Long-term effect of low-dose folic acid intake: potential effect of mandatory fortification on the prevention of neural tube defects.

BACKGROUND: Understanding the full effect of chronic low-dose folic acid is important in interpreting the effect of the mandatory folic acid fortification program in North America. OBJECTIVE: We aimed to describe the rate of attainment and steady state (plateau) of red blood cell (RBC) folate in response to long-term intake of 140 µg (designed to mimic fortification) and 400 µg (recommended dose for the primary prevention of neural tube defects) folic acid/d in reproductive-aged women living in a country with minimal fortification. DESIGN: On the basis of pharmacokinetics principles, it was recently proposed that a steady state should be reached after 40 wk. Thus, 144 women aged 18-40 y were randomly assigned to receive a daily folic acid supplement of 140 (n = 49) or 400 (n = 48) µg or placebo (n = 47) for 40 wk. RBC folate was measured at baseline and at 6, 12, 29, and 40 wk. RESULTS: After 40 wk, RBC folate did not reach a plateau in either treatment group. Kinetic modeling of the data indicated that RBC folate would approximately double from 779 to 1356 nmol/L in response to 140 µg folic acid/d with only ≈50% of model-estimated steady state conditions achieved at 40 wk. An average RBC folate concentration of 1068 nmol/L after 12 wk of supplementation with 400 µg folic acid/d was readily achieved at 36 wk after continuous intake of 140 µg/d. CONCLUSION: Our model shows the considerable length of time required to attain the full effect of low-dose folic acid, which suggests that 140 µg folic acid/d could be as effective as 400 µg folic acid/d taken during the periconceptional period if given sufficient time. This trial is registered at www.anzctr.org.au as ACTRN12609000215224.

Folate status of reproductive age women and neural tube defect risk: the effect of long-term folic acid supplementation at doses of 140 µg and 400 µg per day.

Primary prevention of most folate-responsive neural tube defects (NTDs) may not require 400 µg folic acid/day but may be achieved by attaining a high maternal folate status. Using RBC folate ≥906 nmol/L as a marker for NTD risk reduction, the study aimed to determine the change in blood folate concentrations in reproductive age women in response to long-term folic acid supplementation at 400 µg/day and 140 µg/day (dose designed to mimic the average daily folic acid intake received from New Zealand's proposed mandatory bread fortification program). Participants were randomly assigned to a daily folic acid supplement of 140 µg (n = 49), 400 µg (n = 48) or placebo (n = 47) for 40 weeks. RBC folate concentrations were measured at baseline, and after 6, 12, 29 and 40 weeks. At 40 weeks, the overall prevalence of having a RBC folate <906 nmol/L decreased to 18% and 35% in the 400 µg and 140 µg groups, respectively, while remaining relatively unchanged at 58% in the placebo group. After 40 weeks, there was no evidence of a difference in RBC folate between the two treatment groups (P = 0.340), nor was there evidence of a difference in the odds of a RBC folate <906 nmol/L (P = 0.078). In conclusion, the average daily intake of folic acid received from the proposed fortification program would increase RBC folate concentrations in reproductive age women to levels associated with a low risk of NTDs.

Glycemic index and endurance performance.

The aim of this review is to provide an up-to-date summary of the evidence surrounding glycemic index (GI) and endurance performance. Athletes are commonly instructed to consume low-GI (LGI) carbohydrate (CHO) before exercise, but this recommendation appears to be based on the results of only a few studies, whereas others have found that the GI of CHO ingested before exercise has no impact on performance. Only 1 study was designed to directly investigate the impact of the GI of CHO ingested during exercise on endurance performance. Although the results indicate that GI is not as important as consuming CHO itself, more research in this area is clearly needed. Initial research investigating the impact of GI on postexercise recovery indicated consuming high-GI (HGI) CHO increased muscle glycogen resynthesis. However, recent studies indicate an interaction between LGI CHO and fat oxidation, which may play a role in enhancing performance in subsequent exercise. Despite the fact that the relationship between GI and sporting performance has been a topic of research for more than 15 yr, there is no consensus on whether consuming CHO of differing GI improves endurance performance. Until further well-designed research is carried out, athletes are encouraged to follow standard recommendations for CHO consumption and let practical issues and individual experience dictate the use of HGI or LGI meals and supplements before, during, and after exercise.

Glycemic and insulinemic response to selected snack bars in trained versus sedentary individuals.

The purpose of this study was to determine whether glycemic index (GI) is influenced by training state. Participants were tested in a randomized order: twice with a reference solution containing 50 g glucose and once each with 2 commercially available snack bars (Griffin's Fruitli bar and Peak Fuel's Summit bar) containing 50 g available carbohydrate. Eleven of the participants (6 men and 5 women, M + or - SD age 20.8 + or - 2.0 yr) were endurance trained (ET; VO(2max) 57.5 + or - 8.4 ml x kg(-1) x min(-1) ), and 9 participants (2 men and 7 women, M + or - SD age 22.4 + or - 1.8 yr) were sedentary (SE; VO(2max) 43.7 + or - 9.1 ml x kg(-1) x min(-1) ). After an overnight fast, participants consumed either the glucose solution or snack bar, with blood samples taken before eating and at 15, 30, 45, 60, 90, and 120 min after eating began. The mean incremental area under the curve (IAUC) of the glucose reference was 31% lower (95% CI 3-52%, p = .03), and the Fruitli bar 38% lower (95% CI 0-61%, p = .05) in ET than in SE participants. There was a trend for the IAUC for the Summit bar to be 35% lower in ET than in SE participants (95% CI -7% to 61% p = .09). There was no significant interaction between training state and test food. The GIs of the Fruitli and Summit bars was not significantly different between ET and SE participants (p = .65 and .54, respectively). ET participants had a lower glycemic response than SE participants; however, training state did not influence GI.

Iodine supplementation improves cognition in mildly iodine-deficient children.

BACKGROUND: The effects of severe iodine deficiency during critical periods of brain development are well documented. There is little known about the consequences of milder forms of iodine deficiency on neurodevelopment. OBJECTIVE: The objective was to determine whether supplementing mildly iodine-deficient children with iodine improves cognition. DESIGN: A randomized, placebo-controlled, double-blind trial was conducted in 184 children aged 10-13 y in Dunedin, New Zealand. Children were randomly assigned to receive a daily tablet containing either 150 microg I or placebo for 28 wk. Biochemical, anthropometric, and dietary data were collected from each child at baseline and after 28 wk. Cognitive performance was assessed through 4 subtests from the Wechsler Intelligence Scale for Children. RESULTS: At baseline, children were mildly iodine deficient [median urinary iodine concentration (UIC): 63 microg/L; thyroglobulin concentration: 16.4 microg/L]. After 28 wk, iodine status improved in the supplemented group (UIC: 145 microg/L; thyroglobulin: 8.5 microg/L), whereas the placebo group remained iodine deficient (UIC: 81 microg/L; thyroglobulin: 11.6 microg/L). Iodine supplementation significantly improved scores for 2 of the 4 cognitive subtests [picture concepts (P = 0.023) and matrix reasoning (P = 0.040)] but not for letter-number sequencing (P = 0.480) or symbol search (P = 0.608). The overall cognitive score of the iodine-supplemented group was 0.19 SDs higher than that of the placebo group (P = 0.011). CONCLUSIONS: Iodine supplementation improved perceptual reasoning in mildly iodine-deficient children and suggests that mild iodine deficiency could prevent children from attaining their full intellectual potential. The trial was registered with the Australia New Zealand Clinical Trials Register as ACTRN12608000222347.