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PubMed1992

Concentrations of the water-soluble vitamins thiamin, ascorbic acid, and folic acid in serum and cerebrospinal fluid of healthy individuals.

Thiamin, thiamin monophosphate, ascorbic acid, and folic acid were determined in serum and cerebrospinal fluid (CSF) in 31 outpatients who underwent a myelography because of back-pain. All subjects were otherwise healthy. The CSF concentration (mean +/- SD) was 8.6 +/- 3.9 nmol thiamin/L, 16.9 +/- 8.3 nmol thiamin monophosphate/L, 133 +/- 58.8 mumol ascorbic acid/L, and 44.9 +/- 13.2 nmol folic acid/L. The CSF-serum ratio was 2.1 +/- 0.8 for thiamin, 8.3 +/- 4.3 for thiamin monophosphate, 3.0 +/- 1.4 for ascorbic acid, and 3.3 +/- 0.8 for folic acid; the amount in CSF was significantly higher than in serum for each compound. These results support the existence of a saturated transport mechanism of water-soluble vitamins from serum into CSF for thiamin monophosphate, ascorbic acid, and folic acid. However, low CSF concentrations are correlated with low serum concentrations for the three vitamins. High serum concentrations should therefore be advocated to ensure high CSF concentrations.

Adult↗
PubMed1987

Intestinal absorption, liver uptake, and excretion of 3H-folic acid in folic acid-deficient, alcohol-consuming nonhuman primates.

Nonhuman primates fed folic acid-deficient diets +/- 30% kcal ethanol were used to determine alcohol effects on megaloblastic anemia development and folate bioavailability. Lower hemoglobin (Hb) and red blood cell (RBC) counts and higher mean corpuscular volume (MCV) occurred after 13 wk in alcohol-fed monkeys, later in controls. Plasma, RBC, and liver folate declined and urinary formiminoglutamic acid (FIGLU) was elevated in both groups with FIGLU increasing more among alcohol-fed monkeys at 38 wk. After 40 wk, the bioavailability of oral 3H-folic acid was investigated and showed increased fecal and reduced urinary tritium excretion in alcohol-fed monkeys compared with controls while plasma uptake and liver and whole body tritium retention were similar in both groups. These observations demonstrate that chronic alcohol consumption impairs folate coenzymes, accelerates appearance of hematologic indices of megaloblastic anemia, and causes possible malabsorption of enterohepatically circulated folates in folate deficiency even when other essential nutrients are provided.

Alcohol Drinking↗
PubMed1981

Intrastriatal folic acid mimics the distant but not local brain damaging properties of kainic acid.

Folic acid (pteroyl-L-glutamine acid, PGA), when injected into the rat striatum, has the kainic acid (KA) property of inducing sustained seizures and a disseminated pattern of distant brain damage, but lacks the KA property of destroying neurons locally at the injection site. This suggests the interesting possibility that one component of KA neurotoxicity (seizure-related distant damage) may involve interaction with a folate system. Folates are promising tools for exploring the neurotoxic properties of KA and, more importantly, for studying mechanisms of epilepsy and epileptic brain damage.

Animals↗
PubMed1981

Effect of a folate-binding protein on the plasma transport and tissue distribution of folic acid.

Folic acid (3H-pteroylglutamic acid or 75Se-selenofolate) administered free or bound to folate-binding protein (FABP) was rapidly cleared from the plasma but the plasma survival when bound to FABP was longer than unbound during the initial 5 min. 75Se-folate bound to FABP is more rapidly taken up by the liver than when administered as free 75-Se-folate. 125I-labeled FABP was rapidly cleared from the plasma (90% in 5 min). The rapid uptake of FABP, a sialoglycoprotein, was inhibited by the preadministration of desialyzed fetuin. Following the hepatic uptake of 75Se-folate/FABP, only free 75Se-folate was found in the bile. The total biliary secretion of 75Se-folate over 240 min was 63% when administered bound to FABP and 33% when administered as free 75Se-folate. The liver retained 33.5% of the 125I activity 5 min following the administration of 125I-FABP, while only 4.46% of the 125I activity was secreted into the bile over 180 min. This data suggests that FABP may play an important role in the enterohepatic circulation of folates by directing nonmethylated folates to the liver.

Animals↗
PubMed1999

[Should folic acid be given to women treated with valproic acid and/or carbamazepine? Folic acid and pregnancy in epilepsy].

Fetal exposure to valproic acid or carbamazepine increases the risk of neural tube defect (NTD). The risk of a mother having a baby with spina bifida has been estimated at 1-2 p. 100, close to the rate of risk of recurrent cases. No study has evaluated the effect of folic acid in neonates of women treated with valproic acid or carbamazepine although the protective effect against NTD has been proven in other populations. Periconceptional folic acid supplementation, 0.4 to 1 mg/day, for at least one month prior to conception and until the date of the second missed menstrual period or later decreases the incidence of a first occurrence of neural tube defect. Periconceptional folic acid supplementation, 4 mg/day, decreases the recurrence of NTD in women who had previously had a child with NTD. It seems pertinent to recommend periconceptional folic acid supplementation in women treated with carbamazepine or valporic acid. There are very few data in women on which to base a decision to advise taking 4 mg/day (as used in recurrence prevention) or low doses of 0.4 mg/day (used in primary prevention).

Anticonvulsants↗
PubMed1984

The effect of p-aminobenzoic acid and folic acid on the development of infective larvae of Brugia malayi in Aedes aegypti.

Adult Aedes aegypti mosquitoes, infected with the subperiodic Brugia malayi, were found to enhance the development of the filarial parasites to the infective stage when they were exposed to a cotton pad soaked in 10% sucrose solution containing p-aminobenzoic acid (PABA) in 0.001, 0.005, 0.01, 0.05 and 0.1% concentrations. Similarly, larval development increased when the mosquitoes were fed with folic acid at 0.001, 0.01 and 0.1% concentrations. This stimulation was more when PABA or folic acid was given prior to the infected blood meal through the developmental period of the larvae. The data thus suggest that PABA and folic acid are nutrients for the development of B. malayi-microfilariae to the infective stage in A. aegypti.

4-Aminobenzoic Acid↗
PubMed1989

The diets of pregnant and post-pregnant women in different social groups in London and Edinburgh: calcium, iron, retinol, ascorbic acid and folic acid.

Dietary records were obtained twice in pregnancy and once post-partum, from 265 women in all social classes in London and Edinburgh. Some Edinburgh women, and lactating women, showed the higher levels of calcium intake. For iron, retinol, ascorbic acid and folic acid, there was a consistent and significant regional and social class gradient in intakes. This favoured English women in 'non-manual' social groups, leaving the Scottish 'manual' class, after pregnancy, with the lowest intakes. Mean intakes of Ca and Fe were consistently below the current UK recommended daily amount (RDA). Intakes of retinol were all above it, and ascorbic acid intakes ranged above and below the RDA.

Ascorbic Acid↗
PubMed1978

5-Methyltetrahydrofolic acid, 5-formyltetrahydrofolic acid (folinic acid), and folic acid requirements of normal and Rous sarcoma virus-infected chicken fibroblasts.

Normal and Rous sarcoma virus-infected chicken fibroblasts proliferate maximally in a culture medium containing a physiological (10 ng/ml) concentration of 5-methyltetrahydrofolic acid or folinic acid (5-formyltetrahydrofolic acid), while their maximal proliferation requires a hyperphysiological (1000 ng/ml) concentration of folic acid. The normal and Rous-infected fibroblasts do not differ in their requirements for 5-methyltetrahydrofolate, folinic acid, or folic acid.

Animals↗
PubMed1998

Effects of folic acid and combinations of folic acid and vitamin B-12 on plasma homocysteine concentrations in healthy, young women.

BACKGROUND: Elevated plasma homocysteine concentrations are considered to be a risk factor for vascular disease and fetal malformations such as neural tube defects. Recent studies have shown that plasma homocysteine can be lowered by folic acid in amounts corresponding to 1-2 times the recommended dietary allowance. Preliminary evidence indicates that vitamin B-12 may be beneficial when included in supplements or in a food-fortification regimen together with folic acid. OBJECTIVE: We aimed to compare the homocysteine-lowering potential of a folic acid supplement with that of 2 supplements containing different doses of vitamin B-12 in addition to folic acid. DESIGN: Female volunteers of childbearing age (n = 150) received a placebo for 4 wk followed by a 4-wk treatment with either 400 microg folic acid, 400 microg folic acid + 6 microg vitamin B-12, or 400 microg folic acid + 400 microg vitamin B-12. RESULTS: Significant reductions (P < 0.001) in plasma homocysteine were observed in all groups receiving vitamin treatment. The effect observed with the combination of folic acid + 400 microg vitamin B-12 (total homocysteine, -18%) was significantly larger than that with a supplement containing folic acid alone (total homocysteine, -11%) (P < 0.05). Folic acid in combination with a low vitamin B-12 dose (6 microg) affected homocysteine as well (-15%). CONCLUSIONS: These results suggest that the addition of vitamin B-12 to folic acid supplements or enriched foods maximizes the reduction of homocysteine and may thus increase the benefits of the proposed measures in the prevention of vascular disease and neural tube defects.

Adult↗
PubMed2001

Estimates of the effects of folic-acid fortification and folic-acid bioavailability for women.

OBJECTIVE: With the recent implementation of the folic-acid-fortification program, our objective was to estimate its benefits in adult women and account for the higher bioavailability of synthetic folic acid in fortification programs and supplements. METHODS: The study used a cross-sectional design. Dietary assessment data were collected with a quantitative food-frequency questionnaire, the Nutrition DISCovery program. Fortification was simulated with the use of fortification standards (140 microg/100 g of flour) and new bioavailability standards for synthetic folic acid. Data were collected from 289 women 18 to 89 y old. Subjects were recruited from participants in two health-screening events in autumn of 1997. Chi-square tests were used to estimate the differences between categoric variables, and F tests were used in analysis of variance for continuous outcome measures. Results were considered significant at P < 0.05. RESULTS: Estimated mean dietary intake of folate increased considerably with simulation of fortification (320 to 608 microg of dietary folate equivalents). Women in the lower quartiles for age (18 to 39 and 40 to 46 y) consumed more servings from the bread group than women did in the upper quartile (55 to 89 y). Thus, the improvement in folate intake with fortification was significantly greater for the younger than for the older women (P < 0.05). Despite the limitations of estimating folate intakes, these data suggest that most women met the new estimated average requirement. However, 61% of women of childbearing age had intakes of synthetic folic acid below the recommended level of 400 microg/d, and only those using supplements containing folic acid met the guideline. CONCLUSIONS: Based on this sample of well-educated, adult women, the current level of folic-acid fortification should improve the intakes of a large proportion of women, especially when accompanied by supplements containing folic acid. These improvements in folate intake might not be seen in groups with limited resources, however. Further, under existing standards and practices, many women will not meet current recommendations for prevention of neural-tube defects.

Adolescent↗
PubMed1961

The plasma clearance of injected doses of folic acid as an index of folic acid deficiency.

The folic acid clearance test of Chanarin (1958) has been studied in normal white subjects, patients with megaloblastic anaemia, healthy Bantu males, Bantu females, hospital patients without anaemia, and in patients with scurvy. The test clearly distinguishes patients with megaloblastic anaemia, where clearance from the plasma of injected folic acid is abnormally rapid, from normal subjects. The rate of clearance of folic acid is abnormally rapid both in vitamin B(12) and in folic acid deficiency. Rapid clearance of injected folic acid in patients with primary B(12) deficiency may be the result of a conditioned deficiency of folic acid. The test is sufficiently sensitive to detect body deficiency of folic acid before the development of anaemia. In patients with scurvy, folic acid is cleared from the plasma abnormally rapidly. It is suggested that this may be the result of an associated dietary deficiency of folic acid.

Anemia↗
PubMed2001

Rapid communication: L-folinic acid versus folic acid for the treatment of hyperhomocysteinemia in hemodialysis patients.

BACKGROUND: The hyperhomocysteinemia found in most hemodialysis patients is refractory to combined oral B-vitamin supplementation featuring supraphysiological doses of folic acid (FA). We evaluated whether a high-dose L-folinic acid-based regimen provided improved total homocysteine (tHcy)-lowering efficacy in chronic hemodialysis patients, as suggested by a recent uncontrolled report. METHODS: We block-randomized 48 chronic, stable hemodialysis patients based on their screening predialysis tHcy levels, sex, and dialysis center into two groups of 24 subjects treated for 12 weeks with oral FA at 15 mg/day or an equimolar amount (20 mg/day) of oral L-folinic acid (FNA) [L-5-formyltetrahydrofolate]. All 48 subjects also received 50 mg/day of oral vitamin B6 and 1.0 mg/day of oral vitamin B12. RESULTS: The mean percentage (%) reductions (with 95% CIs) in predialysis tHcy were not significantly different [FNA = 22.1% (11.8 to 31.4%), FA = 20.7% (11.7 to 30.5%), P = 0.950 by paired t test]. Final on-treatment values (mean with 95% CI) were as follows: FNA, 15.9 micromol/L (14.0 to 18.0); FA, 16.9 micromol/L (14.8 to 18.8). Moreover, in those subjects with baseline tHcy levels >/=14 micromol/L, neither treatment resulted in "normalization" of tHcy levels (that is, final on-treatment values <12 micromol/L) among a significantly different or clinically meaningful number of patients [FNA = 2 out of 22 (9.1%); FA = 2 out of 24 (8.3%); Fisher's exact test of between groups difference, P = 1.000]. CONCLUSIONS: Relative to high-dose FA, high-dose oral L-folinic acid-based supplementation does not afford improved tHcy-lowering efficacy in hemodialysis patients. The preponderance of hemodialysis patients (that is,> 90%) exhibits mild hyperhomocysteinemia refractory to treatment with either regimen.

Aged↗
PubMed1991

The 1989 Borden Award Lecture. Some effects of dietary components (amino acids, carbohydrate, folic acid) on brain serotonin synthesis, mood, and behavior.

This review covers three areas in which dietary components may influence brain serotonin synthesis, mood, and behavior. In the first, tryptophan-deficient amino acid mixtures have been used to lower brain tryptophan and serotonin in normal human subjects for experimental purposes. Results suggest that low serotonin can cause lowered mood and increased aggression, but that it is probably not involved in any simple way in carbohydrate craving. Low serotonin levels can block the analgesic effect of morphine in humans. The second area concerns deficiencies of folic acid, which can cause low brain serotonin and lowered mood. Folate supplements may be useful in some depressed patients. The third area concerns the effect of carbohydrate meals. Although it is well established that carbohydrate meals raise brain tryptophan and serotonin in the rat, and that protein meals lower them, any effects of carbohydrate or protein meals on human brain serotonin are likely to be negligible under most circumstances. Carbohydrate meals can have definite effects on mood and behavior in humans, and there are a variety of mechanisms, other than alterations in brain serotonin, that might mediate these effects.

Affect↗
PubMed1984

Substantia nigra cell death from kainic acid or folic acid injections into the pontine tegmentum.

Injections of kainic acid into the rostral pontine tegmentum in rats caused not only local lesions but destruction of GABAergic and dopaminergic cells in the substantia nigra (SN), as indicated histologically and by measurements of tyrosine hydroxylase (TH) and glutamate decarboxylase (GAD). Injections of folic acid caused the nigral damage without local lesions. Pretreatment with scopolamine prevented the losses in GAD without affecting those in TH. The destruction of nigral cells is attributed to pathological stimulation of afferent pathways to the SN, some of which are cholinergic, and it is possible that a similar mechanism may be involved in some forms of Parkinsonism.

Afferent Pathways↗