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Article ; Online: A bidirectional Mendelian randomisation study to evaluate the relationship between body constitution and hearing loss

Yiyan He / Ville Karhunen / Anna Pulakka / Marko Kantomaa / Sylvain Sebert

Scientific Reports, Vol 13, Iss 1, Pp 1-

2023 Volume 10

Abstract: Abstract Hearing loss and hearing disorders represent possible mediating pathways in the associations between noise exposures and non-auditory health outcomes. In this context, we assessed whether the noise-obesity associations should consider hearing ... ...

Abstract	Abstract Hearing loss and hearing disorders represent possible mediating pathways in the associations between noise exposures and non-auditory health outcomes. In this context, we assessed whether the noise-obesity associations should consider hearing functions as possible mediators and applied Mendelian randomisation (MR) to investigate causal relationships between body constitution and hearing impairments. We obtained genetic associations from publicly available summary statistics from genome-wide association studies in European ancestry adult populations (N= from 210,088 to 360,564) for (i) body constitution: body mass index (BMI), waist circumference (WC) and body fat percentage (BFP), and (ii) hearing loss: sensorineural hearing loss, noise-induced hearing loss, and age-related hearing impairment (ARHI). We employed colocalisation analysis to investigate the genetic associations for BMI and ARHI liability within an FTO locus. We conducted bi-directional MR for the ‘forward’ (from body constitution to hearing) and ‘reverse’ directions. We applied the random effects inverse variance-weighted method as the main MR method, with additional sensitivity analyses. Colocalisation analysis suggested that BMI and ARHI shared a causal variant at the FTO gene. We did not find robust evidence for causal associations from body constitution to hearing loss and suggested that some associations may be driven by FTO variants. In the reverse analyses, ARHI was negatively associated with BMI [effect size – 0.22 (95% CI – 0.44 to – 0.01)] and BFP [effect size – 0.23 (95% CI – 0.45 to 0.00)], supporting the notion that ARHI may diminish body constitution. Finally, our data suggest that there is no strong evidence that hearing explains the association between noise exposure and body constitution.
Keywords	Medicine ; R ; Science ; Q
Subject code	390
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Influence of Farm Environment on Asthma during the Life Course

Marko T. Kantomaa / Mimmi Tolvanen / Miia Halonen / Cecilie Svanes / Marjo-Riitta Järvelin / Sylvain Sebert

International Journal of Environmental Research and Public Health, Vol 20, Iss 2128, p

A Population-Based Birth Cohort Study in Northern Finland

2023 Volume 2128

Abstract: We investigated the influence of a farming environment on asthma at three time points from birth to 46 years using the Northern Finland Birth Cohort 1966 (n = 10,926). The prevalence of asthma was investigated by postal questionnaires at 14, 31 and 46 ... ...

Abstract	We investigated the influence of a farming environment on asthma at three time points from birth to 46 years using the Northern Finland Birth Cohort 1966 (n = 10,926). The prevalence of asthma was investigated by postal questionnaires at 14, 31 and 46 years of age. Exposure to a farming environment was assessed by a postal questionnaire at birth and at 31 and 46 years of age. Odds ratios (ORs) and their 95% confidence intervals (95% CIs) for the prevalence of asthma were obtained from multinomial logistic regression, stratified by sex. Being born in a farmer family was potentially causally associated with lower risk of asthma in males at 31 years of age (OR 0.56, 95% CI 0.37, 0.85) and in females at 46 years of age (OR 0.64, 95% CI 0.44, 0.95). Working as a farmer was not associated with asthma. Exposure to a farming environment in childhood may have a lifelong impact on developing asthma from birth through young adulthood and until middle age, indicating that ‘immune deviation’ may persist throughout life.
Keywords	asthma ; asthma epidemiology ; environmental exposures ; farming ; life course ; early life origins ; Medicine ; R
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The association between diabetes and cognitive changes during aging

Sanna Papunen / Anna Mustakallio-Könönen / Juha Auvinen / Markku Timonen / Sirkka Keinänen-Kiukaanniemi / Sylvain Sebert

Scandinavian Journal of Primary Health Care, Vol 38, Iss 3, Pp 281-

2020 Volume 290

Abstract: Background Worldwide, we are observing a rising prevalence of dementia and mild cognitive impairments that often co-occur with the heightened incidence of non-communicable diseases in the elderly. It is suggested that type 2 diabetes and defects in ... ...

Abstract	Background Worldwide, we are observing a rising prevalence of dementia and mild cognitive impairments that often co-occur with the heightened incidence of non-communicable diseases in the elderly. It is suggested that type 2 diabetes and defects in glucose metabolism might predispose to poorer cognitive performances and more rapid decline in old age. Methods to address existing knowledge gaps in this area, we systematically reviewed the literature to identify whether patients with type 2 diabetes (T2DM) and pre-diabetes are at a higher risk of poorer cognitive performance, and whether the risk (if any) might affect specific cognitive abilities. We concentrated the review on elderly individuals (65 years or older) at intake. In total, 3251 original articles were retrieved, of which 17 met our inclusion and quality control criteria, which comprised 12 structured questions used to define the articles. Results 11 of 17 studies found a statistically significant decline in cognition among individuals who had T2DM or pre-diabetes compared to their non-diabetic counterparts. The association between diabetes and cognitive decline was not always clear, and the extent of the cognitive tests used seemed to have the greatest effect on the results. Conclusion Focusing on a population age 65 years and over, we found insufficient evidence to support an association between pre-diabetes stages and mild cognitive impairment. However, there is consistent evidence to support diabetes as an independent risk factor for low cognitive ability in the elderly. Finally, we found insufficient evidence to support effect of T2DM on distinct cognitive ability due to the scarcity of comparable findings.
Keywords	diabetes ; elderly ; cognitive functions ; decline ; systematic review ; Public aspects of medicine ; RA1-1270
Subject code	120
Language	English
Publishing date	2020-07-01T00:00:00Z
Publisher	Taylor & Francis Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Maternal prenatal cholesterol levels predict offspring weight trajectories during childhood in the Norwegian Mother, Father and Child Cohort Study

Linn K. L. Øyri / Jacob J. Christensen / Sylvain Sebert / Magne Thoresen / Trond M. Michelsen / Stine M. Ulven / Hilde K. Brekke / Kjetil Retterstøl / Anne Lise Brantsæter / Per Magnus / Martin P. Bogsrud / Kirsten B. Holven

BMC Medicine, Vol 21, Iss 1, Pp 1-

2023 Volume 11

Abstract: Abstract Background Numerous intrauterine factors may affect the offspring’s growth during childhood. We aimed to explore if maternal and paternal prenatal lipid, apolipoprotein (apo)B and apoA1 levels are associated with offspring weight, length, and ... ...

Abstract	Abstract Background Numerous intrauterine factors may affect the offspring’s growth during childhood. We aimed to explore if maternal and paternal prenatal lipid, apolipoprotein (apo)B and apoA1 levels are associated with offspring weight, length, and body mass index from 6 weeks to eight years of age. This has previously been studied to a limited extent. Methods This parental negative control study is based on the Norwegian Mother, Father and Child Cohort Study and uses data from the Medical Birth Registry of Norway. We included 713 mothers and fathers with or without self-reported hypercholesterolemia and their offspring. Seven parental metabolites were measured by nuclear magnetic resonance spectroscopy, and offspring weight and length were measured at 12 time points. Data were analyzed by linear spline mixed models, and the results are presented as the interaction between parental metabolite levels and offspring spline (age). Results Higher maternal total cholesterol (TC) level was associated with a larger increase in offspring body weight up to 8 years of age (0.03 ≤ P interaction ≤ 0.04). Paternal TC level was not associated with change in offspring body weight (0.17 ≤ P interaction ≤ 0.25). Higher maternal high-density lipoprotein cholesterol (HDL-C) and apoA1 levels were associated with a lower increase in offspring body weight up to 8 years of age (0.001 ≤ P interaction ≤ 0.005). Higher paternal HDL-C and apoA1 levels were associated with a lower increase in offspring body weight up to 5 years of age but a larger increase in offspring body weight from 5 to 8 years of age (0.01 ≤ P interaction ≤ 0.03). Parental metabolites were not associated with change in offspring height or body mass index up to 8 years of age (0.07 ≤ P interaction ≤ 0.99). Conclusions Maternal compared to paternal TC, HDL-C, and apoA1 levels were more strongly and consistently associated with offspring body weight during childhood, supporting a direct intrauterine effect.
Keywords	MoBa ; MBRN ; Cholesterol ; Weight trajectories ; Parental negative control study ; Medicine ; R
Subject code	616
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genetic correlation and causal relationships between cardio-metabolic traits and lung function impairment

Matthias Wielscher / Andre F. S. Amaral / Diana van der Plaat / Louise V. Wain / Sylvain Sebert / David Mosen-Ansorena / Juha Auvinen / Karl-Heinz Herzig / Abbas Dehghan / Debbie L. Jarvis / Marjo-Riitta Jarvelin

Genome Medicine, Vol 13, Iss 1, Pp 1-

2021 Volume 13

Abstract: Abstract Background Associations of low lung function with features of poor cardio-metabolic health have been reported. It is, however, unclear whether these co-morbidities reflect causal associations, shared genetic heritability or are confounded by ... ...

Abstract	Abstract Background Associations of low lung function with features of poor cardio-metabolic health have been reported. It is, however, unclear whether these co-morbidities reflect causal associations, shared genetic heritability or are confounded by environmental factors. Methods We performed three analyses: (1) cardio-metabolic health to lung function association tests in Northern Finland Birth cohort 1966, (2) cross-trait linkage disequilibrium score regression (LDSC) to compare genetic backgrounds and (3) Mendelian randomisation (MR) analysis to assess the causal effect of cardio-metabolic traits and disease on lung function, and vice versa (bidirectional MR). Genetic associations were obtained from the UK Biobank data or published large-scale genome-wide association studies (N > 82,000). Results We observed a negative genetic correlation between lung function and cardio-metabolic traits and diseases. In Mendelian Randomisation analysis (MR), we found associations between type 2 diabetes (T2D) instruments and forced vital capacity (FVC) as well as FEV1/FVC. Body mass index (BMI) instruments were associated to all lung function traits and C-reactive protein (CRP) instruments to FVC. These genetic associations provide evidence for a causal effect of cardio-metabolic traits on lung function. Multivariable MR suggested independence of these causal effects from other tested cardio-metabolic traits and diseases. Analysis of lung function specific SNPs revealed a potential causal effect of FEV1/FVC on blood pressure. Conclusions The present study overcomes many limitations of observational studies by using Mendelian Randomisation. We provide evidence for an independent causal effect of T2D, CRP and BMI on lung function with some of the T2D effect on lung function being attributed to inflammatory mechanisms. Furthermore, this analysis suggests a potential causal effect of FEV1/FVC on blood pressure. Our detailed analysis of the interplay between cardio-metabolic traits and impaired lung function provides the ...
Keywords	Mendelian randomisation ; Metabolic syndrome ; Obesity ; Chronic obstructive pulmonary disease ; UK Biobank ; Medicine ; R ; Genetics ; QH426-470
Subject code	610
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Early exposure to social disadvantages and later life body mass index beyond genetic predisposition in three generations of Finnish birth cohorts

Estelle Lowry / Nina Rautio / Niko Wasenius / Tom A. Bond / Jari Lahti / Ioanna Tzoulaki / Abbas Dehghan / Anni Heiskala / Leena Ala-Mursula / Jouko Miettunen / Johan Eriksson / Marjo-Riitta Järvelin / Sylvain Sebert

BMC Public Health, Vol 20, Iss 1, Pp 1-

2020 Volume 12

Abstract: Abstract Background The study aimed to explore the association between early life and life-course exposure to social disadvantage and later life body mass index (BMI) accounting for genetic predisposition and maternal BMI. Methods We studied participants ...

Abstract	Abstract Background The study aimed to explore the association between early life and life-course exposure to social disadvantage and later life body mass index (BMI) accounting for genetic predisposition and maternal BMI. Methods We studied participants of Helsinki Birth Cohort Study born in 1934–1944 (HBCS1934–1944, n = 1277) and Northern Finland Birth Cohorts born in 1966 and 1986 (NFBC1966, n = 5807, NFBC1986, n = 6717). Factor analysis produced scores of social disadvantage based on social and economic elements in early life and adulthood/over the life course, and was categorized as high, intermediate and low. BMI was measured at 62 years in HBCS1934–1944, at 46 years in NFBC1966 and at 16 years in NFBC1986. Multivariable linear regression analysis was used to explore associations between social disadvantages and BMI after adjustments for polygenic risk score for BMI (PRS BMI), maternal BMI and sex. Results The association between exposure to high early social disadvantage and increased later life BMI persisted after adjustments (β = 0.79, 95% CI, 0.33, 1.25, p < 0.001) in NFBC1966. In NFBC1986 this association was attenuated by PRS BMI (p = 0.181), and in HBCS1934–1944 there was no association between high early social disadvantage and increased later life BMI (β 0.22, 95% CI –0.91,1.35, p = 0.700). In HBCS1934–1944 and NFBC1966, participants who had reduced their exposure to social disadvantage during the life-course had lower later life BMI than those who had increased their exposure (β − 1.34, [− 2.37,-0.31], p = 0.011; β − 0.46, [− 0.89,-0.03], p = 0.038, respectively). Conclusions High social disadvantage in early life appears to be associated with higher BMI in later life. Reducing exposure to social disadvantage during the life-course may be a potential pathway for obesity reduction.
Keywords	Early life ; Social disadvantage ; Body mass index (BMI) ; Maternal ; Polygenic risk score for BMI ; Public aspects of medicine ; RA1-1270
Subject code	300
Language	English
Publishing date	2020-05-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Exploring the causal effect of maternal pregnancy adiposity on offspring adiposity

Tom A. Bond / Rebecca C. Richmond / Ville Karhunen / Gabriel Cuellar-Partida / Maria Carolina Borges / Verena Zuber / Alexessander Couto Alves / Dan Mason / Tiffany C. Yang / Marc J. Gunter / Abbas Dehghan / Ioanna Tzoulaki / Sylvain Sebert / David M. Evans / Alex M. Lewin / Paul F. O’Reilly / Deborah A. Lawlor / Marjo-Riitta Järvelin

BMC Medicine, Vol 20, Iss 1, Pp 1-

Mendelian randomisation using polygenic risk scores

2022 Volume 16

Abstract: Abstract Background Greater maternal adiposity before or during pregnancy is associated with greater offspring adiposity throughout childhood, but the extent to which this is due to causal intrauterine or periconceptional mechanisms remains unclear. Here, ...

Abstract	Abstract Background Greater maternal adiposity before or during pregnancy is associated with greater offspring adiposity throughout childhood, but the extent to which this is due to causal intrauterine or periconceptional mechanisms remains unclear. Here, we use Mendelian randomisation (MR) with polygenic risk scores (PRS) to investigate whether associations between maternal pre-/early pregnancy body mass index (BMI) and offspring adiposity from birth to adolescence are causal. Methods We undertook confounder adjusted multivariable (MV) regression and MR using mother-offspring pairs from two UK cohorts: Avon Longitudinal Study of Parents and Children (ALSPAC) and Born in Bradford (BiB). In ALSPAC and BiB, the outcomes were birthweight (BW; N = 9339) and BMI at age 1 and 4 years (N = 8659 to 7575). In ALSPAC only we investigated BMI at 10 and 15 years (N = 4476 to 4112) and dual-energy X-ray absorptiometry (DXA) determined fat mass index (FMI) from age 10–18 years (N = 2659 to 3855). We compared MR results from several PRS, calculated from maternal non-transmitted alleles at between 29 and 80,939 single nucleotide polymorphisms (SNPs). Results MV and MR consistently showed a positive association between maternal BMI and BW, supporting a moderate causal effect. For adiposity at most older ages, although MV estimates indicated a strong positive association, MR estimates did not support a causal effect. For the PRS with few SNPs, MR estimates were statistically consistent with the null, but had wide confidence intervals so were often also statistically consistent with the MV estimates. In contrast, the largest PRS yielded MR estimates with narrower confidence intervals, providing strong evidence that the true causal effect on adolescent adiposity is smaller than the MV estimates (P difference = 0.001 for 15-year BMI). This suggests that the MV estimates are affected by residual confounding, therefore do not provide an accurate indication of the causal effect size. Conclusions Our results suggest that higher maternal ...
Keywords	Obesity ; BMI ; Pregnancy ; Child ; Maternal ; Offspring ; Medicine ; R
Subject code	150 ; 610
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Fto-Deficiency Affects the Gene and MicroRNA Expression Involved in Brown Adipogenesis and Browning of White Adipose Tissue in Mice

Justiina Ronkainen / Eleonora Mondini / Francesca Cinti / Saverio Cinti / Sylvain Sebért / Markku J. Savolainen / Tuire Salonurmi

International Journal of Molecular Sciences, Vol 17, Iss 11, p

2016 Volume 1851

Abstract: Genetic variants in the fat mass- and obesity-associated gene Fto are linked to the onset of obesity in humans. The causal role of the FTO protein in obesity is supported by evidence obtained from transgenic mice; however, the underlying molecular ... ...

Abstract	Genetic variants in the fat mass- and obesity-associated gene Fto are linked to the onset of obesity in humans. The causal role of the FTO protein in obesity is supported by evidence obtained from transgenic mice; however, the underlying molecular pathways pertaining to the role of FTO in obesity have yet to be established. In this study, we investigate the Fto gene in mouse brown adipose tissue and in the browning process of white adipose tissue. We analyze distinct structural and molecular factors in brown and white fat depots of Fto-deficient mice under normal and obesogenic conditions. We report significant alterations in the morphology of adipose tissue depots and the expression of mRNA and microRNA related to brown adipogenesis and metabolism in Fto-deficient mice. Furthermore, we show that high-fat feeding does not attenuate the browning process of Fto-deficient white adipose tissue as observed in wild-type tissue, suggesting a triggering effect of the FTO pathways by the dietary environment.
Keywords	FTO ; brown adipose tissue (BAT) ; white adipose tissue (WAT) browning ; gene expression ; microRNA expression ; high-fat diet ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2016-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Towards early risk biomarkers

Xiaowei Ojanen, Ph.D / Runtan Cheng, Msc / Timo Törmäkangas, Ph.D / Noa Rappaport, Ph.D / Tomasz Wilmanski, Ph.D / Na Wu, Msc / Erik Fung, M.B.Ch.B., Ph.D / Rozenn Nedelec, MSc / Sylvain Sebert, PhD / Dimitris Vlachopoulos, Ph.D / Wei Yan, Ph.D / Nathan D. Price, Ph.D / Sulin Cheng, Ph.D / Petri Wiklund, Ph.D

EBioMedicine, Vol 72, Iss , Pp 103611- (2021)

serum metabolic signature in childhood predicts cardio-metabolic risk in adulthood

2021

Abstract: Summary: Background: Cardiovascular diseases may originate in childhood. Biomarkers identifying individuals with increased risk for disease are needed to support early detection and to optimise prevention strategies. Methods: In this prospective study, ... ...

Abstract	Summary: Background: Cardiovascular diseases may originate in childhood. Biomarkers identifying individuals with increased risk for disease are needed to support early detection and to optimise prevention strategies. Methods: In this prospective study, by applying a machine learning to high throughput NMR-based metabolomics data, we identified circulating childhood metabolic predictors of adult cardiovascular disease risk (MetS score) in a cohort of 396 females, followed from childhood (mean age 11·2 years) to early adulthood (mean age 18·1 years). The results obtained from the discovery cohort were validated in a large longitudinal birth cohort of females and males followed from puberty to adulthood (n = 2664) and in four cross-sectional data sets (n = 6341). Findings: The identified childhood metabolic signature included three circulating biomarkers, glycoprotein acetyls (GlycA), large high-density lipoprotein phospholipids (L-HDL-PL), and the ratio of apolipoprotein B to apolipoprotein A-1 (ApoB/ApoA) that were associated with increased cardio-metabolic risk in early adulthood (AUC = 0·641‒0·802, all p<0·01). These associations were confirmed in all validation cohorts with similar effect estimates both in females (AUC = 0·667‒0·905, all p<0·01) and males (AUC = 0·734‒0·889, all p<0·01) as well as in elderly patients with and without type 2 diabetes (AUC = 0·517‒0·700, all p<0·01). We subsequently applied random intercept cross-lagged panel model analysis, which suggested bidirectional causal relationship between metabolic biomarkers and cardio-metabolic risk score from childhood to early adulthood. Interpretation: These results provide evidence for the utility of a circulating metabolomics panel to identify children and adolescents at risk for future cardiovascular disease, to whom preventive measures and follow-up could be indicated. Funding: This study was financially supported by the Academy of Finland, Ministry of Education of Finland and University of Jyv€askyl€a, the National Nature Science ...
Keywords	metabolomics ; cardio-metabolic risk ; children ; longitudinal-study ; ALSPAC ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	300
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	Elsevier
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Article ; Online: A Pregnancy and Childhood Epigenetics Consortium (PACE) meta-analysis highlights potential relationships between birth order and neonatal blood DNA methylation

Shaobo Li / Natalia Spitz / Akram Ghantous / Sarina Abrishamcar / Brigitte Reimann / Irene Marques / Matt J. Silver / Sofía Aguilar-Lacasaña / Negusse Kitaba / Faisal I. Rezwan / Stefan Röder / Lea Sirignano / Johanna Tuhkanen / Giulia Mancano / Gemma C. Sharp / Catherine Metayer / Libby Morimoto / Dan J. Stein / Heather J. Zar /

Rossella Alfano / Tim Nawrot / Congrong Wang / Eero Kajantie / Elina Keikkala / Sanna Mustaniemi / Justiina Ronkainen / Sylvain Sebert / Wnurinham Silva / Marja Vääräsmäki / Vincent W. V. Jaddoe / Robin M. Bernstein / Andrew M. Prentice / Marta Cosin-Tomas / Terence Dwyer / Siri Eldevik Håberg / Zdenko Herceg / Maria C. Magnus / Monica Cheng Munthe-Kaas / Christian M. Page / Maja Völker / Maria Gilles / Tabea Send / Stephanie Witt / Lea Zillich / Luigi Gagliardi / Lorenzo Richiardi / Darina Czamara / Katri Räikkönen / Lida Chatzi / Marina Vafeiadi / S. Hasan Arshad / Susan Ewart / Michelle Plusquin / Janine F. Felix / Sophie E. Moore / Martine Vrijheid / John W. Holloway / Wilfried Karmaus / Gunda Herberth / Ana Zenclussen / Fabian Streit / Jari Lahti / Anke Hüls / Thanh T. Hoang / Stephanie J. London / Joseph L. Wiemels

Communications Biology, Vol 7, Iss 1, Pp 1-

2024 Volume 11

Abstract: Abstract Higher birth order is associated with altered risk of many disease states. Changes in placentation and exposures to in utero growth factors with successive pregnancies may impact later life disease risk via persistent DNA methylation alterations. ...

Abstract	Abstract Higher birth order is associated with altered risk of many disease states. Changes in placentation and exposures to in utero growth factors with successive pregnancies may impact later life disease risk via persistent DNA methylation alterations. We investigated birth order with Illumina DNA methylation array data in each of 16 birth cohorts (8164 newborns) with European, African, and Latino ancestries from the Pregnancy and Childhood Epigenetics Consortium. Meta-analyzed data demonstrated systematic DNA methylation variation in 341 CpGs (FDR adjusted P < 0.05) and 1107 regions. Forty CpGs were located within known quantitative trait loci for gene expression traits in blood, and trait enrichment analysis suggested a strong association with immune-related, transcriptional control, and blood pressure regulation phenotypes. Decreasing fertility rates worldwide with the concomitant increased proportion of first-born children highlights a potential reflection of birth order-related epigenomic states on changing disease incidence trends.
Keywords	Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Nature Portfolio
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