1048 results found
Roscoe C, Mackay C, Gulliver J, et al., 2022, Associations of private residential gardens versus other greenspace types with cardiovascular and respiratory disease mortality: observational evidence from UK Biobank, Environment International, ISSN: 0160-4120
BackgroundLongitudinal evidence linking urban greenspace to reduced rates of all-cause and cause-specific mortality has mostly been established using greenness measures of limited specificity such as vegetation indices. Evidence on specific green space types, including private residential gardens is less well established.MethodsWe examined associations of greenspace with all-cause, non-injury, cardiovascular disease (CVD) and respiratory disease deaths in UK Biobank – a national prospective cohort of adults with linked Office for National Statistics mortality records. We included private residential gardens and other greenspace types e.g. public parks, sport facilities, using categories from Ordnance Survey MasterMap™ Greenspace. We used Cox proportional hazards models, adjusted for individual and area-level covariates, and stratified analyses by sex, household income, and area-level deprivation. In sensitivity analyses, we further adjusted for air pollution, road-traffic noise, indirect tobacco smoke exposure, and physical activity, and restricted analyses to non-movers.ResultsIn 232,926 participants, we observed 13,586 all-cause, 13,159 non-injury, 2,796 cardiovascular (CVD), and 968 respiratory disease deaths. Private residential garden cover showed inverse associations with all-cause, non-injury, CVD, and chronic respiratory disease mortality, after adjustment for covariates and other types of greenspace, with hazard ratios and 95% confidence intervals of 0.94 (0.91, 0.97), 0.95 (0.92, 0.97), 0.92 (0.86, 0.98) and 0.87 (0.78, 0.98), respectively, per interquartile range (IQR) increase in private residential garden cover (IQR = 21.6% increase within 100 m buffer). Other greenspace types showed weaker inverse associations with CVD and chronic respiratory disease mortality than private residential gardens. Sex, household income, and area level deprivation modified associations. Findings were robust to sensitivity analyses.ConclusionOur finding that priv
Smith-Byrne K, Cerani A, Guida F, et al., 2022, Circulating Isovalerylcarnitine and Lung Cancer Risk: Evidence from Mendelian Randomization and Pre-Diagnostic Blood Measurements., Cancer Epidemiol Biomarkers Prev
BACKGROUND: Tobacco exposure causes 8 of 10 lung cancers, and identifying additional risk factors is challenging due to confounding introduced by smoking in traditional observational studies. MATERIALS AND METHODS: We used Mendelian randomization (MR) to screen 207 metabolites for their role in lung cancer predisposition using independent genome-wide-association studies (GWAS) of blood metabolite levels (n =7,824) and lung cancer risk (n=29,266 cases / 56,450 controls). A nested case control study (656 cases and 1,309 matched controls) was subsequently performed using pre-diagnostic blood samples to validate MR association with lung cancer incidence data from population-based cohorts (EPIC and NSHDS). RESULTS: An MR-based scan of 207 circulating metabolites for lung cancer risk identified that blood isovalerylcarnitine (IVC) was associated with a decreased odds of lung cancer after accounting for multiple testing (Log10-OR = 0.43, 95% CI: 0.29-0.63). Molar measurement of IVC in pre-diagnostic blood found similar results (Log10-OR = 0.39, 95% CI: 0.21-0.72). Results were consistent across lung cancer sub-types. CONCLUSIONS: Independent lines of evidence support an inverse association of elevated circulating IVC with lung cancer risk through a novel methodological approach that integrates genetic and traditional epidemiology to efficiently identify novel cancer biomarkers. IMPACT: Our results find compelling evidence in favor of a protective role for a circulating metabolite, IVC, in lung cancer aetiology. From the treatment of a Mendelian disease, isovaleric acidemia, we know that circulating IVC is modifiable through a restricted protein diet or glycine and L-carnatine supplementation. IVC may represent a modifiable and inversely associated biomarker for lung cancer.
Heath AK, Muller DC, van den Brandt PA, et al., 2022, Diet-wide association study of 92 foods and nutrients and lung cancer risk in the European Prospective Investigation into Cancer and Nutrition study and the Netherlands Cohort Study., Int J Cancer
It is unclear whether diet, and in particular certain foods or nutrients, are associated with lung cancer risk. We assessed associations of 92 dietary factors with lung cancer risk in 327 790 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC). Cox regression yielded adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) per SD higher intake/day of each food/nutrient. Correction for multiple comparisons was performed using the false discovery rate and identified associations were evaluated in the Netherlands Cohort Study (NLCS). In EPIC, 2420 incident lung cancer cases were identified during a median of 15 years of follow-up. Higher intakes of fibre (HR per 1 SD higher intake/day = 0.91, 95% CI 0.87-0.96), fruit (HR = 0.91, 95% CI 0.86-0.96) and vitamin C (HR = 0.91, 95% CI 0.86-0.96) were associated with a lower risk of lung cancer, whereas offal (HR = 1.08, 95% CI 1.03-1.14), retinol (HR = 1.06, 95% CI 1.03-1.10) and beer/cider (HR = 1.04, 95% CI 1.02-1.07) intakes were positively associated with lung cancer risk. Associations did not differ by sex and there was less evidence for associations among never smokers. None of the six associations with overall lung cancer risk identified in EPIC were replicated in the NLCS (2861 cases), however in analyses of histological subtypes, inverse associations of fruit and vitamin C with squamous cell carcinoma were replicated in the NLCS. Overall, there is little evidence that intakes of specific foods and nutrients play a major role in primary lung cancer risk, but fruit and vitamin C intakes seem to be inversely associated with squamous cell lung cancer.
Fernández-Barrés S, Robinson O, Fossati S, et al., 2022, Urban environment and health behaviours in children from six European countries, Environment International, Vol: 165, ISSN: 0160-4120
Background:Urban environmental design is increasingly considered influential for health and wellbeing, but evidence is mostly based on adults and single exposure studies. We evaluated the association between a wide range of urban environment characteristics and health behaviours in childhood.Methods:We estimated exposure to 32 urban environment characteristics (related to the built environment, traffic, and natural spaces) for home and school addresses of 1,581 children aged 6-11 years from six European cohorts. We collected information on health behaviours including total amount of overall moderate-to-vigorous physical activity, physical activity outside school hours, active transport, sedentary behaviours and sleep duration, and developed patterns of behaviours with principal component analysis. We used an exposure-wide association study to screen all exposure-outcome associations, and the deletion-substitution-addition algorithm to build a final multi-exposure model.Results:In multi-exposure models, green spaces (Normalized Difference Vegetation Index, NDVI) were positively associated with active transport, and inversely associated with sedentary time (22.71 min/day less (95%CI -39.90, -5.51) per interquartile range increase in NDVI). Residence in densely built areas was associated with more physical activity and less sedentary time, and densely populated areas with less physical activity outside school hours and more sedentary time. Presence of a major road was associated with lower sleep duration (-4.80 min/day (95%CI -9.11, -0.48); compared with no major road). Results for the behavioural patterns were similar.Conclusions:This multicohort study suggests that areas with more vegetation, more building density, less population density and without major roads are associated with improved health behaviours in childhood.
Vineis P, Barouki R, 2022, The exposome as the science of social-to-biological transitions, ENVIRONMENT INTERNATIONAL, Vol: 165, ISSN: 0160-4120
Peluso M, Munnia A, Russo V, et al., 2022, Cruciferous Vegetable Intake and Bulky DNA Damage within Non-Smokers and Former Smokers in the Gen-Air Study (EPIC Cohort), NUTRIENTS, Vol: 14
Petrovic D, Bodinier B, Dagnino S, et al., 2022, Epigenetic mechanisms of lung carcinogenesis involve differentially methylated CpG sites beyond those associated with smoking, European Journal of Epidemiology, Vol: 37, Pages: 629-640, ISSN: 0393-2990
Smoking-related epigenetic changes have been linked to lung cancer, but the contribution of epigenetic alterations unrelated to smoking remains unclear. We sought for a sparse set of CpG sites predicting lung cancer and explored the role of smoking in these associations. We analysed CpGs in relation to lung cancer in participants from two nested case–control studies, using (LASSO)-penalised regression. We accounted for the effects of smoking using known smoking-related CpGs, and through conditional-independence network. We identified 29 CpGs (8 smoking-related, 21 smoking-unrelated) associated with lung cancer. Models additionally adjusted for Comprehensive Smoking Index-(CSI) selected 1 smoking-related and 49 smoking-unrelated CpGs. Selected CpGs yielded excellent discriminatory performances, outperforming information provided by CSI only. Of the 8 selected smoking-related CpGs, two captured lung cancer-relevant effects of smoking that were missed by CSI. Further, the 50 CpGs identified in the CSI-adjusted model complementarily explained lung cancer risk. These markers may provide further insight into lung cancer carcinogenesis and help improving early identification of high-risk patients.
Robinson O, 2022, Cord blood metabolites and rapid postnatal growth as multiple mediators in the prenatal propensity to childhood overweight, International Journal of Obesity, Vol: 46, Pages: 1384-1393, ISSN: 0307-0565
BACKGROUND: The mechanisms underlying childhood overweight and obesity are poorly known. Here, we investigated the direct and indirect effects of different prenatal exposures on offspring rapid postnatal growth and overweight in childhood, mediated through cord blood metabolites. Additionally, rapid postnatal growth was considered a potential mediator on childhood overweight, alone and sequentially to each metabolite.METHODS: Within four European birth-cohorts (N=375 mother-child dyads), information on seven prenatal exposures (maternal education, pre-pregnancy BMI, weight gain and tobacco smoke during pregnancy, age at delivery, parity, and child gestational age), selected as obesogenic according to a-priori knowledge, was collected. Cord blood levels of 31 metabolites, associated with rapid postnatal growth and/or childhood overweight in a previous study, were measured via liquid-chromatography-quadrupole-time-of-flight-mass-spectrometry. Rapid growth at 12 months and childhood overweight (including obesity) between four and eight years were defined with reference to WHO growth charts. Single mediation analysis was performed using the imputation approach and multiple mediation analysis using the extended-imputation approach.RESULTS: Single mediation suggested that the effect of maternal education, pregnancy weight gain, parity, and gestational age on rapid postnatal growth but not on childhood overweight was partly mediated by seven metabolites, including cholestenone, decenoylcarnitine(C10:1), phosphatidylcholine(C34:3), progesterone and three unidentified metabolites; and the effect of gestational age on childhood overweight was mainly mediated by rapid postnatal growth. Multiple mediation suggested that the effect of gestational age on childhood overweight was mainly mediated by rapid postnatal growth and that the mediating role of the metabolites was marginal. CONCLUSION: Our findings provide evidence of the involvement of in utero metabolism in the propensity
Jarvelin M-R, 2022, DNA methylation signature of chronic low-gradeinflammation and its role in cardio-respiratorydiseases, Nature Communications, Vol: 13, ISSN: 2041-1723
We performed a multi-ethnic Epigenome Wide Association study on 22,774 individuals to describe the DNA methylation signature of chronic low-grade inflammation as measured by C-Reactive protein (CRP). We find 1,511 independent differentially methylated loci associated with CRP. These CpG sites show correlation structures across chromosomes, and are primarily situated in euchromatin, depleted in CpG islands. These genomic loci are predominantly situated in transcription factor binding sites and genomic enhancer regions. Mendelian randomization analysis suggests altered CpG methylation is a consequence of increased blood CRP levels. Mediation analysis reveals obesity and smoking as important underlying driving factors for changed CpG methylation. Finally, we find that an activated CpG signature significantly increases the risk for cardiometabolic diseases and COPD.
Rothwell JA, Murphy N, Bešević J, et al., 2022, Metabolic signatures of healthy lifestyle patterns and colorectal cancer risk in a European cohort, Clinical Gastroenterology and Hepatology, Vol: 20, Pages: e1061-e1082, ISSN: 1542-3565
Background & AimsColorectal cancer risk can be lowered by adherence to the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) guidelines. We derived metabolic signatures of adherence to these guidelines and tested their associations with colorectal cancer risk in the European Prospective Investigation into Cancer cohort.MethodsScores reflecting adherence to the WCRF/AICR recommendations (scale, 1–5) were calculated from participant data on weight maintenance, physical activity, diet, and alcohol among a discovery set of 5738 cancer-free European Prospective Investigation into Cancer participants with metabolomics data. Partial least-squares regression was used to derive fatty acid and endogenous metabolite signatures of the WCRF/AICR score in this group. In an independent set of 1608 colorectal cancer cases and matched controls, odds ratios (ORs) and 95% CIs were calculated for colorectal cancer risk per unit increase in WCRF/AICR score and per the corresponding change in metabolic signatures using multivariable conditional logistic regression.ResultsHigher WCRF/AICR scores were characterized by metabolic signatures of increased odd-chain fatty acids, serine, glycine, and specific phosphatidylcholines. Signatures were inversely associated more strongly with colorectal cancer risk (fatty acids: OR, 0.51 per unit increase; 95% CI, 0.29–0.90; endogenous metabolites: OR, 0.62 per unit change; 95% CI, 0.50–0.78) than the WCRF/AICR score (OR, 0.93 per unit change; 95% CI, 0.86–1.00) overall. Signature associations were stronger in male compared with female participants.ConclusionsMetabolite profiles reflecting adherence to WCRF/AICR guidelines and additional lifestyle or biological risk factors were associated with colorectal cancer. Measuring a specific panel of metabolites representative of a healthy or unhealthy lifestyle may identify strata of the population at higher risk of colorectal cancer.
Francavilla A, Ferrero G, Pardini B, et al., 2022, FECAL SMALL NON-CODING RNAS AND MICROBIOME CHARACTERIZE PATIENTS WITH CELIAC DISEASE, Publisher: ELSEVIER SCIENCE INC, Pages: S125-S125, ISSN: 1590-8658
Ahmed A, Aune D, Vineis P, et al., 2022, The impact of conditional cash transfers on the control of neglected tropical disease: a systematic review, The Lancet Global Health, Vol: 10, Pages: e640-e648, ISSN: 2214-109X
Background:Neglected tropical diseases (NTDs) are diseases of poverty and affect 1.5 billion people globally. Conditional cash transfer (CCTs) programmes alleviate poverty in many countries, potentially contributing to improved NTD outcomes. This systematic review examines the relationship between CCTs and screening, incidence or treatment outcomes of NTDs.Methods:A systematic review was carried out. MEDLINE, EMBASE, Lilacs, EconLit, Global Health, and grey literature websites were systematically searched in September 2020 with no date or language restrictions. Controlled quantitative studies including randomised controlled trials (RCTs) and observational studies evaluating CCT interventions in low- and middle-income countries (LMICs) were included. Any outcome measures related to the WHO’s 20 diseases classified as NTDs were included. Two authors extracted data from published studies and appraised risk of biases using the Risk of Bias in Non-Randomised Studies of Interventions and Risk of Bias 2 tools. Results were analysed narratively. PROSPERO registration: CRD42020202480.Findings:From the search, 5165 records were identified. Eleven studies were eligible for inclusion covering four CCTs in Brazil, the Philippines, Mexico and Zambia. Most studies were either RCTs or quasi-experimental studies and ten were assessed to be of moderate quality. Seven studies reported improved NTD outcomes associated with CCTs – particularly reduced incidence of leprosy and increased uptake of deworming treatments. There was some evidence of greater benefit in lower socioeconomic groups but sub-group analysis was limited. Methodological weaknesses include self-reported outcomes, missing data, improper randomisation and differences between CCT and comparator populations in observational studies. The available evidence is currently limited, covering a small proportion of CCTs and NTDs. Interpretation:CCTs can be associated with improved NTD outcomes, and could be driven by
Ribeiro AI, Fraga S, Severo M, et al., 2022, Association of neighbourhood disadvantage and individual socioeconomic position with all-cause mortality: a longitudinal multicohort analysis., Lancet Public Health, Vol: 7, Pages: e447-e457
BACKGROUND: Few studies have examined the interactions between individual socioeconomic position and neighbourhood deprivation and the findings so far are heterogeneous. Using a large sample of diverse cohorts, we investigated the interaction effect of neighbourhood socioeconomic deprivation and individual socioeconomic position, assessed using education, on mortality. METHODS: We did a longitudinal multicohort analysis that included six cohort studies participating in the European LIFEPATH consortium: the CoLaus (Lausanne, Switzerland), E3N (France), EPIC-Turin (Turin, Italy), EPIPorto (Porto, Portugal), Melbourne Collaborative Cohort Study (Melbourne, VIC, Australia), and Whitehall II (London, UK) cohorts. All participants with data on mortality, educational attainment, and neighbourhood deprivation were included in the present study. The data sources were the databases of each cohort study. Poisson regression was used to estimate the mortality rates and associations (relative risk, 95% CIs) with neighbourhood deprivation (Q1 being least deprived to Q5 being the most deprived). Baseline educational attainment was used as an indicator of individual socioeconomic position. Estimates were combined using pooled analysis and the relative excess risk due to the interaction was computed to identify additive interactions. FINDINGS: The cohorts comprised a total population of 168 801 individuals. The recruitment dates were 2003-06 for CoLaus, 1989-91 for E3N, 1992-98 for EPIC-Turin, 1999-2003 for EPIPorto, 1990-94 for MCCS, and 1991-94 for Whitehall II. We use baseline data only and mortality data obtained using record linkage. Age-adjusted mortality rates were higher among participants residing in more deprived neighbourhoods than those in the least deprived neighbourhoods (Q1 least deprived neighbourhoods, 369·7 per 100 000 person-years [95% CI 356·4-383·2] vs Q5-most deprived neighbourhoods 445·7 per 100 000 person-years [430·2-461&mid
Roscoe C, Sheridan C, Geneshka M, et al., 2022, Green walkability and physical activity in UK biobank: a cross-sectional analysis of adults in Greater London, International Journal of Environmental Research and Public Health, Vol: 19, Pages: 1-15, ISSN: 1660-4601
Urban greenspace provides opportunities for outdoor exercise and may increase physical activity, with accompanying health benefits. Areas suitable for walking (walkability) are also associated with increased physical activity, but interactions with greenspace are poorly understood. We investigated associations of walkability and green walkability with physical activity in an urban adult cohort. We used cross-sectional data from Greater London UK Biobank participants (n = 57,726) and assessed walkability along roads and footpaths within 1000 m of their residential addresses. Additionally, we assessed green walkability by integrating trees and low-lying vegetation into the walkability index. Physical activity outcomes included self-reported and accelerometer-measured physical activity and active transport. We assessed associations using log-linear, logistic and linear regression models, adjusted for individual- and area-level confounders. Higher green walkability was associated with favourable International Physical Activity Questionnaire responses and achievement of weekly UK government physical activity guideline recommendations. Participants living in the highest versus lowest quintile of green walkability participated in 2.41 min (95% confidence intervals: 0.22, 4.60) additional minutes of moderate-and-vigorous physical activity per day. Higher walkability and green walkability scores were also associated with choosing active transport modes such as walking and cycling. Our green walkability approach demonstrates the utility in accounting for walkability and greenspace simultaneously to understand the role of the built environment on physical activity.
Vineis P, Romanello M, Michelozzi P, et al., 2022, Health co-benefits of climate change action in Italy, LANCET PLANETARY HEALTH, Vol: 6, Pages: E293-E294
Trunfio M, Richiardi L, Alladio F, et al., 2022, Determinants of SARS-CoV-2 Contagiousness in Household Contacts of Symptomatic Adult Index Cases, FRONTIERS IN MICROBIOLOGY, Vol: 13
Papadimitriou N, Bouras E, van den Brandt PA, et al., 2022, A prospective diet-wide association study for risk of colorectal cancer in EPIC, Clinical Gastroenterology and Hepatology, Vol: 20, Pages: 864-873.e13, ISSN: 1542-3565
BACKGROUND & AIMS: Evidence regarding the association of dietary exposures with colorectal cancer (CRC) risk is not consistent with a few exceptions. Therefore, we conducted a diet-wide association study (DWAS) in the European Prospective Investigation into Cancer and Nutrition (EPIC) to evaluate the associations between several dietary exposures with CRC risk. METHODS: The association of 92 food and nutrient intakes with CRC risk was assessed in 386,792 participants, 5,069 of whom developed incident CRC. Correction for multiple comparisons was performed using the false discovery rate, and emerging associations were examined in the Netherlands Cohort Study (NLCS). Multiplicative gene-nutrient interactions were also tested in EPIC based on known CRC-associated loci. RESULTS: In EPIC, alcohol, liquor/spirits, wine, beer/cider, soft drinks, and pork were positively associated with CRC, whereas milk, cheese, calcium, phosphorus, magnesium, potassium, riboflavin, vitamin B6, beta-carotene, fruit, fibre, non-white bread, banana, and total protein intakes were inversely associated. Of these 20 associations, 13 were replicated in NLCS, for which a meta-analysis was performed, namely alcohol (summary HR per 1 SD increment in intake: 1.07; 95%CI:1.04-1.09), liquor/spirits (1.04; 1.02-1.06), wine (1.04;1.02-1.07), beer/cider (1.06;1.04-1.08), milk (0.95;0.93-0.98), cheese (0.96;0.94-0.99), calcium (0.93;0.90-0.95), phosphorus (0.92;0.90-0.95), magnesium (0.95;0.92-0.98), potassium (0.96;0.94-0.99), riboflavin (0.94;0.92-0.97), beta-carotene (0.96;0.93-0.98), and total protein (0.94;0.92-0.97). None of the gene-nutrient interactions were significant after adjustment for multiple comparisons. CONCLUSIONS: Our findings confirm a positive association for alcohol and an inverse association for dairy products and calcium with CRC risk, and also suggest a lower risk at higher dietary intakes of phosphorus, magnesium, potassium, riboflavin, beta-carotene and total protein.
Robinson N, Casement J, Gunter MJ, et al., 2022, Anti-cancer therapy is associated with long-term epigenomic changes in childhood cancer survivors, BRITISH JOURNAL OF CANCER, Vol: 127, Pages: 288-300, ISSN: 0007-0920
McCrory C, Fiorito G, O'Halloran AM, et al., 2022, Early life adversity and age acceleration at mid-life and older ages indexed using the next-generation GrimAge and Pace of Aging epigenetic clocks, PSYCHONEUROENDOCRINOLOGY, Vol: 137, ISSN: 0306-4530
Fiorito G, Pedron S, Ochoa-Rosales C, et al., 2022, The Role of Epigenetic Clocks in Explaining Educational Inequalities in Mortality: A Multicohort Study and Meta-analysis, JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES, ISSN: 1079-5006
Freni Sterrantino A, Fiorito G, D'errico A, et al., 2022, Work-related stress and well-being in association with epigenetic age acceleration: a Northern Finland Birth Cohort 1966 Study, Aging, Vol: 14, Pages: 1128-1156, ISSN: 1945-4589
Recent evidence indicates consistent association of low socioeconomic status with epigenetic age acceleration, measured from DNA methylation. As work characteristics and job stressors are crucial components of socioeconomic status, we investigated their association with various measures of epigenetic age acceleration.The study population included employed and unemployed men and women (n=604) from the Northern Finland Birth Cohort 1966. We investigated the association of job strain, effort-reward imbalance and work characteristics with five biomarkers of epigenetic aging (Hannum, Horvath, PhenoAge, GrimAge, and DunedinPoAm).Our results indicate few significant associations between work stress indicators and epigenetic age acceleration, limited to a range of ±2 years, and smoking recording the highest effect on GrimAge age acceleration biomarker between current and no smokers (median difference 4.73 years (IQR 1.18, 8.41). PhenoAgeAA was associated with job strain active work (β=-1.301 95%CI -2.391, -0.212), slowing aging of less than 1.5 years, and working as white-collar slowed aging six months (GrimAgeAA β=-0.683, 95%CI -1.264, -0.102) when compared to blue collars. Association was found for working for more than 40 hours per week that increased the aging over 1.5 years, (HorvathAA β =2.058 95%CI 0.517,3.599, HannumAA β=1.567, 95%CI 0.415,2.719).The pattern of associations was different between women and men and some of the estimated effects are inconsistent with current literature. Our results provide the first evidence of association of work conditions with epigenetic aging biomarkers. However, further epidemiological research is needed to fully understand how work-related stress affects epigenetic age acceleration in men and women in different societies.
Stratakis N, Siskos AP, Papadopoulou E, et al., 2022, Urinary metabolic biomarkers of diet quality in European children are associated with metabolic health, eLife, Vol: 11, Pages: 1-20, ISSN: 2050-084X
Urinary metabolic profiling is a promising powerful tool to reflect dietary intake and can help understand metabolic alterations in response to diet quality. Here, we used 1H NMR spectroscopy in a multicountry study in European children (1147 children from 6 different cohorts) and identified a common panel of 4 urinary metabolites (hippurate, N-methylnicotinic acid, urea, and sucrose) that was predictive of Mediterranean diet adherence (KIDMED) and ultra-processed food consumption and also had higher capacity in discriminating children’s diet quality than that of established sociodemographic determinants. Further, we showed that the identified metabolite panel also reflected the associations of these diet quality indicators with C-peptide, a stable and accurate marker of insulin resistance and future risk of metabolic disease. This methodology enables objective assessment of dietary patterns in European child populations, complementary to traditional questionary methods, and can be used in future studies to evaluate diet quality. Moreover, this knowledge can provide mechanistic evidence of common biological pathways that characterize healthy and unhealthy dietary patterns, and diet-related molecular alterations that could associate to metabolic disease.
Konstantinoudis G, Cameletti M, Gómez-Rubio V, et al., 2022, Regional excess mortality during the 2020 COVID-19 pandemic in five European countries, Nature Communications, Vol: 13, Pages: 1-11, ISSN: 2041-1723
The impact of the COVID-19 pandemic on excess mortality from all causes in 2020 varied across and within European countries. Using data for 2015-2019, we applied Bayesian spatio-temporal models to quantify the expected weekly deaths at the regional level had the pandemic not occurred in England, Greece, Italy, Spain, and Switzerland. With around 30%, Madrid, Castile-La Mancha, Castile-Leon (Spain) and Lombardia (Italy) were the regions with the highest excess mortality. In England, Greece and Switzerland, the regions most affected were Outer London and the West Midlands (England), Eastern, Western and Central Macedonia (Greece), and Ticino (Switzerland), with 15-20% excess mortality in 2020. Our study highlights the importance of the large transportation hubs for establishing community transmission in thefirst stages of the pandemic. Here, we show that acting promptly to limit transmission around these hubs is essential to prevent spread to other regions and countries.
Alfano R, Robinson O, Handakas E, et al., 2022, Perspectives and challenges of epigenetic determinants of childhood obesity: A systematic review, Obesity Reviews, Vol: 23, Pages: 1-13, ISSN: 1467-7881
The tremendous increase in childhood obesity prevalence over the last few decades cannot merely be explained by genetics and evolutionary changes in the genome, implying that gene–environment interactions, such as epigenetic modifications, likely play a major role. This systematic review aims to summarize the evidence of the association between epigenetics and childhood obesity. A literature search was performed via PubMed and Scopus engines using a combination of terms related to epigenetics and pediatric obesity. Articles studying the association between epigenetic mechanisms (including DNA methylation and hydroxymethylation, non-coding RNAs, and chromatin and histones modification) and obesity and/or overweight (or any related anthropometric parameters) in children (0–18 years) were included. The risk of bias was assessed with a modified Newcastle–Ottawa scale for non-randomized studies. One hundred twenty-one studies explored epigenetic changes related to childhood obesity. DNA methylation was the most widely investigated mechanism (N = 101 studies), followed by non-coding RNAs (N = 19 studies) with evidence suggestive of an association with childhood obesity for DNA methylation of specific genes and microRNAs (miRNAs). One study, focusing on histones modification, was identified. Heterogeneity of findings may have hindered more insights into the epigenetic changes related to childhood obesity. Gaps and challenges that future research should face are herein described.
Handakas E, Lau CH, Alfano R, et al., 2022, A systematic review of metabolomic studies of childhood obesity: State of the evidence for metabolic determinants and consequences, Obesity Reviews, Vol: 23, Pages: 1-13, ISSN: 1467-7881
Childhood obesity has become a global epidemic and carries significant long-term consequences to physical and mental health. Metabolomics, the global profiling of small molecules or metabolites, may reveal the mechanisms of development of childhood obesity and clarify links between obesity and metabolic disease. A systematic review of metabolomic studies of childhood obesity was conducted, following Preferred Reporting Items for Systematic Reviews (PRISMA) guidelines, searching across Scopus, Ovid, Web of Science and PubMed databases for articles published from January 1, 2005 to July 8, 2020, retrieving 1271 different records and retaining 41 articles for qualitative synthesis. Study quality was assessed using a modified Newcastle–Ottawa Scale. Thirty-three studies were conducted on blood, six on urine, three on umbilical cord blood, and one on saliva. Thirty studies were primarily cross-sectional, five studies were primarily longitudinal, and seven studies examined effects of weight-loss following a life-style intervention. A consistent metabolic profile of childhood obesity was observed including amino acids (particularly branched chain and aromatic), carnitines, lipids, and steroids. Although the use of metabolomics in childhood obesity research is still developing, the identified metabolites have provided additional insight into the pathogenesis of many obesity-related diseases. Further longitudinal research is needed into the role of metabolic profiles and child obesity risk.
Vineis P, 2022, [The tragedy of the transfer of research into practice.], Recenti Prog Med, Vol: 113, Pages: 21-23
Alessandro Liberati has been a pioneer of methods for the transfer of research into practice. In the last years this key component of medical practice and decision-making in public health has made one step forward and two steps backward. One forward because the awareness of the need for rational criteria for decision making, based on scientific evidence and literature synthesis, has grown. Two backward because the problems we face have become much more complex. With covid-19 we have seen a rapid acceleration of technological responses and of decision-making, but this has not necessarily followed the recommendations from evidence-based medicine, as testified by the confused bundling up of opinions on the measures to be taken at the bed of patients and at the policy-making level. With the threat of climate change, equally, we face a weak and uncertain process of selection of the best scientific evidence that can guide towards rational policy choices. In both cases the seeds that Alessandro has planted need to be disseminated and reinforced.
This paper is inspired by a thesis on “immune capital” by Kathryn Olivarius. We suggest that the biological capital, which immunity capital is part of, should be considered as an additional component of the life-course experience of individuals, together with the traditional Bourdieu’s social, economic and cultural capitals that drive their lives. Building upon this concept, we consider the relationships between science, society and policy-making in the course of the pandemic. We suggest that we need to ‘reframe problems so that their ethical dimensions are brought to light’ (Jasanoff), with a request for humility extended to political leaders, to ‘look beyond science’ in search for ethical solutions. The present pandemic plays out―and is integral to―the acceleration of the rate of change, Pope Francis’ peculiar word “rapidification”, i.e. a vortex involving technoscience, policy and the new media.
Vineis P, 2021, Deliberative hygiene: how to communicate with those who oppose to vaccines?, EPIDEMIOLOGIA & PREVENZIONE, Vol: 45, Pages: 460-461, ISSN: 1120-9763
Laine J, Huybrechts I, Gunter M, et al., 2021, Co-benefits from sustainable dietary shifts for population and environmental health: an assessment from a large European cohort study, The Lancet Planetary Health, Vol: 5, Pages: e786-e796, ISSN: 2542-5196
Background: Unhealthy diets, the rise of non-communicable diseases, and the declining health of the planet are highly intertwined, where food production and consumption are major drivers of increases in greenhouse gas (GHG) emissions, substantial land use, (LU) and adverse health outcomes such as cancer and mortality. Methods: In the European Prospective Investigation into Cancer and Nutrition (EPIC), a multi-centre prospective cohort study (n=443,991), we estimated associations between dietary contributions to GHG emissions and LU and all-cause and cause-specific mortality and incident cancers using Cox proportional-hazard regression models. Co-benefits, encompassing the potential effects of alternative diets on all-cause mortality and cancer and potential reduction in GHG emissions and LU, were estimated using counterfactual attributable fraction (AF) intervention models, simulating potential effects from dietary shifts based on the EAT-Lancet reference diet. Findings: There was an association between levels of dietary-based GHG emissions and LU and all-cause mortality, with a Hazard Ratio and 95% Confidence Interval (CI) of 1.13 (1.10, 1.16) and 1.18 (95% CI: 1.15, 1.21), respectively, comparing the fourth quartile to the first (HRQ4 vs Q1). Similar associations were observed for cause-specific mortality. There were also associations between overall cancer rates and GHG emissions (HRQ4 vs Q1: 1.11, 95% CI: 1.09, 1.14) and LU (HRQ4 vs Q1: 1.13, 95% CI: 1.10, 1.15); however, estimates differed by cancer type. Through counterfactual AF modelling of shifts in diets, we find that between 19 to 63% of deaths and 10 to 39% of cancers could be prevented, over a 20-year risk period, from adhering to different scores of the EAT-Lancet reference diet. Additionally, switching from a lower score of the EAT-Lancet reference diet to a higher score could reduce food-associated GHG and LU levels by 50% and 62%, respectively.Interpretation: Our results support shifts in diets that
Hanley-Cook GT, Huybrechts I, Biessy C, et al., 2021, Food biodiversity and total and cause-specific mortality in 9 European countries: An analysis of a prospective cohort study, PLoS Medicine, Vol: 18, ISSN: 1549-1277
BackgroundFood biodiversity, encompassing the variety of plants, animals, and other organisms consumed as food and drink, has intrinsic potential to underpin diverse, nutritious diets and improve Earth system resilience. Dietary species richness (DSR), which is recommended as a crosscutting measure of food biodiversity, has been positively associated with the micronutrient adequacy of diets in women and young children in low- and middle-income countries (LMICs). However, the relationships between DSR and major health outcomes have yet to be assessed in any population.Methods and findingsWe examined the associations between DSR and subsequent total and cause-specific mortality among 451,390 adults enrolled in the European Prospective Investigation into Cancer and Nutrition (EPIC) study (1992 to 2014, median follow-up: 17 years), free of cancer, diabetes, heart attack, or stroke at baseline. Usual dietary intakes were assessed at recruitment with country-specific dietary questionnaires (DQs). DSR of an individual’s yearly diet was calculated based on the absolute number of unique biological species in each (composite) food and drink. Associations were assessed by fitting multivariable-adjusted Cox proportional hazards regression models. In the EPIC cohort, 2 crops (common wheat and potato) and 2 animal species (cow and pig) accounted for approximately 45% of self-reported total dietary energy intake [median (P10–P90): 68 (40 to 83) species consumed per year]. Overall, higher DSR was inversely associated with all-cause mortality rate. Hazard ratios (HRs) and 95% confidence intervals (CIs) comparing total mortality in the second, third, fourth, and fifth (highest) quintiles (Qs) of DSR to the first (lowest) Q indicate significant inverse associations, after stratification by sex, age, and study center and adjustment for smoking status, educational level, marital status, physical activity, alcohol intake, and total energy intake, Mediterranean diet score, red
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