Developmental Origins of Disease: Emerging Prenatal Risk Factors and Future Disease Risk

Aris, Izzuddin M.; Fleisch, Abby F.; Oken, Emily

doi:10.1007/s40471-018-0161-0

Cited by 25 publications

(17 citation statements)

References 104 publications

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“…Research has also shown the develop mental origins of adult diseases like diabetes, heart attacks, and strokes. 31,32 Prenatal exposure to envir onmental contaminants is associ ated with epigenetic changes, such as DNAmethylation, linked to the develop ment of diseases later in life. 33 For example, studies in Sweden on the radioactive fallout following the acci dent at the Chernobyl nuclear power plant, Pripyat, Ukraine, show that inutero exposure affected educational attainment and income many years later.…”

Section: Panel 3: Children's Wellbeing In Their Own Wordsmentioning

confidence: 99%

A future for the world's children? A WHO–UNICEF–Lancet Commission

Clark¹,

Coll-Seck

Banerjee³

et al. 2020

The Lancet

699

597

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Despite dramatic improvements in survival, nutrition, and education over recent decades, today's children face an uncertain future. Climate change, ecological degradation, migrating populations, conflict, pervasive inequalities, and predatory commercial practices threaten the health and future of children in every country. In 2015, the world's countries agreed on the Sustainable Development Goals (SDGs), yet nearly 5 years later, few countries have recorded much progress towards achieving them. This Commission presents the case for placing children, aged 0-18 years, at the centre of the SDGs: at the heart of the concept of sustainability and our shared human endeavour. Governments must harness coalitions across sectors to overcome ecological and commercial pressures to ensure children receive their rights and entitlements now and a liveable planet in the years to come.

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Section: Panel 3: Children's Wellbeing In Their Own Wordsmentioning

confidence: 99%

A future for the world's children? A WHO–UNICEF–Lancet Commission

Clark¹,

Coll-Seck

Banerjee³

et al. 2020

The Lancet

699

597

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“…Furthermore, exposures during the prenatal and early postnatal periods may influence long-term chronic disease risk according to the developmental origins of health and disease hypothesis [14]. This hypothesis posits that prenatal and early life exposures may affect future health through inappropriate predictive adaptive responses (based on mismatched prenatal and postnatal environments) [15] or through direct exposure to environmental factors that increase risk of chronic disease [16]. These factors (e.g.…”

Section: Introductionmentioning

confidence: 99%

Prenatal and childhood predictors of hair cortisol concentration in mid-childhood and early adolescence

et al. 2020

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Background Hair cortisol concentration (HCC) is an increasingly used measure of systemic cortisol concentration. However, determinants of HCC in children and adolescents are unclear because few prospective studies have been conducted to date. Study design We followed 725 children in Project Viva, a pre-birth cohort study of mothers and children, who provided hair samples at mid-childhood (median age: 7.7 years) or early adolescence (median age: 12.9 years). We examined associations of various factors measured from pregnancy to mid-childhood with HCC in mid-childhood and early adolescence, as well as change in HCC between these time points (ΔHCC). Results There were 426 children with HCC measurements in both mid-childhood and early adolescence, 173 children with measures only in mid-childhood, and 126 with measures only in early adolescence. HCC was lower in mid-childhood (median 1.0pg/mg [interquartile range, IQR: 0.5, 2.4]) than early adolescence (2.2pg/mg [1.1, 4.4]). In multivariable-adjusted regression models, female sex (β =-0.41, 95% CI:-0.67,-0.15) and birth weight-for-gestational age z-score (β =-0.19, 95% CI:-0.33,-0.04) were associated with lower mid-childhood HCC, while prenatal smoking was associated with higher mid-childhood HCC (β = 0.53, 95% CI: 0.04, 1.01). In early adolescence, child age (β = 0.34 per year, 95% CI: 0.21, 0.46) female sex (β = 0.33, 95% CI: 0.10, 0.57), and maternal pre-pregnancy body mass

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“…According to the Developmental Origins of Health and Disease hypothesis, suboptimal prenatal development likely predisposes to inferior health throughout life. 26 Reduced fetal growth has been associated with among other increased incidences of diabetes mellitus (type 2), obesity and cardiovascular disease. 27 Birth head circumference is an indication of fetal brain growth, and several studies have shown associations between decreased birth head circumference and decreased cognitive skills in childhood, even among the children within the normal range of birth size.…”

Section: Discussionmentioning

confidence: 99%

Cord blood acrylamide levels and birth size, and interactions with genetic variants in acrylamide-metabolizing genes

Hogervorst

Vesper²,

Madhloum

et al. 2019

Preprint

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Background Up to now, 3 epidemiological studies have shown clear inverse associations between prenatal acrylamide exposure and birth size. In addition to studying the association between acrylamide and birth size, we investigated the interaction between acrylamide and polymorphisms in acrylamide-metabolising genes, with the aim of probing the causality of the inverse relationship between acrylamide and fetal growth. Methods We investigated the association between prenatal acrylamide exposure (acrylamide and glycidamide to hemoglobin adduct levels (AA-Hb and GA-Hb) in cord blood) and birth weight, length and head circumference in 443 newborns of the ENVIRONAGE (ENVIRonmental influence ON AGEing in early life) birth cohort. In addition, we studied interaction with single nucleotide polymorphism (SNPs) in CYP2E1, EPHX1 and GSTP1, using multiple linear regression analysis. Results Compared to neonates in the lowest quartile of AA-Hb in cord blood, the body weight, length and head circumference of neonates in the highest quartile were -101 grams (95% CI: -208, 7; p for trend = 0.12), -0.13 centimetres (95% CI: -0.62, 0.36; p for trend = 0.69) and -0.41 centimetres (-0.80, -0.01; p for trend = 0.06) lower, respectively. For GA-Hb, the corresponding effect estimates were -222 grams (95% CI: -337, -108; p for trend = 0.001), -0.85 (95% CI: -1.38, -0.33; p for trend = 0.02) and -0.55 (95% CI: -0.98, -0.11; p for trend = 0.01), respectively. The associations for GA-Hb were similar or stronger in newborns of non-smoking mothers. There was no statistically significant interaction between acrylamide exposure and the studied genetic variations but there was a trend of stronger inverse associations with birth weight and head circumference among newborns with homozygous wildtypes alleles for the CYP2E1 SNPS and with variant alleles for a GSTP1 SNP (rs1138272). Conclusions Prenatal dietary acrylamide exposure, specifically in the form of its metabolite glycidamide, was inversely associated with birth weight, length and head circumference. The interaction pattern with SNPs in CYP2E1, although not statistically significant, is an indication for the causality of this association. Other studies are needed to corroborate this finding.

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Developmental Origins of Disease: Emerging Prenatal Risk Factors and Future Disease Risk

Cited by 25 publications

References 104 publications

A future for the world's children? A WHO–UNICEF–Lancet Commission

A future for the world's children? A WHO–UNICEF–Lancet Commission

Prenatal and childhood predictors of hair cortisol concentration in mid-childhood and early adolescence

Cord blood acrylamide levels and birth size, and interactions with genetic variants in acrylamide-metabolizing genes

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