Genetically predicted dietary intake and risks of colorectal cancer: a Mendelian randomisation study.

BACKGROUND: Effects of confounders on associations between diet and colorectal cancer (CRC) in observational studies can be minimized in Mendelian randomization (MR) approach. This study aimed to investigate observational and genetically predicted associations between dietary intake and CRC using one-sample MR. METHODS: Using genetic data of over 93 million variants, we performed a genome-wide association study to find genomic risk loci associated with dietary intake in participants from the UK Biobank. Then we calculated genetic risk scores of diet-related variants and used them as instrumental variables in the two-stage least square MR framework to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for associations. We also performed observational analyses using age as a time-scale in Cox proportional hazard models. RESULTS: Allele scores were calculated from 399 genetic variants associated with the consumption of of red meat, processed meat, poultry, fish, milk, cheese, fruits, vegetables, coffee, tea, and alcohol in participants from the UK Biobank. In MR analysis, genetically predicted fruit intake was significantly associated with a 21% decreased risk of CRC (HR = 0.79, 95% CI = 0.66-0.95), and there was a marginally inverse association between vegetable intake and CRC (HR = 0.85, 95% CI = 0.71-1.02). However, null findings were observed in multivariable analysis, with HRs (95% CIs) of 0.99 (0.98-1.01) and 0.99 (0.98-1.00) per increment of daily servings of fruits and vegetables, respectively. CONCLUSION: Dietary habits were attributable to genetic variations, which can be used as instrumental variables in the MR framework. Our study supported a causal relationship between fruit intake and a decreased risk of CRC and suggested an effective strategy of consuming fruits in the primary prevention of CRC.

Bidirectional Mendelian randomization explores the causal relationship between dietary habits and rheumatoid arthritis.

Epidemiological and other studies have shown that the occurrence and progression of rheumatoid arthritis (RA) are closely related to diet. To further explore the causal association between dietary habits and RA, we performed a bidirectional Mendelian randomization (MR) analysis. The dataset related to dietary habits is from genome-wide association studies, including 143 dietary habits. The dataset of RA is from the FinnGen database. Inverse variance weighted (IVW), MR-Egger, simple mode, weighted median, and weighted mode were used for the 2-sample, 2-way MR analysis. At the same time, a variety of pleiotropic and heterogeneity tests were used to ensure the accuracy of the results. IVW results show that among current drinkers (drinks usually with meals yes + it varies vs no) was positively correlated with RA (ß, 0.563 [95% confidence interval [CI], 0.286-0.840]; P = 6.7 × 10-5). Spread type (low fat spread vs any other) was negatively correlated with RA (ß, -2.536 [95% CI, -3.725 to -1.346]; P = 2.9 × 10-5). In addition, the reverse MR results showed that RA was positively correlated with milk type (skimmed vs any other; ß, 0.006 [95% CI, 0.000-0.011]; P = 4.5 × 10-2). RA was positively correlated with spread type (tub margarine vs never; ß, 0.016 [95% CI, 0.002-0.029]; P = 2.5 × 10-2). The results of pleiotropy and heterogeneity tests showed that there was no pleiotropy (P > .05) in the obtained results. The analysis results of MR-Egger, simple mode, weighted median, and weighted mode are consistent with our IVW results. This study reveals a potential association between specific dietary habits and RA. Among current drinkers (drinks usually with meals yes + it varies vs no) was positively correlated with RA. Spread type (low fat spread vs any other) was negatively correlated with RA. RA was positively correlated with milk type (skimmed vs any other) and spread type (tub margarine vs never).

[Dietary adaptations and cardiovascular risk factors: what are the evidences ?] / Mesures diététiques et facteurs de risque cardiovasculaire : quelles évidences ?

An inadequate diet, either in its composition, preparation, or even in the processing of its components, plays a crucial role in the development of cardiovascular diseases, particularly through its effects on blood pressure, lipid and carbohydrate metabolism, as well as body weight. Non-pharmacological measures are an integral part of the prevention and management of cardiovascular risk factors, even before the introduction of specific medication. Based on literature, it is established that a so-called "healthy" diet has clear and well-demonstrated benefits, especially in early stages after diagnostic. This article provides a review of the available evidence and its impact regarding different nutritional modalities, particularly for the Mediterranean diet or equivalents.

Une alimentation non adaptée, que ce soit par sa composition, sa préparation ou par l'ultratransformation de ses composants, joue un rôle important dans le développement de maladies cardiovasculaires, notamment par son effet sur la pression artérielle et le métabolisme des lipides et des glucides, ainsi que sur le poids corporel. Les mesures non pharmacologiques font partie intégrante de la prévention et de la prise en charge des facteurs de risque cardiovasculaires, avant même l'introduction d'un traitement médicamenteux spécifique. Une diète dite « saine ¼ a des bénéfices nets et clairement démontrés dans la littérature, en particulier dans les phases précoces de prise en charge. Cet article revoit les évidences et impacts de différentes modalités nutritionnelles, notamment le régime méditerranéen (dietMED) et le DASH (dietary approches to stop hypertension).

The Impact of Japanese Dietary Patterns on Metabolic Dysfunction-Associated Steatotic Liver Disease and Liver Fibrosis.

This study aimed to investigate the effect of Japanese dietary patterns on metabolic dysfunction-associated steatotic liver disease (MASLD) and liver fibrosis. After excluding factors affecting the diagnosis of hepatic steatosis, 727 adults were analyzed as part of the Health Promotion Project. The dietary patterns of the participants were classified into rice, vegetable, seafood, and sweet based on their daily food intake. Liver stiffness measurements and controlled attenuation parameters were performed using FibroScan. Energy and nutrient intake were calculated using the Brief-type Self-administered Diet History Questionnaire. Univariate and multivariate analyses were used to identify the risk factors for liver fibrosis within the MASLD population. The vegetable group had significantly lower liver fibrosis indicators in the MASLD population than the rice group. The multivariate analysis identified a body mass index ≥ 25 kg/m2 (odds ratio [OR], 1.83; 95% confidence interval [CI], 1.01-1.83; p = 0.047) and HOMA-IR ≥ 1.6 (OR, 3.18; 95% CI, 1.74-5.78; p < 0.001) as risk factors for liver fibrosis, and vegetable group membership was a significant low-risk factor (OR, 0.38; 95% CI, 0.16-0.88; p = 0.023). The multivariate analysis of nutrients in low-risk foods revealed high intake of α-tocopherol (OR, 0.74; 95% CI, 0.56-0.99; p = 0.039) as a significant low-risk factor for liver fibrosis. This study suggests that a vegetable-based Japanese dietary pattern, through the antioxidant effects of α-tocopherol, may help prevent liver fibrosis in MASLD and the development of MASLD.

Association between dietary inflammatory index and disease activity in patients with ulcerative colitis.

Considering the influence of dietary factors on inflammatory markers that may affect the disease course in patients with ulcerative colitis (UC), this study aimed to assess the association between dietary inflammatory index (DII) score and disease activity in patients with ulcerative colitis. This cross-sectional study included 158 patients with UC. The Mayo Clinic score was used to determine the disease severity. A food frequency questionnaire was applied to gather the dietary information, then the Shivappa et al. method was used for the calculation of DII. An association between disease severity (dependent factor) and DII score quartiles (independent factors) was conducted by a logistic regression adjusted to different covariates. In this study, 53.8% of participants were in remission or had mild disease activity. The mean DII score was - 0.24 ± 0.66. The mean DII score was significantly lower in patients with remission (-0.34 ± 0.71) compared with patients who were in the active phase (-0.1 ± 0.57) of UC (P = 0.02). The results of the logistic regression analysis showed that after adjusting for confounding factors, the odds of severe disease were 3.33 times higher among patients who had a more pro-inflammatory diet compared with patients who had an anti-inflammatory diet [OR: 3.33 (95%CI: 1.13, 9.76), p = 0.02]. In conclusion, there was a significant association between higher intake of a pro-inflammatory diet and UC severity. So, from a clinical point of view, there is a need to apply an anti-inflammatory diet to decrease disease severity in patients with ulcerative colitis.

Dietary Inflammatory Index and Head and Neck Cancer: A Multicenter Case-Control Study in Iran.

BACKGROUND: The inflammatory potential of diet may affect carcinogenesis. This study aimed to determine the association between dietary inflammatory index (DII) and the risk of head and neck cancer (HNC), as well as the interaction between DII and cigarette smoking in HNC development within the Iranian population. Study Design: This is a case-control study. METHODS: In this multicenter case-control study, participants' dietary intake was assessed using a validated 130-item food frequency questionnaire, from which DII was computed. The study recruited 876 new cases from referral hospitals across 10 provinces and 3409 healthy controls who were frequency-matched based on age, gender, and residential place. Logistic regression was used to obtain odds ratios (ORs) for HNC across tertiles of DII, which were adjusted for confounding variables. RESULTS: A higher pro-inflammatory diet was associated with an increased risk of all HNC (OR T3 vs. T1 [95% CI]: 1.31 [1.06, 1.62]; P-trend=0.013). There was a significant association between lip and oral cavity cancers and DII (OR T3 vs. T1 [95% CI]: 1.56 [1.16, 1.66]; P-trend=0.004). Furthermore, an inflammatory diet was associated with an increased risk of pharynx cancer (OR T3 vs. T1 [95% CI]: 2.08 [1.14, 3.79]; P-trend=0.02). Additionally, no significant association was observed between DII and larynx cancer, while an interaction was found between DII and tobacco use on the risk of HNC (OR T3 vs. T1 [95% CI]: 2.52 [1.78, 3.57]; P-interaction=0.03). CONCLUSION: DII was positively associated with HNC risk. There was a significant association between DII and the risk of lip, oral cavity, and pharynx cancers. Additionally, there was an interaction between tobacco use and DII in determining the risk of HNC.

Incidence and risk factors for colorectal cancer in Africa: a systematic review and meta-analysis.

INTRODUCTION: Colorectal cancer (CRC) is the second leading cause of cancer-related death worldwide. There is a significant burden of mortality from colorectal cancer in Africa. Due to the heterogeneity of dietary and lifestyle practices throughout Africa, our work sought to define risk factors for the development of CRC in the African continent. METHODS: We systematically searched PubMed, Embase, Global Health, CINAHL, Cochrane CENTRAL, and African Index Medicus for studies written in English, examining the incidence and risk factors of CRC in Africa. A systematic analysis was done to compare different risk factors in constituent studies. A meta-analysis random effects model was fitted to estimate the pooled incidence of CRC. RESULTS: Of 2471 studies screened, 26 were included for the quantitative analysis; 20 in the incidence analysis, and six in the risk factor analysis. The overall ASIR per 100,000 person-years of CRC for males and females was 7.51 and 6.22, respectively. The highest incidence rates were observed between 2012 and 2021. Risk factors for CRC in Africa include tobacco smoking, and consumption of red meat, butter, and alcohol. Protective factors included, regular consumption of fruits and regular physical activity. CONCLUSION: The incidence of CRC in Africa is higher than that suggested by previous studies. Our study shows that nonmodifiable and modifiable factors contribute to CRC in Africa. High-quality studies conducted on generalizable populations that examine risk factors in a comprehensive fashion are required to inform primary and secondary prevention initiatives for CRC in Africa.

L-shaped association between dietary niacin intake and chronic kidney disease among adults in the USA: a cross-sectional study.

BACKGROUND: Chronic kidney disease (CKD), which has become a global public health issue, is associated with mitochondrial dysfunction. Niacin is a necessary coenzyme for mitochondrial energy metabolism. However, the association between dietary niacin intake and CKD remains uncertain. This study aimed to investigate the association between dietary niacin intake and CKD in American adults. METHODS: This is a cross-sectional study. 25,608 individuals aged ≥20 years from the National Health and Nutrition Examination Survey from 2007 to 2018 were involved.Dietary niacin intake was estimated based on 24-hour dietary recalls conducted by trained personnel. CKD was determined by an estimated glomerular filtration rate (eGFR) (<60 ml/min/1.73 m2) or a urinary albumin-to-creatinine ratio (ACR) (≥30mg/g). The association between dietary niacin intake and CKD was investigated using multivariable logistic regression analysis. RESULTS: Of 25,608 participants, 17.14% (4388/25,608) had CKD. Compared to individuals with lower niacin intake (quartile [Q]1, ≤15.30 mg/day), those with higher niacin intake in Q2 (15.31-22.07 mg/day), Q3 (22.08-31.09 mg/day), and Q4 (≥31.10 mg/day) exhibited adjusted odds ratios for CKD of 0.89 (95% confidence interval [CI]:0.81-0.99, p = 0.024), 0.83 (95% CI:0.75-0 .92, p < 0 .001), and 0.83 (95% CI:0.75-0.93, p = 0.001) respectively. The relationship between dietary niacin intake and CKD among U.S. adults follows an L-shaped pattern, with an inflection point at approximately 28.04 mg/day. CONCLUSIONS: These results suggest an L-shaped association between dietary niacin intake and CKD. Individuals with low dietary niacin intake levels should be alert to the risk of CKD.

Do Children's Health Behaviors Buffer the Impact of Cumulative Environmental Stress on Emerging Cardiometabolic Risk?

BACKGROUND: Previous studies have found that exposure to childhood environmental stress is associated with cardiometabolic risk. However, it is not known whether individual health behaviors disrupt this relationship. This study prospectively evaluated the relationship between cumulative environmental stress in a low-income sample and cardiometabolic risk in middle childhood and examined whether child health behaviors attenuated this relationship. METHODS AND RESULTS: In a cohort of children (n=338; 57% Hispanic children; 25% Black children), environmental stressors (family and neighborhood factors representing disadvantage/deprivation) and child health behaviors (accelerometry measured physical activity; parent-reported screen time and diet recalls) were measured over 5 time points beginning when children were aged 2 to 4 years and ending when they were aged 7 to 11 years. Children's cardiometabolic risk factors (body mass index, blood pressure, triglyceride/high-density lipoprotein ratio, glucose, hemoglobin A1c, C-reactive protein) were measured at 7 to 11 years. Emerging cardiometabolic risk was defined as having ≥1 elevations that exceeded clinical thresholds. In adjusted path analyses, greater cumulative environmental stress was associated with higher likelihood of emerging cardiometabolic risk in middle childhood (P<0.001). Higher levels of moderate to vigorous physical activity and fewer sedentary minutes attenuated the positive relationship between stress and cardiometabolic risk (P<0.05). Children with >2 hours of average daily screen time had a higher likelihood of elevated cardiometabolic risk (P<0.01), but screen time did not moderate the stress-cardiometabolic risk relationship. Dietary intake was not related to cardiometabolic risk. CONCLUSIONS: Interventions that promote moderate to vigorous physical activity and limit sedentary behavior may have particular importance for the cardiometabolic health of children exposed to high levels of cumulative environmental stress.

Dietary Carbohydrates, Genetic Susceptibility, and Gout Risk: A Prospective Cohort Study in the UK.

This study aimed to investigate the associations between carbohydrate intake and gout risk, along with interactions between genetic susceptibility and carbohydrates, and the mediating roles of biomarkers. We included 187,387 participants who were free of gout at baseline and completed at least one dietary assessment in the UK Biobank. Cox proportional hazard models were used to estimate the associations between carbohydrate intake and gout risk. Over a median follow-up of 11.69 years, 2548 incident cases of gout were recorded. Total carbohydrate intake was associated with a reduced gout risk (Q4 vs. Q1: HR 0.67, 95% CI 0.60-0.74), as were total sugars (0.89, 0.80-0.99), non-free sugars (0.70, 0.63-0.78), total starch (0.70, 0.63-0.78), refined grain starch (0.85, 0.76-0.95), wholegrain starch (0.73, 0.65-0.82), and fiber (0.72, 0.64-0.80), whereas free sugars (1.15, 1.04-1.28) were associated with an increased risk. Significant additive interactions were found between total carbohydrates and genetic risk, as well as between total starch and genetic risk. Serum urate was identified as a significant mediator in all associations between carbohydrate intake (total, different types, and sources) and gout risk. In conclusion, total carbohydrate and different types and sources of carbohydrate (excluding free sugars) intake were associated with a reduced risk of gout.

A U-shaped association between selenium intake and cancer risk.

While selenium is a cofactor of several antioxidant enzymes against cancer and is essential for human health, its excess intake may also be harmful. Though a safe intake of selenium has recently been recommended, it is not well understood in the Asian population. We aimed to determine the association between dietary intake of selenium and cancer risk in a case-control study of 3758 incident cancer cases (i.e., stomach, colon, rectum, lung cancers, and other sites) and 2929 control subjects in Vietnam. Daily intake of selenium was derived from a semiquantitative food frequency questionnaire. The unconditional logistic regression model was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for the association between selenium intake and cancer risk. We observed a U-shaped association between selenium intake and cancer risk. A safe intake ranged from 110.8 to 124.4 µg/day (mean 117.8 µg/day). Compared to individuals with the safe intake of selenium, individuals with the lowest intake (i.e., 27.8-77.2 µg/day) were associated with an increased risk of cancer (OR = 3.78, 95% CI 2.89-4.95) and those with the highest intake (169.1-331.7 µg/day) also had an increased cancer risk (OR = 1.86, 95% CI 1.45-2.39). A U-shaped pattern of association between selenium intake and cancer risk was stronger among participants with body mass index (BMI) < 23 kg/m2 and never smokers than BMI ≥ 23 kg/m2 and ever smokers (P'sheterogeneity = 0.003 and 0.021, respectively) but found in both never and ever-drinkers of alcohol (Pheterogeneity = 0.001). A U-shaped association between selenium intake and cancer risk was seen in cancer sites of the stomach, colon, rectum, and lung cancers. In summary, we found a U-shaped association between selenium intake and cancer risk and a safe selenium intake (mean: 117.8 µg/day) in the Vietnamese population. Further mechanistic investigation is warranted to understand better a U-shaped association between selenium intake and cancer risk.

The association between dietary zinc intake and osteopenia, osteoporosis in patients with rheumatoid arthritis.

BACKGROUND: Diet has been shown to be associated with rheumatoid arthritis (RA), of which osteoporosis is the most common and important complication, and zinc has been shown to inhibit the inflammatory response, but studies on the relationship between dietary zinc and osteoporosis in patients with RA are limited and inconclusive. In this study, we aimed to explore the relationship between dietary zinc intake and osteoporosis or osteopenia in patients with RA. METHODS: Data on RA patients were derived from the National Health and Nutrition Examination Survey (NHANES) 2007 to 2010, 2013 to 2014, and 2017 to 2020. Weighted univariate and multivariate logistic regression models were performed to explore the association between dietary zinc intake and osteoporosis or osteopenia in RA patients. The relationship was further investigated in different age, body mass index (BMI), nonsteroidal use, dyslipidemia, diabetes, and hypertension population. All results were presented as odds ratios (ORs) and confidence intervals (CIs). RESULTS: In total, 905 RA patients aged ≥ 40 years were included. After adjusting all covariates, higher dietary zinc intake was associated with lower odds of osteopenia or osteoporosis (OR = 0.39, 95%CI: 0.18-0.86) in RA patients. The relationship between dietary zinc intake ≥ 19.52 mg and lower odds of osteopenia or osteoporosis were also found in those aged ≥ 60 years (OR = 0.38, 95%CI: 0.16-0.91), BMI normal or underweight (OR = 0.16, 95%CI: 0.03-0.84), nonsteroidal use (OR = 0.14, 95%CI: 0.02-0.82), dyslipidemia (OR = 0.40, 95%CI: 0.17-0.92), diabetes (OR = 0.37, 95%CI: 0.14-0.95), and hypertension (OR = 0.37, 95%CI: 0.16-0.86). CONCLUSION: Higher dietary zinc intake was associated with reduced incidence of osteopenia or osteoporosis in patients with RA. Further longitudinal and randomized trials are necessary to validate our findings and explore the underling mechanisms. Adequate dietary zinc intake may beneficial to the bone health in RA patients.

Food biodiversity and gastrointestinal cancer risk in nine European countries: Analysis within a prospective cohort study.

BACKGROUND: Food biodiversity in human diets has potential co-benefits for both public health and sustainable food systems. However, current evidence on the potential relationship between food biodiversity and cancer risk, and particularly gastrointestinal cancers typically related to diet, remains limited. This study evaluated how dietary species richness (DSR) was associated with gastrointestinal cancer risk in a pan-European population. METHODS: Associations between DSR and subsequent gastrointestinal cancer risk were examined among 450,111 adults enrolled in the European Prospective Investigation into Cancer and Nutrition cohort (EPIC, initiated in 1992), free of cancer at baseline. Usual dietary intakes were assessed at recruitment with country-specific dietary questionnaires. DSR of an individual's yearly diet was calculated based on the absolute number of unique biological species in each food and drink item. Associations between DSR and cancer risk were assessed by multivariable Cox proportional hazards regression models. FINDINGS: During a median follow-up time of 14.1 years (SD=3.9), 10,705 participants were diagnosed with gastrointestinal cancer. Hazard ratios (HRs) and 95 % confidence intervals (CIs) comparing overall gastrointestinal cancer risk in the highest versus lowest quintiles of DSR indicated inverse associations in multivariable-adjusted models [HR (95 % CI): 0.77 (0.69-0.87); P-value < 0·0001] (Table 2). Specifically, inverse associations were observed between DSR and oesophageal squamous cell carcinoma, proximal colon, colorectal, and liver cancer risk (p-trend<0.05 for all cancer types). INTERPRETATION: Greater food biodiversity in the diet may lower the risk of certain gastrointestinal cancers. Further research is needed to replicate these novel findings and to understand potential mechanisms.

The contribution of dietary advanced glycation end-products and genetic risk in the development of inflammatory bowel disease: a prospective cohort study.

BACKGROUND: Dietary advanced glycation end products (AGEs) may promote oxidative stress and inflammation in the gastrointestinal tract. AIMS: The aim of this study is to investigate the association between dietary AGE intake and the risk of inflammatory bowel disease (IBD). METHODS: We included 121,978 participants without IBD at baseline from the UK Biobank. We estimated consumption of three common AGEs (Nε-(carboxymethyl)-lysine (CML), Nε-(1-carboxyethyl)-lysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1)) by matching 24-h dietary questionnaires to a validated dietary AGE database. We used Cox proportional hazards regression models to calculate the hazard ratio (HR) and 95% CI of the association between dietary AGEs and IBD risk. RESULTS: During a median follow-up of 13.72 years, 671 participants developed IBD (192 with Crohn's disease (CD) and 478 with ulcerative colitis (UC)). Among the assessed dietary AGEs, only CEL was associated with an increased risk of IBD (HR = 1.09, 95% CI: 1.01-1.18, p = 0.020) and CD (HR = 1.18, 95% CI: 1.03-1.36, p = 0.014), particularly for participants who were overweight, physically inactive, and non-smokers. Among participants at a high genetic risk of CD, HRs (95% CI) of CD were 1.26 (1.00-1.57) for CML, 1.41 (1.12-1.77) for CEL, and 1.28 (1.01-1.62) for MG-H1 (p < 0.05 for each). However, none of the dietary AGEs was significantly associated with UC risk, irrespective of genetic predisposition. CONCLUSIONS: Dietary CEL was associated with an increased risk of IBD and CD, but not UC. Further interventional studies are required to support the potential benefit of AGE restriction, especially for individuals at a high genetic risk of CD.

An In Vivo Model of Propionic Acid-Rich Diet-Induced Gliosis and Neuro-Inflammation in Mice (FVB/N-Tg(GFAPGFP)14Mes/J): A Potential Link to Autism Spectrum Disorder.

Evidence shows that Autism Spectrum Disorder (ASD) stems from an interplay of genetic and environmental factors, which may include propionic acid (PPA), a microbial byproduct and food preservative. We previously reported that in vitro treatment of neural stem cells with PPA leads to gliosis and neuroinflammation. In this study, mice were exposed ad libitum to a PPA-rich diet for four weeks before mating. The same diet was maintained through pregnancy and administered to the offspring after weaning. The brains of the offspring were studied at 1 and 5 months postpartum. Glial fibrillary acidic protein (astrocytic marker) was significantly increased (1.53 ± 0.56-fold at 1 M and 1.63 ± 0.49-fold at 5 M) in the PPA group brains. Tubulin IIIß (neuronal marker) was significantly decreased in the 5 M group. IL-6 and TNF-α expression were increased in the brain of the PPA group (IL-6: 2.48 ± 1.25-fold at 5 M; TNF-α: 2.84 ± 1.16-fold at 1 M and 2.64 ± 1.42-fold, at 5 M), while IL-10 was decreased. GPR41 and p-Akt were increased, while PTEN (p-Akt inhibitor) was decreased in the PPA group. The data support the role of a PPA-rich diet in glia over-proliferation and neuro-inflammation mediated by the GPR41 receptor and PTEN/Akt pathway. These findings strongly support our earlier study on the role of PPA in ASD.

Consumption of ultra-processed foods and the incidence of hypertension: a cohort study.

The incidence of hypertension (HTN) and consumption of ultra-processed foods are increasing worldwide. However, only a limited amount of research has assessed the causality between ultra-processed foods and the risk of HTN. Therefore, the present study aimed to determine the association between ultra-processed foods and the risk of HTN in a prospective cohort study. In the present study, we included 2399 individuals, aged approximately 19 years, who participated in the Tehran Lipid and Glucose Study (TLGS). The participants had complete dietary data and were free from HTN at baseline. We used the Cox proportional hazards model to determine the association between ultra-processed food intake and the risk of HTN occurrence, reporting the results as the hazard ratio (HR) and 95% confidence interval (95% CI). The mean age of participants was 37.6 years, and we followed them up for an average of 9.21 years. Our results indicated that participants in the highest tertile of ultra-processed foods had a 48% higher risk of HTN development (HR: 1.48; 95% CI: 1.23, 1.79) than those in the lowest tertile. We found a significant association between age and ultra-processed food intake in relation to the risk of HTN. The HR for developing HTN in participants aged <47 years was 1.99 (95% CI: 1.53, 2.58) and in participants aged ≥47 years was 1.26 (95% CI: 0.95, 1.68). Among the ultra-processed food components, consumption of industrial fat products had a positive correlation with the risk of HTN (HR: 1.04; 95% CI: 1.02 to 1.06). Our results suggest that consuming ultra-processed foods is associated with an increased incidence of HTN in adults. This association varied by age and was significant for adults younger than 47 years.

Dietary patterns and risk of Chronic Obstructive Pulmonary Disease (COPD) and clinical outcomes in diagnosed patients: A scoping review.

BACKGROUND & AIMS: Limited research exists on the association between dietary patterns (DP) and COPD risk or health-related outcomes. We reviewed existing literature to identify DP as a potential factor influencing COPD development and associated health outcomes in diagnosed individuals. METHODS: We followed the Joanna Briggs Institute methodology for this scoping review, conducting searches on PubMed, Scopus, Embase, and Web of Science to identify studies meeting our inclusion criteria (P, population - adults from the general population with or without COPD diagnosis; C, concept - DP; C, context - any setting). Two reviewers screened titles and abstracts, confirmed eligibility through full-text examination, extracted data using Redcap®, and assessed bias risk with the Newcastle Ottawa Scale. RESULTS: We analyzed 24 studies with sample sizes ranging from 121 to 421,426 individuals aged 20 to 75. Eighty-three percent investigated the role of DP in the COPD etiology, while 16.7 % examined health-related COPD outcomes. Food frequency questionnaires predominated (75 %) in exploring 23 distinct DP. Sixty-seven percent employed a priori-defined DP, focusing on the Mediterranean Diet (MedDiet) and Healthy Eating Index (HEI), while 33.3 % utilized a posteriori-defined DP, mainly represented by the Prudent and Traditional DP. Sixty percent of the studies reported significant associations between DP and COPD risk/odds. However, studies examining DP and COPD patient outcomes produced varied results. CONCLUSIONS: Most studies focused on assessing COPD risk using a priori-defined DP, particularly emphasizing the Med Diet and HEI. Overall, the studies found that healthy DPs are associated with reduced risk of COPD and improved outcomes in diagnosed patients.

Association between dietary copper intake and constipation in US adults.

Dietary micronutrients are integral to the development and progression of constipation; however, the specific relationship between dietary copper intake and constipation has not been thoroughly investigated. This study aims to examine the correlation between dietary copper intake and constipation among U.S. adults, thereby offering novel insights and recommendations for the clinical management and prevention of constipation. Bowel health data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2005 and 2010 were analyzed. Subjects' dietary information was collected through questionnaire records. Multivariate logistic regression analysis, subgroup analysis, and curve fitting analysis were used to assess the correlation between dietary copper intake and chronic constipation. After adjusting for all possible confounders, each unit increase in dietary copper intake (converted to natural logarithms) was associated with a 20% reduction in the prevalence of constipation (OR = 0.80; 95% CI 0.65-0.98; P = 0.037). The interaction P-values for all subgroups were greater than 0.05, indicating that the findings were stable and consistent across subgroups. The present study showed a significant negative association between dietary copper intake and chronic constipation in adults. This finding raises clinical and healthcare professionals' awareness of the impact of dietary trace elements on intestinal health and has important implications for the development of personalized meal plans and rational supplementation of trace copper in patients with constipation.

A methionine-choline-deficient diet induces nonalcoholic steatohepatitis and alters the lipidome, metabolome, and gut microbiome profile in the C57BL/6J mouse.

The methionine-choline-deficient (MCD) diet-induced non-alcoholic steatohepatitis (NASH) in mice is a well-established model. Our study aims to elucidate the factors influencing liver pathology in the MCD mouse model by examining physiological, biochemical, and molecular changes using histology, molecular techniques, and OMICS approaches (lipidomics, metabolomics, and metagenomics). Male C57BL/6J mice were fed a standard chow diet, a methionine-choline-sufficient (MCS) diet, or an MCD diet for 10 weeks. The MCD diet resulted in reduced body weight and fat mass, along with decreased plasma triglyceride, cholesterol, glucose, and insulin levels. However, it notably induced steatosis, inflammation, and alterations in gene expression associated with lipogenesis, inflammation, fibrosis, and the synthesis of apolipoproteins, sphingolipids, ceramides, and carboxylesterases. Lipid analysis revealed significant changes in plasma and tissues: most ceramide non-hydroxy-sphingosine lipids significantly decreased in the liver and plasma but increased in the adipose tissue of MCD diet-fed animals. Oxidized glycerophospholipids mostly increased in the liver but decreased in the adipose tissue of the MCD diet-fed group. The gut microbiome of the MCD diet-fed group showed an increase in Firmicutes and a decrease in Bacteroidetes and Actinobacteria. Metabolomic profiling demonstrated that the MCD diet significantly altered amino acid biosynthesis, metabolism, and nucleic acid metabolism pathways in plasma, liver, fecal, and cecal samples. LC-MS data indicated higher total plasma bile acid intensity and reduced fecal glycohyodeoxycholic acid intensity in the MCD diet group. This study demonstrates that although the MCD diet induces hepatic steatosis, the mechanisms underlying NASH in this model differ from those in human NASH pathology.