American Journal of Clinical Nutrition最新文献

Background: The associations of sweetened beverages (SBs) and added sugar (AS) intake with adiposity are still debated. Metabolomics could provide insights into the mechanisms linking their intake to adiposity.

Objectives: We aimed to identify metabolomics biomarkers of intake of low- and no-calorie sweetened beverages (LNCSBs), sugar-sweetened beverages (SSBs), and ASs and to investigate their associations with body mass index, body fat percentage, and waist circumference.

Methods: We analyzed 3 data sets from the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) cohort study, of children who provided 2 urine samples (n = 297), adolescents who provided a single urine sample (n = 339), and young adults who provided a single plasma sample (n = 195). Urine and plasma were analyzed using untargeted metabolomics. Dietary intakes were assessed using 3-d weighed dietary records. The random forest, partial least squares, and least absolute shrinkage and selection operator were jointly used for metabolite selection. We examined associations of intakes with metabolites and anthropometric measures using linear and mixed-effects regression.

Results: In adolescents, LNCSB were positively associated with acesulfame (β: 0.0012; 95% confidence interval [CI]: 0.0006, 0.0019) and saccharin (β: 0.0009; 95% CI: 0.0002, 0.0015). In children, the association was observed with saccharin (β: 0.0016; 95% CI: 0.0005, 0.0027). In urine and plasma, SSBs were positively associated with 1-methylxanthine (β: 0.0005; 95% CI: 0.0003, 0.0008; and β: 0.0010, 95% CI 0.0004, 0.0015, respectively) and 5-acetylamino-6-amino-3-methyluracil (β: 0.0005; 95% CI: 0.0002, 0.0008; and β: 0.0009; 95% CI: 0.0003, 0.0014, respectively). AS was associated with urinary sucrose (β: 0.0095; 95% CI: 0.0069, 0.0121) in adolescents. Some of the food-related metabolomics profiles were also associated with adiposity measures.

Conclusions: We identified SBs- and AS-related metabolites, which may be important for understanding the interplay between these intakes and adiposity in young individuals.

Background: There have been mixed results reported internationally when associating vegetarian dietary patterns with all-cause and cause-specific mortalities.

Objectives: This study aimed to extend our previous results by evaluating, with a larger number of deaths (N = 12,515), cause-specific mortalities comparing different vegetarian types with nonvegetarians.

Methods: This prospective study used data from the Adventist Health Study-2 cohort. Mortality was ascertained between study baseline, 2002-2007, and follow-up through 2015. Dietary data were collected at baseline using a validated quantitative food frequency questionnaire and then categorized into 5 dietary patterns: nonvegetarian, semivegetarian, pescovegetarian, lacto-ovovegetarian, and vegan. Main outcomes and measures include all-cause and cause-specific mortalities using Cox proportional hazards regression models and competing risk methods.

Results: The analytic sample included 88,400 participants who provided 971,424 person-years of follow-up. We report results pairwise as estimated at ages 65 and 85 y owing to age dependence of many hazard ratios (HRs). Compared with nonvegetarians, vegetarians had lower risks of mortality, overall (HR: 0.89; 95% confidence interval [CI]: 0.83, 0.95; HR: 0.98; 95% CI: 0.91, 1.04), from renal failure (HR: 0.52; 95% CI: 0.38, 0.70; HR: 0.65; 95% CI: 0.55, 0.76), infectious disease (HR: 0.57; 95% CI: 0.40, 0.82; HR: 0.90; 95% CI: 0.70, 1.17), diabetes (HR: 0.51; 95% CI: 0.33, 0.78; HR: 0.69; 95% CI: 0.53, 0.88), select cardiac (HR: 0.75; 95% CI: 0.65, 0.87; HR: 0.89; 95% CI: 0.83, 0.95), and ischemic heart disease causes (HR: 0.73; 95% CI: 0.59, 0.90; HR: 0.84; 95% CI: 0.75,0.94). Vegans, lacto-ovovegetarians, and pescovegetarians were also observed to have lower risks of total mortality and several similar cause-specific mortalities. However, higher cause-specified neurologic mortalities were observed among older vegetarians (estimated at age 85 y), specifically stroke (HR: 1.17; 95% CI: 1.02, 1.33), dementia (HR: 1.13; 95% CI: 1.00, 1.27), and Parkinson's disease (HR: 1.37; 95% CI: 0.98, 1.91). Results in Black subjects for vegetarian/nonvegetarian comparisons largely followed the same trends, but HRs were less precise owing to smaller numbers.

Conclusions: Vegetarian diets are associated with lower risk for all-cause and many cause-specific mortalities, especially among males and in younger subjects. However, higher risks are observed among older vegetarians for stroke and dementia. These results need further support and investigation.

The participants in this debate agreed that: 1) target-based advocacy is required for ensuring countries' engagement and political commitments toward reducing child malnutrition, and the tools used for monitoring progress should be accurate and pose no risk of harmful consequences; and 2) physical growth is not the only dimension of nutritional status to be monitored in clinical and public health practice; anthropometry is thus only one of the diagnostic indicators of nutritional status. Key disagreements included methodological approaches for developing a single growth standard to evaluate nutritional status globally; the relative utility of universal and contextual growth standards for clinical practice and public health; the balance of benefits, harms, and acceptability among stakeholders; and their use as a screening or a definitive tool in individual and public health nutrition. Noteworthy agreements for research priorities included comparison of benefits and harms of using universal compared with contextual growth standards/references and different stakeholders' perception of expectations from and utility of growth standards.

Background: Low-calorie sweetener (LCS) consumption is prevalent among lactating mothers, yet infants' exposure to LCS in human milk is not well-characterized.

Objectives: Conduct a pharmacokinetic study of sucralose and acesulfame-potassium (ace-K) in mothers' milk and plasma over 72 h and in infants' plasma.

Methods: Following baseline blood and milk collection, mothers (n = 40) consumed 20 oz of diet cranberry juice containing sucralose and ace-K. Blood samples were collected from the mother 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, and 72 h after beverage ingestion, and milk was expressed at 1, 2, 3, 4, 6, 8, 12, and 24 h postingestion. One blood sample was collected from each infant, the timing of which was determined using pharmacokinetics model-based simulation. Concentration-time profiles of LCS from the mother's plasma and milk were analyzed using noncompartmental methods.

Results: Ace-K rapidly entered human milk with the largest observed concentration of 373.0 (coefficient of variation 69%) ng/mL first detected 4 h following diet beverage ingestion. Sucralose appeared in human milk 1-2 h after diet beverage ingestion with the largest observed concentration of 7.2 (coefficient of variation 63%) ng/mL first detected 7 h postingestion. The mean 24-h milk to plasma ratio of ace-K was 1.75 [standard deviation (SD) 1.37] with a mean relative infant dose of 1.59% (SD 1.72%). Ace-K was detected in all infants' plasma with an mean concentration of 9.2 (SD% 14.8) ng/mL ∼6 h after maternal beverage ingestion. The mean 24-h milk to plasma ratio of sucralose was 0.15 (SD 0.06) with a mean relative infant dose of 0.04% (SD 0.02%). Sucralose was detected in only 15 infants' plasma, and the mean concentration was 5.0 (SD% 7.1) ng/mL ∼5 h after diet beverage ingestion.

Conclusions: Ace-K rapidly transfers from human milk into infants' circulation whereas sucralose was detected at much lower concentrations and in some but not all infants. Future research should investigate the effects of early-life sucralose and ace-K exposure via human milk on infants' health. This trial was registered at clinicaltrials.gov as NCT05379270.

Background: Dietary Reference Intake (DRI) Recommendations for total sulfur amino acids (TSAAs; methionine + cysteine) during pregnancy are based on factorial calculations using data from adult males. To date, no data exist on TSAA requirements obtained directly during pregnancy.

Objectives: The objective of this study was to examine whether TSAA requirements during early (11-20 wk) and late (31-40 wk) gestation in healthy females with singleton pregnancies are different than current recommendations, and different between early and late gestation using the indicator amino acid oxidation (IAAO) technique.

Methods: Twenty-five females 20-40 y with a healthy singleton pregnancy were studied using the IAAO technique in a repeated measures design for a total of 70, 8-h d. On each study day a methionine test intake (range: 0-40 mg⋅kg^-1⋅d^-1) was provided in 8 hourly, isonitrogenous and isocaloric meals with cysteine excluded from the diet. Breath samples were collected at baseline and isotopic steady state of orally provided L-1-¹³C-Phenylalanine for measurement of phenylalanine oxidation. The requirement was determined using biphasic linear regression crossover analysis to identify a breakpoint in ¹³CO₂ production, representing the estimated average requirement (EAR).

Results: The TSAA requirement in healthy pregnant participants in early gestation was 11.1 mg⋅kg^-1⋅d^-1 {R²_m = 0.79, R²_c = 0.79; 95% confidence interval [CI] (8.9, 13.3 mg⋅kg^-1⋅d^-1)} and 15.0 mg⋅kg^-1⋅d^-1 (R²_m = 0.72, R²_c = 0.79; 95% CI [13.0, 17.0 mg⋅kg^-1⋅d^-1]) in late gestation. The difference between confidence intervals of the 2 breakpoints was = -3.9 ± 3.0, and statistically different.

Conclusions: We directly measured TSAA requirements in healthy pregnant mothers, and our findings suggest that requirements are lower than current DRI recommendations of 20 and 25 mg⋅kg^-1⋅d^-1, as the EAR, and Recommended Dietary Allowance, respectively. Late gestation TSAA needs are significantly different and increased 35% compared with early gestation. Recommendations for TSAA intake need to be tailored for gestational stage. This clinical trial was registered at clinicaltrials.gov as NCT04326322.

Background: Observational studies have suggested associations between amount of coffee consumption and decreased risk of neurodegenerative diseases. However, these studies do not consider differences among coffee types, including sweetened, unsweetened, caffeinated, and decaffeinated varieties.

Objectives: This study aims to identify associations between the consumption of various coffee types (sugar-sweetened, artificially sweetened, unsweetened, caffeinated, and decaffeinated) and risks of Alzheimer's disease and related dementias (ADRD) and Parkinson's disease (PD), along with related mortality.

Methods: This prospective study included 204,847 participants (44.7% males) from the UK Biobank. Cox proportional hazards models were used to assess the associations of coffee type with neurodegenerative outcome. On the basis of coffee consumption, participants were divided into 5 groups: non-coffee consumers, >0-1 cup/d, ≥1-2 cups/d, ≥2-3 cups/d, and ≥3 cups/d.

Results: Over a median follow-up of 9 y, the study documented 1696 cases of ADRD, 1093 cases of PD, and 419 neurodegenerative-related deaths. In the multivariate analysis, compared with non-coffee consumers, those with the highest intake of unsweetened and caffeinated coffee (≥3 cups/d) showed hazard ratios (95% confidence intervals) of 0.75 (0.62, 0.91) for ADRD, 0.71 (0.56, 0.91) for PD, and 0.67 (0.44, 1.01) for neurodegenerative-related death. However, no significant associations were noted in either decaffeinated or sugar/artificially sweetened coffee groups (P > 0.05).

Conclusions: Higher intake of caffeinated coffee, particularly the unsweetened variety, was associated with reduced risks of ADRD and PD. No such associations were observed for sugar-sweetened or artificially sweetened coffee.

Background: Although serum magnesium deficiency is linked to higher cardiovascular disease risk, its association with chronic kidney disease (CKD) remains unclear.

Objectives: This study aimed to evaluate the relationship between dietary magnesium intake and CKD development in adults with clinically normal kidney function.

Methods: The prospective observational cohort study evaluated 188,510 participants (median age, 57.0 y; female, 54.1%) from the UK Biobank. Dietary magnesium intake was assessed through a 24-h dietary recall questionnaire compromising a list of 206 foods and 32 beverages and categorized into quintiles. The primary outcome was incident CKD diagnosed through International Classification of Diseases-10 and Office of Population Censuses and Surveys 4 codes. Incident CKD, defined as estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 m², was also assessed in a subcohort with creatinine follow-up data.

Results: The median magnesium intake amount per person was 323.2 mg/d [interquartile range (IQR): 269.4-382.7 mg/d]. During 1,826,038.1 person-years of follow-up (median: 9.6 y; IQR: 9.3-10.3 y), CKD developed in 5,878 participants. The incidence of CKD was progressively higher in participants with lower magnesium intake (2.8%, 2.8%, 3.0%, 3.2%, and 3.7% in Q5-Q1, respectively). Cox regression analysis revealed that the hazard ratios (HRs) for incident CKD increased in a stepwise manner toward lower magnesium intake quintiles {adjusted HR (95% confidence interval [CI])-Q4: 0.97 (0.89, 1.06); Q3: 1.05 (0.96, 1.14); Q2: 1.12 (1.03, 1.21); Q1: 1.30 (1.20, 1.41)} relative to Q5 (P-linearity < 0.001). Similar results were observed with eGFR-defined CKD outcome [adjusted HR (95% CI)-Q4: 1.09 (0.92, 1.28); Q3: 1.15 (0.98, 1.35); Q2: 1.21 (1.03, 1.42); Q1: 1.41 (1.20, 1.65) relative to Q5; P-linearity < 0.001].

Conclusions: Lower dietary magnesium intake was associated with higher risk of incident CKD in adults with clinically normal kidney function. Further controlled studies are required to establish the potential benefit of adequate magnesium intake.