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Results for “FOLIC ACID DEFICIENCY”

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At least 1,423 records · Page 79Linked to original sources
PubMed2000

The plasma homocysteine concentration is better than that of serum methylmalonic acid as a marker for sociopsychological performance in a psychogeriatric population.

BACKGROUND: Cobalamin/folate deficiency in elderly subjects may lead to psychiatric symptoms, but more often it increases the severity of various organic and nonorganic mental diseases. A major clinical problem, however, is the uncertainty and controversy concerning biochemical markers of cobalamin/folate deficiency to be used in the diagnostic evaluation of suspected cobalamin/folate deficiency. METHODS: We measured plasma homocysteine (tHcy), blood folate, serum methylmalonic acid, and serum cobalamin in 80 psychogeriatric patients (age, 77.3 +/- 8.6 years) and 50 controls (age, 76.1 +/- 8. 0 years). We assessed associations of these tests with measures of cognitive and behavior performance by use of regression analyses. RESULTS: Plasma tHcy was increased in 45% of the psychogeriatric population (mean, 20.5 +/- 9.2 micromol/L vs 15.3 +/- 4.7 micromol/L for controls; P <0.01). Plasma tHcy correlated with severity of dementia (r = 0.36; P <0.01), the Katz ADL index (r = 0.29; P <0.05), the Berger scale (r = 0.29; P <0.05), and the score of symptoms (r = 0.39; P <0.001) in the psychogeriatric population. Similarly, blood folate was significantly correlated with these measures, but the concentrations of serum cobalamin and methylmalonic acid were not. In a stepwise multiple regression analysis including the biochemical markers, tHcy was the only significant predictor of the severity of dementia (r(2) = 0.11; P <0.01) and the score of symptoms (r(2) = 0.16; P <0.001). CONCLUSION: Plasma tHcy is the best marker of those measured to investigate suspected tissue deficiency of cobalamin/folate.

Aged↗
PubMedDate not supplied

Potential association of thyrotoxicosis with vitamin B and folate deficiencies, resulting in risk for hyperhomocysteinemia and subsequent thromboembolic events.

OBJECTIVE: To describe a patient with severe thyrotoxicosis attributable to Graves' disease who had a thrombotic cerebrovascular accident and hyperhomocysteinuria, which resolved on correction of the thyrotoxicosis, and to present findings in a pilot study undertaken to investigate the relationship among thyrotoxicosis, homocysteine, folate, and vitamin B(12). METHODS: We present a case report of the index case, with clinical and laboratory details. For the investigative analysis, 21 patients who were 18 to 50 years old and had newly diagnosed, untreated Graves' disease and 10 age-and sex-matched euthyroid control subjects were studied. Of the patients with Graves' disease, 11 underwent studies both at diagnosis and after treatment. Fasting blood tests were performed for thyrotropin, free thyroxine, homocys-teine, vitamin B(12), folate, and methylmalonic acid, a marker of vitamin B(12) deficiency. RESULTS: Vitamin B(12), folate, homocysteine, and methylmalonic acid levels were not significantly different between the thyrotoxic and control or posttreatment groups. In patients with thyrotoxicosis, however, free thyroxine was positively correlated with both homocysteine (r = 0.67; P = 0.03) and methylmalonic acid (r = 0.89; P = 0.003). CONCLUSION: The positive correlation between free thyroxine levels and both homocysteine and methylmalonic acid suggests that thyrotoxicosis may be associated with functional vitamin B(12) deficiency. Such a deficiency may result in clinically important hyperhomocysteine-mia.

Adolescent↗
PubMed1994

Folate deficiency and congenital malformations induced by pyrimethamine in the rat.

In order to establish a relationship between the appearance of congenital malformations and the decrease of folic acid in rat mothers and embryos, a folic acid antagonist, pyrimethamine (PY), was administered. On the 12th day of gestation/pregnant rats received an intraperitoneal injection of 12.5, 15.63, 18.75 or 25 mg/kg PY. On the 13th day of gestation folic acid was measured in different maternal and embryonic tissues obtained after surgical hysterectomy of 1 uterine horn. On the 21st day of gestation malformations were studied on live fetuses remaining in the opposite horn. The folate levels were identical in all maternal tissues. The concentration of folic acid significantly decreased (50%) within the embryonic tissues in all PY-treated groups. A decrease of fetal weight occurred in the 18.75 and 25 mg/kg PY groups. Malformations were observed in the same groups. A dysfunction of the placental transfer of folates is hypothesized.

Animals↗
PubMed1975

Prevention of folate deficiency by food fortification. IV. Identification of target groups in addition to pregnant women in an adult rural population.

In a rural Negro population subsisting on a predominantly maize meal diet, the incidence of folate deficiency was 43.8% in nonanaemic women in late pregnancy, 32.1% in nonpregnant women, and 18.6% in adult males. More than one-third of all subjects older than 60 were deficient. No instance of unequivocal vitamin B12 deficiency was revealed in 431 subjects sampled, and it is considered that the hazards of giving a small daily dose of folic acid in this population are negligible. These findings warrant food fortification with folic acid in this and similar population groups.

Adolescent↗
PubMed2003

Long-latency deficiency disease: insights from calcium and vitamin D.

Nutrient intake recommendations and national nutritional policies have focused primarily on prevention of short-latency deficiency diseases. Most nutrient intake recommendations today are based on prevention of the index disease only. However, inadequate intakes of many nutrients are now recognized as contributing to several of the major chronic diseases that affect the populations of the industrialized nations. Often taking many years to manifest themselves, these disease outcomes should be thought of as long-latency deficiency diseases. Sometimes they come about by the same pathophysiologic mechanism that produces the index disease, but sometimes the mechanisms are completely different. Well-documented examples of both short- and long-latency deficiency states involving calcium and vitamin D are described briefly. Then, the insights derived from these nutrients are tentatively applied to folic acid. Discerning the full role of nutrition in long-latency, multifactorial disorders is probably the principal challenge facing nutritional science today. The first component of this challenge is to recognize that inadequate intakes of specific nutrients may produce more than one disease, may produce diseases by more than one mechanism, and may require several years for the consequent morbidity to be sufficiently evident to be clinically recognizable as "disease." Because the intakes required to prevent many of the long-latency disorders are higher than those required to prevent the respective index diseases, recommendations based solely on preventing the index diseases are no longer biologically defensible.

Anemia, Megaloblastic↗
PubMed1993

DNA methylation in folate deficiency: use of CpG methylase.

Folate deficiency produces a marked decrease in the ratio of S-adenosylmethionine to S-adenosylhomocysteine. This ratio regulates the activity of many cellular methylation reactions including that of DNA. We used bacterial CpG methylase to evaluate the effect of folate deficiency on methylation of DNA from livers of weanling rats fed an amino acid-defined folate deficient diet. After 4 weeks, liver DNA from deficient animals was undermethylated compared with DNA from pair-fed control animals.

Animals↗
PubMedDate not supplied

[Homocysteine metabolism and risk of cardiovascular diseases: importance of the nutritional status on folic acid, vitamins B6 and B12].

Homocysteine is a thiol-containing amino acid derived from methionine metabolism that can be degraded through two enzymatic pathways: remethylation and trans-sulfuration. In remethylation, homocysteine regenerates methionine. In the trans-sulfuration pathway, homocysteine forms cysteine. Due to the rapid metabolic utilization, the plasma concentration of this amino acid is low. Homocysteine circulates as free thiol, homocystine, or bound to free cysteine or to cysteine residues of proteins. Genetic defects of some enzymes in the homocysteine metabolism, or nutritional deficiencies of folic acid, vitamin B6 and B12 lead to an increase in homocysteine plasma concentration and is associated to an increment in cardiovascular diseases. On the basis of clinical and epidemiological studies, homocysteine plasma concentration is considered to be an independent risk factor for the development of atherothrombotic and cardiovascular diseases. The present review describes the homocysteine metabolism, the epidemiological evidence showing the association between homocysteine and the incidence of cardiovascular diseases. The mechanisms by which homocysteine produces vascular damage are indicated. Finally, some recommendations are given for the nutritional therapy of patients with hyperhomocysteinemia.

Arteriosclerosis↗
PubMed1983

Importance of vitamin B12 and folate metabolism in malabsorption.

The risk of developing folate deficiency is greatest in patients who have a poor diet and malabsorption secondary to disease of the jejunal mucosa or drugs which interfere with its metabolism. In contrast to cobalamin deficiency, in which body stores delay the onset of major metabolic complications, folate deficiency may develop in a matter of months. It is frequently possible to predict these deficiencies and always possible to reverse them by supplementation.

Diet↗
PubMed1998

Dietary supplements of folic acid during lactation: effects on the performance of dairy cows.

The present experiment was undertaken to determine the effects of dietary supplements of folic acid administered from 4 wk prepartum to 305 d of lactation on lactational performance. Sixty-three Holstein cows were assigned to 22 blocks of 3 cows according to lactation number, milk production, and body weight (BW). Within each block, cows received 0, 2, or 4 mg of folic acid/kg of BW per d. Dietary supplements of folic acid increased serum and milk folates but affected milk production and composition of primiparous and multiparous cows differently. Supplementary folic acid had little effect on milk production and composition of primiparous cows, except that milk production decreased during the first 100 d of lactation. However, during a complete lactation (3 to 305 d after calving), supplementary folic acid was associated with increased milk production by multiparous cows (8284 +/- 560, 8548 +/- 380, and 8953 +/- 191 kg for cows fed diets supplemented with 0, 2, and 4 mg of folic acid/kg of BW per d, respectively). The percentage of ash in milk was decreased for cows fed the highest amount of dietary folic acid. During the first 100 d of lactation, supplementary folic acid was associated with a lower concentration of nonprotein nitrogen in the milk of multiparous cows. The present study confirms results obtained previously, suggesting that, although the supply of folates from an unsupplemented diet and the ruminal microflora is sufficient to avoid a deficiency in folic acid, supplementary folic acid may increase the milk production of cows in the second lactation or greater.

Animals↗