Folate Status Response to Controlled Folate Intake in Pregnant Women

Caudill, Marie A.; Cruz, Amelia C.; Gregory, Jesse F.; Hutson, Alan D.; Bailey, Lynn B.

doi:10.1093/jn/127.12.2363

Cited by 62 publications

(49 citation statements)

References 35 publications

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“…This higher demand may be explained by accelerated folate breakdown (Kownacki Brown et al 1993;McPartlin et al 1993). However, Caudill et al (1997) found no differences between pregnant and non-pregnant women with respect to increase in serum folate or erythrocyte folate concentrations or in urinary excretion of 5-methyltetrahydrofolate after supplementation with 450 and 850 g folate/d. Although the same research group suggested, from results of a controlled dietary trial, that pregnant women made more efficient use of 450 g folic acid than of 850 g folic acid, they found no significant difference in catabolism between pregnant and non-pregnant women .…”

Section: Host-related Factorsmentioning

confidence: 99%

Bioavailability and bioefficacy of folate and folic acid in man

et al. 2001

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Folic acid is important because supplementation around the time of conception has been proven to lower the risk of having offspring with a neural-tube defect. Furthermore, both dietary folate and folic acid decrease plasma total homocysteine concentrations. Elevated plasma homocysteine concentrations are considered to be an independent risk factor for cardiovascular disease. The aim of the present review is to give an overview of factors influencing bioavailability and bioefficacy (the proportion of ingested nutrient converted to its active form) of food folate and folic acid, and to discuss the functional bioefficacy of folate and folic acid in decreasing plasma homocysteine concentrations. We use the mnemonic SLAMENGHI to group factors influencing bioavailability and bioefficacy: Species of folate; Linkage at molecular level; Amount of folate and folic acid consumed; Matrix; Effect modifiers; Nutrient status; Genetic factors; Host-related factors; mathematical Interactions between the various factors. Bioefficacy of folate from some foods is <50 % that of folic acid. This factor is most probably explained by the matrix factors, encapsulation and binding. However, often such effects cannot be distinguished from factors such as species, chain length of folate in food, effect modifiers and the amount of folate consumed in a meal. Folic acid provided as a supplement is well absorbed. However, the homocysteine-lowering capacity of doses of folic acid >500 g is limited. It is unclear whether unmetabolised folic acid poses health risks. This factor is of importance, because food fortification is now implemented in many countries and folic acid supplements are freely available. In particular circumstances host-related factors, such as gastrointestinal illness and pH of the jejunum, can influence

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Section: Host-related Factorsmentioning

confidence: 99%

Bioavailability and bioefficacy of folate and folic acid in man

et al. 2001

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“…Serum folate may be better able to discriminate between different levels of folate intake. For instance, in a study using controlled daily intake of 450 μ g versus 850 μ g folic acid over 12 weeks, the 850 μ g group had higher serum folate concentrations but the same red cell folate levels as the 450 μ g group [ 86 ]. A meta-analysis of supplementation studies has shown a 2.13 nmol/L increase in serum folate concentration for every 0.1 mg/ day increase in folic acid intake in women 20 -25 [ 87 ].…”

Section: Response To Supplementation and Fortificationmentioning

confidence: 99%

Red cell or serum folate: what to do in clinical practice?

Farrell¹,

Kirsch

Herrmann

2013

Clinical Chemistry and Laboratory Medicine

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Folate deficiency has been linked to diverse clinical manifestations and despite the importance of accurate assessment of folate status, the best test for routine use is uncertain. Both serum and red cell folate assays are widely available in clinical laboratories; however, red cell folate is the more time-consuming and costly test. This review sought to evaluate whether the red cell assay demonstrated superior performance characteristics to justify these disadvantages. Red cell folate, but not serum folate, measurements demonstrated analytical variation due to sample pre-treatment parameters, oxygen saturation of haemoglobin and haematocrit. Neither marker was clearly superior in characterising deficiency but serum folate more frequently showed the higher correlation with homocysteine, a sensitive marker of deficiency. Similarly, both serum and red cell folate were shown to increase in response to folic acid supplementation. However, serum folate generally gave the greater response and was able to distinguish different supplementation doses. The C677T polymorphism of methylenetetrahydrofolate reductase alters the distribution of folate forms in red cells and may thereby cause further analytical variability in routine red cell folate assays. Overall, serum folate is cheaper and faster to perform than red cell folate, is influenced by fewer analytical variables and provides an assessment of folate status that may be superior to red cell folate.

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“…Most importantly, excessive folic acid is eliminated through the urine primarily in its metabolic forms, 20 especially 5-methyltetrahydrofolate, 75 and thus results in a waste of SAM and the methyl donors. Folic acid supplementation and fortification have been found to significantly increase the urinary excretion of 5-methyltetrahydrofolate.…”

Section: Folic Acidmentioning

confidence: 99%

“…Folic acid supplementation and fortification have been found to significantly increase the urinary excretion of 5-methyltetrahydrofolate. 75 Theoretically, excessive folic acid may worsen rather than alleviate methyl-group deficiency. In fact, studies have demonstrated that folic acid supplementation neither lowers SAH, nor increases SAM, nor alters SAM/SAH ratio.…”

Section: Folic Acidmentioning

confidence: 99%

Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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The metabolic syndrome, a major risk factor for type 2 diabetes and cardiovascular disease, is a cluster of metabolic abnormalities including obesity, insulin resistance, hypertension and dyslipidemia. Although systemic oxidative stress and aberrant methylation status are known to have important roles in the development of metabolic syndrome, how they occur remains unclear. The metabolism of methyl-consuming compounds generates reactive oxygen species and consumes labile methyl groups; therefore, a chronic increase in the levels of methyl-consuming compounds in the body can induce not only oxidative stress and subsequent tissue injury, but also methyl-group pool depletion and subsequent aberrant methylation status. In the past few decades, the intake amount of methyl-consuming compounds has substantially increased primarily due to pollution, food additives, niacin fortification and high meat consumption. Thus, increased methyl consumers might have a causal role in the development and prevalence of metabolic syndrome and its related diseases. Moreover, factors that decrease the elimination/ metabolism of methyl-consuming compounds and other xenobiotics (for example, sweat gland inactivity and decreased liver function) or increase the generation of endogenous methyl-consuming compounds (for example, mental stress-induced increase in catecholamine release) may accelerate the progression of metabolic syndrome. Based on current nutrition knowledge and the available evidence from epidemiological, ecological, clinical and laboratory studies on metabolic syndrome and its related diseases, this review outlines the relationship between methyl supply-consumption imbalance and metabolic syndrome, and proposes a novel mechanism for the pathogenesis and prevalence of metabolic syndrome and its related diseases.

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Folate Status Response to Controlled Folate Intake in Pregnant Women

Cited by 62 publications

References 35 publications

Bioavailability and bioefficacy of folate and folic acid in man

Bioavailability and bioefficacy of folate and folic acid in man

Red cell or serum folate: what to do in clinical practice?

Dietary methyl-consuming compounds and metabolic syndrome

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