Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FOLIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed2001

Influence of folic acid supplements on the carry-over of folates from the sow to the piglet.

This experiment aimed to investigate the influence of folic acid supplements on the carry-over of folates from the sow to the fetus during late gestation and to the suckling piglet. Two groups of sixteen German Landrace sows received, during gestation and lactation, a diet supplemented with either 0 or 10 mg folic acid/kg. Increased folic acid concentrations in the serum of sows were detected only at the end of gestation (day 100) and at the end of lactation (day 28). The supplementation with folic acid to the sows' diet improved the folic acid supply of the fetus compared with unsupplemented controls; values were respectively 92.6 v. 56.2 nmol folates/l serum in newborn piglets and 171.9 v. 76.3 micromol folates/g fresh liver in stillborn piglets (P < 0.05). Folate concentrations in colostrum and milk (day 28) were 3.6- and 5.0-times higher in supplemented than unsupplemented sows. This treatment effect was also reflected in the serum of piglets until weaning. Therefore, the folic acid supply for the suckling piglet is dependent mainly upon the carry-over of maternal folates via colostrum and milk.

Animals↗
PubMed2006

Folic acid pretreatment prevents the reduction of Na(+),K(+)-ATPase and butyrylcholinesterase activities in rats subjected to acute hyperhomocysteinemia.

The main objective of the present study was to evaluate the effect of folic acid pretreatment on parietal cortex Na(+),K(+)-ATPase and serum butyrylcholinesterase activities in rats subjected to acute hyperhomocysteinemia. Animals were pretreated daily with an intraperitoneal injection of folic acid (5 mg/kg) or saline from the 22th to the 28th day of age. Twelve hours after the last injection of folic acid or saline, the rats received a single subcutaneous injection of homocysteine (0.6 micromol/g of weight body) or saline and were killed 1h later. Serum was collected and the brain was quickly removed and parietal cortex dissected. Results showed that acute homocysteine administration significantly decreased the activities of Na(+),K(+)-ATPase and butyrylcholinesterase on parietal cortex and serum, respectively. Furthermore, folic acid pretreatment totally prevented these inhibitory effects. We also evaluated the effect of acute homocysteine administration on some parameters of oxidative stress, namely thiobarbituric acid-reactive substances and total thiol content in parietal cortex of rats. No alteration of these parameters were observed in parietal cortex of homocysteinemic animals, indicating that these oxidative stress parameters were probably not responsible for the reduction of Na(+),K(+)-ATPase and butyrylcholinesterase activities. The presented results confirm previous findings that acute hyperhomocysteinemia produces an inhibition of Na(+),K(+)-ATPase and butyrylcholinesterase activities and that pretreatment with folic acid prevents such effects. Assuming that homocysteine might also reduce the activities of these enzymes in human beings, our results support a new potential therapeutic strategy based on folic acid supplementation to prevent the neurological damage found in hyperhomocysteinemia.

Animals↗
PubMedDate not supplied

Iron, but not folic acid, combined with effective antimalarial therapy promotes haematological recovery in African children after acute falciparum malaria.

Whether children with malarial anaemia should receive supplementation with iron or folic acid is uncertain. Therefore, the effects of supplementary treatment with iron or folic acid, given together with chloroquine or pyrimethamine-sulfadoxine (Fansidar), has been assessed in 600 Gambian children with uncomplicated falciparum malaria. After one month, haematological recovery was significantly better in the group treated with Fansidar than in the chloroquine-treated group (difference in mean haemoglobin level = 0.54 g/dL, P = 0.01). Children who received iron had a significantly better response than those given placebo (differences in mean haemoglobin level after one month and at dry season follow-up = 0.70 g/dL, P = 0.006, and 0.81 g/dL, P = 0.001, respectively). Iron supplementation was not associated with increased prevalence of malaria. Supplementation with folic acid did not improve the haematological response but, among children who received Fansidar, the treatment failure rate was significantly higher among those given folic acid than among those given placebo. Thus, supplementation with iron, but not folic acid, improves haematological recovery without increasing susceptibility to malaria.

Acute Disease↗
PubMed2003

The etiology of neural tube defects: the role of folic acid.

DISCUSSION: While the cause of neural tube defects in humans is considered to be multifactorial, it is apparent that folic acid can prevent 70% of open neural tube defects. Even in laboratory animals with known genetic defects, folic acid can prevent the genetic expression. CONCLUSION: While some of the metabolic pathways for folic acid are known, the true effects of folic acid on closure of the neural tube have yet to be discovered.

Female↗
PubMed2002

Prevalence of spina bifida and anencephaly during the transition to mandatory folic acid fortification in the United States.

BACKGROUND: In 1992, the United States Public Health Service recommended that all women of childbearing age consume 400 microg of folic acid daily. The Food and Drug Administration authorized the addition of synthetic folic acid to grain products in March 1996 with mandatory compliance by January 1998. The impact of these public health policies on the prevalence of neural tube defects needs to be evaluated. We sought to determine the prevalences of spina bifida and anencephaly during the transition to mandatory folic acid fortification. METHODS: Twenty-four population-based surveillance systems were used to identify 5,630 cases of spina bifida and anencephaly from 1995-99. Cases were divided into three temporal categories depending on whether neural tube development occurred before folic acid fortification (January 1995 to December 1996), during optional fortification (January 1997 to September 1998), or during mandatory fortification (October 1998 to December 1999). Prevalences for each defect were calculated for each time period. Data were also stratified by programs that did and did not ascertain prenatally diagnosed cases. RESULTS: The prevalence of spina bifida decreased 31% (prevalence ratio [PR] = 0.69, 95% confidence interval [CI] = 0.63-0.74) from the pre- to the mandatory fortification period and the prevalence of anencephaly decreased 16% (PR = 0.84, 95% CI = 0.75-0.95). Stratification by prenatal ascertainment did not alter results for spina bifida but did impact anencephaly trends. CONCLUSIONS: The decline in the prevalence of spina bifida was temporally associated with folic acid fortification of US grain supplies. The temporal association between fortification and the prevalence of anencephaly is unclear.

Anencephaly↗
PubMedDate not supplied

Folic acid knowledge and use among relatives in Irish families with neural tube defects: an intervention study.

BACKGROUND: Relatives in families where a child has a neural tube defect (NTD) may be at higher risk of having an affected child. Little is known of their level of knowledge and use of folic acid. AIM: To carry out an intervention study intended to increase knowledge and use of folic acid among relatives. METHODS: One hundred aunts and female first cousins (relatives of the proband) were interviewed by telephone before and after receiving an information pack. RESULTS: At baseline, although knowledge of the benefits of folic acid was high (73%), use of folic acid was low (8.8%). After the intervention, knowledge increased and use went up to 19% (p < 0.05). CONCLUSIONS: This study suggests that relatives in Irish NTD families have a high level of information about folic acid benefits. This awareness may not translate into action since the intervention produced only a modest increase in folic acid use overall. Future studies focussing on women who are planning a pregnancy may show larger benefits from intervention.

Adolescent↗
PubMed1981

Intestinal absorption of [3H]folic acid in the chronic alcoholic monkey.

The intestinal absorption of labeled folic acid ([3H]pteroylmonoglutamate) was determined from urinary and fecal recoveries of tritium in pairs of monkeys fed control liquid diets or diets containing 50% of energy as ethanol for a 24-mo period. Weight gain, fecal fat excretion, nitrogen balance, D-xylose absorption, serum folate levels, jejunal histology, and intestinal enzyme activities were similar in each group. Liver biopsies obtained after 12 and 24 mo of feeding demonstrated steatosis and megamitochondria in the ethanol-fed group, with decreased hepatic levels of folate at 24 mo. Intestinal malabsorption of labeled folic acid in the ethanol-fed monkeys was indicated by decreased urinary recovery of tritium but increased fecal recovery of tritium after intragastric administration of [3H]pteroylmonoglutamate. These studies suggest that folic acid malabsorption follows the chronic administration of ethanol together with a nutritious diet.

Alcoholism↗
PubMed1984

Electroencephalographic, behavioral, and histopathologic features of seizures induced by intra-amygdala application of folic acid in cats.

The effects of intracerebral injection of folic acid are still controversial. We studied the electroencephalographic, behavioral, and histopathologic consequences of the seizures induced by intra-amygdala administration of various doses of FA in freely moving cats. The severity of the seizures was dose-dependant. For doses of 25 and 50 nmol, single low-amplitude spikes appeared in the amygdala 15 to 20 min after injection and a typical amygdala symptomatology was observed. From doses of 100 nmol recurrent limbic seizures occurred 40 to 80 min after injection. Finally, from doses of 150 nmol secondarily generalized seizures were induced, which could be followed by death 4 to 6 h after injection. The severity of the cerebral lesions was related to both the dose and the paroxysmal manifestations. In cases with short survival time (6 h) and few seizures the pathology was restricted to a lymphocytic and glial reaction with some ischemic cells at the injected site. In cases with status epilepticus, edema and neuronal degeneration was observed in the hippocampus, amygdala, thalamic nuclei of the midline, entorhinal cortex, and cerebellum. No neuronal alteration at the injected site was observed. For longer survival times (8 days) edema was less severe, but hyperchromatic cells were still numerous. These results, compared with those of intra-amygdala administration of kainic acid, suggest that pathologic lesions induced in cats by folic acid more closely resemble those described in man after some status epilepticus.

Amygdala↗
PubMed1993

Recommendations on the use of folic acid supplementation to prevent the recurrence of neural tube defects. Clinical Teratology Committee, Canadian College of Medical Geneticists.

OBJECTIVE: To prevent the recurrence of neural tube defects (NTDs) in families at increased risk of having offspring with NTDs with the use of periconceptional folic acid supplementation. OPTIONS: Genetic counselling and prenatal diagnosis of NTDs. OUTCOMES: NTDs cause stillbirth, neonatal death and severe disabilities. The cost for medical care and rehabilitation in the first 10 years of life of a child with spina bifida cystica was estimated to be $42,507 in 1987. EVIDENCE: The authors reviewed the medical literature, communicated with investigators from key studies, reviewed policy recommendations from other organizations and drew on their own expertise. A recent multicentre randomized controlled trial showed that among women at high risk of having a child with an NTD those who received 4 mg/d of folic acid had 72% fewer cases of NTD-affected offspring than nonsupplemented women. Two previous intervention studies also demonstrated that folic acid supplementation was effective in reducing the rate of NTD recurrence. Several retrospective studies support this conclusion. VALUES: Recommendations are the consensus of the Clinical Teratology Committee of the Canadian College of Medical Geneticists (CCMG) and have been approved by the CCMG Board. The committee believes that primary prevention of NTDs is preferable to treatment or to prenatal detection and abortion. BENEFITS, HARMS AND COSTS: Folic acid supplementation should result in fewer NTDs among infants in Canada and ancillary savings in medical costs. The recommended dosage of folic acid is not known to be associated with adverse effects. Higher dosages of folic acid may make vitamin B12 deficiency difficult to diagnose and may alter seizure frequency in patients with epilepsy due to drug interactions with anticonvulsants. RECOMMENDATIONS: A minimum dosage of folic acid of 0.8 mg/d, not to exceed 5.0 mg/d, is recommended along with a well-balanced, nutritious diet for all women who are at increased risk of having offspring with NTDs and who are planning a pregnancy or may become pregnant. Supplementation should begin before conception and continue for at least 10 to 12 weeks of pregnancy. VALIDATION: These guidelines are similar to those of the Society of Obstetricians and Gynaecologists of Canada, the US Centers for Disease Control and Prevention and the Department of Health in Britain. SPONSORS: These guidelines were developed by the CCMG Clinical Teratology Committee and endorsed by the Board of the CCMG. No funding for the development of these guidelines was obtained from any other sources.

Female↗
PubMed2004

Atherosclerosis and folic acid supplementation trial in chronic renal failure: baseline results.

BACKGROUND: Atherosclerosis and Folic Acid Supplementation Trial (ASFAST) is a randomized placebo controlled trial assessing whether high-dose folic acid can reduce cardiovascular events and atherosclerosis progression in patients with chronic renal failure (CRF). Here we report the baseline results and compare indices of arterial structure (carotid intima-medial thickness (IMT)) and function (systemic arterial compliance (SAC)), pressure augmentation index (AI(x)) and pulse wave velocity (PWV a-f and PWV f-d)) to age- and sex-matched controls. METHODS: Three hundred and fifteen subjects with CRF (serum creatinine > or = 0.40 mmol/L) aged 24-79 years (mean +/- SD: 56.6 +/- 13.6 years) and 213 healthy controls (58.2 +/- 10.2 years) were studied. Fasting blood samples were assayed for lipids (both groups), total homocysteine (tHcy), red cell folate, cobalamin and fibrinogen (CRF group). Ultrasound B mode measurements were used to determine mean carotid IMT and applanation tonometry techniques to determine SAC, AI(x), PWV (a-f), PWV (f-d) and central pressures. RESULTS: Ninety-six per cent of the CRF group had at least one of: hypertension, hypercholesterolaemia, diabetes or smoking; 35% had established cardiovascular disease. The mean IMT was greater in CRF patients than in controls (0.86 +/- 0.19 vs 0.68 +/- 0.11 mm, P < 0.001). The SAC was significantly lower, and PWV (a-f) and AI(x) significantly higher. The tHcy was increased in 97% of the CRF group (27.3 +/- 2.9 micromol/L (normal < 13)). Total homocysteine did not correlate with IMT or any other measure of arterial function. However, those in the upper quantile of tHcy (> or =25 micromol/L) did have higher PWV (a-f) and lower SAC than those in the lower quantile. CONCLUSIONS: Compared to normals, patients with CRF exhibited a 10-15-year shift to the right in age-related increases in carotid IMT and PWV (a-f), and significantly increased central pressure augmentation. This 5-year study is examining the impact of high-dose folic acid therapy on cardiovascular end-points, IMT progression and arterial function in CRF.

Adult↗
PubMedDate not supplied

Folic acid and human malformations: a summary and evaluation.

A large body of evidence gathered over the past 30 or more years has led to the firmly established belief that deficiency of the vitamin folic acid is a cause of congenital malformations of neural tube closure. Beginning with studies showing folic acid levels of mothers of children with such defects to be low, this belief has been solidified by epidemiologic studies revealing that this consequence is prevented by maternal supplements of the vitamin from early pregnancy. The present article reviews this evidence for the purpose of examining the claims of the efficacy of folic acid in this respect. This seems to be an advantageous moment to do so, because no clear impact of folic acid supplementation and fortification on the prevalence of neural tube defects has as yet been documented; and furthermore a pause seems to have been reached in such studies. It is felt that a historical, i.e. a chronologic approach will best describe the findings, and therefore they will be considered as they unfolded.

Abnormalities, Drug-Induced↗
PubMed2003

Effects of maternal ethanol consumption during pregnancy or lactation on intestinal absorption of folic acid in suckling rats.

A fostering/crossfostering analysis of the effects of maternal ethanol exposure on jejunal and ileal folate absorption was performed. Male and female rats were randomized into two groups. In the first group, ethanol-treated rats received ad libitum 5, 10 and 15% ethanol in the drinking fluid during three successive weeks. A consumption of 20% was maintained in this group for 5 additional weeks. Ethanol-treated rats were mated. Group 2 served as the control. To study the effect of chronic alcoholism during lactation or gestation separately, at birth (2nd day postpartum) control newborns were cross-fostered to ethanol dams (EG), and the pups issued from the ethanol treated mothers were cross-fostered to control dams (CG). Thus, three experimental groups of pups were formed: (1) control pups receiving no treatment during gestation and lactation (CG); (2) pups exposed to ethanol only during gestation (GG); and (3) pups exposed to ethanol only during lactation (LG). At 21 days postpartum the jejunal and distal ileum folate absorption was determined in the offspring rats by a perfusion technique. Milk folic acid levels were determined by an immunoluminometric assay. The results showed an increase in jejunal folic acid absorption in offsprings exposed to ethanol only during the lactation period (LG). However, in pups exposed to ethanol only during the gestation period (GG), the jejunal folic acid absorption was significantly increased only at concentrations of 0.25, 0.5 and 2.5 microM. No free folic acid absorption occurred in the distal ileum of control pups (CG) at day 21 at all assayed concentrations but in offsprings exposed to ethanol only during the gestation or lactation periods absorption did take place. Pups exposed to ethanol during the gestation period (GG) showed decreased values in ileum folic acid absorption at the lowest assayed concentration (0.25 microM) compared to values obtained for pups exposed to ethanol only during lactation (LG). Milk folic acid levels were significantly decreased in the ethanol-fed dams on day 21 of lactation. These results indicate that exposure of rats to ethanol during the lactation period affects more severely postnatal development of intestinal functions than ethanol exposure only during gestation. In summary, both the exposure to ethanol itself and the decrease in folic acid intake caused alterations in the function of the intestinal mucosa in the offspring, which in turn altered absorption time and development. However, the present results do not explain how ethanol stimulated intestinal absorption of folic acid in pups exposed to ethanol during the gestation or lactation periods. Further studies are needed.

Administration, Oral↗
PubMed1989

Effects of intramuscular injections of folic acid during lactation on folates in serum and milk and performance of sows and piglets.

In order to determine the effect of folic acid on serum and milk folates in lactating sows as well as on serum folates and growth rate of the piglets, sows (n = 25) received either saline or 15 mg folic acid i.m. each week from d 2 after parturition to weaning, 26 d later. Blood samples were drawn from all sows at 110 d of gestation and every week during lactation. Milk samples were taken at d 7 and 21 of lactation. Piglets were weighed and blood samples were collected weekly during lactation. Serum folates of sows increased during lactation. The rate of increase was more pronounced (P less than .0002) after folic acid injections. Milk folates concentrations decreased (P less than .0007) from d 7 to 21 of lactation but were higher (P less than .0001) in treated sows (11.8 +/- .7 ng/ml) than in control sows (7.9 +/- .4 ng/ml). Serum folates of piglets in control litters increased from 55.0 +/- 2.2 ng/ml at 2 d of age to a peak value of 86.3 +/- 3.1 ng/ml 2 wk later, and then gradually decreased. In piglets from treated dams, the time response curve was similar to that of the controls, but values were about 15% higher (P less than .01). The growth rate of piglets until 8 wk of age was not changed (P greater than .47) by folic acid injection of sows. More studies are needed to evaluate the practical importance of changes in folates status in establishing the folic acid requirements of lactating sows.

Animals↗
PubMed2005

Folic Acid does not limit endothelial dysfunction induced by ischemia and reperfusion: a human study.

Nitric oxide synthase (NOS) uncoupling is a condition of increased production of superoxide anion associated with a decreased production of nitric oxide (NO) by this enzyme. Folic acid can prevent and/or reverse NOS uncoupling in the setting of diabetes, smoking, hypercholesterolemia, and nitrate tolerance. Whereas animal studies showed a protective effect of folic acid in ischemia and reperfusion (IR) injury, no study tested whether folic acid administration limits IR-induced endothelial dysfunction in humans. In a double-blind, parallel study, 20 healthy young male volunteers were randomized to receive folic acid, 10 mg/d for 7 days, or matching placebo. At the end of the treatment period, endothelium-dependent, flow-mediated dilation (FMD) of the radial artery was measured before and after IR injury (15 minutes of ischemia at the level of the brachial artery followed by 15 minutes of reperfusion). There was no difference at baseline between groups in any variable. In the placebo group, IR significantly blunted FMD (before IR, 6.7+/-1.0%; after IR, 1.5+/-1.3%, P<0.01). A similar effect was observed in the folic acid group (before IR, 6.3+/-1.1%; after IR, 2.1+/-1.0%, P=ns compared with placebo). As opposed to animal studies, high-dose folic acid does not protect the vascular endothelium from IR injury in humans.

Blood Flow Velocity↗
PubMed1991

Effects of a parenteral supplement of folic acid and its interaction with level of feed intake on hepatic tissues and growth performance of young dairy heifers.

Forty-seven dairy heifers of approximately 10 d of age were assigned to a factorial experiment in which a supplement of folic acid (0 or 40 mg) administered weekly by i.m. injection and level of feed intake were the two factors studied. The heifers were weaned after 5 wk of experimentation. Following weaning, and until the end of the experiment, 11 wk later, they had ad libitum access to grass hay and concentrates at two different levels, ad libitum or restricted, to allow a body weight gain of 700 g/d. A supplement of folic acid (P less than .05) and ad libitum access to feed (P less than .05) increased the mean concentration of serum folates. Blood hemoglobin and packed cell volume were not affected by the level of feed intake. However, they were both increased (P less than .05) by the supplement of folic acid. Average daily gain was analyzed over three different periods: 0 to 5 wk (before weaning), 5 to 10 wk, and 10 to 16 wk. Average daily gain was increased by the supplement of folic acid during the second period (P less than .05) and by ad libitum access to feed during the last two periods (P less than .05). Ad libitum access to feed increased (P less than .05) weight of the liver, decreased the (P less than .05) concentrations of RNA and DNA, and increased (P less than .05) the ratios of protein/DNA and RNA/DNA. The supplement of folic acid decreased (P less than .05) weight of the liver and increased the ratio RNA/DNA (P less than .05). These effects of supplement of folic acid on growth performance and on hematological cells may reflect a lack of folic acid during the weeks after weaning.

Animals↗
PubMed2004

The effect of folic acid and folinic acid supplements on purine metabolism in methotrexate-treated rheumatoid arthritis.

OBJECTIVE: To determine if folinic acid supplementation during methotrexate (MTX) therapy for rheumatoid arthritis (RA) reduces both urinary 5-aminoimidazole-4-carboxamide (AICA) and urinary adenosine excretion more than does folic acid supplementation. AICA and adenosine are markers for MTX interference with purine metabolism. METHODS: Forty patients with RA who received MTX for 6 weeks were randomized to receive either daily folic acid or folinic acid supplements during an additional week of MTX therapy. Colorimetric and radioimmunocompetition assays were used to measure 24-hour urinary AICA and adenosine excretion levels, respectively. RESULTS: At the end of 6 weeks, 24-hour urinary levels of AICA, but not adenosine, were elevated as compared with baseline levels (i.e., prior to MTX therapy). Folinic acid, but not folic acid, supplementation normalized urinary AICA levels during MTX therapy. Relatively high urinary levels of AICA were correlated with reduced disease activity. No similar correlations were seen with urinary adenosine levels. CONCLUSION: The blockade of purine nucleotide biosynthesis by MTX at the AICA ribonucleotide transformylase-catalyzed step may be related to the efficacy of MTX, and this blockade is effectively relieved by folinic acid, but not by folic acid, supplementation.

Adenosine↗