Background Phenylalanine is an indispensable amino acid and, via tyrosine, is the precursor for the neurotransmitters dopamine, norepinephrine, and epinephrine. Currently, dietary requirements for phenylalanine during pregnancy are unknown. Objectives This study's aim was to determine phenylalanine requirements (in the presence of excess tyrosine) during early and late gestation using direct amino acid oxidation (DAAO; with l-[1-13C]phenylalanine) and indicator amino acid oxidation (IAAO; with l-[1-13C]leucine). Methods Twenty-three healthy women (age: 30.4 ± 3.1 y, mean ± SD) were studied at a range of phenylalanine intakes (5.5–30.5 mg · kg−1 · d−1 in early and late pregnancy using DAAO, and 2.5–30.5 mg · kg−1 · d−1 in late pregnancy using IAAO) for a total of 76 study days. Test intakes were provided as 8 isocaloric and isonitrogenous meals with 1.5 g · kg−1 · d−1 protein and energy at 1.7 times the measured resting energy expenditure. Breath samples were analyzed on an isotope ratio mass spectrometer for 13C enrichment. Phenylalanine requirement was determined using a 2-phase linear regression crossover model to identify a breakpoint in 13CO2 production (representing the mean requirement) in response to phenylalanine intakes. Results Phenylalanine requirement during early pregnancy was determined to be 15 mg · kg−1 · d−1 (95% CI: 10.4, 19.9 mg · kg−1 · d−1); during late pregnancy, it was determined to be 21 mg · kg−1 · d−1 by DAAO (95% CI: 17.4, 24.7 mg · kg−1 · d−1) and IAAO (95% CI: 10.5, 32.2 mg · kg−1 · d−1). Conclusions Our results suggest a higher requirement (40%) for phenylalanine during late pregnancy than during early pregnancy. Moreover, the early pregnancy requirements are higher than the previous adult male requirement (9.1 mg · kg−1 · d−1; 95% CI: 4.6, 13.6 mg · kg−1 · d−1), although the 95% CIs overlap. Both DAAO and IAAO methods provided similar breakpoints in late pregnancy, showing that the DAAO method was appropriate even though low phenylalanine intakes could not be tested. These results have potential implications for gestation stage–specific dietary phenylalanine recommendations in future. This trial was registered at clinicaltrials.gov as NCT02669381.

Lutein and zeaxanthin are xanthophyll carotenoids present in highly pigmented vegetables and fruits. Lutein is selectively accumulated in the brain relative to other carotenoids. Recent evidence has linked lutein to cognition in older adults, but little is known about lutein in young children, despite structural brain development. We determined lutein intake using FFQ, one 24 h recall and three 24 h recalls, plasma lutein concentrations and their association with cognition in 160 children 5·6–5·9 years of age, at low risk for neurodevelopmental delay. Plasma lutein was skewed, with a median of 0·23 (2·5th to 95th percentile range 0·11–0·53) µmol/l. Plasma lutein showed a higher correlation with lutein intake estimated as the average of three 24 h recalls (r 0·479; P = 0·001), rather than one 24 h recall (r 0·242; P = 0·003) or FFQ (r 0·316; P = 0·001). The median lutein intake was 697 (2·5th to 95th percentile range 178–5287) µg/d based on three 24 h recalls. Lutein intake was inversely associated with SFA intake, but dietary fat or SFA intakes were not associated with plasma lutein. No associations were found between plasma lutein or lutein intake and any measure of cognition. While subtle independent effects of lutein on child cognition are possible, separating these effects from covariates making an impact on both child diet and cognition may be difficult.

Leucine, a branched-chain amino acid, has been shown to stimulate muscle protein synthesis and has been suggested to play a role in the prevention of age-related muscle atrophy (sarcopenia). Although leucine supplementation may be beneficial, the efficacious dose of leucine is unknown. Before conducting studies with increased doses of leucine, the Tolerable Upper Intake Level (UL) for leucine needs to be determined. The objective of this review is to describe 2 current studies to determine the UL for leucine in young and elderly men. Initially, in young men we tested the conceptual model of determining the maximum oxidative capacity of an amino acid to be an ideal marker for identifying the UL. Leucine oxidation, measured with the use of l-[1-C]leucine, increased with increasing leucine intakes and reached a plateau at higher intakes. Two-phase linear regression analysis identified a breakpoint of 550 mg ⋅ kg ⋅ d (95% CI: 454, 646 mg ⋅ kg ⋅ d), with a simultaneous increase in blood ammonia concentrations above normal values (35 μmol/L). Recently, a similar study was conducted in elderly men (∼72 y old). A breakpoint in leucine oxidation was observed at 431 mg ⋅ kg ⋅ d (95% CI: 351, 511 mg ⋅ kg ⋅ d), with blood ammonia concentrations above normal (35 μmol/L) at leucine intakes >550 mg ⋅ kg ⋅ d Taking the data together, the UL for leucine intake in healthy elderly men could be set at a value similar to young men, at 500 mg ⋅ kg ⋅ d, or ∼35 g/d for an individual weighing 70 kg; or, as a cautious estimate, the leucine UL could also be considered as 351 mg ⋅ kg ⋅ d (the lower 95% CI), which would be ∼24.5 g/d for an elderly individual weighing 70 kg. These studies to determine the UL for leucine in humans are acute diet studies, and future studies with additional biomarkers and long-term supplementation of leucine will be necessary.