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PubMed1983

Relationship between adaptation of the folic acid and the cAMP mediated cGMP response in Dictyostelium.

Chemotactic stimulation of post-vegetative Dictyostelium cells with folic acid or aggregative cells with cAMP results in a fast transient cGMP response which peaks at 10 s; basal levels are recovered in about 30-40 s. Stimulation with folic acid or cAMP rapidly desensitizes the cells for equal or lower concentrated stimuli. However, cells remain responsive for stimuli with higher concentration, which indicates that desensitization is caused by an adaptation process. Removal of the stimulus induces deadaptation, which for both cAMP and folic acid has first order kinetics with a half-life of 1.5 min. Cells were prepared which are simultaneously sensitive to folic acid and to cAMP. The cGMP responses to saturated folic acid and cAMP stimuli are not additive, which suggests that the transduction pathways of these signals meet each other at or before the guanylate cyclase. Cells which are adapted to folic acid are not adapted to cAMP and vice versa. This demonstrates that adaptation of Dictyostelium cells to chemotactic stimuli is localized at a step in the transduction chain before the transduced folic acid and cAMP signals combine in one pathway.

Acclimatization↗
PubMed1997

Folic acid and food fortification: implications for the primary care practitioner.

Folic acid will soon be added to cereal-grain products as a result of a new public health measure enacted by the Food and Drug Administration. This fortification program will target women of childbearing age with the goal of increasing folic acid intake, a B vitamin shown to reduce the incidence of neural tube defects. This measure may benefit the health of the general population, as recent research demonstrates that folic acid may be associated with the prevention of coronary artery disease and some cancers. This article will review the key concepts related to folic acid and provide an overview of the implications of the fortification program for the primary care practitioner. The clinician working with women and families must be prepared to provide individualized nutritional intervention to assist individuals to reach the goal of 400 mcg of folate per day.

Coronary Disease↗
PubMed2002

Folic acid supplementation use among women who contact a teratology information service.

OBJECTIVE: The purpose of this study was to determine the percentage of the women who call a teratology information service who take folic acid before conception. STUDY DESIGN: A pilot-tested questionnaire was used to survey women who called a teratology information service about their use of folic acid supplementation. Frequencies were generated by pregnancy status, age, race, and parity. RESULTS: Of the 693 pregnant callers, 42% of the women initiated folic acid use 6 weeks before pregnancy, 35% of the women initiated folic acid use during pregnancy. Thirty-seven percent of the total caller population reported taking folic acid. Forty-seven percent of pregnant white women versus 27% of pregnant black women reported preconceptional folic acid use (P =.005). Thirty-nine percent of pregnant women who were <30 years old reported preconceptional folic acid use versus 48% of women who were >30 years old (P =.018). CONCLUSION: Most pregnant women take folic acid; however, only a minority of them start before conception. The use of preconceptional folic acid, although higher than the national average of 30%, was still low. Many women start taking folic acid in their pregnancy after the neural tube is closed.

Black or African American↗
PubMed2006

The effect of folic acid supplementation in beta-thalassemia major: a randomized placebo-controlled clinical trial.

Folic acid is a coenzyme for many important biochemical reactions including synthesis of purines, pyrimidines, and nucleoproteins. The recommended daily allowance of folic acid is 65 - 200 microg/day for infants and children. The recommended dose for deficiency states is 1000 microg/day; the effects of excess amounts of folic acid are unknown. The role of folic acid in preventing progression of arteriosclerosis is rather a new issue. Thrombotic events related to slightly elevated levels of homocystein in adults may be decreased by daily consumption of 1 mg of folic acid together with 5 - 100 mg of pyridoxine.

Adolescent↗
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↗
PubMedDate not supplied

[Environment and genetics in the etiology of cleft lip and cleft palate with reference to the role of folic acid].

The combined birth prevalence of cleft palate [CP] and cleft lip with or without cleft palate [CL(P)] in Europe is approximately one in 700 with characteristic regional variations. Orofacial clefting (OC) is therefore now one of the most frequent congenital anomalies, with a higher birth prevalence that Down's Syndrome or Neural Tube defects, but still lower than cardiovascular malformation. Babies with OC require a multidisciplinary medical approach, surgery and rehabilitative treatments over time. This means an important effort in terms of social organization as well as economical costs for the health care system. In Italy, the health care costs for approximately 800 children born with orofacial clefting per year has been estimated at around 150 billion Lire (80 million Euros). The etiology of OC is complex and heterogeneous both for isolated and associated defects; causes linked to environment, genetics and gene-environment interaction are known, although there is still a lot to do, especially in clarifying the role of genetics in producing susceptibility to the environment. Four categories of genes for which there are results suggestive of a genetic susceptibility to OCs are: 1) genes expressed in a particular area of the embryo or in a particular period of the palatine arch development, such as the transforming growth factors alpha and beta (TGF alpha, TGF beta 2, TGF beta 3); 2) genes having biological activities linked to the OC's pathogenesis without direct involvement (e.g. the retinoic acid receptor (RARA), the methylenetetrahydrofolate reductase receptor (MTHFR) and the folic acid receptor (FOLR1); 3) genes or locus identified in experimental animals as the homeotic genes MSX-1 and MSX-2; 4) genes involved in the interaction with the xenobiotics metabolism as those in P-450 cytochrome system. Several environmental factors have been implicated in the OC etiology; among those, the folic acid supplementation during the periconceptional period that was found effective in the prevention of neural tube defects. In fact, folic acid deficiency may be responsible for different malformations through a common mechanism that interferes with the embryonic development, depending on the maternal or embryo genotype. Further investigation is required to study in depth how the genotype would modify the role of environmental factors like folic acid. Well-designed and conducted epidemiological studies seem to be able to give worthwhile information. Studies carried out in Europe on these issues are a few, particularly those on gene-environment interaction. Recent results obtained in molecular biology and the availability of wealth of data can allow to perform ad hoc investigations, being important not only for the basic research but also for their public health implications. For this objective a specific scientific network at the European level has been set by the European Science Foundation (ESF), whose first step will be to establish consistent case ascertainment and data collection across Europe and to develop standardized protocols and methods of analysis. It is hoped that in the longer term such multicentre collaborative research will enable combined analysis and lead to the identification of genetic susceptibility to certain environmental factors, including nutrition. Such studies would inform the current debate about the efficacy of folic acid and other nutritional factors in prevention of disease in the developing embryo. Subsequent public health measures targeted according to risk might reduce the prevalence of disorders such as orofacial clefting.

Adult↗
PubMed2006

Synthesis and preclinical evaluation of a folic acid derivative labeled with 18F for PET imaging of folate receptor-positive tumors.

UNLABELLED: Folic acid was linked regioselectively through its alpha- and gamma-carboxyl groups to 4-fluorobenzylamine (FBA), and the alpha- and gamma-FBA-folate regioisomers were evaluated for their ability to bind to folate receptor-positive cells. The 18F-labeled alpha/gamma-FBA-folate counterpart was examined for in vivo tumor targeting efficiency in nude mice bearing folate receptor-positive tumor cells. METHODS: 18F-alpha/gamma-FBA-folate was prepared in a 4-step reaction sequence starting from folic acid. The relative binding affinities of the alpha- and gamma-FBA-folates to the folate receptor with respect to parent folic acid were determined in cultured KB-31 cells (nasopharyngeal epidermal carcinoma cell line) overexpressing the folate receptor using 3H-folic acid. Tumor accumulation of the 18F-labeled alpha/gamma-FBA-folate and 18F-FDG was analyzed in vivo by high-resolution PET. Biodistribution and PET studies were performed under baseline and blockage conditions. RESULTS: The radiochemical yield of the coupling step ranged from 15% to 44%, and the maximum specific radioactivity was 24 GBq/micromol. The in vitro binding affinities of the alpha- and gamma-isomers and folic acid were 71, 62, and 41 nmol/L, respectively. PET revealed heterogeneous uptake of the radioligand, with the highest activity concentrations found in the tumor rim. In contrast, 18F-FDG uptake in a nude mouse bearing KB-31 folate receptor-positive tumors was negligible. Radioligand uptake in tumors at 125 min after injection amounted to 6.56% of the injected dose per gram of tissue (%ID/g) in control animals, whereas radioactivity accumulation in the tumors of folic acid-treated animals was significantly reduced by more than 80%-to 1.07 %ID/g (P = 0.001). CONCLUSION: This new 18F-labeled folic acid derivative is a promising tool for PET imaging of folate receptor-positive tumors.

Animals↗
PubMed2001

Motherisk alert: Folic acid fortification of flour--three years later.

Fortification of flour with folic acid aims to prevent neural tube defects. In Canada, flour fortification began in 1997. The objective of this study was to quantify the changes in women's erythrocyte folic acid levels. Comparing these levels among normocytic women revealed an almost twofold increase (from 517+/-215 nmol/L in 1995 to 901+/-318 nmol/L in 1998) (P<0.00001). While the mean value increased substantially, even now, women at the low range of measured values (367 nmol/L) confer a relative risk of 3.2 for neural tube defects. For these women, higher intake of nutritional folic acid and perinatal supplementation of folic acid tablets continue to be crucial.

Adolescent↗
PubMed2002

Folic acid supplementation and prevention of birth defects.

Based on animal studies, epidemiologic studies and intervention trials, maternal folic acid is known to be protective for neural tube defects (NTD), primarily spina bifida and anencephalus. To reduce the risk of NTD, the U.S. Food and Drug Administration mandated that all enriched cereal grain products be fortified with folic acid as of January 1998. Recent data demonstrate that this public health action is associated with increased folate blood levels among U.S. women of childbearing age and that the national rate of spina bifida has decreased by 20%. Rates of anencephaly appear not to have declined. Epidemiologic data on use of folate and folate antagonists have also implicated folic acid in prevention of other birth defects such as facial clefts and cardiac and limb defects. Dietary folic acid is likely to be inadequate for maximal protection against NTD. Because about half of pregnancies in the U.S. are unplanned, according to the March of Dimes, birth defect prevention includes a recommended daily dose of 400 micro g synthetic folic acid for women of childbearing age. Uniform compliance is estimated to decrease the incidence of NTD by up to 70%. This could reduce the overall incidence from 2 to 0.6 per 1000 pregnancies and prevent disease in approximately 2000 babies per year in the U.S. Four thousand micrograms of folic acid per day is recommended for women with previous pregnancies affected by NTD.

Female↗
PubMed1994

Folic acid and neural tube defects: the current evidence and implications for prevention.

The results of the MRC Vitamin Study have established the specific role of folic acid in the prevention of neural tube defects. Folic acid supplementation (4 mg/day) at the time of conception reduced the recurrence rate by about 70%. Evidence from observational studies and the Hungarian randomized trial (that used 0.4-0.8 mg/day supplemental folic acid) indicates that a similar level of prevention can be achieved among women who have not already had an affected pregnancy and that this may be achieved with a lower dose of folic acid. The medical implications of these results are important. (1) Women planning a pregnancy should take folic acid supplements. (2) Because a large proportion of pregnancies are unplanned and many of those that are planned will occur in women who will not have taken folic acid supplements, a complementary general public health strategy is needed, based on dietary advice and food fortification designed to achieve the benefit with adequate safety. (3) Any public health prevention strategy needs to be monitored for efficacy and possible harm. (4) Research is needed on the dose-response relationship between folic acid and neural tube defect prevention and the mechanism of action.

Dose-Response Relationship, Drug↗
PubMed2004

Supplementation with [6S]-5-methyltetrahydrofolate or folic acid equally reduces plasma total homocysteine concentrations in healthy women.

BACKGROUND: Increased plasma total homocysteine (tHcy) is a risk factor for vascular disease and adverse pregnancy outcomes. Health authorities recommend periconceptional supplementation with 400 micro g folic acid to prevent neural tube defects. Several countries have implemented food fortification with folic acid. However, excessive intake of folic acid could mask an undiagnosed vitamin B-12 deficiency. The biologically active [6S]-5-methyltetrahydrofolate ([6S]-5-MTHF) may be an alternative to folic acid because it is unlikely to mask vitamin B-12 deficiency symptoms. OBJECTIVE: We compared the tHcy-lowering potential of 2 dosages of [6S]-5-MTHF with that of 400 micro g folic acid during 24 wk of supplementation. DESIGN: In this double-blind, randomized, controlled intervention trial, 144 female participants were supplemented daily with 400 micro g folic acid, 416 micro g [6S]-5-MTHF, 208 micro g [6S]-5-MTHF, or placebo. Concentrations of tHcy and plasma folate were measured at baseline and at 4-wk intervals. RESULTS: After supplementation, there was a significant interaction between time and treatment with respect to changes in tHcy and plasma folate (both P < 0.001 by two-factor repeated-measures analysis of variance). The decrease in tHcy did not differ significantly between the 3 supplemented groups (P > 0.05; Tukey's post hoc test). The increase in plasma folate in the group receiving 208 micro g [6S]-5-MTHF was significantly lower than that in the groups receiving 400 micro g folic acid (P < 0.001) or 416 micro g [6S]-5-MTHF (P < 0.05). CONCLUSIONS: [6S]-5-MTHF was shown to be an adequate alternative to folic acid in reducing tHcy concentrations. Supplementation with 416 micro g [6S]-5-MTHF was no more effective than that with 208 micro g [6S]-5-MTHF.

Adult↗
PubMed1980

Folic acid deaminase activity during development in Dictyostelium discoideum.

Folic acid attracts vegetative amoebae of Dictyostelium discoideum. Secreted by bacteria, it may act as a food-seeking device. The inactivation of this attractant is catalyzed by a deaminase. As assay has been developed to measure the folic acid deaminase activity. In addition to cell-surface an intracellular deaminase, the amoebae of D. discoideum release the enzyme into the medium. The pH optimum of the extracellular enzyme was 6.0, and higher for the cell-associated deaminases. The extracellular enzyme was secreted maximally by vegetative amoebae, and its activity diminished during cell differentiation. The cell-surface bound enzyme was less active than the extracellular enzyme, and its activity decreased twofold during a 6-h starvation period. The enzyme activity of homogenates and 48,000 x g pellets diminished during this period 35 to 40%. The supernatant of a homogenate had a higher deaminase activity than the homogenate itself or its pellet; this suggests the presence of an inhibitor in the particulate fraction. The underlying mechanism for inactivation of folic acid has similar characteristics as that for inactivation of cyclic adenosine monophosphate.

Aminohydrolases↗
PubMed1993

[Folic acid supply in pregnancy--results of a prospective longitudinal study].

After discussing the problem of folic acid requirements and supply during pregnancy, the results of a longitudinal study on 162 pregnant women are presented. By measuring biochemical and morphological changes in two subgroups (non-substituted vs unspecifically substituted), the necessity of a substitution with folic acid is discussed, as there might be additional requirements for the pregnant and the foetal organism. Concentrations of folic acid in the maternal plasma and in the erythrocytes as well as the segmentation rate and hypersegmentation of the granulocytes show a clear decrease in pregnancy. At the same time there was a significant difference between the subjects substituted and not substituted; the foetus and newborn levels were much higher than their mothers' concentrations. Moreover, there was a correlation between red cells folic acid levels in the last trimester and duration and outcome of pregnancy. These results indicate a substitution with folic acid for certain populations in pregnancy, which are highlighted.

Adolescent↗
PubMed1976

[Folic acid determination in the serum and erythrocytes by means of a competitive binding method with 125 iodine labeling].

Folic acid concentration in serum and erythrocytes was measured by radio assay according to the principle of competitive binding to proteins with 125I as marker. The method yielded a linear regression with readily reproducible results. The mean value in controls was 7.05 -+/ 3.4 ng/ml in serum and 386.8 -+/ 215.1 ng/ml in erythrocytes. In chronic alcoholics the respective values were significantly lower: 4.79 -+/ 2.02 ng/ml for serum and 344.4 -+/ 198.9 ng/ml for erythrocytes. The clinical importance of folic acid estimations arises from the general frequency of folic aicd deficits. Latent folic acid deficiency is associated with lowered folic acid concentrations in serum and normal values in red cells. In manifest folic acid deficiency both concentrations are decreased.

Alcoholism↗
PubMed2001

[Netherlands Health Council report:'Risks associated with folic acid fortification': those who don't risk, don't win].

Because the advice to take folic acid supplements is insufficiently followed by women who wish to become pregnant, a committee of the Health Council of the Netherlands investigated the possible risks associated with increasing folic acid intake through fortification of food products. The committee concludes that the risk of inducing or exacerbating neurological abnormalities by increasing the intake of folic acid in people with a vitamin B12 deficiency cannot be excluded. Therefore the fortification of food products should, for the time being, be limited to those foods which are especially aimed at women who wish to become pregnant. It is unlikely, however, that such a restricted food fortification program will lead to a decrease in the incidence of neural tube defects. Like the use of folic acid supplements, the purchase of special food products presupposes that the individual woman will undertake a positive action. Moreover, most women do not want their shopping to reveal their wish to have a child, and the need to cook their own meals will meet practical difficulties. The hypothetical and avoidable side-effects of food fortification have to be balanced against the certain benefit of preventing neural tube defects in unplanned pregnancies and pregnancies in women unaware of the benefits of folic acid supplementation. A revision of the report is recommended.

Adult↗
PubMed2006

Cardiovascular morbidity and mortality in the Atherosclerosis and Folic Acid Supplementation Trial (ASFAST) in chronic renal failure: a multicenter, randomized, controlled trial.

OBJECTIVES: The Atherosclerosis and Folic Acid Supplementation Trial (ASFAST) aimed to establish whether high-dose folic acid would slow the progression of atherosclerosis and reduce cardiovascular events in patients with chronic renal failure (CRF). BACKGROUND: Hyperhomocysteinemia is a potential contributor to the high rates of cardiovascular morbidity and mortality in patients with CRF. METHODS: A total of 315 subjects with CRF, mean age 57 years (range 24 to 79 years) were randomized to 15 mg folic acid daily or placebo and followed for a median of 3.6 years. The primary intima-media thickness (IMT) and clinical end points were: rate of progression of mean maximum carotid IMT and a composite of myocardial infarction (MI), stroke, and cardiovascular death. Secondary end points included all cardiovascular events and change in pulse wave velocity, systemic arterial compliance and augmentation index. Data were analyzed by intention-to-treat. RESULTS: Plasma total homocysteine was reduced by 19% in the folic acid group. There was no significant difference between the treatment groups in rate of change of IMT or any measure of artery function. Seventy-seven events occurred in the folic acid group (14.9 per 100 patient-years) as compared with 86 in the placebo group (16.3 per 100 patient-years). The rates of the primary and secondary clinical end points at five years were not significantly different after adjustment for baseline differences between the groups (adjusted hazard ratio for MI, stroke, and cardiovascular death: 0.98 [95% confidence interval: 0.66 to 1.47]; p = 0.94; for all cardiovascular events: 0.95 [95% confidence interval: 0.69 to 1.30]; p = 0.75). CONCLUSIONS: High-dose folic acid does not slow atheroma progression or improve cardiovascular morbidity or mortality in patients with CRF.

Adult↗
PubMed2006

Folic acid supplementation delays atherosclerotic lesion development in apoE-deficient mice.

Folic acid is a vitamin that when used as a dietary supplementation can improve endothelial function. To assess the effect of folic acid on the development of atherosclerosis, male apolipoprotein E-deficient mice fed a standard chow diet received either water (control group) or an aqueous solution of folic acid that provided a dose of 75 microg/kg/day, for ten weeks. At the time of sacrifice, blood was drawn and the heart removed. The study measured plasma homocysteine, lipids, lipoproteins, low-density lipoprotein (LDL) oxidation, isoprostane, paraoxonase, and apolipoproteins, and aortic atherosclerotic areas. In folic acid-treated animals, total cholesterol, mainly carried in very low-density and low-density lipoproteins, increased significantly, and homocysteine, HDL cholesterol, paraoxonase, and triglyceride levels did not change significantly. Plasma isoprostane and apolipoprotein (apo) B levels decreased. The resistance of LDL to oxidization and plasma apoA-I and apoA-IV levels increased with a concomitant decrease in the area of atherosclerotic lesions. The administration of folic acid decreased atherosclerotic lesions independently of plasma homocysteine and cholesterol levels, but was associated with plasma levels of apolipoproteins A-I, A-IV and B, and decreased oxidative stress.

Animals↗
PubMed1998

Preventing neural tube defects: the importance of periconceptional folic acid supplements.

OBJECTIVE: To inform the obstetrician-gynecologist of recent scientific evidence regarding the use of supplemental folic acid for prevention of neural tube defects (NTDs). DATA SOURCES: We selected English language articles via MEDLINE published from January 1990 through February 1997, using the search terms "folic acid" and "neural tube defect." Additional sources were identified through cross-referencing and through searching selected journals published from March through October 1997. METHODS OF STUDY SELECTION: Articles were selected on the basis of their relevance to the relationship between folate intake and NTD incidence, mechanisms of folate responsive NTD formation, and folate provision strategy. We referenced 55 papers in total. TABULATION, INTEGRATION, AND RESULTS: The majority of evidence demonstrates a decreased incidence of NTDs with increased folic acid consumption. The most convincing trials were performed in Europe among women who were planning pregnancy by using multivitamin or folic acid supplements. Some studies suggest that the protective effect of folate is explained, in many cases, not through correction of dietary deficiencies, but through correction of metabolic defects. Other evidence implies that it reduces NTDs by causing abortion of affected conceptuses. Supplemental folic acid tablets are the most proven means of improving an individual's folate status, but ensuring compliance with a strategy using vitamin tablets is problematic. CONCLUSION: Women of reproductive age should be advised to take multivitamin supplements containing 0.4 mg folic acid daily. Women with previously affected offspring who intend to become pregnant should take daily supplementation containing 4 mg of folic acid in the periconceptional period to reduce the risk of recurrence.

Female↗