Journal of Nutrition最新文献

Background: Pistachios are a bioavailable source of the xanthophyll lutein. Along with zeaxanthin, these plant pigments are major components of macular pigment (MP) in the human retina. MP can be non-invasively measured and is referred to as MP optical density (MPOD). MPOD is modifiable with dietary interventions that include lutein and zeaxanthin (L/Z). Higher MPOD protects the eye from light damage and is positively associated with eye health.

Objectives: This dietary intervention study aimed to evaluate the effect of pistachio consumption on MPOD.

Methods: This single-blinded, randomized controlled trial compared a 12-week pistachio intervention (2 oz/d) with usual diet (UD) on MPOD and serum L/Z in middle-aged to older healthy adults (n = 36) in a 1:1 randomization scheme. Participants were selected for habitually low L/Z intake and low baseline MPOD. MPOD was measured using heterochromatic flicker photometry at 4 retinal eccentricities during baseline, week 6, and week 12 study visits. Serum L/Z was analyzed using high-performance liquid chromatography. Primary statistical analysis was conducted on an intent-to-treat basis using repeated-measure analysis of variance.

Results: Compared with UD, MPOD of the participants in the pistachio intervention group (PIS) had significantly increased (P < 0.001) at all eccentricities over the initial 6-wk period. This increase was maintained at week 12. MPOD in the UD participants did not change during the 12-week period. Serum lutein concentration followed a similar pattern to MPOD; serum cis-lutein and zeaxanthin did not change in either group over the 12-wk intervention.

Conclusions: The results of our study demonstrate that a dietary intervention with pistachios is efficacious in increasing MPOD in healthy adults selected for habitually low intake of L/Z and low baseline MPOD. This suggests that pistachio consumption could be an effective dietary strategy for preserving eye health. Future studies need to evaluate the generalizability of our findings to other populations. This trial was registered at clinicaltrials.gov as NCT05283941.

Background: High gluten and low dietary fiber in pregnancy intake is associated with an increased risk of celiac disease (CeD) in the child. Early life higher dietary quality is suggested to reduce the subsequent risk of CeD.

Objectives: The aim was to investigate associations of pregnancy dietary quality and diversity with child risk of CeD.

Methods: In The Norwegian Mother, Father and Child Cohort Study, 85,122 mother-child pairs had available data from a validated pregnancy food frequency questionnaire. Pregnancy dietary quality and diversity were estimated by a Pregnancy Healthy Eating Index [mean 99.3, standard deviation (SD) 9.9, range 48.8-128.3], and a Diet Diversity Score (mean 7.0, SD 1.0, range 1.6-9.8), respectively. Child CeD was captured by ≥2 diagnostic codes in the Norwegian Patient Registry. Logistic regression was used to estimate associations between pregnancy dietary quality, diversity and child CeD, adjusted for socioeconomic factors, and parents CeD [adjusted odds ratio (aOR), 95% confidence intervals (CI)]. CeD-susceptible human leukocyte antigen haplotypes (DQ2/DQ8) were present in 30,718 (45.5%).

Results: Up to mean age 16.0 (SD 1.8, 12.4-19.8) y, 1363 (1.6%) children were diagnosed with CeD. Lower as well as higher pregnancy dietary quality associated with a reduced risk of CeD in the child (<5th percentile aOR = 0.67, 95% CI: 0.48, 0.93, >95th percentile aOR = 0.71, 95% CI: 0.52, 0.98, respectively, nonlinear squared term P = 0.011). Analyses on genetically susceptible children, adjustments for pregnancy iron supplementation, gluten, and dietary fiber intake, and child early life dietary quality, gluten intake and iron supplementation, supported the finding. Pregnancy dietary diversity was not associated with child CeD (aOR = 1.00, 95% CI: 0.94, 1.07/score).

Conclusions: In this population-based study, lower as well as higher pregnancy dietary quality associated with a reduced risk of CeD diagnosis in the child. In contrast, no such association was observed with maternal dietary diversity.

Background: Current systems for assessing protein quality such as the Digestible Indispensable Amino Acid Score correct apparent amino acid (AA) digestibility for basal endogenous protein losses (bEPL), ignoring the potential influence of the diet on these losses. However, the quantification of total endogenous protein losses (tEPL) poses a challenge.

Objectives: To evaluate different methods for quantifying tEPL and bEPL, and to assess their potential in discriminating between tEPL originating from bacteria and host.

Methods: Using an incomplete Youden square design, 12 ileal cannulated pigs received 10 different protein sources, and a nitrogen-free (NF) diet. Ileal digesta were collected on days 6 and 7 of each 1-wk feeding period, to quantify endogenous protein losses (EPL) and analyze apparent ileal digestibility. Ileal EPL were estimated based on 1) 16S-+18S gene copy quantitative polymerase chain reaction, 2) diaminopimelic acid (DAPA)+18S, 3) differential AA profiles in digesta, EPL, and bacteria, equaling tEPL, and 4) an NF diet and 5) whey protein isolate (WPI), equaling bEPL.

Results: Ileal bEPL based on the NF and WPI method correlated moderately to highly (r = 0.69, P < 0.05), but the NF method probably underestimated bEPL. In pigs fed the WPI diet, EPL based on the WPI and AA profile method were highly correlated (r = 0.88, P < 0.01). Overall, tEPL based on the AA profile method were moderately correlated with the 16S+18S method (r = 0.58, P < 0.001), and DAPA+18S (r = 0.57, P < 0.001). Low correlations were observed between bacterial tEPL based on the AA profile method and 16S or DAPA. Host tEPL based on the AA profile method and 18S were weakly correlated (r = 0.39, P < 0.001).

Conclusions: The AA profile method seems the most appropriate method for tEPL quantification, whereas the WPI method is preferred for bEPL quantification. Despite challenges in distinguishing between bacterial and host EPL, it is evident that bacterial proteins substantially (on average 37%-83%, depending on method) contribute to the EPL.

Background: Cardiometabolic multimorbidity (CMM), defined as the co-occurrence of 2 or more cardiometabolic diseases, including myocardial infarction (MI), stroke, and type 2 diabetes (T2D), is an increasing public health challenge. Although poor diet is a known risk factor for a first cardiometabolic disease (FCMD), the relationship with subsequent occurrence of CMM is less studied.

Objectives: This study aims to investigate the prospective association between baseline adherence to the Mediterranean diet and the onset of CMM across various follow-up durations.

Methods: We used data from the European Prospective Investigation into Cancer-Norfolk cohort study of 21,900 adults, aged 40-79 free of prevalent MI, stroke, and T2D at baseline (1993-1997). A median-based Mediterranean diet score and a pyramid-based MDS (pyr-MDS) were used to measure baseline adherence to the Mediterranean diet. Multistate modeling was employed to investigate associations with the FCMD and the subsequent CMM event.

Results: Over the entire follow-up period of 21.4 y (median), we observed 5028 FCMD and 734 CMM events. Multistate analysis indicated that the association between baseline Mediterranean diet and the risk of CMM may be stronger in shorter follow-up durations. Particularly, baseline pyr-MDS was significantly associated with the risk of subsequent CMM transitioning from FCMD when follow-up durations were limited to 10 and 15 y, with hazard ratio (95% confidence interval) being 0.67 (0.53, 0.84) and 0.80 (0.70, 0.92) per SD increase in pyr-MDS, respectively. Additionally, we observed that the risk of CMM transitioning from FCMD was modified by social class across shorter to longer follow-ups, where the impact of baseline Mediterranean diet was only significant in nonmanual workers.

Conclusions: Baseline adherence to the Mediterranean diet was potentially associated with a lower risk of CMM transitioning from FCMD, particularly during shorter follow-up periods.

Background: Nicotinamide adenine dinucleotide (NAD⁺) levels decline with age, and boosting it can improve multi-organ functions and lifespan.

Objectives: Nicotinamide mononucleotide (NMN) is a natural NAD⁺ precursor with the ability to enhance NAD⁺ biosynthesis. Numerous studies have shown that a high-fat diet (HFD) can accelerate the process of aging and many diseases. We hypothesized that long-term administration of NMN could exert protective effects on adipose, muscle, and kidney tissues in mice on an HFD act by affecting the autophagic pathway.

Methods: Mice at 14 mo of age were fed an HFD, and NMN was added to their drinking water at a dose of 400 mg/kg for 7 mo. The locomotor ability of the mice was assessed by behavioral experiments such as grip test, wire hang test, rotarod, and beam-walking test. At the end of the behavioral experiments, the pathological changes of each peripheral organ and the expression of autophagy-related proteins, as well as the markers of the senescence and inflammaging were analyzed by pathological staining, immunohistochemical staining, and western blotting, respectively.

Results: We found that NMN supplementation increased NAD⁺ levels and ultimately attenuated age- and diet-related physiological decline in mice. NMN inhibited HFD-induced obesity, promoted physical activity, improved glucose and lipid metabolism, improved skeletal muscle function and renal damage, as well as mitigated the senescence and inflammaging as demonstrated by p16, interleukin 1β, and tumor necrosis factor α levels. In addition, the present study further emphasizes the potential mechanisms underlying the bidirectional relationship between NAD⁺ and autophagy. We detected changes in autophagy levels in various tissue organs, and NMN may play a protective role by inhibiting excessive autophagy induced by HFD.

Conclusions: Our findings demonstrated that NMN administration attenuated HFD-induced metabolic disorders and physiological decline in aging mice.

The lungs are a mucosal organ constantly exposed to potentially harmful compounds and pathogens. Beyond their role in gas exchange, they must perform a well-orchestrated protective response against foreign invaders. The lungs identify these foreign compounds, respond to them by eliciting an inflammatory response, and restore tissue homeostasis after inflammation to ensure the lungs continue to function. In addition, lung function can be affected by genetics, environmental exposures, and age, leading to pulmonary diseases that infringe on quality of life. Recent studies indicate that diet can influence pulmonary health including the incidence and/or severity of lung diseases. Specifically, long-chain omega-3 polyunsaturated fatty acids (n-3 PUFAs) have gained attention because of their potential to reduce inflammation and promote resolution of inflammation. Docosahexaenoic acid and eicosapentaenoic acid are 2 potentially beneficial n-3 PUFAs primarily acquired through dietary intake. Here we review current literature examining the role of n-3 PUFAs and the biological mechanisms by which these fatty acids alter the incidence and pathologies of chronic lung diseases including asthma, chronic obstructive pulmonary disease, and interstitial lung disease. We also highlight the role of n-3 PUFAs in vulnerable populations such as pre/postnatal children, those with obesity, and the elderly. Lastly, we review the impact of n-3 PUFA intake and supplementation to evaluate if increasing consumption can mitigate mechanisms driving chronic lung diseases.

Iodine is essential for the synthesis of thyroid hormones, which regulate cell metabolism, growth, and development. Although iodine deficiency (ID) causes adverse health effects across the lifespan, it is particularly problematic in pregnancy, when it can lead to irreversible fetal brain damage. A high prevalence of severe ID, manifesting as endemic goiter and cretinism, predated the arrival of European explorers in the Americas. Early 20th century surveys showed that most countries in the Western Hemisphere had regions with a goiter prevalence >50%. In North America, the introduction of iodized salt led to the elimination of ID by the 1950s. Although most Latin American countries passed laws mandating salt iodization in the 1950s-1960s, initial programs met with limited success because laws were unenforced, monitoring was absent, and the importance of iodine nutrition was inadequately communicated. A renewed interest in ID prevention arose in the 1970s-1980s, when 3 Andean countries were the first in Latin America to implement effective salt iodization programs. Over the last 3 decades there has been a stronger political commitment to ID prevention across the region, alignment with the broader nutrition and development agenda, and a widespread recognition of optimal iodine nutrition as a fundamental human right. Currently, 92% of households in Latin America consume adequately iodized salt, and urinary iodine concentrations in schoolchildren reflect optimal iodine nutrition across the region. However, additional work remains. It is essential to ensure ongoing government commitment; to monitor population iodine status and the production, quality, and household consumption of iodized salt; and to maintain advocacy and communication strategies. Universal salt iodization programs must be harmonized with efforts to reduce salt intake for cardiovascular disease prevention. Ensuring optimal iodine nutrition in pregnant women, who may remain deficient even when intakes in schoolchildren are optimized, requires particular attention.

Background: Eggs are rich in bioactive compounds, including choline and carotenoids that may benefit cardiometabolic outcomes. However, little is known about their relationship with nonalcoholic fatty liver disease (NAFLD).

Objectives: We investigated the association between intakes of eggs and selected egg-rich nutrients (choline, lutein, and zeaxanthin) and NAFLD risk and changes in liver fat over ∼6 y of follow-up in the Framingham Offspring and Third Generation cohorts.

Methods: On 2 separate occasions (2002-2005 and 2008-2011), liver fat was assessed using a computed tomography scan to estimate the average liver fat attenuation relative to a control phantom to create the liver phantom ratio (LPR). In 2008-2011, cases of incident NAFLD were identified as an LPR ≤0.33 in the absence of heavy alcohol use, after excluding prevalent NAFLD (LPR ≤0.33) in 2002-2005. Food frequency questionnaires were used to estimate egg intakes (classified as <1, 1, and ≥2 per week), dietary choline (adjusted for body weight using the residual method), and the combined intakes of lutein and zeaxanthin. Multivariable modified Poisson regression and general linear models were used to compute incident risk ratios (RR) of NAFLD and adjusted mean annualized liver fat change.

Results: NAFLD cumulative incidence was 19% among a total of 1414 participants. We observed no associations between egg intake or the combined intakes of lutein and zeaxanthin with an incident NAFLD risk or liver fat change. Other diet and cardiometabolic risk factors did not modify the association between egg intake and NAFLD risk. However, dietary choline intakes were inversely associated with NAFLD risk (RR for tertile 3 compared with tertile 1: 0.69, 95% CI: 0.51, 0.94).

Conclusions: Although egg intake was not directly associated with NAFLD risk, eggs are a major source of dietary choline, which was strongly inversely associated with NAFLD risk in this community-based cohort.

Background: Postprandial vascular endothelial dysfunction is an early marker of atherosclerosis. Meal protein has been reported to reduce endothelial dysfunction in adults, and the effect could be mediated by the amino acid content.

Objectives: This trial aims to assess the effect of a specifically designed plant-protein blend that contains high leucine, arginine, and cysteine on postprandial endothelial function in the elderly.

Methods: In a randomized, double-blind, 3-period crossover (2-wk washout), controlled trial, we compared the vascular effects of 3 high-saturated-fat high-sucrose (HFHS) meals containing either our specific plant-protein blend, or milk protein, or without added protein. The trial was conducted on 29 healthy adults aged >65 y presenting ≥2 cardiometabolic risk factors. Postprandial vascular function was evaluated at fasting, 3 h, and 5 h postprandially, using brachial flow-mediated dilation (FMD), hand microvascular reactivity (using Flowmetry Laser Doppler, FLD), and finger reactive hyperemia index (using Peripheral Arterial Tonometry, RHI). Immune cell count and gene expression in peripheral blood mononuclear cells (PBMCs) were also assessed postprandially. Data were analyzed using mixed linear models with repeated measurements on participants for meal composition and time of sampling. This trial was registered at clinicaltrials.gov as NCT04923555.

Results: FMD incremental AUC value decreased after meals (time effect P < 0.01), with no significant differences between meals. RHI also decreased with time (P < 0.01). PBMC count and monocyte chemoattractant protein-1 (MCP1), IL-1β, and IL-6 expression increased after meals showing postprandial endothelial activation (P < 0.05). Overall, meal composition had no effect on any of the postprandial changes (Ps>0.10).

Conclusions: In healthy adults aged >65 y presenting cardiometabolic risk, adding protein to an HFHS challenge meal does not mitigate postprandial impairments in vascular endothelial function and inflammatory activation. Further studies are needed to explore the potential differences with younger adults.