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Ning Chen,1,2 Iram Faqir Muhammad,2 Zhibin Li,3 Peter M Nilsson,2,4 Yan Borné2 1Department of Endocrinology, Xiamen Branch, Zhongshan Hospital, Fudan University, Xiamen, People’s Republic of China; 2Department of Clinical Sciences in Malmö, Lund University, Malmö, Sweden; 3Epidemiology Research Unit, The First Affiliated Hospital, Xiamen University, Xiamen, People’s Republic of China; 4Department of Internal Medicine, Skåne University Hospital, Malmö, SwedenCorrespondence: Yan Borné; Ning Chen Email yan.borne@med.lu.se; ningchen8080@outlook.comObjective: To explore the longitudinal, as well as sex-specific, associations between circulating uric acid (UA) and diabetes incidence.Methods: A cohort study of the Malmö Diet Cancer-cardiovascular Cohort (Malmö, Sweden) consisting of 3140 individuals without diabetes at baseline, was followed up until the end of 2018. Incident diabetes cases were identified by linking to local and national diabetes registers. Cox proportional hazard regression was used to assess plasma UA levels in relation to diabetes incidence with adjustment for established confounders.Results: At baseline, with increasing levels of UA, subjects were more likely to be older and have significantly higher body mass index, waist circumference, triglycerides, C-reactive protein, fasting glucose and 2-h plasma glucose postoral glucose tolerance test, and lower levels of high-density lipoprotein. During a mean follow-up period of 8.09± 2.24 years, 315 (10.0%) participants developed diabetes, and diabetes incidence rates were 7.89, 9.48 and 18.11 per 1000 person-years for subjects in the 1st, 2nd, and 3rd tertiles of UA, respectively (log-rank test: p< 0.001). With adjustment for potential confounders, elevated UA levels were significantly associated with increased risks of diabetes incidence, with the adjusted hazard ratio (HR) (95% confidence interval) for per standard deviation increment of UA of 1.22 (1.08– 1.39, p=0.002). Compared with the 1st tertile of UA, the 3rd tertile showed significantly increased risk of diabetes incidence with the adjusted HR of 1.74 (1.24– 2.45, p=0.002), and there was a significant trend between increasing tertiles of UA and diabetes incidence (trend test: p< 0.001). Stratified analyses showed that elevated circulating UA levels were independently associated with increased risks of diabetes incidence in men but not in women, although the interaction between sex and UA was not statistically significant.Conclusion: Elevated circulating UA was independently associated with increased risk of diabetes incidence, especially for men.Keywords: cohort study, diabetes incidence, longitudinal, stratified analysis, uric acid

Objectives Red blood cell distribution width ( RDW), a measure of variation in erythrocyte volume, has been associated with several cardiovascular disorders, but the relationship with atrial fibrillation ( AF) remains unclear. We investigated the association between RDW and incidence of first hospitalization due to AF in a population-based cohort. Design Red blood cell distribution width was measured in 27 124 subjects from the general population (age 45-73 years, 62% women) with no history of AF, heart failure, myocardial infarction or stroke. The association between baseline RDW and incidence of AF identified from the Swedish Hospital Discharge Register was evaluated. Results During a mean follow-up of 13.6 years, 1894 subjects (53% men) were hospitalized with a diagnosis of AF. After adjustment for potential confounding factors, including cardiovascular disease risk factors, nutrient intake (iron, vitamin B12 and folate) and several haematological parameters (haemoglobin concentration, mean corpuscular volume and corpuscular haemoglobin content), the hazard ratio ( HR) for incidence of AF was 1.33 [95% confidence interval ( CI) 1.16-1.53] for the fourth versus first quartile of RDW ( P for trend <0.001). The results were essentially unchanged when subjects with incident myocardial infarction or hospitalizations because of heart failure were censored from the analysis ( HR 1.30, 95% CI 1.13-1.51; P for trend = 0.001). Conclusion Red blood cell distribution width was associated with incidence of AF independently of several cardiovascular, nutritional and haematological factors in this study of middle-aged subjects from the general population. [ABSTRACT FROM AUTHOR]

Abstract Background Studies from Sweden have reported association between immigrant status and incidence of cardiovascular diseases. The nature of this relationship is unclear. We investigated the relationship between immigrant status and risk of heart failure (HF) hospitalization in a population-based cohort, and to what extent this is mediated by hypertension and life-style risk factors. We also explored whether immigrant status was related to case-fatality after HF. Methods 26,559 subjects without history of myocardial infarction (MI), stroke or HF from the community-based Malmö Diet and Cancer (MDC) cohort underwent a baseline examination during 1991-1996. Incidence of HF hospitalizations was monitored during a mean follow-up of 15 years. Results 3,129 (11.8%) subjects were born outside Sweden. During follow-up, 764 subjects were hospitalized with HF as primary diagnosis, of whom 166 had an MI before or concurrent with the HF. After adjustment for potential confounding factors, the hazard ratios (HR) for foreign-born were 1.37 (95% CI: 1.08-1.73, p = 0.009) compared to native Swedes, for HF without previous MI. The results were similar in a secondary analysis without censoring at incident MI. There was a significant interaction (p < 0.001) between immigrant status and waist circumference (WC), and the increased HF risk was limited to immigrants with high WC. Although not significant foreign-born tended to have lower one-month and one-year mortality after HF. Conclusions Immigrant status was associated with long-term risk of HF hospitalization, independently of hypertension and several life-style risk factors. A significant interaction between WC and immigrant status on incident HF was observed.

Background & Aims: Epidemiological evidence on ultra-processed food (UPF) and cause-specific mortality remains limited and mixed. Molecular mechanisms underlying UPF intake and mortality remain unexplored. This study aimed to evaluate the associations between UPF consumption, metabolic signatures, and all-cause, premature, and cause-specific mortality., Methods: This study included 27670 participants (mean age 58.1 years) from the Malmö Diet and Cancer (MDC) cohort study. Consumption of UPF was assessed using a food frequency questionnaire and a 7-day food diary. In a subset of the MDC (n = 879), the associations of UPF with 991 plasma metabolites were investigated. An elastic net regression model was used to establish the metabolic signature of UPF. Cox proportional hazards regression model was used to determine the association between UPF intake, metabolic signature, and mortality risk., Results: During a median follow-up of 23.3 years, a total of 11333 participants died. UPF intake showed a nonlinear positive association with all-cause mortality, with more pronounced associations found in females (P interaction  = 0.044); in females, UPF was linked to a higher mortality risk in a linear manner, while the association was J-shaped in males. Each standard deviation (SD) increment in UPF intake was associated with an increased risk of premature mortality (HR, 1.06; 95 % CI, 1.03-1.09), cardiovascular disease (CVD) mortality (HR, 1.05; 95 % CI, 1.01-1.08) or respiratory disease mortality (HR, 1.08; 95 % CI, 1.01-1.15), but not cancer mortality. The metabolic signature for UPF consumption (with 93 metabolites) was positively associated with all-cause mortality risk (HR per 1 SD, 1.23; 95 % CI, 1.06-1.42)., Conclusions: Our results suggest that higher UPF intake is associated with increased risk of all-cause, premature, CVD, and respiratory disease mortality, with the association varying across sex for all-cause mortality. The plasma metabolic signature of UPF showed a positive association with all-cause mortality., Competing Interests: Conflict of interest The authors declare no conflict of interest., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Context: Cardiometabolic multimorbidity (CM) is an increasing public health concern. Previous observational studies have suggested inverse associations between coffee, tea, and caffeine intake and risks of individual cardiometabolic diseases; however, their associations with CM and related biological markers are unknown., Methods: This prospective study involved 172 315 (for caffeine analysis) and 188 091 (tea and coffee analysis) participants free of any cardiometabolic diseases at baseline from the UK Biobank; 168 metabolites were measured among 88 204 and 96 393 participants. CM was defined as the coexistence of at least 2 of the following conditions: type 2 diabetes, coronary heart disease, and stroke., Results: Nonlinear inverse associations of coffee, tea, and caffeine intake with the risk of new-onset CM were observed. Compared with nonconsumers or consumers of less than 100 mg caffeine per day, consumers of moderate amount of coffee (3 drinks/d) or caffeine (200-300 mg/d) had the lowest risk for new-onset CM, with respective hazard ratios (95% CIs) of 0.519 (0.417-0.647) and 0.593 (0.499-0.704). Multistate models revealed that moderate coffee or caffeine intake was inversely associated with risks of almost all developmental stages of CM, including transitions from a disease-free state to single cardiometabolic diseases and subsequently to CM. A total of 80 to 97 metabolites, such as lipid components within very low-density lipoprotein, histidine, and glycoprotein acetyls, were identified to be associated with both coffee, tea, or caffeine intake and incident CM., Conclusion: Habitual coffee or caffeine intake, especially at a moderate level, was associated with a lower risk of new-onset CM and could play important roles in almost all transition phases of CM development. Future studies are warranted to validate the implicated metabolic biomarkers underlying the relation between coffee, tea, and caffeine intake and CM., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com. See the journal About page for additional terms.)

Background: Epidemiological evidence on weight change and atrial fibrillation (AF) remains limited and inconsistent. Previous studies on body mass index (BMI) in youth and AF rarely considered subsequent BMI. This study aimed to assess the associations of AF with weight change and BMI in youth, as well as modified effect by genetic susceptibility of AF., Methods: The study included 21,761 individuals (mean age 57.8 years) from the Malmö Diet and Cancer cohort. Weight information was obtained at three time points, including recalled weight at age 20 years, measured weight at baseline (middle adulthood), and reported weight at 5-year follow-up examination (late middle adulthood). A weighted genetic risk score of AF was created using 134 variants., Results: During a median follow-up of 23.2 years, a total of 4038 participants developed AF. The association between weight change from early to middle adulthood and AF risk was modified by sex (P interaction  = 0.004); weight loss was associated with a lower AF risk in females, but not in males. Conversely, weight gain was positively associated with AF risk in a linear manner in females, whereas increased AF risk appeared only when weight gain exceeded a threshold in males. Participants with weight gain of > 5 kg from middle to late middle adulthood had a 19% higher risk of AF relative to those with stable weight, whereas weight loss showed a null association. Compared to individuals with a lower BMI at age 20 years, those with a BMI above 25 kg/m 2 had an increased risk of AF (HR = 1.14; 95% CI: 1.02-1.28), after controlling for baseline BMI; this association was more pronounced in males or those with a lower genetic risk of AF., Conclusions: Weight gain in middle adulthood was associated with higher AF risk. Weight loss from early to middle adulthood, but not from middle to late middle adulthood, was associated with a lower risk of AF only in females. Higher BMI in youth was associated with an increased risk of AF, particularly among males or those with a lower genetic risk of AF., (© 2024. The Author(s).)

Background and Aims: The EAT-Lancet Commission devised a globally sustainable dietary pattern to jointly promote human health and sustainability. However, the extent to which this diet supports metabolic dysfunction-associated steatotic liver disease (MASLD) has not yet been assessed. This study aimed to investigate the association between the EAT-Lancet diet and the risk of MASLD and its severity., Approach and Results: This prospective multicohort study included 15,263 adults from the Tianjin Chronic Low-grade Systemic Inflammation and Health (TCLSIH) cohort, 1137 adults from the Guangzhou Nutrition and Health Study (GNHS) cohort, and 175,078 adults from the UK Biobank. In addition, 228 Chinese adults from the Prospective Epidemic Research Specifically of Non-alcoholic Steatohepatitis (PERSONS) with biopsy-proven MASLD were included. An EAT-Lancet diet index was created to reflect adherence to the EAT-Lancet reference diet. The TCLSIH cohort recorded 3010 MASLD cases during 53,575 person-years of follow-up, the GNHS cohort documented 624 MASLD cases during 6454 person-years of follow-up, and the UK Biobank developed 1350 MASLD cases during 1,745,432 person-years of follow-up. In multivariable models, participants in the highest tertiles of the EAT-Lancet diet index had a lower risk of MASLD compared with those in the lowest tertiles (TCLSIH: HR = 0.87, 95% CI: 0.78, 0.96; GNHS: HR = 0.79, 95% CI: 0.64, 0.98; UK Biobank: HR = 0.73, 95% CI: 0.63, 0.85). Moreover, liver-controlled attenuation parameter decreased with increasing the diet index in individuals with biopsy-proven MASLD (β = -5.895; 95% CI: -10.014, -1.775)., Conclusions: Adherence to the EAT-Lancet reference diet was inversely associated with the risk of MASLD as well as its severity., (Copyright © 2024 American Association for the Study of Liver Diseases.)

High-quality diets have been increasingly acknowledged as a promising candidate to counter the growing prevalence of mental health disorders. This study aims to investigate the prospective associations of adhering to the EAT-Lancet reference diet with incident depression, anxiety and their co-occurrence in 180,446 UK Biobank participants. Degrees of adherence to the EAT-Lancet diet were translated into three different diet scores. Over 11.62 years of follow-up, participants in the highest adherence group of the Knuppel EAT-Lancet index showed lower risks of depression (hazard ratio: 0.806, 95% CI: 0.730-0.890), anxiety (0.818, 0.751-0.892) and their co-occurrence (0.756, 0.624-0.914), compared to the lowest adherence group. The corresponding hazard ratios (95% CIs) were 0.711 (0.627-0.806), 0.765 (0.687-0.852) and 0.659 (0.516-0.841) for the Stubbendorff EAT-Lancet index, and 0.844 (0.768-0.928), 0.825 (0.759-0.896) and 0.818 (0.682-0.981) for the Kesse-Guyot EAT-Lancet diet index. Our findings suggest that higher adherence to the EAT-Lancet diet is associated with lower risks of incident depression, anxiety and their co-occurrence., (© 2024. The Author(s).)

Background: The landmark EAT-Lancet Commission proposed that a planetary health diet is comprised mainly of plant-based foods. However, studies examining whether this diet is associated with heart failure (HF) are currently lacking. In addition, the potential proteomics mechanism on the association between diet and HF warrants further elucidation., Objectives: This study aims to both examine the association between the EAT-Lancet diet index and risk of HF and identify plasma proteins underlying such an association., Methods: This prospective cohort study included 23,260 participants. HF cases during the follow-up were identified through the Swedish national register. An EAT-Lancet diet index (score range: 0-42) was created to assess adherence to the EAT-Lancet reference diet. In a subcohort (n = 4,742), fasting plasma proteins were quantified., Results: During a median follow-up of 25.0 years, 1,768 incident HF cases were documented. After adjusting for sociodemographic, lifestyle, diabetes, hypertension, use of lipid-lowering drugs, and body mass index, the HR per 3-point increase of the EAT-Lancet diet index was 0.93 (95% CI: 0.88-0.97). This association was robust in several sensitivity analyses. Among the included 136 plasma proteins, a total of 8 proteins (AM, GDF15, IL-6, TIM, CTSD, CCL20, FS, and FUR) were both inversely associated with the EAT-Lancet diet index and positively associated with risk of HF; the overall proteomic score mediated 9.4% (95% CI: 2.2%-32.1%) of the association., Conclusions: Higher adherence to the EAT-Lancet diet was associated with a lower risk of HF. The identified eight plasma proteins provide information on potential pathways mediating such an association., Competing Interests: Funding Support and Author Disclosures This study was funded by the Swedish Research Council (2020-01412), Heart and Lung Foundation (20190555 and 20200482), and Crafoord Foundation (20210674). The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: Various lifestyle factors including smoking, alcohol, physical activity, sedentary behavior, diet quality, sleep behavior, and overweight have been related to metabolic dysfunction-associated steatotic liver disease (MASLD); however, their joint impact on risk of MASLD is not well known. We prospectively investigated the association between a combination of lifestyle factors and risk of MASLD., Methods: This prospective cohort study included 13,303 participants (mean age: 39.1 ± 11.3 years, female: 60.1%) in China. A novel healthy lifestyle score was created combining seven healthy factors: not smoking, no alcohol intake, regular physical activity, short sedentary time, healthy diet, healthy sleep, and healthy weight. Incident MASLD cases were ascertained annually by liver ultrasound and cardiometabolic risk factors. Multivariable Cox proportional hazards regression models were used to estimate the association of healthy lifestyle score with risk of MASLD., Results: Within 48,036 person-years of follow-up, 2823 participants developed MASLD. After adjusting for age, sex, education, occupation, household income, personal and family history of disease, and total energy intake, compared with participants with 0-2 healthy lifestyle factors, the multivariable hazard ratios (95% confidence interval) of MASLD were 0.81 (0.73, 0.89), 0.67 (0.61, 0.75), and 0.55 (0.49, 0.62) for healthy lifestyle score of 3, 4, and 5-7, respectively (P for trend <0.0001). Such associations were consistent across subgroup and sensitivity analyses., Conclusion: Our results indicate that a higher healthy lifestyle score is associated with a lower risk of MASLD., Competing Interests: Declaration of competing interest The authors declared no conflict of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Dicarbonyl compounds are highly reactive precursors of advanced glycation end products (AGE), produced endogenously, present in certain foods and formed during food processing. AGE contribute to the development of adverse metabolic outcomes, but health effects of dietary dicarbonyls are largely unexplored. We investigated associations between three dietary dicarbonyl compounds, methylglyoxal (MGO), glyoxal (GO) and 3-deoxyglucosone (3-DG), and body weight changes in European adults. Dicarbonyl intakes were estimated using food composition database from 263 095 European Prospective Investigation into Cancer and Nutrition-Physical Activity, Nutrition, Alcohol, Cessation of Smoking, Eating Out of Home in Relation to Anthropometry participants with two body weight assessments (median follow-up time = 5·4 years). Associations between dicarbonyls and 5-year body-weight changes were estimated using mixed linear regression models. Stratified analyses by sex, age and baseline BMI were performed. Risk of becoming overweight/obese was assessed using multivariable-adjusted logistic regression. MGO intake was associated with 5-year body-weight gain of 0·089 kg (per 1-sd increase, 95 % CI 0·072, 0·107). 3-DG was inversely associated with body-weight change (-0·076 kg, -0·094, -0·058). No significant association was observed for GO (0·018 kg, -0·002, 0·037). In stratified analyses, GO was associated with body-weight gain among women and older participants (above median of 52·4 years). MGO was associated with higher body-weight gain among older participants. 3-DG was inversely associated with body-weight gain among younger and normal-weight participants. MGO was associated with a higher risk of becoming overweight/obese, while inverse associations were observed for 3-DG. No associations were observed for GO with overweight/obesity. Dietary dicarbonyls are inconsistently associated with body weight change among European adults. Further research is needed to clarify the role of these food components in overweight and obesity, their underlying mechanisms and potential public health implications.

Different approaches have been used for translation of the EAT-Lancet reference diet into dietary scores that can be used to assess health and environmental impact. Our aim was to compare the different EAT-Lancet diet scores, and to estimate their associations with all-cause mortality, stroke incidence, and greenhouse gas emissions. We did a systematic review (PROSPERO, CRD42021286597) to identify different scores representing adherence to the EAT-Lancet reference diet. We then qualitatively compared the diet adherence scores, including their ability to group individuals according the EAT-Lancet reference diet recommendations, and quantitatively assessed the associations of the diet scores with health and environmental outcome data in three diverse cohorts: the Danish Diet, Cancer and Health Cohort (DCH; n=52 452), the Swedish Malmö Diet and Cancer Cohort (MDC; n=20 973), and the Mexican Teachers' Cohort (MTC; n=30 151). The DCH and MTC used food frequency questionnaires and the MDC used a modified diet history method to assess dietary intake, which we used to compute EAT-Lancet diet scores and evaluate the associations of scores with hazard of all-cause mortality and stroke. In the MDC, dietary greenhouse gas emission values were summarised for every participant, which we used to predict greenhouse gas emissions associated with varying diet adherence scores on each scoring system. In our review, seven diet scores were identified (Knuppel et al, 2019; Trijsburg et al, 2020; Cacau et al, 2021; Hanley-Cook et al, 2021; Kesse-Guyot et al, 2021; Stubbendorff et al, 2022; and Colizzi et al, 2023). Two of the seven scores (Stubbendorff and Colizzi) were among the most consistent in grouping participants according to the EAT-Lancet reference diet recommendations across cohorts, and higher scores (greater diet adherence) were associated with decreased risk of mortality (in the DCH and MDC), decreased risk of incident stroke (in the DCH and MDC for the Stubbendorff score; and in the DCH for the Colizzi score), and decreased predicted greenhouse gas emissions in the MDC. We conclude that the seven different scores representing the EAT-Lancet reference diet had differences in construction, interpretation, and relation to disease and climate-related outcomes. Two scores generally performed well in our evaluation. Future studies should carefully consider which diet score to use and preferably use multiple scores to assess the robustness of estimations, given that public health and environmental policy rely on these estimates., Competing Interests: Declaration of interests AS, UE, and ES were all involved in constructing one of the EAT–Lancet diet scores investigated (Stubbendorff et al(8)). All other authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

The receptor for advanced glycation endproducts (RAGE) has pro-inflammatory and pro-atherogenic effects. Low plasma levels of soluble RAGE (sRAGE), a decoy receptor for RAGE ligands, have been associated with increased risk for major adverse coronary events (MACE) in the general population. We performed a genome-wide association study to identify genetic determinants of plasma sRAGE in 4338 individuals from the cardiovascular arm of the Malmö Diet and Cancer study (MDC-CV). Further, we explored the associations between these genetic variants, incident first-time MACE and mortality in 24,640 unrelated individuals of European ancestry from the MDC cohort. The minor alleles of four single nucleotide polymorphisms (SNPs): rs2070600, rs204993, rs116653040, and rs7306778 were independently associated with lower plasma sRAGE. The minor T (vs. C) allele of rs2070600 was associated with increased risk for MACE [HR 1.13 95% CI (1.02-1.25), P = 0.016]. Neither SNP was associated with mortality. This is the largest study to demonstrate a link between a genetic sRAGE determinant and CV risk. Only rs2070600, which enhances RAGE function by inducing a Gly82Ser polymorphism in the ligand-binding domain, was associated with MACE. The lack of associations with incident MACE for the other sRAGE-lowering SNPs suggests that this functional RAGE modification is central for the observed relationship., (© 2024. The Author(s).)

Background: Lead exposure is associated with cardiovascular disease. Atherosclerosis has been hypothesized to be one of the underlying mechanisms behind this association., Aim: To investigate whether lead exposure is associated with an increased risk of atherosclerosis in the carotid arteries in a large Swedish population-based cohort., Methods: We performed a cross-sectional study using data from the population-based Swedish CardioPulmonary bioImage Study (SCAPIS), including 5622 middle-aged men and women, enrolled 2013-2018. Blood lead (B-Pb), measured by inductively coupled plasma mass spectrometry, was used as exposure biomarker. The presence of atherosclerotic plaque in the carotid arteries (yes/no), total plaque area (mm 2 ) and the presence of large plaques (>25 mm 2 ) were determined by ultrasonography. Associations between B-Pb and the different outcomes were analysed using Poisson and linear regression models, adjusted for potential confounders., Results: Atherosclerotic plaque was present in 57% of the individuals, for whom the median total plaque area was 16 mm 2 (range: 0.2-222). The median B-Pb concentration was 14 μg/L (range: 0.75-203). After adjusting for potential confounders, individuals in the fourth quartile of B-Pb (Q4) had a prevalence ratio (PR) for plaque of 1.08 (95% CI: 1.01, 1.16) when compared with the first quartile (Q1). A 10 μg/L increase in B-Pb concentrations was associated with an increase of 0.92 mm 2 (95% CI: 0.14, 1.71) in total plaque area. The PR for large plaque was 1.09 (95% CI: 0.84, 1.42 for Q4 vs Q1)., Conclusions: This study shows an association between B-Pb and atherosclerosis in the carotid arteries providing some support for the hypothesis that atherosclerosis is one of the mechanisms underlying the association between lead exposure and cardiovascular disease., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Purpose: To investigate the role of adiposity in the associations between ultra-processed food (UPF) consumption and head and neck cancer (HNC) and oesophageal adenocarcinoma (OAC) in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort., Methods: Our study included 450,111 EPIC participants. We used Cox regressions to investigate the associations between the consumption of UPFs and HNC and OAC risk. A mediation analysis was performed to assess the role of body mass index (BMI) and waist-to-hip ratio (WHR) in these associations. In sensitivity analyses, we investigated accidental death as a negative control outcome., Results: During a mean follow-up of 14.13 ± 3.98 years, 910 and 215 participants developed HNC and OAC, respectively. A 10% g/d higher consumption of UPFs was associated with an increased risk of HNC (hazard ratio [HR] = 1.23, 95% confidence interval [CI] 1.14-1.34) and OAC (HR = 1.24, 95% CI 1.05-1.47). WHR mediated 5% (95% CI 3-10%) of the association between the consumption of UPFs and HNC risk, while BMI and WHR, respectively, mediated 13% (95% CI 6-53%) and 15% (95% CI 8-72%) of the association between the consumption of UPFs and OAC risk. UPF consumption was positively associated with accidental death in the negative control analysis., Conclusions: We reaffirmed that higher UPF consumption is associated with greater risk of HNC and OAC in EPIC. The proportion mediated via adiposity was small. Further research is required to investigate other mechanisms that may be at play (if there is indeed any causal effect of UPF consumption on these cancers)., (© 2023. The Author(s).)

The association between the consumption of dairy products and risk of CVD has been inconsistent. There is a lack of studies in populations with high intakes of dairy products. We aimed to examine the association between intake of dairy products and risk of incident major adverse coronary events and stroke in the Swedish Malmö Diet and Cancer cohort study. We included 26 190 participants without prevalent CVD or diabetes. Dietary habits were obtained from a modified diet history, and endpoint data were extracted from registers. Over an average of 19 years of follow-up, 3633 major adverse coronary events cases and 2643 stroke cases were reported. After adjusting for potential confounders, very high intakes of non-fermented milk (>1000 g/d) compared with low intakes (<200 g/d) were associated with 35 % (95 % CI (8, 69)) higher risk of major adverse coronary events. In contrast, moderate intakes of fermented milk (100-300 g/d) were associated with a lower risk of major adverse coronary events compared with no consumption. Intakes of cheese (only in women) and butter were inversely associated with the risk of major adverse coronary events. We observed no clear associations between any of the dairy products and stroke risk. These results highlight the importance of studying different dairy foods separately. Further studies in populations with high dairy consumption are warranted.

Recent epidemiological studies have suggested a positive association between ultra-processed food consumption and breast cancer risk, although some studies also reported no association. Furthermore, the evidence regarding the associations between intake of food with lower degrees of processing and breast cancer risk is limited. Thus, we investigated the associations between dietary intake by degree of food processing and breast cancer risk, overall and by breast cancer subtypes in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Dietary intake of EPIC participants was assessed via questionnaires at baseline. More than 11,000 food ingredients were classified into four groups of food processing levels using the NOVA classification system: unprocessed/minimally processed (NOVA 1), culinary ingredients (NOVA 2), processed (NOVA 3) and ultra-processed (NOVA 4). Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of breast cancer per standard deviation increase in daily consumption (grams) of foods from each NOVA group. The current analysis included 14,933 breast cancer cases, diagnosed among the 318,686 EPIC female participants, (median follow-up of 14.9 years). No associations were found between breast cancer risk and the level of dietary intake from NOVA 1 [HR per 1 SD =0.99 (95% CI 0.97 - 1.01)], NOVA 2 [HR per 1 SD =1.01 (95% CI 0.98 - 1.03)] and NOVA 4 [HR per 1 SD =1.01 (95% CI 0.99 - 1.03)] foods. However, a positive association was found between NOVA 3 and breast cancer risk [HR per 1 SD =1.05 (95% CI 1.03 - 1.07)] which became non-significant after adjustment for alcohol intake [HR per 1 SD =1.01 (95% CI 0.98 - 1.05)] or when beer and wine were excluded from this group [HR per 1 SD =0.99 (95% CI 0.97 - 1.01)]. The associations did not differ by breast cancer subtype, menopausal status or body mass index. Findings from this large-scale prospective study suggest that the positive association between processed food intake and breast cancer risk was likely driven by alcoholic beverage consumption., Supplementary Information: The online version contains supplementary material available at 10.1186/s43014-024-00264-2., Competing Interests: Competing interestsThe authors declare no potential conflicts of interest., (© The Author(s) 2024.)

Background: About one in ten adults are living with diabetes worldwide. Intake of carbohydrates and carbohydrate-rich foods are often identified as modifiable risk factors for incident type 2 diabetes. However, strong correlation between food variables can make it difficult to identify true associations. The purpose of this study was to identify clusters of carbohydrate-rich foods and analyse their associations with type 2 diabetes incidence in the Malmö Diet and Cancer Study cohort in southern Sweden., Methods: Dietary intake of 26 622 participants was assessed using a validated three-part diet history method: a 7-day food diary, a 168-item food frequency questionnaire, and a 60-minute interview. K-means clustering analysis identified five clusters from 21 food variables. The Cox proportional hazard regression model was applied to calculate hazard ratios (HR) and 95% confidence intervals (CI) of the association between clusters and incident type 2 diabetes., Results: The cluster analysis resulted in five clusters; high vegetables/low added sugar, high sugar-sweetened beverages, high juice, high fruit, and high refined carbohydrates/low fruit & vegetables (reference). During mean follow-up of 18 years, 4046 type 2 diabetes cases were identified. After adjustment for potential confounding (including lifestyle, body mass index, and diet), a high fruit cluster (HR 0.86; 95% CI 0.78, 0.94) was inversely associated with type 2 diabetes compared to the reference cluster. No other significant associations were identified., Conclusions: A dietary pattern defined by a high intake of fruits was associated with a lower incidence of type 2 diabetes. The findings provide additional evidence of a potential protective effect from fruit intake in reducing type 2 diabetes risk. Future studies are needed to explore this association further., (© 2023. The Author(s).)

Background: It is currently unknown whether ultra-processed foods (UPFs) consumption is associated with a higher incidence of multimorbidity. We examined the relationship of total and subgroup consumption of UPFs with the risk of multimorbidity defined as the co-occurrence of at least two chronic diseases in an individual among first cancer at any site, cardiovascular disease, and type 2 diabetes., Methods: This was a prospective cohort study including 266,666 participants (60% women) free of cancer, cardiovascular disease, and type 2 diabetes at recruitment from seven European countries in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Foods and drinks consumed over the previous 12 months were assessed at baseline by food-frequency questionnaires and classified according to their degree of processing using Nova classification. We used multistate modelling based on Cox regression to estimate cause-specific hazard ratios (HR) and their 95% confidence intervals (CI) for associations of total and subgroups of UPFs with the risk of multimorbidity of cancer and cardiometabolic diseases., Findings: After a median of 11.2 years of follow-up, 4461 participants (39% women) developed multimorbidity of cancer and cardiometabolic diseases. Higher UPF consumption (per 1 standard deviation increment, ∼260 g/day without alcoholic drinks) was associated with an increased risk of multimorbidity of cancer and cardiometabolic diseases (HR: 1.09, 95% CI: 1.05, 1.12). Among UPF subgroups, associations were most notable for animal-based products (HR: 1.09, 95% CI: 1.05, 1.12), and artificially and sugar-sweetened beverages (HR: 1.09, 95% CI: 1.06, 1.12). Other subgroups such as ultra-processed breads and cereals (HR: 0.97, 95% CI: 0.94, 1.00) or plant-based alternatives (HR: 0.97, 95% CI: 0.91, 1.02) were not associated with risk., Interpretation: Our findings suggest that higher consumption of UPFs increases the risk of cancer and cardiometabolic multimorbidity., Funding: Austrian Academy of Sciences, Fondation de France, Cancer Research UK, World Cancer Research Fund International, and the Institut National du Cancer., Competing Interests: None of the authors declared a competing interest., (© 2023 Published by Elsevier Ltd.)

Background: We aim to examine the association between ultra-processed foods (UPF) consumption and cardiovascular disease (CVD) risk and to identify plasma proteins associated with UPF., Methods: This prospective cohort study included 26,369 participants from the Swedish Malmö Diet and Cancer Study, established in 1991-1996. Dietary intake was assessed using a modified diet history method, and UPF consumption was estimated using the NOVA classification system. A total of 88 selected CVD-related proteins were measured among 4475 subjects. Incident CVD (coronary heart disease and ischemic stroke) was defined as a hospital admission or death through registers. Cox proportional hazards regression models were performed to analyze the associations of UPF intake with risks of CVD. Linear regression models were used to identify the plasma proteins associated with UPF intake., Results: During 24.6 years of median follow-up, 6236 participants developed CVD, of whom 3566 developed coronary heart disease and 3272 developed ischemic stroke. The adjusted hazard ratio (95% confidence interval) in the 4th versus 1st quartile of UPF was 1.18 (1.08, 1.29) for CVD, 1.20 (1.07, 1.35) for coronary heart disease, and 1.17 (1.03, 1.32) for ischemic stroke. Plasma proteins interleukin 18, tumor necrosis factor receptor 2, macrophage colony-stimulating factor 1, thrombomodulin, tumor necrosis factor receptor 1, hepatocyte growth factor, stem cell factor, resistin, C-C motif chemokine 3, and endothelial cell-specific molecule 1 were positively associated with UPF after correcting for multiple testing., Conclusions: Our study showed that high UPF intake increased the risk of CVD and was associated with several protein biomarkers. Future studies are warranted to validate these findings and assess the potential pathways between UPF intake and CVD., (© 2023. The Author(s).)

Background and aims : Previous studies of primarily Western populations have consistently documented a lower risk of type 2 diabetes (T2D) among people with a higher yogurt intake, but an inconsistent association with milk intake. However, little is known about the association between dairy intake and risk of T2D among Chinese adults who consume considerably less dairy (mainly milk and yogurt) compared with Western populations. The aim is to investigate the associations of dairy intake with the risk of incident T2D in the general adult population in China. Methods : This cohort study consisted of 22 843 participants without prevalent cardiovascular disease, cancer, or diabetes at the baseline. Dietary data were collected using a validated food frequency questionnaire at the baseline (2013-2018); dairy intake was categorized into tertiles after zero consumers were taken as the reference. Incident T2D was ascertained by medical examinations and self-report of physician-diagnosed diabetes during follow-up visits. Cox proportional hazards models were performed to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs). Results : In total, 735 incident T2D cases were recorded over a median follow-up of 4.0 years. Relative to zero consumers, the HRs (95% CIs) for incident T2D among participants in the highest tertiles were 0.70 (0.57, 0.87) for total dairy, 0.73 (0.60, 0.90) for milk, and 0.81 (0.66, 1.00) for yogurt. Such associations were slightly attenuated by additional adjustment for the body mass index. In addition, such inverse associations were robust in sensitivity analyses and consistent in most of the subgroups defined by baseline characteristics. Conclusion : Higher intakes of total dairy, milk, and yogurt were all associated with a lower risk of T2D among Chinese adults.

Carbohydrate quality might be more important than quantity to reduce type 2 diabetes (T2D) risk. Various metrics of carbohydrate quality exist; however, their associations with T2D have only been studied to a limited extent. Consequently, the aim was to investigate the association between four different pre-defined carbohydrate quality indices, with various amounts of fiber (≥1 g) and free sugar (<1 or <2 g) per 10 g of carbohydrates, and T2D risk among 26,622 individuals without diabetes from the Malmö Diet and Cancer cohort. Dietary data were collected through a food diary, diet frequency questionnaire, and interview. After a mean follow-up of 18 years, 4046 cases were identified through registers. After adjusting for potential confounders, no statistically significant associations were found for any of the indices. When excluding individuals with past dietary changes and potential misreporting of energy (36% of the population), lower risk was found for the following intake ratios: 10:1:2 carbohydrate:fiber:free sugar (HR = 0.82; 95% CI = 0.70-0.97), and 10:1&1:2 carbohydrate:fiber and fiber:free sugar, respectively (HR = 0.84; 95% CI = 0.72-0.97). Our findings indicate that adherence to a diet with high amounts of fiber and moderate amounts of free sugar in relation to total carbohydrate intake may be associated with a lower risk of T2D.

Purpose: Added sugar is associated with a variety of adverse health outcomes, but its association with kidney stones is unclear. This study was to determine whether added sugar is associated with kidney stones., Materials and Methods: This nationally representative study used National Health and Nutrition Examination Survey (NHANES) datasets from 2007 to 2018 for analysis. People aged ≥20 years who reported a history of kidney stones and provided dietary recall data on added sugars were included. Weighted proportions, multivariable logistic regression analysis and stratified logistic regression were used to evaluate the associations between added sugars and kidney stones by adjusting potential confounders., Results: Totally 28,303 adults were included, with weighted mean age [95% confidence interval (CI)] of 48.03 (47.56, 48.51) years, 47.74% (47.09, 48.40%) males and 52.26% (51.60, 52.91%) females. The overall mean (95% CI) energy intake from added sugars was 272.10 (266.59, 277.60) kilocalories. In the fully-adjusted multivariable model, the percentage of energy intake from added sugars was positively correlated with kidney stones. Compared to the first quartile of added sugar energy intake percentage, the population in the fourth quartile had a higher prevalence of kidney stones (OR = 1.39; 95% CI 1.17 to 1.65). Compared with the less than 5% calories from added sugar population, the more than or equal to 25% calories from added sugar had a higher kidney stone prevalence (OR = 1.88; 95% CI 1.52 to 2.32)., Conclusion: A higher percentage of energy intake from added sugars is significantly associated with a higher prevalence of kidney stones. This study provides cross-sectional evidence for the relationship between added sugars and health outcomes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Yin, Yang, Zhu, Du, Yu, Tang and Borné.)

Background: The EAT-Lancet Commission proposed a global reference diet with both human health benefits and environmental sustainability in 2019. However, evidence regarding the association of such a diet with the risk of atrial fibrillation (AF) is lacking. In addition, whether the genetic risk of AF can modify the effect of diet on AF remains unclear. This study aimed to assess the association of the EAT-Lancet diet with the risk of incident AF and examine the interaction between the EAT-Lancet diet and genetic susceptibility of AF., Methods: This prospective study included 24,713 Swedish adults who were free of AF, coronary events, and stroke at baseline. Dietary habits were estimated with a modified diet history method, and an EAT-Lancet diet index was constructed to measure the EAT-Lancet reference diet. A weighted genetic risk score was constructed using 134 variants associated with AF. Cox proportional hazards regression models were applied to estimate the hazard ratio (HR) and 95% confidence interval (CI)., Results: During a median follow-up of 22.9 years, 4617 (18.7%) participants were diagnosed with AF. The multivariable HR (95% CI) of AF for the highest versus the lowest group for the EAT-Lancet diet index was 0.84 (0.73, 0.98) (P for trend < 0.01). The HR (95% CI) of AF per one SD increment of the EAT-Lancet diet index for high genetic risk was 0.92 (0.87, 0.98) (P for interaction = 0.15)., Conclusions: Greater adherence to the EAT-Lancet diet index was significantly associated with a lower risk of incident AF. Such association tended to be stronger in participants with higher genetic risk, though gene-diet interaction was not significant., (© 2023. The Author(s).)

Background: Since the first version of the dietary inflammatory index (DII®) developed in the past decade, several other versions have been developed. However, to date no study has attempted to compare these versions with respect to their associations with biomarkers of inflammation., Objective: We aimed to investigate the relationship between four dietary inflammatory scores [DII, two energy-adjusted derivatives (E-DII and E-DII r ), and the Inflammatory Score of the Diet (ISD)], and circulating levels of several inflammatory markers and adipokines., Methods: This study included 17 637 participants from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort with at least one marker of inflammation measured in blood. Associations between the four scores and C-reactive protein (CRP), interleukin (IL)6, IL10, IL1RA, tumor necrosis factor-α (TNFα), soluble tumor necrosis factor receptor-1 (sTNFR1), sTNFR2, leptin, soluble leptin receptor (sLeptin R), adiponectin, and High Molecular Weight (HMW) adiponectin were evaluated using multivariable linear regressions adjusted for potential confounders., Results: Positive associations were observed between the four dietary inflammatory scores and levels of CRP, IL6, sTNFR1, sTNFR2 and leptin. However, only the DII and the ISD were positively associated with IL1RA levels and only the DII and the E-DII r were positively associated with TNFα levels. The proportion of variance of each biomarker explained by the scores was lower than 2%, which was equivalent to the variance explained by smoking status but much lower than that explained by body mass index., Conclusions: Our results suggest that the four dietary inflammatory scores were associated with some biomarkers of inflammation and could be used to assess the inflammatory potential of diet in European adults but are not sufficient to capture the inflammatory status of an individual. These findings can help to better understand the inflammatory potential of diet, but they need to be replicated in studies with repeated dietary measurements., Competing Interests: Conflicts of Interest Dr. James R. Hébert owns controlling interest in Connecting Health Innovations LLC (CHI), a company that has licensed the right to his invention of the dietary inflammatory index (DII®) from the University of South Carolina in order to develop computer and smartphone applications for patient counseling and dietary intervention in clinical settings. Dr. Nitin Shivappa is an employee of CHI. The subject matter of this paper will not have any direct bearing on that work, nor has CHI-related activity exerted any influence on this project., (Crown Copyright © 2023. Published by Elsevier Ltd. All rights reserved.)

It has been suggested that added sugar intake is associated with non-alcoholic fatty liver disease (NAFLD). However, previous studies only focused on sugar-sweetened beverages; the evidence for associations with total added sugars and their sources is scarce. This study aimed to examine the associations of total added sugars, their physical forms (liquid v . solid) and food sources with risk of NAFLD among adults in Tianjin, China. We used data from 15 538 participants, free of NAFLD, other liver diseases, CVD, cancer or diabetes at baseline (2013-2018 years). Added sugar intake was estimated from a validated 100-item FFQ. NAFLD was diagnosed by ultrasonography after exclusion of other causes of liver diseases. Multivariable Cox proportional hazards models were fitted to calculate hazard ratios (HR) and corresponding 95 % CI for NAFLD risk with added sugar intake. During a median follow-up of 4·2 years, 3476 incident NAFLD cases were documented. After adjusting for age, sex, BMI and its change from baseline to follow-up, lifestyle factors, personal and family medical history and overall diet quality, the multivariable HR of NAFLD risk were 1·18 (95 % CI 1·06, 1·32) for total added sugars, 1·20 (95 % CI 1·08, 1·33) for liquid added sugars and 0·96 (95 % CI 0·86, 1·07) for solid added sugars when comparing the highest quartiles of intake with the lowest quartiles of intake. In this prospective cohort of Chinese adults, higher intakes of total added sugars and liquid added sugars, but not solid added sugars, were associated with a higher risk of NAFLD.

Scope: Evidence suggests a positive association between ultra-processed food (UPF) consumption and the incidence of cardiovascular disease (CVD). The study aims to investigate associations between UPF intake and respiratory disease, CVD, and their multimorbidity in a large prospective cohort., Methods and Results: Within the UK Biobank, participants who are free from respiratory disease or CVD at baseline and completed at least two times 24-h dietary records are included in this study. After adjusting for socioeconomic status and lifestyle factors, the hazard ratios (95% confidence interval) for each 10% increase in UPF are 1.06 (1.04, 1.09) for CVD, 1.04 (1.02, 1.06) for respiratory disease, 1.15 (1.08, 1.22) for CVD mortality, and 1.06 (1.01, 1.12) for their multimorbidity, respectively. In addition, replacing 20% of UPF weight in diet with an equivalent proportion of unprocessed or minimally processed foods is estimated to be associated with 11% lower risk of CVD, 7% lower risk of respiratory disease, 25% lower risk of CVD mortality, and 11% lower risk of CVD and respiratory disease multimorbidity., Conclusion: In this prospective cohort study, higher consumption of UPF is associated with higher risks of CVD and respiratory disease multimorbidity. Further longitudinal studies are needed to confirm these findings., (© 2023 Wiley-VCH GmbH.)

Background: Mood disorders and strokes are often comorbid, and their health toll worldwide is huge. This study characterizes prognostic and causal roles of mood disorders in stroke., Methods: We tested if genetic susceptibilities for mood disorders were associated with all strokes, ischemic strokes in the Malmö Diet and Cancer cohort (24 631 individuals with a median follow-up of 21.3 (interquartile range: 16.6-23.2) years. We further examined the causal effects for mood disorders on all strokes and ischemic strokes using summary statistics from large genome-wide association studies of mood disorders (up to 609 424 individuals, Psychiatric Genomics Consortium), all strokes and ischemic strokes (up to 446 696 individuals, MEGASTROKE Consortium)., Results: Among 24 366 stroke-free participants at baseline, 2632 individuals developed strokes, 2172 of them ischemic, during follow-up. After properly adjusting for well-known risk factors, participants in the highest quintile of polygenic risk scores for mood disorders had 1.45× (95% CI, 1.21-1.74) higher risk of strokes and 1.44× (95% CI, 1.18-1.76) higher risk of ischemic strokes compared with the lowest quintile in women. Mendelian randomization analyses suggested that mood disorders had a causal effect on strokes (odds ratio, 1.07 [95% CI, 1.03-1.11]) and ischemic strokes (odds ratio, 1.09 [95% CI, 1.04-1.13])., Conclusions: Our results suggest a causal role of mood disorders in the risk of stroke. High-risk women could be identified early in life using polygenic risk scores to ultimately prevent mood disorders and strokes.

Background: The EAT-Lancet Commission proposed a globally environmentally sustainable dietary pattern featuring mainly plant-based foods in 2019. However, evidence on this dietary pattern in preventing coronary events is minimal., Objectives: We aimed to examine the association between the EAT-Lancet diet and risk of coronary events., Methods: The Malmö Diet and Cancer cohort study (recruited between 1991 and 1996) included 23,877 participants aged 44.5-73.6 y (62.5% women) without CVDs and diabetes at baseline. A modified diet history was used to collect the dietary data. An EAT-Lancet diet index (range, 0-42 points) was applied on the basis of 14 food components scored 0 (nonadherence) to 3 (adherence). Coronary events were extracted from the registers. Cox proportional hazards models were used to estimate the HRs and 95% confidential intervals (CIs)., Results: Over a median of 24.9 y of follow-up, 3031 coronary events occurred (incidence rate: 5.89/1000 person-years). After adjusting for age, sex, dietary assessment methods, season, total energy intake, leisure-time physical activity, alcohol consumption, smoking status, educational level, and BMI, the multivariable HR (95% CI) for coronary events among participants who had the highest adherence to the EAT-Lancet diet index (≥23 points, 8.1%) was 0.80 (0.67, 0.96) compared with those who had the lowest adherence (≤13 points, 9.7%) (P-trend = 0.01 across 5 groups of the EAT-Lancet diet). The inverse association was consistent in men and women and was robust after excluding those with misreported energy and significant diet changes or excluding coronary events occurred within the first 2 y of follow-up., Conclusions: Our data indicate that adherence to the EAT-Lancet diet was associated with a lower risk of coronary events., (Copyright © 2023. Published by Elsevier Inc.)

Background and Aims: In 2019, the EAT-Lancet Commission proposed a mainly plant-based diet that nurtures human health and supports environmental sustainability. However, its association with type 2 diabetes (T2D) has not been widely studied, and it remains unclear whether genetic susceptibility for T2D can modify this association. The aim was therefore to investigate the association between the EAT-Lancet diet and risk of T2D and assess whether the association differs by the genetic predisposition to T2D., Methods: A total of 24,494 participants from the Malmö Diet and Cancer study were analyzed. Dietary intake was assessed using a modified diet history methodology, and an EAT-Lancet diet index (range from 0 to 42 points) was constructed based on the EAT-Lancet reference diet. National and local registers were used to identify T2D cases during follow-up. Cox proportional hazards regression model was applied to estimate the association between the EAT-Lancet diet index and risk of T2D. Genetic predisposition to T2D was captured based on 116 single nucleotide polymorphisms., Results: During a median of 24.3 years of follow-up, 4197 (17.1 %) T2D cases were documented. Compared with those with the lowest adherence to the EAT-Lancet diet (≤13 points), participants who had the highest adherence (≥23 points) showed an 18 % (95 % CI: 4 %-30 %) lower risk of T2D (P for trend <0.01). There was no significant multiplicative interaction between genetic predisposition to T2D and the EAT-Lancet diet index (P = 0.59). Also, no significant additive interaction between the genetic risk and the EAT-Lancet diet was seen (P = 0.44). The highest risk was observed among the 22.9 % of the individuals with high genetic risk and low EAT-Lancet diet score (HR = 1.79; 95 % CI: 1.63, 1.96)., Conclusions: Our findings indicate that high adherence to the EAT-Lancet diet was associated with decreased risk of incident T2D among people with different genetic risks., Competing Interests: Declaration of competing interest None., (Copyright © 2023. Published by Elsevier Inc.)

Background: Emerging evidence suggests that animal protein foods may increase the risk of nonalcoholic fatty liver disease (NAFLD). We therefore examined the NAFLD risk reduction related to substituting plant protein foods for animal protein foods., Methods: The cohort in North China included 14,541 participants from the Tianjin Chronic Low-Grade Systemic Inflammation and Health (TCLSIH) study, and the cohort in South China included 1297 participants from the Guangzhou Nutrition and Health Study (GNHS). Dietary intake was assessed using validated food frequency questionnaires. NAFLD was ascertained by abdominal ultrasound. The Cox model was used to fit the substitution analysis., Results: In the TCLSIH cohort, when replacing one type of animal protein food (eggs, processed meat, unprocessed red meat, poultry, and fish) with an equivalent serving of plant protein foods (nuts, legumes, and whole grains), the replacement of animal protein foods with whole grains showed the strongest benefit; substituting one serving per day of whole grains for an equal amount of eggs (hazard ratio [HR] = 0.89; 95% confidence interval [CI]: 0.79, 1.00), processed meat (HR = 0.76; 95% CI: 0.64, 0.91), unprocessed red meat (HR = 0.90; 95% CI: 0.81, 1.00), poultry (HR = 0.81; 95% CI: 0.72, 0.92), or fish (HR = 0.87; 95% CI: 0.78, 0.97) was associated with a lower risk of NAFLD. In both the TCLSIH and GNHS cohorts, replacing poultry with fish, nuts, legumes, or whole grains was associated with a lower risk of NAFLD. When different numbers of protein foods were simultaneously replaced, the risk reduction of NAFLD was stronger., Conclusions: Our findings suggest that replacing animal protein foods with plant protein foods is related to a significant reduction in NAFLD risk., (© 2022 The Association for the Publication of the Journal of Internal Medicine.)

To investigate the associations of milk intake (non-fermented and fermented milk), lactase persistence (LCT-13910 C/T) genotype (a proxy for long-term non-fermented milk intake), and gene-milk interaction with risks of cardiovascular disease (CVD) and CVD mortality. Also, to identify the CVD-related plasma proteins and lipoprotein subfractions associated with milk intake and LCT-13910 C/T genotype. The prospective cohort study included 20,499 participants who were followed up for a mean of 21 years. Dietary intake was assessed using a modified diet history method. Cox proportional hazards regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). After adjusting for sociodemographic and lifestyle factors, higher non-fermented milk intake was significantly associated with higher risks of coronary heart disease (CHD) and CVD mortality, whereas higher fermented milk intake was significantly associated with lower risks of CVD and CVD mortality. The genotype associated with higher milk (mainly non-fermented) intake was positively associated with CHD (CT/TT vs. CC HR = 1.27; 95% CI: 1.03, 1.55) and CVD (HR = 1.22; 95% CI: 1.05, 1.42). The association between rs4988235 genotype and CVD mortality was stronger in participants with higher milk intake than among participants with lower intake (P for interaction < 0.05). Furthermore, leptin, HDL, and large HDL were associated with non-fermented milk intake, while no plasma proteins or lipoprotein subfractions associated with fermented milk intake and LCT-13910 C/T genotype were identified. In conclusion, non-fermented milk intake was associated with higher risks of CHD and CVD mortality, as well as leptin and HDL, whereas fermented milk intake was associated with lower risks of CVD and CVD mortality., (© 2023. The Author(s).)

Background: Many ultraprocessed food (UPF)-derived by-products may play a role in the development of chronic kidney disease (CKD). Although several studies have assessed the association of UPFs with kidney function decline or CKD in various countries, no evidence has been shown in China and the United Kingdom., Objectives: This study aims to evaluate the association between UPF consumption and risk of CKD in 2 large cohort studies from China and the United Kingdom., Methods: In total, 23,775 and 102,332 participants without baseline CKD were enrolled in the Tianjin Chronic Low-Grade Systemic Inflammation and Health (TCLSIH) and UK Biobank cohort studies, respectively. Information on UPF consumption was obtained from a validated food frequency questionnaire in the TCLSIH and 24-h dietary recalls in the UK Biobank cohort. CKD was defined as an estimated glomerular filtration rate of <60 mL/min/1.73 m 2 , albumin-to-creatinine ratio ≥30 mg/g, or as having a clinical diagnosis of CKD in both cohorts. Multivariable Cox proportional hazard models were used to examine the association between UPF consumption and the risk of CKD., Results: After a median follow-up of 4.0 and 10.1 y, the incidence rates of CKD were around 1.1% and 1.7% in the TCLSIH and UK Biobank cohorts, respectively. The multivariable hazard ratio [95% confidence interval] of CKD across increasing quartiles (quartiles 1-4) of UPF consumption were 1 (reference), 1.24 (0.89, 1.72), 1.30 (0.91, 1.87), and 1.58 (1.07, 2.34) (P for trend = 0.02) in the TCLSIH cohort and 1 (reference), 1.14 (1.00, 1.31), 1.16 (1.01, 1.33), and 1.25 (1.09, 1.43) (P for trend < 0.01) in the UK Biobank cohort, respectively., Conclusions: Our finding indicated that higher UPF consumption is associated with a higher risk of CKD. Moreover, restricting UPF consumption may potentially benefit the prevention of CKD. Further clinical trials are required to clarify the causality. This trial was registered at UMIN Clinical Trials Registry as UMIN000027174 (https://upload.umin.ac.jp/cgi-open-bin/ctr&#95;e/ctr&#95;view.cgi?recptno=R000031137)., (Copyright © 2022 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)

Background: Salivary amylase, encoded by the AMY1 gene, initiate the digestion of starch. Whether starch intake or AMY1 copy number is related to disease risk is currently rather unknown. The aim was to investigate the association between starch intake and AMY1 copy number and risk of cardiovascular disease (CVD) and mortality and whether there is an interaction. In addition, we aim to identify CVD-related plasma proteins associated with starch intake and AMY1 copy number., Methods: This prospective cohort study used data from 21,268 participants from the Malmö Diet and Cancer Study. Dietary data were collected through a modified diet history method and incident CVD and mortality were ascertained through registers. AMY1 gene copy number was determined by droplet digital polymerase chain reaction, a risk score of 10 genetic variants in AMY1 was measured, and a total of 88 selected CVD-related proteins were measured. Cox proportional hazards regression was used to analyze the associations of starch intake and AMY1 copy number with disease risk. Linear regression was used to identify plasma proteins associated with starch intake and AMY1 copy number., Results: Over a median of 23 years' follow-up, 4443 individuals developed CVD event and 8125 died. After adjusting for potential confounders, a U-shape association between starch intake and risk of CVD (P-nonlinearity = 0.001) and all-cause mortality (P-nonlinearity = 0.03) was observed. No significant association was found between AMY1 copy number and risk of CVD and mortality, and there were no interactions between starch intake and AMY1 copy number (P interaction > 0.23). Among the 88 plasma proteins, adrenomedullin, interleukin-1 receptor antagonist protein, fatty acid-binding protein, leptin, and C-C motif chemokine 20 were associated with starch intake after adjusting for multiple testing., Conclusions: In this large prospective study among Swedish adults, a U-shaped association between starch intake and risk of CVD and all-cause mortality was found. Several plasma proteins were identified which might provide information on potential pathways for such association. AMY1 copy number was not associated with CVD risk or any of the plasma proteins, and there was no interaction between starch intake and AMY1 copy number on disease risk., (© 2023. The Author(s).)

Background: Epidemiological studies have demonstrated an association between the degree of food processing in our diet and the risk of various chronic diseases. Much of this evidence is based on the international Nova classification system, which classifies food into four groups based on the type of processing: (1) Unprocessed and minimally processed foods, (2) Processed culinary ingredients, (3) Processed foods, and (4) "Ultra-processed" foods (UPF). The ability of the Nova classification to accurately characterise the degree of food processing across consumption patterns in various European populations has not been investigated so far. Therefore, we applied the Nova coding to data from the European Prospective Investigation into Cancer and Nutrition (EPIC) in order to characterize the degree of food processing in our diet across European populations with diverse cultural and socio-economic backgrounds and to validate this Nova classification through comparison with objective biomarker measurements., Methods: After grouping foods in the EPIC dataset according to the Nova classification, a total of 476,768 participants in the EPIC cohort (71.5% women; mean age 51 [standard deviation (SD) 9.93]; median age 52 [percentile (p)25-p75: 58-66] years) were included in the cross-sectional analysis that characterised consumption patterns based on the Nova classification. The consumption of food products classified as different Nova categories were compared to relevant circulating biomarkers denoting food processing, measured in various subsamples (N between 417 and 9,460) within the EPIC cohort via (partial) correlation analyses (unadjusted and adjusted by sex, age, BMI and country). These biomarkers included an industrial transfatty acid (ITFA) isomer (elaidic acid; exogenous fatty acid generated during oil hydrogenation and heating) and urinary 4 - methyl syringol sulfate (an indicator for the consumption of smoked food and a component of liquid smoke used in UPF)., Results: Contributions of UPF intake to the overall diet in % grams/day varied across countries from 7% (France) to 23% (Norway) and their contributions to overall % energy intake from 16% (Spain and Italy) to >45% (in the UK and Norway). Differences were also found between sociodemographic groups; participants in the highest fourth of UPF consumption tended to be younger, taller, less educated, current smokers, more physically active, have a higher reported intake of energy and lower reported intake of alcohol. The UPF pattern as defined based on the Nova classification (group 4;% kcal/day) was positively associated with blood levels of industrial elaidic acid ( r = 0.54) and 4 - methyl syringol sulfate ( r = 0.43). Associations for the other 3 Nova groups with these food processing biomarkers were either inverse or non-significant (e.g., for unprocessed and minimally processed foods these correlations were -0.07 and -0.37 for elaidic acid and 4 - methyl syringol sulfate, respectively)., Conclusion: These results, based on a large pan-European cohort, demonstrate sociodemographic and geographical differences in the consumption of UPF. Furthermore, these results suggest that the Nova classification can accurately capture consumption of UPF, reflected by stronger correlations with circulating levels of industrial elaidic acid and a syringol metabolite compared to diets high in minimally processed foods., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Huybrechts, Rauber, Nicolas, Casagrande, Kliemann, Wedekind, Biessy, Scalbert, Touvier, Aleksandrova, Jakszyn, Skeie, Bajracharya, Boer, Borné, Chajes, Dahm, Dansero, Guevara, Heath, Ibsen, Papier, Katzke, Kyrø, Masala, Molina-Montes, Robinson, Santiuste de Pablos, Schulze, Simeon, Sonestedt, Tjønneland, Tumino, van der Schouw, Verschuren, Vozar, Winkvist, Gunter, Monteiro, Millett and Levy.)

Background and Objectives: There has been a growing body of evidence associating consumption of ultraprocessed foods (UPF) with adverse health outcomes including depression, cardiovascular disease, and all-cause mortality. However, whether UPF are associated with dementia is unknown. The authors investigated the associations between UPF and dementia incidence in the UK Biobank., Methods: We included 72,083 participants (55 years or older) who were free from dementia at baseline and provided at least 2 times 24-hour dietary assessments from the UK Biobank study. Follow-up occurred through March 2021. UPF were defined according to the NOVA classification. Incident all-cause dementia comprising Alzheimer disease (AD) and vascular dementia was ascertained through electronic linkages to hospital and mortality records. Cox proportional hazards were used to estimate the association between the proportion (%) of UPF in the diet and the subsequent risk of dementia. In addition, substitution analysis was used to estimate the risk of dementia when substituting UPF with an equivalent proportion of unprocessed or minimally processed foods., Results: During a total of 717,333 person-years of follow-up (median 10.0 years), 518 participants developed dementia, of whom 287 developed AD and 119 developed vascular dementia. In the fully adjusted model, consumption of UPF was associated with higher risk of dementia (hazard ratio [HR] for 10% increase in UPF 1.25; 95% CI 1.14-1.37), AD (HR 1.14; 95% CI 1.00-1.30), and vascular dementia (HR 1.28; 95% CI 1.06-1.55), respectively. In addition, replacing 10% of UPF weight in diet with an equivalent proportion of unprocessed or minimally processed foods was estimated to be associated with a 19% lower risk of dementia (HR 0.81; 95% CI 0.74-0.89)., Discussion: In this prospective cohort study, higher consumption of UPF was associated with higher risk of dementia, whereas substituting unprocessed or minimally processed foods for UPF was associated with lower risk of dementia., (© 2022 American Academy of Neurology.)