Summary of the workshop

Field, Catherine J.

doi:10.3945/ajcn.2009.27113h

Cited by 19 publications

(4 citation statements)

References 28 publications

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“…Moreover, defining the critical window of epigenetic susceptibility into postnatal life needs more clarification [22]. It is likely that the critical window time frame depends not only on the genes of interest, but also on the target tissue; for example, late developing organs like the brain likely experience epigenetic alterations into adolescence [23].…”

Section: Non-communicable Diseases Perinatal Diet and Epigeneticsmentioning

confidence: 99%

“…For example, rodents are altricial species and much more developmental maturation occurs postnatally compared to precocial species such as pigs and humans. Moreover, different organ systems mature at different developmental stages, so some disease outcomes are programmed prenatally (i.e., hypertension, Type 2 diabetes) and others postnatally (i.e., cognition, obesity) [23].…”

Section: Effects Of Postnatal Dietary Methyl Related Nutrients On Adult Phenotypementioning

confidence: 99%

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The Effects of Maternal and Postnatal Dietary Methyl Nutrients on Epigenetic Changes that Lead to Non-Communicable Diseases in Adulthood

Randunu

Bertolo

2020

IJMS

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The risk for non-communicable diseases in adulthood can be programmed by early nutrition. This programming is mediated by changes in expression of key genes in various metabolic pathways during development, which persist into adulthood. These developmental modifications of genes are due to epigenetic alterations in DNA methylation patterns. Recent studies have demonstrated that DNA methylation can be affected by maternal or early postnatal diets. Because methyl groups for methylation reactions come from methionine cycle nutrients (i.e., methionine, choline, betaine, folate), deficiency or supplementation of these methyl nutrients can directly change epigenetic regulation of genes permanently. Although many studies have described the early programming of adult diseases by maternal and infant nutrition, this review discusses studies that have associated early dietary methyl nutrient manipulation with direct effects on epigenetic patterns that could lead to chronic diseases in adulthood. The maternal supply of methyl nutrients during gestation and lactation can alter epigenetics, but programming effects vary depending on the timing of dietary intervention, the type of methyl nutrient manipulated, and the tissue responsible for the phenotype. Moreover, the postnatal manipulation of methyl nutrients can program epigenetics, but more research is needed on whether this approach can rescue maternally programmed offspring.

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Section: Non-communicable Diseases Perinatal Diet and Epigeneticsmentioning

confidence: 99%

Section: Effects Of Postnatal Dietary Methyl Related Nutrients On Adult Phenotypementioning

confidence: 99%

The Effects of Maternal and Postnatal Dietary Methyl Nutrients on Epigenetic Changes that Lead to Non-Communicable Diseases in Adulthood

Randunu

Bertolo

2020

IJMS

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“…In order to develop effective interventions it is important to understand the genetic and environmental determinants of obesity. There is evidence suggesting critical windows during fetal and early postnatal life, within which altered development may predispose the individual to obesity in later life [2] , [3] .…”

Section: Introductionmentioning

confidence: 99%

Relation of FTO gene variants to fetal growth trajectories: Findings from the Southampton Women's survey

et al. 2016

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IntroductionPlacental function is an important determinant of fetal growth, and fetal growth influences obesity risk in childhood and adult life. Here we investigated how FTO and MC4R gene variants linked with obesity relate to patterns of fetal growth and to placental FTO expression.MethodsSouthampton Women's Survey children (n = 1990) with measurements of fetal growth from 11 to 34 weeks gestation were genotyped for common gene variants in FTO (rs9939609, rs1421085) and MC4R (rs17782313). Linear mixed-effect models were used to analyse relations of gene variants with fetal growth.ResultsFetuses with the rs9939609 A:A FTO genotype had faster biparietal diameter and head circumference growth velocities between 11 and 34 weeks gestation (by 0.012 (95% CI 0.005 to 0.019) and 0.008 (0.002–0.015) standard deviations per week, respectively) compared to fetuses with the T:T FTO genotype; abdominal circumference growth velocity did not differ between genotypes. FTO genotype was not associated with placental FTO expression, but higher placental FTO expression was independently associated with larger fetal size and higher placental ASCT2, EAAT2 and y + LAT2 amino acid transporter expression. Findings were similar for FTO rs1421085, and the MC4R gene variant was associated with the fetal growth velocity of head circumference.DiscussionFTO gene variants are known to associate with obesity but this is the first time that the risk alleles and placental FTO expression have been linked with fetal growth trajectories. The lack of an association between FTO genotype and placental FTO expression adds to emerging evidence of complex biology underlying the association between FTO genotype and obesity.

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“…Emerging evidence from both animal and experimental studies has demonstrated that increased chronic inflammation, oxidative stress, insulin resistance and glucose related to maternal obesity create an in utero environment that can lead to altered fetal growth 4–8 . Accumulating data from human epidemiological studies corroborates that fetuses born to obese women are of greater risk for overgrowth, which may predispose them to obesity and cardio-metabolic disorders in later life 9 .…”

mentioning

confidence: 98%

Association of Maternal Obesity With Longitudinal Ultrasonographic Measures of Fetal Growth

et al. 2018

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IMPORTANCE Despite the increasing prevalence of pregravid obesity, systematic evaluation of the association of maternal obesity with fetal growth trajectories is lacking.OBJECTIVE To characterize differences in fetal growth trajectories between obese and nonobese pregnant women, and to identify the timing of any observed differences. DESIGN, SETTING, AND PARTICIPANTSThe Eunice Kennedy Shriver National Institute of Child Health and Human Development Fetal Growth Studies-Singletons study enrolled cohorts of pregnant women at 12 US health care institutions. Obese women (with prepregnancy body mass index > 30) and nonobese women (prepregnancy body mass indexes, 19-29.9) without major chronic diseases were recruited between 8 weeks and 0 days' gestation and 13 weeks and 6 days' gestation. A mixed longitudinal randomization scheme randomized participants into 1 of 4 schedules for 2-dimensional and 3-dimensional ultrasonograms to capture weekly fetal growth data throughout the remainder of their pregnancies. MAIN OUTCOMES AND MEASURESOn each ultrasonogram, fetal humerus length, femur length, biparietal diameter, head circumference, and abdominal circumference were measured. Fetal growth curves were estimated using linear mixed models with cubic splines. Median differences in the fetal measures at each gestational week of the obese and nonobese participants were examined using the likelihood ratio and Wald tests after adjustment for maternal characteristics. RESULTSThe study enrolled 468 obese and 2334 nonobese women between 8 weeks and 0 days' gestation and 13 weeks and 6 days' gestation. After a priori exclusion criteria, 443 obese and 2320 nonobese women composed the final cohort. Commencing at 21 weeks' gestation, femur length and humerus length were significantly longer for fetuses of obese woman than those of nonobese women. Differences persisted in obese and nonobese groups through 38 weeks' gestation (median femur length, 71.0 vs 70.2 mm; P = .01; median humerus length, 62.2 vs 61.6 mm; P = .03). Averaged across gestation, head circumference was significantly larger in fetuses of obese women than those of nonobese women (P = .02). Fetal abdominal circumference was not greater in the obese cohort than in the nonobese cohort but was significantly larger than in fetuses of normal-weight women (with body mass indexes between 19.0-24.9) commencing at 32 weeks (median, 282.1 vs 280.2 mm; P = .04). Starting from 30 weeks' gestation, estimated fetal weight was significantly larger for the fetuses of obese women (median, 1512 g [95% CI, 1494-1530 g] vs 1492 g [95% CI, 1484-1499 g]) and the difference grew as gestational age increased. Birth weight was higher by almost 100 g in neonates born to obese women than to nonobese women (mean, 3373.2 vs 3279.5 g). CONCLUSIONS AND RELEVANCEAs early as 32 weeks' gestation, fetuses of obese women had higher weights than fetuses of nonobese women. The mechanisms and long-term health implications of these findings are not yet established.

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Summary of the workshop

Cited by 19 publications

References 28 publications

The Effects of Maternal and Postnatal Dietary Methyl Nutrients on Epigenetic Changes that Lead to Non-Communicable Diseases in Adulthood

The Effects of Maternal and Postnatal Dietary Methyl Nutrients on Epigenetic Changes that Lead to Non-Communicable Diseases in Adulthood

Relation of FTO gene variants to fetal growth trajectories: Findings from the Southampton Women's survey

Association of Maternal Obesity With Longitudinal Ultrasonographic Measures of Fetal Growth

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