Ultra-processed food and drink consumption and lipoprotein subclass profiles: A cross-sectional study of a middle-to older-aged population.

BACKGROUND AND AIMS: Studies have consistently demonstrated associations between ultra-processed food and drink (UPFD) consumption and non-communicable diseases. However, there is a lack of data investigating relationships between UPFD intake and intermediate cardiometabolic disease markers. In this study we explored UPFD associations with lipoprotein subclasses. METHODS: This was a cross-sectional study of 1986 middle-to older-aged men and women randomly selected from a large primary care centre. The percentage contribution of UPFDs to total energy intake was calculated for each participant using the NOVA classification. Lipoprotein particle subclass concentrations and size were determined using nuclear magnetic resonance spectroscopy. Correlation and multivariate-adjusted linear regression analyses were performed to examine UPFD intake relationships with lipoprotein subclasses. RESULTS: In fully adjusted regression models, higher UPFD consumption was associated with reduced high-density lipoprotein (HDL) cholesterol concentrations (ß = -0.024, p = 0.001), large low-density lipoprotein (LDL) levels (ß = -18.645, p = 0.002), total and medium HDL concentrations (ß = -0.328, p = 0.012; ß = -0.510, p < 0.001), smaller LDL and HDL size (ß = -0.026, p = 0.023; ß = -0.023, p = 0.024), and increased medium very low-density lipoprotein levels (ß = 0.053, p = 0.022), small LDL and HDL concentrations (ß = 20.358, p = 0.02; ß = 0.336, p = 0.011), and higher lipoprotein insulin resistance scores (ß = 0.048, p = 0.012), reflecting greater lipoprotein-related insulin resistance. CONCLUSIONS: Findings from this research suggest that increased intake of UPFDs is associated with a more pro-atherogenic, insulin-resistant metabolic profile in middle-to older-aged adults which may be a potential mechanism underlying reported associations between UPFD consumption and chronic disease risk and mortality.

The Nutri-Score nutrition label: Associations between the underlying nutritional profile of foods and lipoprotein particle subclass profiles in adults.

BACKGROUND AND AIMS: Lipoprotein particle concentrations and size are associated with increased risk for atherosclerosis and premature cardiovascular disease. Certain dietary behaviours may be cardioprotective and public health strategies are needed to guide consumers' dietary choices and help prevent diet-related disease. The Food Standards Agency nutrient profiling system (FSAm-NPS) constitutes the basis of the five-colour front-of-pack Nutri-Score labelling system. No study has examined FSAm-NPS index associations with a wide range of lipoprotein particle subclasses. METHODS: This was a cross-sectional study of 2006 middle-to older-aged men and women randomly selected from a large primary care centre. Individual participant FSAm-NPS dietary scores were derived from validated food frequency questionnaires. Lipoprotein particle subclass concentrations and size were determined using nuclear magnetic resonance spectroscopy. Multivariate-adjusted linear regression analyses were performed to examine FSAm-NPS relationships with lipoprotein particle subclasses. RESULTS: In fully adjusted models which accounted for multiple testing, higher FSAm-NPS scores, indicating poorer dietary quality, were positively associated with intermediate-density lipoprotein (ß = 0.096, p = 0.005) and small high-density lipoprotein (HDL) (ß = 0.492, p = 0.006) concentrations, a lipoprotein insulin resistance score (ß = 0.063, p = 0.02), reflecting greater lipoprotein-related insulin resistance, and inversely associated with HDL size (ß = -0.030, p = 0.045). CONCLUSIONS: A higher FSAm-NPS score is associated with a less favourable lipoprotein particle subclass profile in middle-to older-aged adults which may be a potential mechanism underlying reported health benefits of a healthy diet according to Nutri-Score rating.

Plant-based diet adherence is associated with metabolic health status in adults living with and without obesity.

PURPOSE: Metabolic health phenotypes exist across the body mass index spectrum. Diet may be an important modifiable risk factor, yet limited research exists on dietary patterns in this context. We investigated associations between dietary patterns, reflecting dietary quality, healthfulness and inflammatory potential, and metabolic health phenotypes in adults living with and without obesity. METHODS: This cross-sectional study included 2,040 middle- to older-aged men and women randomly selected from a large primary care centre. The Dietary Approaches to Stop Hypertension score, Healthy Eating Index, Dietary Inflammatory Index, overall, healthful and unhealthful plant-based dietary indices and Nutri-Score were derived from validated food frequency questionnaires. Descriptive and logistic regression analyses were used to examine diet score relationships with metabolic health phenotypes (Metabolically Healthy/Unhealthy Obese (MHO/MUO) and Non-Obese (MHNO/MUNO)), defined using three separate metabolic health definitions, each capturing different aspects of metabolic health. RESULTS: In fully adjusted models, higher unhealthful plant-based dietary scores were associated with a lower likelihood of MHO (OR = 0.96, 95% CI: 0.93-1.00, p = 0.038) and MHNO (OR = 0.97, 95% CI: 0.95-0.99, p = 0.006). Higher Nutri-Score values were associated with an increased likelihood of MHNO (OR = 1.06, 95% CI: 1.01-1.13, p = 0.033). CONCLUSION: These findings provide evidence that more unhealthful plant-based diets may be linked with unfavourable metabolic health status, irrespective of BMI.

Lifestyle factors and BMI attenuate relationships between biomarkers of inflammation and depressive symptoms and well-being: A cross-sectional study.

Background: Mental disorders are a growing public health concern and evidence has linked chronic low-grade inflammation with depression and well-being. Research also suggests that certain modifiable lifestyle factors such as smoking, alcohol use, physical activity, diet quality and BMI are related to psychological health. These may modulate the relationship between low-grade inflammation and mental health conditions. In this study we examined inflammatory biomarker associations with two psychological health scores and investigated whether relationships are influenced by lifestyle factors and BMI. Methods: This was a cross-sectional study of 1824 middle-to older-aged men and women randomly selected from a large primary care centre. Depressive symptoms and well-being were assessed using the 20-item Centre for Epidemiologic Studies Depression (CES-D) Scale and the World Health Organization-Five (WHO-5) Well-Being Index. Linear regression analyses were performed to examine depression and well-being score relationships with six inflammatory biomarkers, and a composite inflammatory biomarker score, adjusting for demographic characteristics, health conditions, lifestyle factors and BMI. Results: Depression and well-being score associations with complement component 3 (CES-D only) c-reactive protein, interleukin 6, leptin, white blood cell counts, neutrophils and the inflammatory biomarker score were observed. These relationships survived adjustment for demographic variables and health conditions but were attenuated in models which included lifestyle factors and BMI. In final models, only leptin (ß = 0.566, p = 0.018) and inflammatory score (ß = 0.137, p = 0.004) associations with the CES-D score remained. Conclusions: These findings suggest that the relationship between systemic low-grade inflammation and depressive symptoms and well-being may be largely explained by lifestyle factors and adiposity, highlighting the potential importance of promoting a healthy lifestyle in the treatment of depressive disorders.

Sociodemographic factor associations with maternal and placental outcomes: A cluster and partial least squares regression analysis.

INTRODUCTION: Maternal social disadvantage adversely affects maternal and offspring health, with limited research on placental outcomes. Therefore, we examined maternal sociodemographic factor associations with placental and birth outcomes in general (Lifeways Cross-Generation Cohort) and at-risk (PEARS Study of mothers with overweight or obesity) populations of pregnant women. METHODS: TwoStep cluster analysis profiled Lifeways mothers (n = 250) based on their age, parity, marital status, household income, private healthcare insurance, homeowner status, and education. Differences in placental and birth outcomes (untrimmed placental weight (PW), birthweight (BW) and BW:PW ratio) between clusters were assessed using one-way ANOVA and chi-square tests. Partial least squares regression analysed individual effects of sociodemographic factors on placental and birth outcomes in Lifeways and PEARS mothers (n = 461). RESULTS: Clusters were classified as "Married Homeowners" (n = 140, 56 %), "Highest Income" (n = 58, 23.2 %) and "Renters" (n = 52, 20.8 %) in the Lifeways Cohort. Renters were younger, more likely to smoke, have a means-tested medical card and more pro-inflammatory diets compared to other clusters (p < 0.01). Compared to Married Homeowners, renters' offspring had lower BW (-259.26 g, p < 0.01), shorter birth length (-1.31 cm, p < 0.01) and smaller head circumference (-0.59 cm, p = 0.02). PLS regression analyses identified nulliparity as having the greatest negative effect on PW (Lifeways and PEARS) while being a homeowner had the greatest positive effect on PW (Lifeways). CONCLUSION: Certain combinations of sociodemographic factors (particularly homeownership) were associated with less favourable lifestyle factors, and with birth, but not placental outcomes. When explored individually, parity contributed to the prediction of placental and birth outcomes in both cohorts of pregnant women.

Associations between a paternal healthy lifestyle score and its individual components with childhood overweight and obesity.

BACKGROUND: Maternal healthy lifestyle behaviors during pregnancy have been associated with reduced risk of offspring overweight and obesity (OWOB). However, there has been little investigation, in the context of the Paternal Origins of Health and Disease (POHaD) paradigm, of the potential influence of the paternal lifestyle on offspring OWOB. OBJECTIVES: To describe paternal healthy lifestyle factors around pregnancy and investigate their associations, individually and combined, with offspring risk of OWOB during childhood. MATERIALS AND METHODS: Participants included 295 father-child pairs from the Lifeways Cross-Generation Cohort Study. A composite paternal healthy lifestyle score (HLS) based on having a high dietary quality (top 40% of the Healthy Eating Index-2015), meeting physical activity guidelines (≥450 MET-min/week of moderate-to-vigorous physical activity), having a healthy body mass index (BMI) (18.5-24.9 kg/m2 ), being a non-smoker, and having no/moderate alcohol intake, was calculated (range 0-5). Paternal HLS (and individual components) associations with child BMI and waist-to-height ratio (WHtR) at age 5 and 9 years were assessed using linear (BMI z-scores and WHtR) and logistic (IOTF categories) regression analyses, adjusted for sociodemographic characteristics. RESULTS: At age 5 and 9 years, 23.5% and 16.9% of children were classified as living with OWOB, respectively. Of the 160 pairs with a complete HLS, 45.0% of the fathers had unfavorable lifestyle factors, determined by a low HLS between 0 and 2 points. Although a low paternal HLS was not significantly associated with a higher risk of childhood OWOB measured using either BMI z-scores and IOTF categories, it was associated with a greater child WHtR, an indicator of central adiposity, at 9 years of age (ß [95% CI] = 0.04 [0.01,0.07]). DISCUSSION AND CONCLUSION: Almost half of the fathers had unfavorable lifestyle factors around pregnancy. A low paternal HLS was associated with a greater child WHtR at 9 years but not with a higher risk of childhood OWOB when measured by BMI z-scores or IOTF categories.

Relationships between childhood adversity and inflammatory biomarkers in adulthood: A cross-sectional analysis of a middle-to older-aged population.

Background: Exposure to adverse childhood experiences (ACEs) has been linked with increased cardiometabolic risk in adulthood. Low-grade systemic inflammation may underlie this association. Thus far, however, there has been limited investigation of later life inflammatory biomarkers in the context of childhood adversity. Objectives: To assess ACE history, and ACE subcategory, relationships with a broad range of inflammatory biomarkers in middle-to older-aged adults to test the hypothesis that ACE exposure is associated with an unfavourable inflammatory profile in adulthood and determine whether associations vary by ACE subtype and sex. Methods: This study used data from a random sample of 1,839 men and women aged 46-74 years. Participant exposure to ACEs (overall and subtypes including abuse, neglect and household dysfunction) was determined using a validated 10-item ACE questionnaire. Inflammatory biomarkers (pro-inflammatory cytokines, adipocytokines, acute-phase response proteins, white blood cell counts and their constituents, coagulation factors and glycoprotein acetyl) were measured from participant blood samples. Linear regression analyses examined relationships between ACE history (overall and each subcategory) and inflammatory biomarkers in adulthood, controlling for potential confounders. Sex-stratified and mediation analyses were also conducted. Results: In age and sex-adjusted models, ACE history was significantly associated with higher c-reactive protein (p = 0.027), resistin (p = 0.024), white blood cell count (WBC) (p = 0.034), monocyte (p = 0.044), eosinophil (p = 0.031) and plasminogen activator inhibitor-1 (p = 0.047) concentrations, and lower adiponectin (p = 0.025) levels. Results from stratified analyses indicated sex differences and ACE subtype specific associations, with household dysfunction identified as the main driver of positive ACE associations with WBCs and constituents (all p < 0.05). Mediation analyses suggested that BMI and smoking mediate relationships between ACE exposures and increased inflammation. Conclusions: This study provides evidence that ACE exposure may be associated with more pro-inflammatory and pro-thrombotic profiles in adulthood. Associations differed according to ACE subtype, and sex differences exist, which may influence cardiometabolic risk.

Anthropometric measures, predicted visceral adipose tissue and biomarkers of chronic inflammation.

BACKGROUND: Evidence has linked low-grade systemic inflammation and visceral adipose tissue (VAT) with development of chronic conditions. Cytokines and select proteins released by VAT may promote a low-grade inflammatory response. A number of equations have been developed to estimate VAT levels. In this study, we compared predicted VAT equation relationships with biomarkers of inflammation. METHODS: This was a cross-sectional study of 2038 men and women aged 46-73 years. Correlation and linear regression analyses were performed to examine inflammatory biomarker relationships with four commonly assessed anthropometric measures and 10 predicted VAT equations. RESULTS: Compared with anthropometric measures, predicted VAT equations were found to explain a greater proportion of variance in CRP (R2 = .075, p = .001), IL-6 (R2 = .060, p = .001), TNF-α (R2 = .017, p = .005), resistin (R2 = .011, p = .012), monocyte (R2 = .027, p = .001), eosinophil (R2 = .012, p = .01) and basophil (R2 = .015, p = .002) levels in males, and a greater variance in concentrations of C3 (R2 = .175, p = .001), IL-6 (R2 = .090, p = .001), TNF-α (R2 = .036, p = .001), adiponectin (R2 = .121, p = .001), the adiponectin-to-leptin ratio (R2 = .444, p = .001), resistin (R2 = .025, p = .001), white blood cell count (R2 = .057, p = .001), neutrophils (R2 = .061, p = .001) and lymphocytes (R2 = .020, p = .001) in females. CONCLUSION: Equations for assessing VAT levels might be useful to characterise metabolic health. Further studies that examine predicted VAT relationships with disease and mortality outcomes are warranted.

The impact of macrosomia on cardiometabolic health in preteens: findings from the ROLO longitudinal birth cohort study.

BACKGROUND: Macrosomia (birthweight ≥ 4 kg or ≥ 4.5 kg) is strongly associated with a predisposition to childhood obesity, which in turn is linked with adverse cardiometabolic health. Despite this, there is a lack of longitudinal investigation on the impact of high birthweight on cardiometabolic outcomes in youth. The preteen period represents an important window of opportunity to further explore this link, to potentially prevent cardiometabolic profiles worsening during puberty. METHODS: This is a secondary analysis of 9-11-year-olds (n = 405) born to mothers in the ROLO longitudinal birth cohort study, who previously delivered an infant with macrosomia. Preteens were dichotomised into those born with and without macrosomia, using two common cut-off criteria (birthweight ≥ 4 kg (n = 208) and < 4 kg; ≥ 4.5 kg (n = 65) and < 4.5 kg). Cardiometabolic health was assessed using anthropometry, dual-energy x-ray absorptiometry, blood pressure, heart rate, cardiorespiratory endurance (20-m shuttle run test), and non-fasting serum biomarkers for a subgroup (n = 213). Statistical comparisons between the two groups were explored using independent t-tests, Mann-Whitney U tests, and Chi-square tests. Crude and adjusted linear regression models investigated associations between macrosomia and preteen cardiometabolic outcomes. RESULTS: In total, 29.3% (n = 119) of preteens had overweight/obesity based on their BMI z-score. Preteens born ≥ 4 kg had lower median (IQR) C3 concentrations (1.38 (1.22, 1.52) g/L vs. 1.4 (1.26, 1.6) g/L, p = 0.043) and lower median (IQR) ICAM-1 concentrations (345.39 (290.34, 394.91) ng/mL vs. 387.44 (312.91, 441.83) ng/mL, p = 0.040), than those born < 4 kg. Those born ≥ 4.5 kg had higher mean (SD) BMI z-scores (0.71 (0.99) vs. 0.36 (1.09), p = 0.016), and higher median (IQR) lean mass (24.76 (23.28, 28.51) kg vs. 23.87 (21.9, 26.79) kg, p = 0.021), than those born < 4.5 kg. Adjusted linear regression analyses revealed birthweight ≥ 4 kg was negatively associated with C3 concentration (g/L) (B = - 0.095, 95% CI = - 0.162, - 0.029, p = 0.005) and birthweight ≥ 4.5 kg was positively associated with weight z-score (B = 0.325, 95% CI = 0.018, 0.633, p = 0.038), height z-score (B = 0.391, 95% CI = 0.079, 0.703, p = 0.014), lean mass (kg) (B = 1.353, 95% CI = 0.264, 2.442, p = 0.015) and cardiorespiratory endurance (B = 0.407, 95% CI = 0.006, 0.808, p = 0.047). CONCLUSION: This study found no strong evidence to suggest that macrosomia is associated with adverse preteen cardiometabolic health. Macrosomia alone may not be a long-term cardiometabolic risk factor. Trial registration ISRCTN54392969 registered at  www.isrctn.com .

Plant-based dietary indices and biomarkers of chronic low-grade inflammation: a cross-sectional analysis of adults in Ireland.

PURPOSE: There is increasing interest in the health benefits of plant-based diets (PBDs). Evidence reports favourable associations with inflammatory profiles and reduced cardiovascular disease risk. However, limited studies have examined relationships between PBD indices (PDIs) and inflammatory biomarkers. We explored overall PDI, healthful PDI (hPDI) and unhealthful PDI (uPDI) associations with inflammatory biomarker profiles. METHODS: This cross-sectional analysis included 1986 middle- to older-aged adults from the Mitchelstown Cohort. PDI scores were calculated using validated food frequency questionnaires. PDI score associations with inflammatory biomarkers were assessed via linear regression analysis, with adjustment for potential confounders. RESULTS: Comparison of quintiles (Q5 vs Q1) revealed lower concentrations of C-reactive protein (CRP), interleukin 6 (IL-6), white blood cells (WBCs), neutrophils and monocytes, and the leptin-to-adiponectin ratio (PDI and hPDI P < 0.05); lower leptin (PDI, P < 0.05), and complement component 3 (C3), tumour necrosis factor alpha (TNF-α), plasminogen activator inhibitor 1, lymphocytes and eosinophils (hPDI, P < 0.05); and higher concentrations of adiponectin (PDI and hPDI, P < 0.05). Conversely, higher concentrations of C3, CRP, IL-6, TNF-α, resistin, WBCs, neutrophils, lymphocytes, monocytes and eosinophils, and the neutrophil-to-lymphocyte ratio, and lower adiponectin concentrations were observed comparing uPDI quintiles (P < 0.05). In fully adjusted regression models, higher hPDI scores were associated with lower concentrations of C3, TNF-α, WBCs, neutrophils and monocytes (all P < 0.01). Higher uPDI scores were associated with higher C3 and TNF-α concentrations (all P < 0.01). CONCLUSION: This study provides evidence that a more healthful PBD is associated with a more favourable inflammatory profile and that a more unhealthful PBD is associated with the reverse.

Plant-based diet indices and lipoprotein particle subclass profiles: A cross-sectional analysis of middle- to older-aged adults.

BACKGROUND AND AIMS: Plant-based diets (PBDs) are associated with favourable lipid profiles and cardiometabolic outcomes. However, limited data regarding PBD indices (PDIs) and lipoprotein subclasses exist. We examined overall PDI, healthful PDI (hPDI) and unhealthful PDI (uPDI) associations with lipid and lipoprotein profiles. METHODS: This cross-sectional analysis includes 1,986 middle- to older-aged adults from the Mitchelstown Cohort. The PDI, hPDI and uPDI scores were calculated from validated food frequency questionnaires. Higher PDI, hPDI and uPDI scores indicate a more PBD, healthful PBD and unhealthful PBD, respectively. Lipoprotein particle size and subclass concentrations were measured using nuclear magnetic resonance spectroscopy. Relationships between PDIs and lipid and lipoprotein profiles were examined via correlation and regression analyses adjusted for covariates. RESULTS: In fully adjusted regression analyses, higher PDI scores were associated with lower high-density lipoprotein (HDL) cholesterol concentrations and more triglyceride-rich lipoprotein and small very low-density lipoprotein (VLDL) particles. Higher hPDI scores were negatively associated with non-HDL cholesterol concentrations, large VLDL and small HDL particles, the Lipoprotein Insulin Resistance Index (LP-IR) score and VLDL particle size. Higher uPDI scores were associated with lower HDL cholesterol and greater triglyceride concentrations and more medium and large VLDL, total LDL, small LDL and total non-HDL particles, less large LDL and large HDL particles, a greater LP-IR score, greater VLDL particle size and smaller LDL and HDL particle size. CONCLUSIONS: This study provides novel evidence regarding associations between PBD quality and lipoprotein subclasses. A more unhealthful PBD was robustly associated with a more pro-atherogenic lipoprotein profile.

Associations between the maternal healthy lifestyle score and its individual components during early pregnancy with placental outcomes.

INTRODUCTION: The influence of maternal lifestyle behaviours on placental growth have been investigated individually, but with conflicting results, and their combined effect is under-researched. Therefore, we examined associations between a composite maternal healthy lifestyle score (HLS), and its individual components, during early pregnancy with placental outcomes. METHODS: Participants included Lifeways Cross-Generational Cohort mother-child pairs (n = 202). A composite HLS based on a less inflammatory diet (bottom 40% of the energy-adjusted Dietary Inflammatory Index (E-DII™)), moderate-to-vigorous physical activity (MVPA), healthy pre-pregnancy BMI (18.5-24.9 kg/m2), never smoking, and non-/moderate alcohol intake was calculated. Quantile regression analysed HLS (and individual components) associations with measures of placental development (untrimmed placental weight (PW)) and function (birth weight:placental weight (BW:PW) ratio) at the 10th, 25th, 50th, 75th and 90th centiles. RESULTS: A more pro-inflammatory diet was positively, and smoking and heavy alcohol consumption were negatively, associated with PW at median centiles (B: 41.97 g, CI: 3.71, 80.22, p < 0.05; B: -58.51 g, CI: -116.24, -0.77, p < 0.05; B: -120.20 g, CI: -177.97, -62.43, p < 0.05 respectively). Low MVPA was inversely associated with BW:PW ratio at the 10th and 90th centiles (B: -0.36, CI: -0.132, -0.29, p < 0.01 and B: -0.45, CI: -0.728, -0.182, p < 0.01, respectively). Heavy alcohol intake was positively associated with BW:PW ratio at the 10th centile (B: 0.54, CI: 0.24, 0.85, p < 0.01). Results of sex-stratified analysis provide evidence of sexual dimorphism. DISCUSSION: Associations of certain lifestyle factors, but not the composite HLS, during early pregnancy with measures of placental development (PW) and function (BW:PW ratio) varied by quantiles and by sex.

Impact of parental lifestyle patterns in the preconception and pregnancy periods on childhood obesity.

Introduction: High prevalence of overweight and obesity already observed in preschool children suggests the involvement of early-life risk factors. Preconception period and pregnancy are crucial windows for the implementation of child obesity prevention interventions with parental lifestyle factors as relevant targets. So far, most studies have evaluated their role separately, with only a few having investigated their potential synergistic effect on childhood obesity. Our objective was to investigate parental lifestyle patterns in the preconception and pregnancy periods and their association with the risk of child overweight after 5 years. Materials and methods: We harmonized and interpreted results from four European mother-offspring cohorts participating in the EndObesity Consortium [EDEN, France; Elfe, France; Lifeways, Ireland; and Generation R, Netherlands] with data available for 1,900, 18,000, 1,100, and 9,500 families, respectively. Lifestyle factors were collected using questionnaires and included parental smoking, body mass index (BMI), gestational weight gain, diet, physical activity, and sedentary behavior. We applied principal component analyses to identify parental lifestyle patterns in preconception and pregnancy. Their association with risk of overweight (including obesity; OW-OB) and BMI z-scores between 5 and 12 years were assessed using cohort-specific multivariable logistic and linear and regression models (adjusted for potential confounders including parental age, education level, employment status, geographic origin, parity, and household income). Results: Among the various lifestyle patterns derived in all cohorts, the two explaining the most variance were characterized by (1) "high parental smoking, low maternal diet quality (and high maternal sedentary behavior in some cohorts)" and, (2) "high parental BMI and low gestational weight gain." Patterns characterized by high parental BMI, smoking, low diet quality or high sedentary lifestyle before or during pregnancy were associated with higher risk of OW-OB in children, and BMI z-score at any age, with consistent strengths of associations in the main cohorts, except for lifeways. Conclusion: This project provides insight into how combined parental lifestyle factors in the preconception and pregnancy periods are associated with the future risk of child obesity. These findings are valuable to inform family-based and multi-behavioural child obesity prevention strategies in early life.

Socio-ecological predictors of dietary inflammatory scores and associations with childhood and adolescent adiposity: A protocol for a rapid scoping review of observational studies.

INTRODUCTION: Diet-related inflammation is associated with adiposity. Obesity and inflammation in early life may have adverse health outcomes in later life; however, the socio-ecological predictors of a pro-inflammatory diet in childhood and adolescence are not well understood. This rapid scoping review aims to summarise the current state of research from observational studies investigating socio-ecological predictors (childhood, parental, familial, demographic and chronobiological risk factors) and their association with diet-associated inflammation and adiposity in children and adolescents. METHODS: This scoping review will be conducted using the frameworks based on the Joanna Briggs Institute and Arksey and O'Malley and the Population, Concept and Context (PCC) mnemonic. Searches were conducted in OVID Medline, Cinahl and Embase, with adaptations as required. The piloted study selection process will utilise two reviewers for study selection, with reference lists checked for included studies. A third reviewer will moderate disagreements. Data will be extracted by one reviewer and calibrated by a second reviewer. RESULTS: The results will be reported using the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) checklist and PRISMA-ScR flow diagram. The main findings will be synthesised into themes and concepts narratively. Tables and graphs will present frequencies, study details and categorical descriptions. DISCUSSION: This scoping review will provide an overview of the research conducted to date regarding predictors of diet-related inflammation in childhood and their associations with adiposity. Better understanding of the factors associated with a more inflammatory diet in childhood may be useful for clinicians and policy makers when designing and implementing health interventions.

Association of adverse childhood experiences with lipid profiles and atherogenic risk indices in a middle-to-older aged population.

Background: Adverse childhood experiences (ACE) have been associated with poor later life health outcomes, including cardiovascular disease (CVD). Limited research investigating potential underlying biological mechanisms linking ACE to CVD exists, particularly regarding lipid biomarkers. Objectives: The aim of this study was to examine the associations between childhood adversity and unfavourable lipid profiles and derived atherogenic risk indices in a middle-to-older aged population. Methods: This cross-sectional study includes 1820 participants from the Mitchelstown cohort (49% male) in Ireland. Participants' self-reported history of childhood adversity (overall and by subtypes household dysfunction, abuse and neglect) were assessed through a validated 10-item ACE questionnaire. Lipid profiles were determined and atherogenic risk indices including Castelli's Risk Index 1 and 2 (CRI-I and CRI-II), Atherogenic Coefficient (AC) and Atherogenic Index Plasma (AIP) were generated. Logistic regression analysed ACE associations with unfavourable lipid outcomes, controlling for potential confounders. Results: ACE history (reported by 23% of sample), in particular childhood exposure to household dysfunction, was associated with later-life non-optimal TG and HDL-C concentrations and atherogenic risk indices CRI-II and AC in age and sex-adjusted models (all p < 0.05). In fully adjusted models, adults reporting ACE or exposure to household dysfunction were approximately twice as likely to have pro-atherogenic CRI-II relative to adults with no ACE (OR = 1.86, 95% CI: 1.19-2.92, p = 0.006 and OR = 2.19, 95% CI: 1.33-3.61, p = 0.002, respectively). Sex-stratified analysis demonstrated sex-specific associations. Conclusions: This study provides evidence that ACEs are common among older adults in Ireland and are associated with unfavourable lipid profiles and derived atherogenic risk indices.

Why do preconception and pregnancy lifestyle interventions show little evidence of success in preventing overweight and obesity in children? A scoping review.

BACKGROUND: Adverse lifestyle factors in the periconception and early life period, including high maternal prepregnancy BMI and excessive gestational weight gain, are important risk factors for childhood obesity. Early prevention is key, but results from systematic reviews of preconception and pregnancy lifestyle interventions have shown mixed success in improving children's weight outcomes and adiposity. We aimed to investigate the complexity of these early interventions and process evaluation components and authors' statements to improve our understanding regarding their limited success. METHODS: We did a scoping review, guided by frameworks of the Joanna Briggs Institute and Arksey and O'Malley. Eligible articles (with no language restriction) were identified between July 11 and Sept 12, 2022, by searching PubMed, Embase, and CENTRAL; consulting previous reviews; and conducting CLUSTER searches. A thematic analysis was conducted with NVivo in which process evaluation components and authors' interpretations were coded as reasons. Intervention complexity was evaluated with the Complexity Assessment Tool for Systematic Reviews. FINDINGS: 40 publications corresponding to 27 eligible preconception or pregnancy lifestyle trials with child data beyond age 1 month were included. Most interventions started during pregnancy (n=25) and focused on multiple lifestyle factors (eg, diet and exercise). The preliminary results show that almost no interventions involved the participants' partner or social network. Potential reasons for limited success in the interventions preventing overweight or obesity in children included the start time of the intervention, duration and intensity, and sample size or dropout rates. The results will be discussed with an expert group as part of a consultation stage. INTERPRETATION: The results and discussions with an expert group are expected to uncover gaps and inform the design or adaptation of future interventions and approaches to potentially increase success rates in preventing childhood obesity. FUNDING: Funded by the Irish Health Research Board through the transnational JPI HDHL ERA-NET HDHL-INTIMIC-2020 call (PREPHOBES): EU Cofund action (number 727565; EndObesity project).

Parental lifestyle patterns around pregnancy and risk of childhood obesity in four European birth cohort studies.

BACKGROUND: A high prevalence of excess weight in children younger than 5 years suggests the involvement of early-life risk factors. The preconception and pregnancy periods are crucial stages for the implementation of interventions to prevent childhood obesity. Most studies so far have evaluated the effects of early-life factors separately, with only a few investigating the combined effect of parental lifestyle factors. Our objective was to fill the literature gap regarding parental lifestyle factors in the preconception and pregnancy periods and to study their association with the risk of overweight in children after the age of 5 years. METHODS: We harmonised and interpreted data from four European mother-offspring cohorts (EDEN [comprising 1900 families], Elfe [comprising 18 000 families], Lifeways [comprising 1100 families], and Generation R [comprising 9500 families]). Written informed consent was obtained from parents of all involved children. Lifestyle factor data collected through questionnaires comprised parental smoking, BMI, gestational weight gain, diet, physical activity, and sedentary behaviour. We applied principal component analyses to identify multiple lifestyle patterns in preconception and pregnancy. Their association with child BMI z-score and risk of overweight (including obesity, overweight and obesity, as defined by the International Task Force reference) between the ages of 5 and 12 years were assessed using cohort-specific multivariable linear and logistic regression models (adjusted for confounders including parental age, education level, employment status, geographic origin, parity, and household income). FINDINGS: Among the various lifestyle patterns identified in all cohorts, the two that better explained variance were high parental smoking plus low maternal diet quality or high maternal sedentary behaviour, and high parental BMI plus low gestational weight gain. Overall, we observed that patterns characterised by high parental BMI, smoking, low-quality diet, or sedentary lifestyle before or during pregnancy were associated with higher BMI z-scores and risk of overweight and obesity in children aged 5-12 years. INTERPRETATION: Our data contribute to a better understanding of how parental lifestyle factors might be associated with the risk of childhood obesity. These findings are valuable to inform future family-based and multi-behavioural child obesity prevention strategies in early life. FUNDING: European Union's Horizon 2020 under the ERA-NET Cofund action (reference 727565) and European Joint Programming Initiative "A Healthy Diet for a Healthy Life" (JPI HDHL, EndObesity).

Maternal and Paternal Dietary Quality and Dietary Inflammation Associations with Offspring DNA Methylation and Epigenetic Biomarkers of Aging in the Lifeways Cross-Generation Study.

BACKGROUND: Early-life nutritional exposures may contribute to offspring epigenetic modifications. However, few studies have evaluated parental dietary quality effects on offspring DNA methylation (DNAm). OBJECTIVES: We aim to fill this gap by elucidating the influence of maternal and paternal whole-diet quality and inflammatory potential on offspring DNAm in the Lifeways Cross-generation cohort. METHODS: Families (n = 1124) were recruited around 16 weeks of gestation in the Republic of Ireland between 2001 and 2003. Maternal dietary intake during the first trimester and paternal diet during the 12 previous months were assessed with an FFQ. Parental dietary inflammatory potential and quality were determined using the energy-adjusted Dietary Inflammatory Index (E-DII), the Healthy Eating Index-2015 (HEI-2015), and the maternal DASH score. DNAm in the saliva of 246 children at age nine was measured using the Illumina Infinium HumanMethylationEPIC array. DNAm-derived biomarkers of aging, the Pediatric-Buccal-Epigenetic clock and DNAm estimator of telomere length, were calculated. Parental diet associations with the DNAm concentrations of 850K Cytosine-phosphate-guanine sites (CpG sites) and with DNAm-derived biomarkers of aging were examined using an epigenome-wide association study and linear regressions, respectively. RESULTS: Maternal HEI-2015 scores were inversely associated with DNAm at CpG site (cg21840035) located near the PLEKHM1 gene, whose functions involve regulation of bone development (ß = -0.0036, per 1 point increase in the score; P = 5.6 × 10-8). Higher paternal HEI-2015 score was related to lower methylation at CpG site (cg22431767), located near cell signaling gene LUZP1 (ß = -0.0022, per 1 point increase in the score, P = 4.1 × 10-8). There were no associations with parental E-DII and DASH scores, and no evidence of major effects on biomarkers of aging. CONCLUSIONS: Parental dietary quality in the prenatal period, evaluated by the HEI-2015, may influence offspring DNAm during childhood. Further research to improve our understanding of parental nutritional programming is warranted.

Associations between maternal dietary scores during early pregnancy with placental outcomes.

Background and aims: Individual macronutrient and micronutrient effects on placental growth have been widely investigated. However, the influence of overall maternal diet is relatively unknown. Therefore, the aim of this study is to examine associations between a range of maternal dietary scores during early pregnancy with placental outcomes, and to investigate whether there is evidence of sexual dimorphism. Methods: This analysis of the Lifeways Cross-Generational Cohort includes 276 mother-child pairs. A validated 148-item semi-quantitative food frequency questionnaire assessed maternal diet in early pregnancy. Dietary scores reflecting dietary quality [Healthy Eating Index (HEI-2015), Dietary Approaches to Stop Hypertension (DASH)], dietary inflammatory potential [Dietary Inflammatory Index (DII) and the energy adjusted DII (E-DII)], dietary antioxidant status [Dietary Antioxidant Quality (DAQ)], and glycemic and insulinemic loads/indices (GL/GI, IL/II) were calculated. Linear regression analyses assessed maternal dietary score relationships with untrimmed placental weight (PW) and birth weight:placental weight (BW:PW) ratio. Results: In fully adjusted models, maternal E-DII and GI were positively associated, and HEI-2015 and DAQ were negatively associated with PW (B: 12.31, 95% CI: 0.41, 24.20, p = 0.04, B: 4.13, 95% CI: 0.10, 8.17, p = 0.04, B: -2.70, 95% CI: -5.03, -0.35, p = 0.02 and B: -15.03, 95% CI: -28.08, -1.98, p = 0.02, for E-DII, GI, HEI-2015 and DAQ respectively). Maternal DAQ associations with BW:PW ratio were attenuated. When stratified by sex, maternal GI and pregnancy-specific DAQ were associated with PW in female offspring (B: 5.61, 95% CI: 0.27, 10.96, p = 0.04 and B: -15.31, 95% CI: -30.35, -0.27, p = 0.046). Maternal E-DII and HEI-2015 were associated with PW in males (B: 24.31, 95% CI: 5.66, 42.96, p = 0.01 and B: -3.85, 95% CI: -7.47, -0.35, p = 0.03 respectively). Conclusion: The results of this novel investigation suggest that maternal diet may influence placental development. Female fetuses may be more sensitive to increased glucose levels whereas male fetuses may be more susceptible to in-utero stresses that are regulated by inflammatory pathways and overall diet quality. Hence, early pregnancy offers an opportune time for a mother to prioritize dietary changes that focus on reducing inflammatory and glycemic responses.

Plant-Based Diets and Lipid, Lipoprotein, and Inflammatory Biomarkers of Cardiovascular Disease: A Review of Observational and Interventional Studies.

Plant-based diets (PBDs) are becoming increasingly popular. Thus far, the literature has focused on their association with lipid profiles, with less investigation of lipoprotein and inflammatory profiles. Because pro-atherogenic lipid, lipoprotein, and inflammatory processes may facilitate the development of atherosclerosis, understanding the relation between PBDs and these processes is important to inform risk mitigation strategies. Therefore, the objective of this paper was to review the literature on PBDs and lipid, lipoprotein, and inflammatory biomarkers of cardiovascular disease (CVD). A structured literature search was performed, retrieving 752 records, of which 43 articles were included. Plant-based diets generally associated with favourable lipid and lipoprotein profiles, characterised by decreased total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B concentrations, and less low-grade inflammation, characterised by decreased C-reactive protein concentrations. Effect sizes from PBD interventions were greatest compared to habitual dietary patterns, and for non-low-fat vegan and tightly controlled dietary interventions. Associations between PBD indices and the reviewed biomarkers were less consistent. Findings are discussed with reference to the literature on PBDs and PBD indices and CVD risk, the associations between specific plant food groups and CVD outcomes and the reviewed biomarker outcomes, and the potential mechanisms underpinning associations between PBDs and reduced CVD risk.