Nutrition & Metabolism最新文献

Background: The Planetary Health Diet proposed by the EAT-Lancet Commission aims to promote global health and environmental sustainability through a predominantly plant-based, carbohydrate-rich nutritional model. Despite its appeal, its universal application raises concerns regarding human metabolic compatibility, nutrient sufficiency, and evolutionary coherence.

Objectives: This article critically evaluates the Planetary diet through the lenses of evolutionary biology, clinical nutrition, cancer metabolism, and anthropological diversity. An alternative framework is proposed: The autogenous diet, which aligns more with human physiological and ecological heritage.

Methods: A narrative synthesis was conducted of peer-reviewed literature from evolutionary nutrition, clinical trials, oncology, and chronobiology. Comparative analysis highlights the metabolic divergence between high-carbohydrate, standardized diets and fat-adapted, ancestral nutritional models.

Results: The planetary diet fails to meet several human biological requirements. It neglects nutrient-dense animal foods rich in DHA, vitamin B12, and bioavailable iron; promotes chronic glycemic load and insulin signaling; and ignores interindividual genetic and epigenetic variability. By contrast, the autogenous diet contains a species-appropriate macronutrient distribution (moderate protein, high fat, low carbohydrate), prioritizes local and minimally processed foods, aligns with circadian biology and fasting cycles, and elicits tumor-suppressive mechanisms.

Conclusion: The universalization of the planetary diet represents a biological and cultural oversimplification. Nutritional strategies must account for evolutionary metabolism, regional diversity, and clinical outcomes. Ancestral, autogenous diets may offer a more effective and ecological solution that can meet nutritional requirements based on fundamental physiology.

Background: The complex interaction of food habits, stress levels, and gut microbiota is instrumental in shaping global human well-being. Lifestyle indicators like diet, stress, and exercise have immense potential to drive gut health but are usually plagued by the divide between knowledge and action.

Methodlogy: This research compared lifestyle variables and awareness of gut health in 51 participants on a standardized questionnaire. It analyzed variables such as frequency of meals, intake of processed foods, intake of dietary fiber and probiotics, history of digestive diseases, perceived influence of stress, and knowledge of the gut-brain axis.

Results: Results indicated that 69.05% of the participants ate only 1-2 meals a day, and 71.43% had moderate consumption (1-2 times per week) of fast or processed foods. A concerning fact is that only 7.14% ate probiotic foods daily, and only 28.57% had high-fiber foods in their daily diet. Gastrointestinal problems were prevalent, with 56.41% having issues and 51.28% having occasional problems (1-2 times per week). In addition, 66.67% thought that stress influences their digestion, and 74.36% experienced changes in diet influencing their gut. Just 13.16% were physically active daily, and 44.74% slept for less than six hours daily, both are known to influence the gut microbiome. While 76.32% understood the diet-stress-microbiota connection, just 57.89% were of the view that dietary modifications can help manage stress.

Conclusion: The research points to an important gap between knowledge and practical behaviors concerning gut health and stress management. There is a need for public health programs to enhance sustainable lifestyle and dietary changes to improve microbial diversity, digestive well-being, and mental health.

Background: Metabolic comorbidities related to obstructive sleep apnoea (OSA) are a major concern in regarding OSA prognosis and complexity. However, few studies have investigated the interrelationships among these metabolic comorbidities. We explored the associations among insulin resistance (IR), the waist-to-hip ratio (WHR), and OSA using innovative and rigorous statistical methods.

Methods: We enrolled 5,326 subjects after meticulous recording anthropometric, biochemical, and standard polysomnographic parameters. The relationships among IR, WHR, and OSA were analyzed using confirmatory factor analysis (CFA) as well as moderation and mediation analyses.

Results: CFA showed that IR and obesity were strongly correlated (loading = 0.73, p < 0.001). OSA was associated with both obesity and IR (loading = 0.57, p < 0.001; loading = 0.46, p < 0.001, respectively). Obesity was strongly associated with both the body mass index (BMI) and the WHR (loading = 0.82, p < 0.001; loading = 0.67, p < 0.001, respectively). WHR served as a moderator; the interaction effect between WHR and IR on the apnoea-hypopnea index (AHI) was significant (coefficient = - 2.451; p = 0.023). Mediation analyses showed that WHR explained 14.93%, 14.02%, and 13.10% of the associations between IR and AHI, the oxygen desaturation index, and the micro-arousal index, respectively.

Conclusion: Multifactorial relationships are apparent among IR, WHR, and OSA. The complex interrelationships highlight the intricate clinical interactions among metabolic dysfunction, central obesity, and sleep-disordered breathing, emphasizing the multifaceted nature of OSA and its related health implications.

Introduction: The association between calcium (Ca) intake and incidence of type 2 diabetes mellitus (T2DM) remains still inconclusive. We investigated the association of total and food source-specific Ca intake and the incidence of T2DM in Iranian adults.

Methods: This cohort study was conducted on adult Iranian men and women (n = 2,458 subjects, mean age 39.3 ± 13.4 years, 1130 men (46%) and 1328 women (54%)), free of T2DM, who were assessed for Ca intake at baseline (2006-2008) and were followed up to 2018-2022. To evaluate potential non-linear associations between dietary calcium intake and T2DM risk, we employed univariate unrestricted regression spline analysis. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the risk of developing T2DM across quartiles and per each 100 mg/d of total and food-specific Ca intake.

Results: During the study follow-up, 353 subjects with T2DM were diagnosed. Mean daily Ca intake was 1,313 ± 526 mg/day, mainly from dairy and plant-based foods (51.62 and 40.08%, respectively), and the remaining from the processed and ultra-processed foods (UPFs) and animal sources (2.23 and 6.07%, respectively). Dairy sources contributed a Ca intake of 704 ± 393 mg/day. Higher intake of dietary Ca from plant-based foods (> 640 vs. <322 mg/day) was associated with a decreased risk of T2DM by 40% (HR = 0.60, 95% CI = 0.41-0.87). Conversely, higher Ca intake from processed and UPFs (> 100 vs. <28.6 mg/day) increased T2DM risk (HR = 1.53, 95%CI = 1.10-2.13). Furthermore, each 100 mg/day increase in dietary Ca from processed and UPFs raised the risk of T2DM (HR = 1.26, 95% CI = 1.04-1.52). Intake of Ca from dairy was not associated with the incidence of T2DM (HR = 0.98, 95% CI = 0.95-1.01).

Conclusion: A higher intake of dietary Ca from plant-based foods shows an inverse association with risk of T2DM. Conversely, increased consumption of Ca from processed and UPFs seems to be a risk factor for developing T2DM. These findings suggest that the source of dietary Ca may play a significant role in T2DM risk, highlighting the importance of food choices in managing health outcomes.

Background: Few studies, with inconsistent results, have been conducted to examine the effect of protein and amino acid consumption on non-alcoholic fatty liver disease (NAFLD). Therefore, this study aimed to assess the relationship between dietary intake of amino acids or groups of amino acids and the risk of NAFLD.

Methods: This case-control study included 171 participants with NAFLD and 730 controls from Tehran, Iran. A validated Food frequency questionnaire (FFQ) with 168 items, was used to evaluate dietary information. Odds ratios (ORs) and corresponding confidence intervals (CIs) were calculated by regression models, adjusted for potential confounders including age, sex, body mass index (BMI), smoking status, physical activity, history of diabetes mellitus, and total energy intake.

Results: The mean ± standard deviation (SD) age of participants was 43.26 ± 13.9 years. Intake of total protein and all amino acids was significantly higher in patients with NAFLD than in the control group (P < 0.001). Increased risk of developing NAFLD compared to the reference quartile was observed in the highest quartiles of dietary isoleucine (OR, 4.72; 95%CI, 1.57-14.19), tyrosine (OR, 5.11, 95%CI, 1.73-15.05), threonine (OR, 3.47; 95%CI, 1.16-10.33), and valine (OR, 4.51; 95%CI, 1.45-14.02) intake. Subgroup analysis by sex revealed that in the females, the OR for NAFLD were 0.36 (95%CI, 0.13-0.98) among those with the highest intake of non-essential amino acids, and 2.78 (95%CI, 1.02-7.50) among those with the highest intake of essential amino acids compared to those in the first quartile. However, there was no significant trend among male cases.

Conclusion: Consumption of specific amino acids might be associated with odds of NAFLD.

Background: Although nutritional support is crucial in intensive care, the impact of protein intake remains unclear, emphasizing the need for further randomized controlled trials. This study aimed to evaluate the effects of high-protein versus conventional-protein nutritional support on clinical outcomes in critically ill patients, with 60-day mortality as the primary endpoint.

Method: In this double-blind, two-arm, parallel-group randomized controlled trial, 56 adult patients admitted to the intensive care unit [1] were enrolled. Participants received either high-protein support (2.2 g/kg/day, actual body weight [ABW]) or conventional-protein support (1.0 g/kg/day, ABW) for 12 days. Both groups targeted 25 kcal/kg/day energy intake. Patients and data analysts were blinded. Mortality was assessed at ICU discharge, on days 28 and 60, and at hospital discharge. Hospital mortality was defined as any death occurring during the hospital stay, including both the ICU and post-ICU periods. Mid-arm circumference (MAC) was measured as an indicator of muscle attenuation.

Results: Mean protein intake was 1.67 ± 0.33 vs. 0.93 ± 0.10 g/kg/day in high- vs. conventional-protein groups (P < 0.05). In-hospital mortality was significantly lower in the high-protein group (8 patients [28.6%]) compared to the conventional-protein group (16 patients [57.1%]; adjusted P = 0.049). Although 60-day mortality was also lower in the high-protein group (28.6% vs. 53.6%), the difference did not reach statistical significance (adjusted P = 0.07). A significant reduction in MAC attenuation was observed in the high-protein group (P < 0.001).

Conclusion: High-protein intake (1.67 g/kg/day) significantly reduced in-hospital mortality and improved preservation of muscle mass. Although 60-day mortality reduction was not significant, the trend suggests a meaningful benefit warranting further study.

Irct registration id: IRCT20180619040151N4.

Bone, a vital component of the human body, plays a crucial role in maintaining mobility and systemic health. Growing evidence underscores the complex interplay between a high-fat diet (HFD), intestinal microecology, and bone loss. This review consolidates findings across three interconnected mechanisms: (1) HFD compromises bone homeostasis by reducing bone mineral density (BMD) and disrupting microarchitecture, driven by bone marrow adiposity, oxidative stress, and chronic inflammation; (2) HFD disrupts intestinal microecology through microbiota dysbiosis (e.g., elevated Firmicutes/Bacteroidetes ratio, depletion of Bifidobacterium), epithelial barrier impairment (e.g., suppressed Mucin2 secretion, downregulated tight junction proteins), and immune dysregulation (e.g., Th17/Treg imbalance, diminished IL-10 production); and (3) intestinal microecology imbalances exacerbate bone loss through microbial metabolite alterations (e.g., a deficiency of short-chain fatty acids impairing Treg-mediated Wnt10b signaling), systemic inflammation from barrier leakage, and intestinal immune cell trafficking (e.g., Th17 migration to bone marrow). These interconnected mechanisms point to an indirect pathway by which HFD contributes to bone loss through alterations in intestinal microecology. While this indirect relationship remains insufficiently validated, accumulating evidence highlights the important roles of HFD and intestinal microecology in bone regulation. This review aims to comprehensively examine the connections between HFD, intestinal microecology, and bone loss, with a focus on elucidating these potential mechanisms. Given diet's profound impact on intestinal microecology, optimizing dietary patterns to rebalance intestinal microecology offers a promising strategy for preventing and treating bone-related disorders.

Background: Lipid accumulation product (LAP) has recently gained attention as a novel indicator of metabolic dysfunction. However, the association between LAP and sarcopenia, a metabolic condition characterized by loss of muscle mass, strength, and function, remains unclear. This study aimed to explore the relationship between LAP and both the prevalence and incidence of sarcopenia using data from the China Health and Retirement Longitudinal Study (CHARLS).

Methods: Sarcopenia was defined according to the criteria established by the Asian Working Group for Sarcopenia in 2019. LAP was calculated using waist circumference and triglyceride levels. A cross-sectional analysis was performed with 7,004 participants from the baseline survey, utilizing logistic regression models to evaluate the association between LAP and sarcopenia prevalence. Additionally, a longitudinal cohort analysis involved 4,484 individuals who were free of sarcopenia at baseline and followed from 2011 to 2015. Cox proportional hazards models were employed to assess the longitudinal association between baseline LAP levels and incident sarcopenia. Furthermore, restricted cubic spline regression (RCS) and subgroup analyses were conducted to explore potential nonlinear relationships and differences across various subgroups. Receiver operating characteristic (ROC) curves was used to evaluate the discriminatory ability of LAP for identifying sarcopenia.

Results: Cross-sectional analyses and RCS revealed a significant inverse linear relationship between LAP and the prevalence of sarcopenia [odds ratio (OR) = 0.95, 95% confidence interval (CI): 0.94-0.96]. Participants within the highest LAP tertile demonstrated substantially lower odds of sarcopenia compared to those in the lowest tertile (OR = 0.21, 95% CI: 0.14-0.31). Longitudinal analyses similarly indicated that elevated LAP levels were associated with reduced sarcopenia incidence, with the highest LAP tertile associated with notably decreased risk (HR = 0.17, 95% CI: 0.11-0.27). The nonlinear pattern identified through RCS analysis indicated significant risk reductions up to a LAP threshold of 27.577. Furthermore, subgroup analyses consistently supported this inverse association across various demographic and clinical subgroups. Finally, diagnostic performance of LAP was assessed using the ROC curve (0.763 ([CI]: 0.744-0.783) in the longitudinal study).

Conclusions: Elevated LAP levels are inversely associated with both the prevalence and incidence of sarcopenia among middle-aged and elderly adults in China. These findings suggest LAP could serve as a useful metabolic indicator for predicting reduced sarcopenia risk, warranting additional studies to confirm and further elucidate these relationships.

Background: This study investigated the association of specific sweet-taste and obesity-related genes with sweetener consumption patterns among children and the interaction between these genetic factors and sweetener intake on the risk of childhood obesity. By leveraging data from the Taiwanese Pubertal Longitudinal Study (TPLS), the current study minimized the influence of environmental confounders commonly encountered in adult studies, offering a more precise understanding of these relationships in pediatric and adolescent populations.

Methods: Participants in the TPLS underwent genetic sampling, anthropometric measurements, puberty stage assessments, dietary recall, and measurements of relevant lifestyle variables. Nonnutritive sweetener (NNS) intake was assessed using the validated Nonnutritive Sweetener Food Frequency Questionnaire (NNS-FFQ). The statistical analysis employs logistic regression to investigate the correlations between genotypes and sweetener consumption, while accounting for potential confounders such as parental education and household income. Simultaneously, the study examines gene-sweetener interactions to assess the association between specific alleles and particular sweetener consumption patterns.

Results: Higher consumption of specific artificial sweeteners-acesulfame potassium, sucralose, and steviol-was associated with lower body mass index (BMI) Z-scores and reduced body fat percentage. The interaction analyses indicated a significantly positive association of the interaction between sucralose consumption and sweet-taste genes on the waist-hip ratio. Genetic analysis revealed significant associations between obesity-related genes (e.g., ADCY9 and TFAP2B) and sweet-taste receptor genes (e.g., TAS1R2 and TAS1R3) with sweetener consumption, which may influence susceptibility to obesity. Notably, rs7498665 was significantly associated with BMI Z-scores, underscoring its role in obesity predisposition.

Conclusions: These findings highlight the genetic underpinnings of sweetener consumption and its interactive effects with genetic variants on childhood obesity risk, providing valuable insights for promoting public health and developing personalized nutrition strategies. Future research involving larger samples and consideration of genetic and environmental factors is required to develop personalized nutrition strategies aimed at effectively combating childhood obesity.