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PubMed2006

Maternal folic acid supplementation to dams on marginal protein level alters brain fatty acid levels of their adult offspring.

Studies on fetal programming of adult diseases have highlighted the importance of maternal nutrition during pregnancy. Folic acid and long-chain essential polyunsaturated fatty acids (LC-PUFAs) have independent effects on fetal growth. However, folic acid effects may also involve alteration of LC-PUFA metabolism. Because marginal deficiency of LC-PUFAs during critical periods of brain growth and development is associated with risks for adult diseases, it is highly relevant to investigate how maternal supplementation of such nutrients can alter brain fatty acid levels. We examined the impact of folic acid supplementation, conventionally used in maternal intervention, on brain essential fatty acid levels and plasma corticosterone concentrations in adult offspring at 11 months of age. Pregnant female rats from 4 groups (6 in each) were fed with casein diets either with 18 g protein/100 g diet (control diet) or treatment diets that were marginal in protein (MP), such as 12 g protein/100 g diet supplemented with 8 mg folic acid (FAS/MP), 12 g protein/100 g diet without folic acid (FAD/MP), or 12 g protein/100 g diet (MP) with 2 mg folic acid. Pups were weaned to a standard laboratory diet with 18 g protein/100 g diet. All male adult offspring in the FAS/MP group showed lower docosahexaenoic acid (P<.05) as compared with control adult offspring (6.04+/-2.28 vs 10.33+/-0.86 g/100 g fatty acids) and higher n-6/n-3 ratio (P<.05). Docosahexaenoic acid levels in FAS/MP adult offspring were also lower (P<.05) when compared with the MP group. Plasma corticosterone concentrations were higher (P<.05) in male adult offspring from the FAS/MP group compared with control as well as the MP adult offspring. Results suggest that maternal folic acid supplementation at MP intake decreased brain docosahexaenoic acid levels probably involving corticosterone increase.

Animals↗
PubMed2006

Folic acid awareness and supplementation among Texas women of childbearing age.

OBJECTIVE: Neural tube defects (NTDs) affect about seven of every 10,000 deliveries in Texas. To reduce the risk for NTDs, women are encouraged to supplement with 400 mcg folic acid daily during their reproductive years. This study examines folic acid awareness, knowledge, and supplementation practices among women of childbearing age (WCBA), including residents of Texas-Mexico border as well as women of Hispanic origin/ethnicity, populations that have NTD rates up to three times higher than the national average. METHODS: We conducted a statewide multistage sample telephone survey among Texas women of childbearing age in 2001. In total 1,196 women age 18 to 44 were interviewed. RESULTS: About 78% of WCBA knew about folic acid, 28% knew that folic acid prevents birth defects, and 25% knew to take folic acid before pregnancy. The prevalence of daily folic acid supplementation among all women of childbearing age was 33%. Education was the strongest predictor of folic acid awareness followed by race/ethnicity and age. Significant predictors of daily folic acid supplementation were education and ethnicity. CONCLUSIONS: Our findings suggest the need for more emphases on strategies to improve the level of folic acid supplementation among low educated women, and race ethnic minority populations.

Adolescent↗
PubMedDate not supplied

College women's awareness and consumption of folic acid for the prevention of neural tube defects.

PURPOSE: Awareness and consumption of folic acid in the context of neural tube defect prevention among college women were assessed. METHODS: Subjects documented folic acid awareness and multivitamin consumption. Beliefs about folic acid before and after an educational intervention were characterized using the Health Belief Model (HBM) and the Fetal Health Locus of Control Scale (FHLCS). RESULTS: Awareness of folic acid was not associated with multivitamin consumption. Belief variables were not associated with awareness or consumption of folic acid. CONCLUSION: This study does not support educational interventions based on the HBM or FHLCS to increase multivitamin consumption among college women.

Adolescent↗
PubMed2004

[Blood concentration of homocysteine, vitamin B (12), and folic acid in patients with exudative age related macular degeneration].

PURPOSE: Recent studies have shown a relationship between elevated levels of Hcy and vascular disease including cerebrovascular accidents and myocardial infarctions. Elevated Hcy plasma is considered as an independent risk factor for atherosclerosis and trombosis. MATERIAL AND METHODS: This study included 30 patients with diagnosed exudative form of AMD. We evaluated plasma homocysteine levels, by high performance liquid chromatography and red blood cell folic acid, plasma folic acid and plasma vitamin B12 concentration by radioassay method. RESULTS: The plasma concentration of Hcy in AMD patients had significantly increased when compared with control group. We found not significant decrease of the plasma vitamin B12, red blood cell folic acid and plasma folic acid concentration in AMD group, when compared with the control group.

Aged↗
PubMed1998

Drug and environmental factors associated with adverse pregnancy outcomes. Part III: Folic acid: pharmacology, therapeutic recommendations, and economics.

OBJECTIVE: To review folic acid's mechanism of action, adverse effects, therapeutic recommendations, compliance, and cost. DATA SOURCES: A MEDLINE search was conducted through December 1997. Additional sources were obtained from Current Contents and citations from the references obtained. Search terms included folate, folic acid, neural tube defect, homocysteine, and methylenetetrahydrofolate reductase. STUDY SELECTION: Animal and human studies examining the effects of folate were reviewed. DATA EXTRACTION: Data collected included mechanism of action, safety issues, dosing recommendations, compliance with recommendations, and economics. DATA SYNTHESIS: Folic acid decreases neural tube defect risk through an effect on methionine-homocysteine metabolism. In addition, increased folate intake may reduce cardiovascular morbidity and mortality. Since toxicity is minimal, everyone can potentially benefit from increased folate consumption. To help achieve this, the Food and Drug Administration has mandated that cereal grain be fortified with 140 micrograms of folic acid per 100 g of grain, which will add approximately 0.1 mg of folate to the average diet. Studies recommend supplementing with 0.2 mg to promote optimal homocysteine concentrations and for preventing neural tube defects. CONCLUSIONS: Despite fortification, most women will still receive less folate than the 0.4 mg/d recommended by the Public Health Service. All population groups would benefit from increased folate intake. Current studies indicate 200 micrograms/d may be the minimum effective amount of fortification needed for normalizing homocysteine concentrations and preventing a significant number of neural tube defects; thus, a higher level of food fortification may be warranted.

Environmental Exposure↗
PubMed2005

Degradation kinetics of folic acid in cowpea (Vigna catjang L.) during cooking.

Kinetics of folic acid degradation in cowpea (Vigna catjang L.) as well as in pure folic acid solutions at initial concentrations present in cowpea over a temperature range of 50-120 degrees C (isothermal conditions) followed first order reaction kinetics, where the rate constant increased with an increase in temperature. The temperature dependence of degradation was adequately modeled by Arrhenius equation. The degradation was also evaluated in normal open pan cooking, pressure-cooking and a newly developed and patented fuel-efficient Eco Cooker (non-isothermal heating process). A mathematical model was developed using the isothermal kinetic parameters obtained to predict the losses of folic acid from the time-temperature data of the non-isothermal heat processing method. The results obtained indicate the folic acid degradation is of a similar order of magnitude in all the methods of cooking.

Cooking↗
PubMed2000

Trans-stimulation effects of folic acid derivatives on methotrexate transport by rat renal organic anion transporter, OAT-K1.

We examined the pharmacological role of the renal organic anion transporter OAT-K1, which localizes predominantly in the brush-border membranes of proximal straight tubules, in the urinary excretion of methotrexate and the possibility of its contribution to "folinic acid rescue." With Madin-Darby canine kidney (MDCK) cells stably transfected with OAT-K1 cDNA, OAT-K1-mediated methotrexate accumulation was inhibited in the presence of various folic acid derivatives. These derivatives included aminopterin, 5-methyltetrahydrofolic acid, unlabeled methotrexate, folinic acid (citrovorum factor, leucovorin), and folic acid with apparent inhibition constant values of 0.5, 1.2, 1.8, 8.2, and 14.1 microM, respectively. In contrast, 10 microM taurocholic acid and sulfobromophthalein did not inhibit OAT-K1-mediated methotrexate accumulation. In addition, methotrexate efflux was stimulated in the presence of inwardly directed gradients of aminopterin, 5-methyltetrahydrofolic acid, unlabeled methotrexate, folinic acid, and folic acid, but not of uric acid, taurocholic acid, and glutathione, indicating that OAT-K1-mediated methotrexate efflux is stimulated by a folic acid derivatives exchange. In conclusion, OAT-K1 was suggested to enhance the apical efflux of highly accumulated methotrexate in tubular epithelial cells and contribute at least in part to folinic acid rescue by exchanging intracellular methotrexate for extracellular folinic acid.

Aminopterin↗
PubMed2006

The impact of folate status and folic acid supplementation on the micronucleus frequency in human erythrocytes.

Folic acid has a well-documented stabilising effect on chromosomes. A correlation between folate status and chromosome stability in humans has been reported in studies that were restricted to certain subpopulations, e.g., folate-deficient persons. The goal of the present investigation was to clarify if there also is a correlation between folate status and chromosome stability among individuals without any folate deficiency. The method used here is the recently developed flow cytometry-based micronucleus assay in human transferrin-positive reticulocytes (MN-Trf-Ret). In a blood sample, separation of the very young reticulocytes from the mature erythrocytes makes this micronucleus assay possible. This investigation comprises three studies (cross-sectional, giving baseline data), two of which are connected to an intervention study. In the three cross-sectional studies (total number of subjects, 99) the frequency of MN-Trf-Ret (fMN-Trf-Ret) was measured and compared with the serum folate status. In two of the studies also serum homocysteine and Vitamin B12 were measured and compared with the baseline fMN-Trf-Ret. Combining the results from the three cross-sectional studies, a negative correlation between folate status and fMN-Trf-Ret was obtained (p<0.05). The goal of the intervention studies was to clarify if different nutritional supplementations had any effect on the fMN-Trf-Ret and the cell proliferation (percentage polychromatic erythrocytes, PCE). Each of the two studies involved two groups, one placebo and one supplemented group. In one of the studies the supplementation was folic acid, 1000 microg/day during 1 week (n=30, both sexes); in the other intervention study, folic acid (800 microg/day), B12 (20 microg/day) and B6 (4 mg/day) were taken during 1 week (n=29, both sexes). No significant difference in %PCE or fMN-Trf-Ret between the two groups was found in either of the two intervention studies.

Adult↗
PubMed1998

No change in impaired endothelial function after long-term folic acid therapy of hyperhomocysteinaemia in haemodialysis patients.

BACKGROUND: Hyperhomocysteinaemia is frequent in chronic haemodialysis patients. Because of its potential role in athero- and thrombogenesis, the effects of long-term homocysteine-lowering treatment on endothelial function are of interest. METHODS: We conducted a randomized, controlled trial in 35 haemodialysis patients. In phase 1, patients were treated with 5 mg folic acid or 5 mg folic acid and 4 g betaine per day for 12 weeks, and in phase 2 with 1 or 5 mg folic acid daily for 40 weeks. In phase 3, all patients received 15 mg folic acid daily for four weeks. Endothelial function was assessed before and after 52 weeks of treatment by determination of flow-mediated vasodilatation of the brachial artery, and by measuring plasma levels of endothelium-derived proteins. RESULTS: Non-fasting predialysis plasma total homocysteine was markedly elevated at baseline (46.9 +/- 6.3 mumol/l) and decreased rapidly after initiation of therapy. Significant differences in plasma homocysteine between the groups were found neither during phase 1 nor phase 2. Plasma total homocysteine had normalized in only two out of 30 patients at the end of phase 2. Increasing the daily folic acid dose to 15 mg did not further reduce plasma total homocysteine. Endothelial function parameters did not improve. CONCLUSIONS: We concluded that betaine is not effective in conjunction with folic acid in the treatment of hyperhomocysteinaemia in haemodialysis patients. Normalization of plasma total homocysteine is seldom achieved with 1, 5 or 15 mg folic acid daily, which may explain why long-term homocysteine-lowering treatment with 1 or 5 mg folic acid does not ameliorate endothelial function.

Adult↗
PubMed2004

[Relationship of plasma homocysteine and folic acid levels and 5,10-methylenetetrahydrofolate reductase gene mutation with venous thromboembolism].

OBJECTIVE: To investigate the association between concentrations of plasma homocysteine and folic acid, 5,10-methylenetetrahydrofolate reductase (MTHFR) C667T mutation and venous thromboembolism (VTE) and to analyze the effect of MTHFR C667T mutation on concentrations of plasma homocysteine and folic acid. METHODS: In 58 patients with VTE and 58 sex and age matched controls, epidemiological risk factors were surveyed. The concentration of plasma homocysteine was measured by high performance liquid chromatography, and the concentration of plasma folic acid was measured by radioimmunoassay. MTHFR C667T genotype was measured by PCR-RFLP. RESULTS: The concentrations of plasma homocysteine and folic acid showed significant difference between the case group and the control group (OR = 1.5, 95% CI: 1.216 - 2.213 and OR = 0.396, 95% CI: 0.149 - 0.709, respectively). There was no significant difference in the frequency of mutant alleles in site 667 of MTHFR gene between the cases and the controls (P > 0.05). The concentration of plasma folic acid was associated with the concentration of plasma homocysteine (multiple correlation coefficient = -2.061, P < 0.05). The MTHFR C667T polymorphism was associated with the concentration of plasma folic acid but not with the concentration of plasma homocysteine in both the case group and the control group. The multiple correlation coefficient between the MTHFR C667T polymorphism and the concentration of plasma folic acid is 0.5856 (P < 0.01). CONCLUSIONS: The results of our study demonstrate that hyperhomocysteinemia and folic acid deficiency are independent risk factors for VTE. Folic acid deficiency is a cause of hyperhomocystinemia while the MTHFR C667T mutation is one of the possible genetic factors causing folic acid deficiency in this Chinese population.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗
PubMed2000

Erythropoietin, folic acid deficiency and hyperhomocysteinemia: is there a possible relationship in chronically hemodialyzed patients?

AIMS: To examine the possible relationships between recombinant human erythropoietin (rhEPO) therapy, serum folic acid and homocysteine levels in a cohort of stable, chronically hemodialyzed patients. MATERIAL AND METHODS: The study was cross-sectional in its first phase and consisted of 3 groups of subjects (group 1:6 healthy controls; group 2:7 dialyzed patients not receiving rhEPO; group 3: 14 patients on rhEPO therapy). Hematological and biochemical parameters were taken after an overnight fast in all subjects. The second phase of the study was prospective, and included 8 dialyzed patients, and investigated the effects of a 6-month period of folic acid supplementation (10 mg, 3 times a week) on the same parameters examined in the first phase of the study. RESULTS: In the first part of the study hemoglobin levels were near-normal, or normal, in all patients. No differences in hemoglobin or hematocrit values were observed in the 3 groups. 80% of all hemodialyzed patients had low serum folic acid levels, irrespective of whether they were receiving rhEPO. Serum erythropoietin level was elevated in group 3 (23.3+/-10.4 mIU/ml). In group 2, serum erythropoietin level was not different from that of the healthy controls (13.5+/-11.2 vs. 8.0+/-5.4 mIU/ml, p = n.s.). Total serum homocysteine levels were elevated in all dialyzed patients (group 2: 24.7+/-9.2 micromol/l; group 3: 31.6+/-14.4 micromol/l), with a significant difference seen when comparing controls and those dialyzed patients on rhEPO therapy (8.7+/-2.2 vs. 31.6+/-14.4 micromol/l; p<0.05). Significant correlations (ANOVA) were observed between serum erythropoietin and folic acid levels (r = -0.382; p = 0.049), and between folic acid and homocysteine levels (r = -0.560; p = 0.002). In the second part of the study folic acid supplementation led to a highly significant reduction in homocysteine levels (20.9+/-4.9 vs. 11.9+/-2.5 micromol/l; p<0.0005). Two of 3 patients receiving rhEPO therapy, had rhEPO discontinued after commencing folic acid, as hemoglobin levels remained adequate, even without rhEPO. CONCLUSIONS: In hemodialyzed patients, the presence of a near-normal hemoglobin level, irrespective of rhEPO therapy, implies efficient erythropoiesis. Without adequate folic acid reserves, folic acid deficiency may develop in these patients and this will aggravate already high homocysteine levels. Therefore, folic acid supplementation is warranted in hemodialyzed patients, especially in those patients with hemoglobin levels approaching normal. This treatment is safe and effective in reducing homocysteine levels, especially when given in high doses for prolonged periods of time.

Analysis of Variance↗
PubMed2004

Efficacy of folic acid when added to statin therapy in patients with hypercholesterolemia following acute myocardial infarction: a randomised pilot trial.

BACKGROUND: Folic acid is assumed to have favourable effects on vascular endothelium, directly as well as indirectly through its effect on homocysteine metabolism. However, the clinical value of folic acid in secondary prevention after acute myocardial infarction (MI) has never been tested. Thus, a randomised, open-label, multicentre trial was performed in order to study the effect of folic acid 5 mg o.d. when added to statin therapy on the incidence of recurrent major clinical events up to 1 year post-MI. METHODS: A total of 283 patients with a total cholesterol >6.5 mmol/l (251 mg/dl) (mean 7.3 mmol/l) were included. All patients received 40 fluvastatin. In 140 of the 283 patients, folic acid (5 mg o.d.) was instituted at discharge, and the remaining 143 patients served as controls. Other secondary prevention measures for both groups were advocated. The primary endpoint was a composite consisting of all vascular events, including death, recurrent MI, strokes, and unplanned invasive coronary interventions. RESULTS: At baseline, the two groups were well-matched for all clinical and demographic parameters. After 1 year of treatment, no difference was noticed in the primary endpoint between the two groups. These endpoints occurred in 43 patients (31%) in the folic acid group, as opposed to 45 patients (31%) in the control group. All separate cardiovascular events were also equally distributed between both groups. Total cholesterol levels decreased to a similar extent in the two groups (to 5.5 and 5.7 mmol/l, in folic acid and control groups, respectively). CONCLUSIONS: In this medium-size pilot study, folic acid did not demonstrate any beneficial additive effects on cardiovascular mortality or morbidity in post-MI patients with hypercholesterolemia who were treated with statin therapy. Larger trials, possibly targeting at selected populations, must be awaited before definitive conclusions regarding the potentially favourable effects of folic acid supplementation in secondary prevention can be drawn.

Anticholesteremic Agents↗
PubMed2001

Effect of folic acid supplements on homocysteine concentration in plasma of gestating sows.

An experiment comprising 19 German Landrace sows was established to evaluate the effect of folic acid supplements (10 mg/kg concentrate) on homocysteine and folic acid concentration in plasma and serum, respectively, of highly pregnant sows as compared to an unsupplemented control (basal diet contained 0.62 mg folic acid/kg concentrate). Blood samples were taken between day 75 and 110 of gestation for homocysteine analysis and on day 100 of gestation for folic acid determination. Due to the folic acid supplements serum folic acid concentration increased significantly (104 nmol/l in controls and 140 nmol/l in supplemented sows). In contrast, homocysteine concentration in the plasma was not significantly influenced by folic acid supplements (16.6 mumol/l in controls and 15.2 mumol/l in supplemented sows). Further investigations seem to be necessary to clarify the physiology of homocysteine metabolism in swine.

Animals↗
PubMed2006

Trends in folic Acid awareness and behavior in the United States: the Gallup Organization for the March of Dimes Foundation surveys, 1995-2005.

OBJECTIVE: To summarize changes in folic acid awareness, knowledge, and behavior among women of childbearing age in the United States since the U.S. Public Health Service (USPHS) 1992 folic acid recommendation and later fortification. METHODS: Random-digit dialed telephone surveys were conducted of approximately 2000 women (per survey year) aged 18-45 years from 1995-2005 in the United States. RESULTS: The percentage of women reporting having heard or read about folic acid steadily increased from 52% in 1995 to 84% in 2005. Of all women surveyed in 2005, 19% knew folic acid prevented birth defects, an increase from 4% in 1995. The proportion of women who reported learning about folic acid from health care providers increased from 13% in 1995 to 26% in 2005. The proportion of all women who reported taking a vitamin supplement containing folic acid increased slightly from 28% in 1995 to 33% in 2005. Among women who were not pregnant at the time of the survey in 2005, 31% reported taking a vitamin containing folic acid daily compared with 25% in 1995. CONCLUSIONS: The percentage of women taking folic acid daily has increased modestly since 1995. Despite this increase, the data show that the majority of women of childbearing age still do not take a vitamin containing folic acid daily. Health care providers and maternal child health professionals must continue to promote preconceptional health among all women of childbearing age, and encourage them to take a vitamin containing folic acid daily.

Adolescent↗
PubMed1999

The 'Folic Acid Campaign': has the message got through? A questionnaire study.

There is now clear evidence that folic acid reduces the risk of neural tube defects. In February 1996 the Health Education Authority launched a publicity campaign to inform women of the benefits of periconceptual folic acid. We have surveyed 1000 women to assess the compliance of pregnant women with the Department of Health's recommendations about taking folic acid. Of the women, 761 (76%) said they knew about the benefits of folic acid but only 433 (43%) of them took it before pregnancy. Of the 567 women who did not take folic acid before conception, 227 had not planned their pregnancy and 239 did not know about the benefits. Of the 644 women who planned their pregnancy and knew about the benefits of folic acid before conception 211 still did not take folic acid pre-pregnancy. These findings have important implications for public policy and health professionals if the incidence of neural tube defect is to be reduced further.

Journal Article↗
PubMedDate not supplied

Application of the social ecological model in folic acid public health initiatives.

All women of childbearing age who are capable of becoming pregnant should consume 0.4 mg/400 microg of folic acid daily. Folic acid decreases the incidence of neural tube defects in newborns. Despite continued public health initiatives, many women still do not consume the recommended daily requirement. This article analyzes the use of the social ecological model in folic acid public health initiatives and emphasizes assessing the outcomes of such initiatives.

Adolescent↗
PubMed1997

Loss of folic acid exporter function with markedly augmented folate accumulation in lipophilic antifolate-resistant mammalian cells.

We previously described a 1,000-fold pyrimethamine-resistant Chinese hamster ovary cell line (PyrR100) which retains parental dihydrofolate reductase activity and methotrexate (MTX) sensitivity. This study characterizes the basis for the 14-fold decrease in folic acid and leucovorin concentrations required for clonogenic growth of PyrR100 cells relative to parental AA8 cells. Under conditions in which folic acid reduction was blocked by trimetrexate, PyrR100 cells displayed relative to parental AA8 cells a: 1) 17- and 5-fold increase in the net transport of folic acid and MTX, respectively; 2) 23- and 5-fold decrease in the efflux rate constant for folic acid and MTX, respectively; and 3) 2-fold increase in folic acid influx with no significant change in MTX influx. The markedly increased net folic acid transport in PyrR100 cells could not be explained by cellular folic acid binding, mitochondrial sequestration, polyglutamylation, nor by a decreased membrane potential. The effect of energy deprivation on folic acid and MTX transport in both cell lines was quite different. Glucose and pyruvate deprivation nearly abolished the increase in net folic acid transport in PyrR100 cells. In contrast, energy deprivation increased net MTX transport in AA8 cells, whereas no change was seen with PyrR100 cells. Furthermore, while folic acid influx in PyrR100 and AA8 cells was markedly reduced with energy deprivation, MTX influx was not affected. Provision of glucose and pyruvate to energy-deprived cells resulted in a rapid onset of MTX efflux from parental AA8 cells but not from PyrR100 cells. Taken together these results indicate that the markedly enhanced net transport of folic acid and MTX in PyrR100 cells is largely due to the complete loss of exit pump activity. Furthermore, the energy source that sustains the augmented levels of folic acid appears linked to the influx process and is distinct from the energy source that sustains MTX gradients under these conditions. We conclude that the loss of folic acid efflux is an efficient means of augmenting cellular uptake of folate cofactors and subsequent survival on picomolar folate concentrations. This constitutes the first demonstration of the loss of folic acid exporter activity in mammalian cells as a response to lipophilic antifolate selective pressure.

Animals↗