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At least 973 records · Page 54Linked to original sources
PubMed1975

Calcium and folic acid absorption in patients taking anticonvulsant drugs.

Calcium and folic acid absorption were studied in 28 adult male epileptics on chronic anticonvulsant therapy. In 16 patients on diphenylhydantoin alone, calcium absorption was abnormal in 9. In 12 patients on both diphenylhydantoin and phenobarbital, calcium absorption was abnormal in 3 patients. Folic acid (3H-PGA) absorption was normal in all but one patient, while serum folate (less than 6.4 ng/ml) was reduced in all patients. Hypocalcemia (less than 8.5 mg/100 ml) occurred in only 2 patients, while serum alkaline phosphatase was elevated in 7 patients. These findings support the proposal that rickets and osteomalacia reported in patients on chronic anticonvulsant therapy results from reduced calcium absorption. The effect of these drugs appears to be the acceleration of the metabolism of vitamin D and an increase in the excretion of polar metabolites. This may result in reduced levels of 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol which are necessary for normal absorption of calcium. Since calcium absorption may be impaired secondary to a relative vitamin D deficiency, a supplemental increase in vitamin D intake by patients on anticonvulsant drugs is recommended.

Adult↗
PubMed1989

Survival rate and development of fetuses during the first 30 days of gestation after folic acid addition to a swine diet.

At weaning, 162 sows were assigned randomly to six treatments (27 in each treatment) according to a 2 X 3 factorial arrangement: two levels of supplementary folic acid (0 and 5 mg/kg of diet) and three treatments to stimulate ovulation (none, flushing and pregnant mare serum gonadotropin [PMSG] injection). All sows were mated twice within 7 d after weaning. Of the 162 animals originally selected, 123 sows were pregnant and used in this trial. The flushing treatment consisted of allowing sows ad libitum access to feed from the day after weaning through the 1st day of behavioral estrus, whereas control animals received 2.4 kg of feed daily. The hormonal treatment consisted of one i.m. injection of 1,250 IU of PMSG the day after weaning. The commercial-type diet used as the control was computed to contain .6 mg folates per kilogram. Folic acid supplementation elevated (P less than .001) serum folates between weaning and 30 d of gestation. Fetuses of sows fed the diet supplemented with folic acid had a higher (P less than .05) total protein concentration than fetuses of control sows, whereas RNA and DNA concentrations and protein:DNA ratio were not affected. The PMSG treatment elevated (P less than .05) ovulation rate, whereas the flushing or folic acid treatments had no effect on this trait. The addition of 5 mg/kg folic acid to the commercial-type diet improved (P less than .05) the survival rate of fetuses during early gestation and tended (P = .096) to increase the number of fetuses presumably living at 30 d of gestation when this treatment was associated with high ovulation rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1982

Effects of dietary fiber on the bioavailability of folic acid monoglutamate.

Low bioavailability of folacin has been previously reported for a variety of foods of plant origin. This study was conducted to examine the possible role of various types of dietary fiber on the bioavailability of folic acid monoglutamate. Cellulose, pectin, lignin, sodium alginate and wheat bran were selected for their differing physical and chemical properties. In vitro binding studies by equilibrium dialysis showed no evidence of physical or chemical binding of folic acid under physiological conditions. In vivo effects were evaluated by a chick bioassay with graded levels of folic acid in semipurified diets containing the fiber materials at 3% (weight/weight). Total liver and plasma folacin concentration and chick growth were used as response indicators. Dose-response curves indicated that pectin, lignin and alginate significantly reduced chick growth at all levels of dietary folacin. Plasma and liver folacin dose-response curves were not significantly different for any of the fiber materials, which indicated that the growth impairment was not due to a fiber effect on folic acid absorption. These results suggest that added dietary fiber has little or no effect on the bioavailability of folic acid monoglutamate.

Alginates↗
PubMed1977

Serum vitamin B12 and folate levels, vitamin B12 and folic acid binding proteins in patients with primary carcinoma of the liver.

Serum vitamin B12, folic acid, vitamin B12 and folic acid binding protein concentration were determined in 31 patients with primary carcinoma of the liver. Serum vitamin B12 level was found to be higher in 16 of 31 (52%) patients with carcinoma of the liver and the mean value was also significantly higher than that of the control group. There was no significant difference between the mean values of serum UBBC of these 2 groups. TCI and TCIII increased while TCII decreased considerably in the patient group. Serum folate level in patients with primary carcinoma of the liver was significantly lower than that of the control group. About 39% of these patients had serum folate level lower than the lowest value of the control group. Serum FABP in the former group was also significantly higher than that of the latter group.

Adult↗
PubMed1999

[Folic acid protects against neural tube defects. But how many women of reproductive age have been informed about this fact?].

The involvement of folic acid in the aetiology of neural tube defects (NTDs) has been discussed for decades. Both observational and controlled intervention trials have shown periconceptional folic acid supplementation (PFAS) to significantly reduce the incidence both of first-time and recurrent NTDs. PFAS may also be associated with reduction in the incidence of certain other congenital malformations, preterm delivery, and intra-uterine growth retardation. However, the mechanism whereby folic acid exerts its protective effect remains unclear. Thermolabile 5,10-methyl-enetetrahydrofolate reductase was the first folate-related enzyme to be associated with an increased risk of NTDs. This genetic variant may result in increased plasma homocysteine levels, which have been linked to an increased risk of NTDs. The folate-dependent genetic variants known today can explain no more than 30-50 per cent of the observed protective effect of folate. However, available evidence suggests low maternal folate status itself to be the major determinant of NTD risk. Since the vast majority of NTDs are first occurrences, and in Sweden a large proportion of fetuses with spina bifida remain undetected at routine ultrasonography during pregnancy, primary prevention by means of PFAS represents a major potential public health asset, capable of reducing both mortality and morbidity due to NTDs. Accordingly, implementation of a national strategy to reduce the incidence of NTDs, and promote awareness among health care providers and women of reproductive age of the benefits of PFAS is strongly to be recommended. Although supplemental folic acid tablets are the best proven means of improving folate status, compliance may be a problem, which emphasises the importance of considering a nutrient fortification programme as a complementary strategy for reducing the incidence of NTDs.

Female↗
PubMedDate not supplied

Folic acid and the prevention of neural tube defects (NTDs). Challenges and recommendations for public health.

OBJECTIVE: To outline specific challenges facing public health in Canada that need to be addressed to ensure that all women of childbearing years can attain optimal folate status for prevention of NTDs. METHODS: The new Dietary Reference Intake (DRI) for folate was examined in terms of the literature on the effective form of the vitamin, the level of folic acid provided by the Canadian food supply and the folic acid content of available supplements. FINDINGS: There are six major challenges facing public health in Canada on this issue. These include confusion among health professionals and the general public on the effective form of the vitamin, requirements, and the necessity of taking supplements. Further obstacles to ensuring optimal folate status in all women of childbearing age in Canada include the limited amounts of folic acid that are currently permitted in foods and the difficulties involved in identifying the amount of folic acid provided in these foods in relation to needs. INTERPRETATION: These challenges must be addressed to enable women in Canada to make an informed choice about folic acid. This has the potential to prevent up to 70% of the 300 births affected by NTDs each year.

Canada↗
PubMed1983

A possible relationship between folic acid neurotoxicity and cholinergic receptors in the pyriform cortex and amygdala.

The substantia innominata complex (SI) is the major source of cholinergic innervation to the amygdala, entorhinal and pyriform cortices, and the neocortex. Immunohistochemical studies using both monoclonal and polyclonal antibodies to choline acetyltransferase (ChAT) have clearly identified that the large size neurons of this area are cholinergic. We have lesioned this area by three methods: electrocoagulation, kainic acid (KA) injection and folic acid (FA) injection. Biochemical (GAD, ChAT and QNB binding) and histological studies of the SI and its known target areas as well as the hippocampus, thalamus and striatum were undertaken. Histologically, electrolytic and KA (2 nmol) lesions produced extensive local damage, but local damage was minimal with FA (100-250 nmol). Electrolytic lesions produced no remote neuronal damage. KA injections produced mild to moderate damage in the amygdala and cortex, while FA produced severe damage in the amygdala and pyriform cortex, with less severe damage in the entorhinal cortex and neocortex. Biochemically, electrolytic lesions produced drops in ChAT only in remote areas. Kainic acid produced moderate drops in ChAT, GAD and QNB binding. FA, on the other hand, produced only a minimal change in ChAT, but very heavy reductions in GAD and QNB binding. Thus, GABA neurons of the cortex were damaged. They may also be the cholinoceptive neurons that were damaged. The remote damage following KA and, particularly, FA, is presumed to be due to the epileptiform activity induced by the local injection of these agents. Reduction in both seizures and remote damage was brought about by pre-treatment of the animals with valium (20 mg/kg) or scopolamine (50 mg/kg). Injection of FA into the amygdala or striatum produced some remote damage but it was much less in magnitude than after SI injection.

Amygdala↗
PubMed1984

Folic acid therapy in the fragile X syndrome.

Two brothers with fra(X) positive X-linked mental retardation (XLMR) were treated with folic acid. Initially a double blind cross-over design was employed followed by a long-term high dose trial. A decrease in the frequency of fra(X) positive cells was observed when low folic acid culture medium was used but not when an FUdR induction system was employed. Selected behavioral characteristics improved in both while receiving folic acid. Decreased hyperactivity, greater attention span, increased motor coordination, increased quantity and quality of speech were noted. Improvement in Leiter mental age and regression after cessation of treatment was seen in one subject but not in the other. Further controlled trials with larger numbers of subjects using high doses of folic acid over longer periods of time are needed to assess the possible benefits of this experimental form of treatment.

Adolescent↗
PubMed1998

A structurally altered human reduced folate carrier with increased folic acid transport mediates a novel mechanism of antifolate resistance.

CEM/MTX is a subline of human CCRF-CEM leukemia cells which displays >200-fold resistance to methotrexate (MTX) due to defective transport via the reduced folate carrier (RFC). CEM/MTX-low folate (LF) cells, derived by a gradual deprivation of folic acid from 2.3 microM to 2 nM (LF) in the cell culture medium of CEM/MTX cells, resulted in a >20-fold overexpression of a structurally altered RFC featuring; 1) a wild type Km value for MTX transport but a 31-fold and 9-fold lower Km values for folic acid and leucovorin, respectively, relative to wild type RFC; 2) a 10-fold RFC1 gene amplification along with a >20-fold increased expression of the main 3.1-kilobase RFC1 mRNA; 3) a marked stimulation of MTX transport by anions (i.e. chloride); and 4) a G --> A mutation at nucleotide 227 of the RFC cDNA in both CEM/MTX-LF and CEM/MTX, resulting in a lysine for glutamate substitution at amino acid residue 45 predicted to reside within the first transmembrane domain of the human RFC. Upon transfer of CEM/MTX-LF cells to folate-replete medium (2.3 microM folic acid), the more efficient folic acid uptake in CEM/MTX-LF cells resulted in a 7- and 24-fold elevated total folate pool compared with CEM and CEM/MTX cells, respectively (500 versus 69 and 21 pmol/mg of protein, respectively). This markedly elevated intracellular folate pool conferred a novel mechanism of resistance to polyglutamatable (e.g. ZD1694, DDATHF, and AG2034) and lipophilic antifolates (e.g. trimetrexate and pyrimethamine) by abolishing their polyglutamylation and circumventing target enzyme inhibition.

Affinity Labels↗
PubMed2005

Influence of serum folic acid levels on plasma homocysteine concentrations in patients with rheumatoid arthritis.

The purpose of this study was to investigate whether negative effects of methotrexate (mtx) on blood homocysteine (hmc) levels can be prevented with the replacement of folic acid. 42 female patients with rheumatoid arthritis (RA) were studied. Patients were separated into two groups according to their treatment status with mtx (group I: 27 patients taking mtx and folic acid; group II: 15 patients not using mtx). The level of hmc was found to be 6.3+/-2.4 micromol/l in group I and 7.87+/-3.2 micromol/l in group II (p>0.05). Folic acid levels of group I and II were found to be 21.3+/-15.9 ng/ml and 8.41+/-2.86 ng/ml respectively (p<0.001). There was a statistically-significant correlation between age and hmc levels (r=0.386, p=0.012). Negative statistically-significant correlations were observed between folic acid and hmc levels. The effects of mtx on hmc can be prevented with the replacement of folic acid.

Adolescent↗
PubMedDate not supplied

[Megalocytic anemia of alcoholics and folic acid (author's transl)].

Megalocytic anemia of alcoholics is due to the deficiency of folic acid: the proof is the serum hypofolemia. The mechanism is complex and due to : a dietary deficiency; a malabsorption; an insufficiency of conversion of polyglutamate to monoglutamate; a liver deficiency; a specific effect of alcohol on the folate absorption. Alcohol has a toxic effect on the marrow and inhibits the folic acid.

Adult↗
PubMed2006

Validity of protein, retinol, folic acid and n-3 fatty acid intakes estimated from the food-frequency questionnaire used in the Danish National Birth Cohort.

OBJECTIVE: To validate intakes of protein, folic acid, retinol and n-3 fatty acids estimated from a food-frequency questionnaire in week 25 of pregnancy (FFQ-25). DESIGN: Validation was done against a 7-day weighed food diary (FD) and biomarkers of the nutrients in gestation week 32-38. SUBJECTS AND SETTING: The FFQ-25 to be validated was used in the Danish National Birth Cohort comprising 101 042 pregnant Danish women, of whom 88 participated in the present validation study. RESULTS: Estimated intakes of protein, retinol and folic acid did not differ significantly between the two dietary methods, but intake of n-3 fatty acids was one third larger when estimated from the FFQ-25. The intakes estimated from the two dietary methods were all significantly correlated, ranging from 0.20 for retinol intake to 0.57 for folic acid intake. Sensitivities of being correctly classified into low and high quintiles were between 0.22 and 0.77, and specificities were between 0.62 and 0.89. Urinary protein content did not correlate significantly with protein estimated from the FFQ (r = 0.17, P > 0.05), but did with intake estimated from the FD (r = 0.56, P < 0.0001). Erythrocyte folate correlated significantly with the estimated total intake from the FFQ (r = 0.55, P < 0.0001) and the FD (r = 0.52, P < 0.0001). No correlations with plasma retinol were found. Erythrocyte eicosapentaenoic acid (C20:5n-3) correlated significantly with n-3 fatty acids intake estimated from both the FFQ-25 (r = 0.37, P < 0.001) and the FD (r = 0.62, P < 0.0001). CONCLUSION: The FFQ-25 gives reasonable valid estimates of protein, retinol and folic acid intakes, but seems to overestimate intake of n-3 fatty acids.

Adult↗
PubMed1999

Periconceptional use of folic acid amongst women of advanced maternal age.

Between February 1994 and February 1997 a group of 881 women completed a questionnaire on the use of folic acid. During the study period the percentage of women who had been informed about the benefits of folic acid rose from 41 per cent to 90 per cent and the percentage taking supplementation rose from 18 per cent to 60 per cent. Nevertheless, few women used folic acid at the right time and dose and although 90 per cent would have been willing to follow recommendations, correct use did not exceed 25 per cent. It is concluded that effective folic acid supplementation requires food fortification rather than information provided by healthcare workers.

Adult↗
PubMed2001

Oral vitamin B(12) and high-dose folic acid in hemodialysis patients with hyper-homocyst(e)inemia.

BACKGROUND: Hyper-homocyst(e)inemia is an independent risk factor for atherosclerotic vascular disease in patients with end-stage renal disease (ESRD), although optimal treatment remains unknown. This randomized, double-blind, placebo-controlled study was designed to measure the effect of high-dose oral vitamin B(12) and folic acid on predialysis total homocyst(e)ine levels in patients with ESRD. METHODS: We studied 81 hemodialysis patients who had hyper-homocyst(e)inemia (>16 micromol/L) on varied doses of a multivitamin containing 1 mg of folic acid/day. After screening blood work, all patients were switched to daily multivitamin therapy, including 1 mg of folic acid for four weeks. For all patients, vitamin B(12), 1 mg/day, was added for an additional four weeks. Patients were then randomized to receive four weeks of 0, 5, or 20 mg of folic acid in addition to the multivitamin and vitamin B(12) (all given daily). RESULTS: Screening homocyst(e)ine levels (mean 27.7 micromol/L) decreased by 19.2% after four weeks of treatment with a daily multivitamin containing 1 mg of folic acid (P < 0.001). Homocyst(e)ine levels were reduced further from 22.3 to 18.6 micromol/L (mean reduction 16.7%, 95% CI 11.8 to 21.6%, P < 0.001) after four weeks of therapy with vitamin B(12) (1 mg/day). There was no significant difference in mean reduction of homocyst(e)ine levels after therapy with high-dose folic acid compared with placebo (P = 0.35). CONCLUSIONS: The optimal oral treatment of hyper-homocyst(e)inemia in hemodialysis patients consists of 1 mg of folic acid and 1 mg of oral vitamin B(12) daily. Whether this treatment will lower the risk of future atherosclerotic vascular events remains to be investigated.

Administration, Oral↗
PubMed2005

Effect of folic acid supplementation on genomic DNA methylation in patients with colorectal adenoma.

BACKGROUND AND AIMS: A low dietary folate intake can cause genomic DNA hypomethylation and may increase the risk of colorectal neoplasia. The hypothesis that folic acid supplementation increases DNA methylation in leucocytes and colorectal mucosa was tested in 31 patients with histologically confirmed colorectal adenoma using a randomised, double blind, placebo controlled, parallel design. METHODS: Subjects were randomised to receive either 400 microg/day folic acid supplement (n = 15) or placebo (n = 16) for 10 weeks. Genomic DNA methylation, serum and erythrocyte folate, and plasma homocysteine concentrations were measured at baseline and post intervention. RESULTS: Folic acid supplementation increased serum and erythrocyte folate concentrations by 81% (95% confidence interval (CI) 57-104%; p<0.001 v placebo) and 57% (95% CI 40-74%; p<0.001 v placebo), respectively, and decreased plasma homocysteine concentration by 12% (95% CI 4-20%; p = 0.01 v placebo). Folic acid supplementation resulted in increases in DNA methylation of 31% (95% CI 16-47%; p = 0.05 v placebo) in leucocytes and 25% (95% CI 11-39%; p = 0.09 v placebo) in colonic mucosa. CONCLUSIONS: These results suggest that DNA hypomethylation can be reversed by physiological intakes of folic acid.

Adenoma↗
PubMed1993

[Pharmacokinetics and relative bioavailability of iron and folic acid in healthy volunteers].

The pharmacokinetics and the relative bioavailability of iron and of folic acid was investigated in a randomized, balanced 2-way cross-over study with 14 healthy male participants. The drugs were given in a combined preparation dragée (Ferro-Folsan) containing 100 mg of ferrous-II-sulfate x 1.5 H2O (CAS 13463-43-9) and 0.85 mg of folic acid (CAS 59-30-3). Other established preparations were used as reference drugs. All subjects had a normal iron body level and were brought to a saturated folic acid level prior to the investigation. After administration of 2 dragées of the test medication and determination of serum iron level until 9 h p.a., a relative bioavailability of 64%, compared to an equal dose of a ferrous-II-sulfate-ascorbic acid reference solution, was calculated. From the serum folate AUC (0-9 h) the relative bioavailability was evaluated with 97% for the oral formulation compared to the i.m. administration. The ratio of the cumulative renal folate excretion in the 0-9 h interval amounted to 76% for the oral compared to the i.m. administration. However, in order to understand this differing result it should be kept in mind that during the first hours following parenteral administration a greater amount of the unchanged compound is renally excreted than after oral dosing. This is presumably based upon the different rate of absorption following both administrations with a steeper absorption phase following the parenteral dose.

Administration, Oral↗