Journal of Nutrition最新文献

Background: Aspartame, one of the most widely used low-calorie sweeteners, was recently classified by the International Agency for Research on Cancer as possibly carcinogenic to humans. Epidemiologic evidence remains inconsistent, particularly for specific and obesity-related cancers (ObCa), highlighting the need for further large prospective studies.

Objectives: We examined the association between aspartame intake and risk of all cancers combined, non-ObCa, ObCa, and 2 ObCa subgroups (digestive and female reproductive), in the Cancer Prevention Study-II Nutrition Cohort (CPS-II NC).

Methods: Among 100,004 U.S. adults (98% non-Hispanic White; mean age: 69 y), aspartame intake from low-calorie carbonated beverages (70‒180 mg per 12-oz serving depending on type) and single-serving packets (20 mg/packet) was assessed in 1999 and 2003 using a modified Willett food frequency questionnaire. Participants were categorized as nonconsumers (0 to less than once per month) or consumers (at least once per month). Total intake estimates were converted to daily equivalents, and consumers were further grouped into 3 categories: >0 to <20 mg/d, 20 to <80 mg/d, and ≥80 mg/d. A total of 21,356 cancer cases were verified, including 8087 ObCa (2976 digestive; 2756 female reproductive) through June 2017. Multivariable-adjusted Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) overall and by baseline weight status (overweight/obesity compared with under/normal weight).

Results: At baseline, 74.3% of the participants were aspartame consumers. Compared with nonconsumers, consumers had higher risks of developing all cancers combined [adjusted HR (aHR): 1.13; 95% CI: 1.08, 1.18; P < 0.0001], non-ObCa (aHR: 1.10; 95% CI: 1.05, 1.16; P = 0.0003), ObCa (aHR: 1.17; 95% CI: 1.09, 1.26; P < 0.0001); digestive ObCa (aHR: 1.19; 95% CI: 1.06, 1.33; P = 0.004) and female reproductive ObCa (aHR: 1.13; 95% CI: 1.00, 1.28, P = 0.05). No clear dose-response relationship was observed for any of the cancer outcomes. Associations were not modified by weight status.

Conclusions: In the CPS-II NC, aspartame consumption is associated with higher cancer risk, including ObCa and non-ObCa, regardless of weight status. However, the lack of dose-response underscores the need for cautious interpretation and replication in future studies.

Background: n-3 (ω-3) long-chain polyunsaturated fatty acids (n-3 LCPUFAs) have anti-inflammatory effects that may influence immune-mediated diseases.

Objectives: We investigated whether higher maternal pregnancy intake of n-3 LCPUFA is associated with a lower incidence of infections in young children.

Methods: We used data from 3 Nordic cohorts: the Norwegian Mother, Father and Child Cohort study (MoBa, n = 76,026), the Finnish Diabetes Prediction and Prevention Study (DIPP, n = 560), and the Copenhagen Prospective Studies on Asthma in Childhood 2010 cohort (COPSAC₂₀₁₀, n = 680). Childhood infections up to age 36 mo were assessed using questionnaires in MoBa, coxsackievirus B 1-6 (CVB1-6) neutralizing antibodies in DIPP, and pathogenic viral PCR identification from acute respiratory episodes in COPSAC₂₀₁₀. Maternal n-3 LCPUFA intake was assessed through validated food frequency questionnaires in MoBa and DIPP, whereas COPSAC₂₀₁₀ used a randomized trial design where pregnant women received fish oil capsules or a placebo.

Results: Higher n-3 LCPUFA intake was not significantly associated with lower respiratory tract infection (adjusted incidence rate ratio [aIRR]: 0.99; 95% CI: 0.94-1.03) but was associated with a reduced risk of upper respiratory tract infections (aIRR: 0.99; 95% CI: 0.98-0.99) and gastroenteritis (aIRR: 0.96; 95% CI: 0.95-0.98) per g/d up to age 36 mo in MoBa. The DIPP study found no association between n-3 LCPUFA intake and having ≥1 CVB infection (adjusted odds ratio: 1.74; 95% CI: 0.64-4.72, per g/d). The COPSAC₂₀₁₀ trial found no significant effects of the intervention for pathogen-specific respiratory episodes (IRR: 0.86; 95% CI: 0.69-1.07).

Conclusions: This study does not provide consistent evidence that higher maternal n-3 LCPUFA pregnancy intake reduces the risk of infections in early childhood.

Clinical trial registry: This trial was registered as NCT00798226, https://clinicaltrials.gov/study/NCT00798226.

Background: Coffee is one of the most widely consumed beverages and has been associated with various health benefits. However, the relationship between coffee consumption and body composition remains unclear, particularly in Asian populations.

Objectives: This study aimed to investigate the association between coffee consumption frequency and body composition indicators-fat mass index (FMI), lean body mass index (in kg/m²) (LBMI), and appendicular skeletal muscle mass index (ASMI)-in a nationally representative sample of Korean adults.

Methods: Data were obtained from the Korea National Health and Nutrition Examination Survey between 2008 and 2011. A total of 15,457 adults aged ≥20 y or were included in the analysis. Coffee consumption was assessed via a food frequency questionnaire and categorized into 4 groups: <1 per day, 1 per day, 2 per day, and 3 per day. Body composition was measured using dual-energy X-ray absorptiometry, and FMI, LBMI, and ASMI were calculated. Multivariable linear regression analyses were performed, adjusting for sociodemographic, lifestyle, and dietary factors. Stratified analyses were conducted by age.

Results: In multivariable-adjusted models, higher coffee consumption was associated with favorable body composition indices, particularly lean mass-related measures. Among men, consuming coffee 3 times per day was associated with higher ASMI and LBMI compared with consuming coffee less than once per day, whereas no clear association with FMI was observed. Among women, higher coffee consumption was associated with lower FMI and higher ASMI and LBMI. Specifically, women who consumed coffee 3 times per day had lower FMI (7.64 compared with 7.83) and higher ASMI (5.94 compared with 5.86) and LBMI (15.56 compared with 15.39) than those who consumed coffee less than once per day.

Conclusions: Consumption of coffee, 3 times per day, was associated with more modestly more favorable body composition profiles in Korean adults. These findings indicate an association between habitual coffee consumption and body composition at the population level. However, longitudinal and interventional studies are warranted to establish causality and elucidate underlying biological mechanisms.

Background: Rating a person's diet as a whole, as opposed to rating individual food items, could help better inform consumers about the health value of their diet.

Objectives: Our goal was to develop an automated health rating of grocery shopping baskets, based on the nutrient composition of all the food items contained within the basket, and without knowing how many people consume the food items over what period of time. It is envisaged that the rating, or score, can be deployed by retailers on top of existing loyalty or digital shopping basket programs.

Methods: We developed a novel model for calculating Grocery Basket Scores (GBS) that uses nutrient energy densities rather than absolute quantities. It was based on self-reported daily food intake from the National Health and Nutrition Examination Survey as well as mortality follow-up data. We conducted a validation against the Alternate Healthy Eating Index (AHEI) as well as the Nutri-Score.

Results: The nutrient energy density (GBS) model penalized consuming calories from sugar and saturated fats, high salt intake, as well as consuming calories from beverages. Furthermore, a penalty was applied to foods that have a low ratio of protein, vitamin C, or iron relative to the total number of calories. Fiber consumption was rewarded. The model showed a high degree of correlation with the AHEI (Pearson correlation coefficient: 0.62 for the AHEI without the protective effect of moderate alcohol consumption and 0.60 with it) and the Nutri-Score (PCC: -0.60).

Conclusions: The proposed nutrient energy density model is aligned with the recommendations formulated in nutritional guidelines, as indicated by a high degree of correlation with the AHEI and Nutri-Score. Long-term use of a GBS from a single or multiple grocery stores could help consumers adhere to dietary guidelines.

Background: Long-term high-fat diet (HFD) consumption is associated with the development of metabolic cardiomyopathy and contributes to accelerated cardiac aging. Nicotinamide mononucleotide (NMN), a key NAD⁺ precursor, has shown promise in ameliorating age-related cardiac decline, but its mechanisms are not fully understood.

Objective: To investigate the protective effects of nicotinamide mononucleotide (NMN) against high-fat diet-induced myocardial injury and elucidate the underlying molecular mechanisms.

Methods: Male C57BL/6J mice (14-month-old) were assigned to 3 groups: normal diet, HFD, and HFD + NMN. NMN was added to their drinking water at a dose of 400 mg/kg for 7 mo. Cardiac tissues were collected and analyzed using hematoxylin and eosin staining, Masson's trichrome staining, Western blotting, quantitative real-time polymerase chain reaction, and immunohistochemistry. In vitro, H9c2 cardiomyocytes were exposed to palmitic acid (PA) to establish a lipotoxicity model, and the effects of NMN on cell viability and autophagy flux were assessed by the Methyl Thiazol Tetrazolium (MTT) assay and mRFP-GFP-LC3 adenoviral transfection.

Results: Compared with the HFD group, NMN treatment significantly reduced the heart index, ameliorated myocardial fibrosis, and decreased the expression concentrations of senescence-associated secretory phenotype markers (Serpine1, MMP3, CXCL-1, CXCL-10, and P16; P < 0.05), senescence markers (P21 and β-galactosidase (β-gal); P < 0.01), proinflammatory cytokines [interleukin (IL)-1β and tumor necrosis factor α; P < 0.05], and apoptotic indicators (Bax/Bcl-2 ratio and cleaved caspase-3; P < 0.01). Conversely, NMN treatment upregulated the concentrations of anti-inflammatory factor IL-10 (P < 0.01) in cardiac tissue. Furthermore, NMN treatment increased protein concentrations of Sirt3, PINK1, and Parkin (P < 0.01), and enhanced autophagy-lysosomal markers, including LC3-II/LC3-I ratio and transcription factor EB (TFEB) (P < 0.05), and decreased p62 concentrations (P < 0.01) in cardiac tissue. In H9c2 cardiomyocytes, NMN treatment significantly attenuated PA-induced cytotoxicity (P < 0.01) and enhanced PA-induced impairment of autophagy flux. Notably, these protective effects were abolished by cotreatment with 3-TYP, a selective Sirt3 inhibitor.

Conclusions: NMN alleviates HFD-induced myocardial damage in aging mice by activating the Sirt3/PINK1/Parkin signaling pathway and enhancing autophagy-lysosomal function. These findings indicate that NMN is a promising therapeutic candidate for the treatment of metabolic cardiomyopathy.

α-linolenic acid (ALA) is a naturally occurring omega-3 (ω-3) PUFA that is essential for human health but cannot be synthesized by the body and must be obtained through the diet. Studies have demonstrated that ALA offers a variety of health benefits, particularly showing potential in the prevention and adjunctive treatment of metabolic syndrome. In terms of lipid-lowering effects, ALA suppresses the expression of genes involved in cholesterol and triglyceride synthesis, while promoting the expression of genes related to fatty acid oxidation. In cardiovascular protection, ALA prevents or ameliorates atherosclerosis by improving endothelial function, inhibiting thrombosis, and reducing oxidative stress and inflammation. Although some clinical studies show that ALA can lower lipids, regulate blood glucose, and provide cardiovascular protection, other studies suggest that its effects may not be entirely consistent. Therefore, although ALA has potential value in regulating lipid metabolism, inflammatory responses, and cellular signaling pathways, especially in metabolic diseases and cardiovascular protection, its clinical effects still exhibit certain heterogeneity.

Background: Several risk factors for severe outcomes of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and vaccine responsiveness are related to aging and lifestyle-related conditions, like obesity-associated diabetes. Although vaccination reduces the risk of coronavirus disease 2019 symptoms, vaccine responsiveness in older or metabolically impaired individuals remains variable.

Objectives: This study examined the effects of quercetin glycoside (QG), a bioactive compound with anti-inflammatory and antiaging properties, taken before mRNA vaccination in older or metabolically at-risk individuals, focusing primarily on immune responses and secondarily on vaccine-related reactions.

Methods: In this randomized, double-blind, placebo-controlled, parallel-group study, participants consumed QG or a placebo daily for 4 wk before a mRNA SARS-CoV-2 booster. Each QG capsule contained 280 mg ± 5% of QG complex; 2 capsules were taken per day. Immune profiles were assessed for 3 mo post vaccination. Linear mixed-effects models evaluated changes in antibody titers and antigen-specific T-cell activation, including group, time, and their interaction as fixed effects, with age, sex, and BMI as covariates.

Results: A total of 50 participants (QG = 24; placebo = 26) were analyzed. Vaccine-induced antibody responses rose markedly after the booster in both groups, with similar kinetics and magnitudes. No significant differences were found between groups in neutralizing antibody titers or spike-specific immunoglobin G. Likewise, spike-specific cluster of differentiation 4 (CD4⁺) and CD8⁺ T-cell responses were comparable. The frequency and intensity of local and systemic vaccine-related reactions were also similar. The QG group showed a slightly lower median peak temperature (37.3°C compared with 37.9°C), though not significant.

Conclusions: Oral QG supplementation did not significantly alter vaccine immunogenicity or reactogenicity. A minor numerical trend toward lower temperature responses was observed, but it was not significant. These findings confirm that QG supplementation was well tolerated and highlight the exploratory nature of this trial. This trial was registered at UMIN as UMIN000046945.

Background: Zinc (Zn) is an essential trace element for bone growth and development and for maintaining bone mineral density (BMD). Although Zn deficiency is known to disrupt calcium (Ca) metabolism, it remains unclear whether this metabolic disturbance directly underlies the associated reduction in BMD.

Objectives: The study aimed to clarify how Zn deficiency affects BMD by disrupting systemic Ca metabolism.

Methods: This study consisted of 2 animal experiments. In experiment 1, 35-day-old male Wistar rats were fed a normal Zn diet (30 mg/kg; NZG), a low Zn diet (10 mg/kg; LZG), or a pair-fed Zn diet (30 mg/kg; PZG) for 4 wk. In experiment 2, 28-d-old male Wistar rats received the same dietary treatments for 5 wk. Femoral weight, length, morphology; and BMD; as well as Ca and calmodulin (CaM) concentrations were measured. Complementary cellular and molecular experiments were conducted to validate the in vivo findings and explore the underlying mechanisms. Group differences were evaluated using independent t-tests and analysis of variance.

Results: In both animal experiments, the LZG group demonstrated significantly lower femoral weight and BMD than the NZG and PZG groups (P < 0.05). In experiment 2, LZG rats additionally showed shorter femoral length, reduced trabecular number, and decreased cortical thickness. Furthermore, these rats exhibited lower Ca concentrations in urine, feces, and liver but higher concentrations in serum and skeletal muscle (P < 0.05), indicating that Zn deficiency perturbs systemic Ca distribution across tissues. Serum and skeletal muscle CaM concentrations were also reduced (P < 0.05). Corroborating these in vivo findings, low Zn culture conditions in mouse skeletal muscle cells elevated intracellular Ca concentrations and downregulated CaM expression at both mRNA and protein concentrations. Notably, overexpression of CaM1 reversed the intracellular Ca dysregulation induced by Zn deficiency.

Conclusions: Our results indicate that CaM plays a key role in Ca dysregulation and BMD reduction caused by Zn deficiency.