because of its potential clinical importance, rapid onset, and attendent diagnostic difficulties, prophylactic folic acid is recommended in the clinical setting described.
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