At current fortification levels, US adults who do not consume supplements or who consume an average of < or =400 microg folic acid/d from supplements are unlikely to exceed the UL in intake for folic acid.

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Background Red blood cell (RBC) folate concentrations are a potential biomarker of folate-sensitive neural tube defect (NTD) risk in the population. The purpose of this analysis was to describe women in the U.S. population with RBC folate concentrations below those associated with optimal NTD prevention. Methods We used data from the 2007 to 2012 National Health and Nutrition Examination Survey (NHANES) to assess the RBC folate status of U.S. women of childbearing age relative to risk categories for NTD risk based on RBC folate concentrations. We defined suboptimal RBC folate concentrations as those associated with a prevalence of _9 NTDs per 10,000 live births. Results Among nonpregnant women age 12 to 49 years, 22.8% (95% Confidence Interval: 21.1, 24.6) had suboptimal RBC folate concentrations. Women had greater odds of having a suboptimal RBC folate concentration if they did not use dietary supplements containing folic acid; had mandatorily fortified enriched cereal grain products as their only source of folic acid; were non-Hispanic black or Hispanic; or were current smokers. Conclusion Based on RBC folate concentrations, we would predict that the majority of U.S. women of reproductive age are not at increased risk for folate sensitive NTDs in the presence of mandatory folic acid fortification. Prevention policies and programs can be aimed at population subgroups identified as having higher predicted risk for folate-sensitive NTDs based on RBC folate concentrations.

Serum and red blood cell (RBC) total folate are indicators of folate status. No nationally representative population data exist for folate forms. We measured serum folate forms [5-methyltetrahydrofolate (5-methylTHF), unmetabolized folic acid (UMFA), non-methyl folate (sum of THF, 5-formylTHF, 5,10-methenylTHF), and MeFox (5-methylTHF oxidation product)] by HPLC-MS/MS and RBC total folate by microbiologic assay in US persons ≥1 year (n ~7500) participating in the National Health and Nutrition Examination Survey 2011–2. Data analysis for serum total folate was conducted including and excluding MeFox. Concentrations (geometric mean; detection rate) of 5-methylTHF (37.5 nmol/L; 100%), UMFA (1.21 nmol/L; 99.9%), MeFox (1.53 nmol/L; 98.8%), and THF (1.01 nmol/L; 85.2%) were mostly detectable. 5-FormylTHF (3.6%) and 5,10-methenylTHF (4.4%) were rarely detected. The biggest contributor to serum total folate was 5-methylTHF (86.7%); UMFA (4.0%), non-methyl folate (4.7%), and MeFox (4.5%) contributed smaller amounts. Age was positively related to MeFox but showed a U-shaped pattern for other folates. We generally noted sex and race-ethnic biomarker differences and weak (Spearman r <0.4) but significant (P <0.05) correlations with physiologic and lifestyle variables. Fasting, kidney function, smoking, and alcohol intake showed negative associations. BMI and body surface area showed positive associations with MeFox but negative associations with other folates. All biomarkers showed significantly higher concentrations with recent folic acid-containing dietary supplement use. These first-time population data for serum folate forms generally show similar associations with demographic, physiologic, and lifestyle variables as serum total folate. Patterns observed for MeFox may suggest altered folate metabolism dependent on biological characteristics.

Meta-analysis results (limited to the MA, the recommended population assessment method) indicated a consistent percentage difference in S/P and RBC folate concentrations across MTHFR C677T genotypes. Lower blood folate concentrations associated with this polymorphism could have implications for a population-level risk of neural tube defects.

Background Folate cutpoints for risk of deficiency vs. possible deficiency were originally derived differently (experimental vs. epidemiologic data) and their interpretation is different. Matching cutpoints derived from one assay with population-based data derived from another assay requires caution. Objective We assessed the extent of folate status misinterpretation using inappropriate cutpoints. Methods In the cross-sectional NHANES, serum and red blood cell (RBC) folate were first measured using a radioproteinbindingassay (RPBA, 1988–2006), then using a microbiologic assay (MBA, 2007–2010). We compared prevalence estimates for assay-matched (e.g., using RPBA cutpoint with RPBA data) and assay-mismatched (e.g., using MBA cutpoint with RPBA data) cutpoints for risk of deficiency based on megaloblastic anemia as a hematologic indicator in persons ≥4 y [e.g., <7 nmol/L serum folate, <305 nmol/L RBC folate, derived by MBA], possible deficiency based on rising homocysteine as a metabolic indicator in persons ≥4 y (e.g., <10 nmol/L serum folate, <340 nmol/L RBC folate, derived by RPBA), and insufficiency based on elevated risk of neural tube defects in women 12–49 y (e.g., <906 nmol/L RBC folate, derived by MBA). Results Pre-folic acid fortification (1988–1994), risk of deficiency for assay-matched vs. assay-mismatched cutpoints was 5.6% vs. 16% (serum folate) and 7.4% vs. 28% (RBC folate); it declined post-fortification (1999–2006) to <1% vs. <1% (serum folate) and <1% vs. 2.5% (RBC folate). Pre-fortification (1988–1994), risk of possible deficiency for assay-matched vs. assay-mismatched cutpoints was 35% vs. 56% (serum folate) and 37% vs. 84% (RBC folate); it declined post-fortification (1999–2006) to 1.9% vs. 7.0% (serum folate) and 4.8% vs. 53% (RBC folate). Post-fortification (2007–2010), risk of insufficiency was 23% (assay-matched) vs. 39% (assay-mismatched). Conclusions Applying assay-mismatched cutpoints leads to misinterpretation of folate status. This likely applies to clinical assays as no comparability data are available.

Despite using a broader definition of complementary foods, this analysis found a lower prevalence of early introduction in this nationally representative sample than previous studies that included only solids. However, many young children were still introduced to complementary foods earlier than recommended. Strategies to support caregivers to adhere to infant feeding guidelines may be needed.

Background: Total-body iron stores (TBI), which are calculated from serum ferritin and soluble transferrin receptor concentrations, can be used to assess the iron status of populations in the United States.Objective: This analysis, developed to support workshop discussions, describes the distribution of TBI and the prevalence of iron deficiency (ID) and ID anemia (IDA) among toddlers, nonpregnant females, and pregnant females. Design: We analyzed data from NHANES; toddlers aged 12-23 mo (NHANES 2003(NHANES -2010, nonpregnant females aged 15-49 y (NHANES 2007(NHANES -2010, and pregnant females aged 12-49 y (NHANES 1999(NHANES -2010. We used SAS survey procedures to plot distributions of TBI and produce prevalence estimates of ID and IDA for each target population. All analyses were weighted to account for the complex survey design.Results: According to these data, ID prevalences (6 SEs) were 15.1% 6 1.7%, 10.4% 6 0.5%, and 16.3% 6 1.3% in toddlers, nonpregnant females, and pregnant females, respectively. ID prevalence in pregnant females increased significantly with each trimester (5.3% 6 1.5%, 12.7% 6 2.3%, and 27.5% 6 3.5% in the first, second, and third trimesters, respectively). Racial disparities in the prevalence of ID among both nonpregnant and pregnant females exist, with Mexican American and non-Hispanic black females at greater risk of ID than non-Hispanic white females. IDA prevalence was 5.0% 6 0.4% and 2.6% 6 0.7% in nonpregnant and pregnant females, respectively. Conclusions: Available nationally representative data suggest that ID and IDA remain a concern in the United States. Estimates of ironreplete status cannot be made at this time in the absence of established cutoffs for iron repletion based on TBI. The study was registered at clinicaltrials.gov as NCT03274726.Am J Clin Nutr 2017;106 (Suppl):1640S-6S.