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In vivo methylation capacity is not impaired in healthy men during short-term dietary folate and methyl group restriction.

Ten healthy adult men were fed a diet low in folate and exogenous methyl groups to study the effects on in vivo methylation capability. The men were housed in a metabolic unit for the entire 108 d of the study. After a 9-d baseline period (Period 1), the men were fed a soy-product-amino acid defined diet for 45 d, which provided 25 micrograms/d of folate for 30 d (Period 2) and, with a folate supplement, 99 micrograms/d for 15 d (Period 3). During Period 2 and Period 3, the low methionine and choline diet was supplemented with methionine for half the subjects to vary the dietary methyl group intake. The periods were then repeated over the next 54 d (Periods 4-6), with a crossover of methionine intakes in Period 5 and Period 6. A 1-g oral dose of nicotinamide was given at the end of each period and methylated urine metabolites determined. Other measures related to in vivo methylation capability included urine creatinine, and plasma and urine carnitine. Even with moderate folate depletion, none of these measures was decreased by low methionine and choline intakes. Plasma methionine concentrations were unchanged throughout. Limiting exogenous methyl group intake by restricting dietary methionine and choline did not impair in vivo methylation capabilities for the variables tested, even at low folate intake.

Administration, Oral↗

[Deficiency of folates in pregnancy: effect of supplementary folic acid].

Higher folate needs are present during pregnancy, which may lead to tissular deficiency in the mother and to depleted newborn folate reserves. The aim of this work was to assess the prevalence of folate deficiency and to establish the rates of serum and red cell folate in two groups of mothers and newborn infants, one receiving only iron and the other iron and folate during pregnancy. The rates of serum and red cell folate found at the end of pregnancy were significantly higher in the group which received folate; however, the percentage of cases with tissular folate deficiency was low in both groups, with no significant difference (3.8% and 1.3%, respectively). These findings, along with the lack of effect of supplemental folate on erythropoiesis, pose some questions on the usefulness of supplemental folate during pregnancy in our country.

Adult↗

Drugs and folate metabolism.

Folates are a group of compounds which are required in the diet and are important in DNA, amino acids and possibly also amine metabolism. The biologically active folates are in the tetrahydro form. Tetrahydrofolates are produced from unreduced dietary folates by the enzyme dihydrofolate reductase. A number of drugs such as aminopterin, methotrexate (amethopterin), pyrimethamine, trimethoprim and triamterene act as folate antagonists and produce folate deficiency by inhibiting this enzyme. With other drugs which produce low serum and tissue concentrations of folate such as anticonvulsants, antituberculosis drugs, alcohol and oral contraceptives, the mechanism of this effect is uncertain. Possible mechanism include reduced absorption, prevention of release of folate from tissue stores, altered plasma protein binding, or increased folate metabolism in the liver. Treatment with folic acid antagonists such as methotrexate readily causes megaloblastic anaemia; this can be prevented by therapy with folinic acid (5-formyltetrahydrofolate). The role of other drugs in producing megaloblastic anaemia is less certain, e.g. it occurs in less than 0.75% of patients receiving anticonvulsants. The possible neurological and psychiatric effects of folate deficiency are also uncertain. However, in patients with folate deficiency who have neuropsychiatric symptoms, neuropathy or myelopathy, and normal vitamin B12 levels, it may be of value to try therapy with folic or folinic acid.

Amines↗

[Advances in the study of the etiologic relationship between reduced folate carrier gene (RFC1) and neural tube and craniofacial defects].

Neural tube and craniofacial defects are common birth defects which are ascribed to the combination of genetic and environmental factors. The population epidemiological studies suggested that periconceptional use of multivitamins containing folic acid can reduce a woman's risk of having a child with neural tube and craniofacial defects. It's a major environmental factor that periconceptional women with deficiency of folic acid may increase their risk for delivering babies with neural tube and craniofacial defects, but the mechanism by which folic acid facilitates this risk reduction is unknown. This paper reviews folate transport carrier, Reduced Folate Carrier (RFC)'s characteristics in biological chemistry, physiological function, the folate transport mechanism, structure, function, regulation and expression of reduced folate carrier gene (RFC1), and the relationship between RFC1 with plasm or erythrocyte folate level and neural tube defects, et al. It is suggested a etiologic hypothesis in investigation of candidate gene encoding specific folate-related pathways of neural tube and craniofacial defects.

Carrier Proteins↗

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↗

Folate deficiency is associated with nutritional anaemia in Lebanese women of childbearing age.

OBJECTIVE: The objective of this study was to identify the determinants of anaemia in Lebanese women of childbearing age attending health centres in Lebanon. DESIGN: Cross-sectional study carried out between May and December 2003. Anthropometric measurements as well as sociodemographic, health and dietary intake data were collected using a questionnaire. Haemoglobin (Hb), plasma ferritin, plasma folate and vitamin B12 were assessed using standard laboratory methods. SETTING: Governmental health centres in Lebanon. SUBJECTS: Four hundred and seventy non-pregnant Lebanese women aged 15-45 years. RESULTS: Anaemia (Hb <12 g dl(-1)) and iron deficiency (ferritin <15 microg l(-1)) were prevalent in 16.0 and 27.2% of the study sample, respectively. Of the total sample, 7.7% had iron-deficiency anaemia. The percentage of women with either Hb or ferritin deficiency or both was 35.6%. Plasma folate and vitamin B12 deficiency was reported in 25.1 and 39.4%, respectively, and 12.6% of the women had both folate and vitamin B12 deficiencies. Of the anaemic group, 48.0% of the women had iron deficiency. The intake of iron was lower in iron-deficient than in non-deficient women and a positive relationship was shown between folate intake and its corresponding serum levels. Regression analysis showed that ferritin, plasma folate and family history of anaemia were significant determinants of the anaemia in the sample of women. CONCLUSIONS: Anaemia not related to iron deficiency was partly explained by plasma folate deficiency. Measures to control folate and iron deficiency should be considered.

Adolescent↗