Prenatal exposure to a natural disaster increases risk for obesity in 5½-year-old children

Dancause, Kelsey Needham; Laplante, David P.; Fraser, Sarah; Brunet, Alain; Ciampi, Antonio; Schmitz, N.; King, Suzanne

doi:10.1038/pr.2011.18

Cited by 97 publications

(144 citation statements)

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“…Despite the importance of G 3 E models in explaining the majority of VMR-CpGs, we failed to find VMR-CpGs that were best explained by environmental conditions independently of genotype. This finding emerged despite the considerable evidence for the effects of environmental factors in pregnancy on both epigenetic states (Barker et al 1989;Roseboom et al 2001;Gillman et al 2003;Hofman et al 2004;Boney et al 2005;Hillier et al 2007;BouhoursNouet et al 2008;Painter et al 2008;Broekman et al 2009;Alisi et al 2011;Skilton et al 2011;Sohi et al 2011;Dancause et al 2012;Schwarze et al 2012) and health outcomes (Godfrey et al 2011). Our data suggest that genotype exerts a moderating influence on such environmental effects.…”

Section: Discussioncontrasting

confidence: 42%

“…Epidemiological data link disease risk directly to the in utero environment (Roseboom et al 2001;Gillman et al 2003;Hillier et al 2007;Painter et al 2008;Alisi et al 2011;Sohi et al 2011;Dancause et al 2012;Schwarze et al 2012) or to birth outcomes as a surrogate for the in utero environment (Barker et al 1989;Hofman et al 2004;Boney et al 2005;Bouhours-Nouet et al 2008;Broekman et al 2009;Skilton et al 2011). This phenomenon is often called fetal programming and defines, in part, the developmental origins of health and disease (Bjornsson et al 2004;Gluckman et al 2008).…”

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confidence: 99%

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The effect of genotype and in utero environment on interindividual variation in neonate DNA methylomes

et al. 2014

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Integrating the genotype with epigenetic marks holds the promise of better understanding the biology that underlies the complex interactions of inherited and environmental components that define the developmental origins of a range of disorders. The quality of the in utero environment significantly influences health over the lifecourse. Epigenetics, and in particular DNA methylation marks, have been postulated as a mechanism for the enduring effects of the prenatal environment. Accordingly, neonate methylomes contain molecular memory of the individual in utero experience. However, interindividual variation in methylation can also be a consequence of DNA sequence polymorphisms that result in methylation quantitative trait loci (methQTLs) and, potentially, the interaction between fixed genetic variation and environmental influences. We surveyed the genotypes and DNA methylomes of 237 neonates and found 1423 punctuate regions of the methylome that were highly variable across individuals, termed variably methylated regions (VMRs), against a backdrop of homogeneity. MethQTLs were readily detected in neonatal methylomes, and genotype alone best explained~25% of the VMRs. We found that the best explanation for 75% of VMRs was the interaction of genotype with different in utero environments, including maternal smoking, maternal depression, maternal BMI, infant birth weight, gestational age, and birth order. Our study sheds new light on the complex relationship between biological inheritance as represented by genotype and individual prenatal experience and suggests the importance of considering both fixed genetic variation and environmental factors in interpreting epigenetic variation.

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confidence: 42%

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confidence: 99%

The effect of genotype and in utero environment on interindividual variation in neonate DNA methylomes

et al. 2014

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“…[17][18][19][20][21][22][23] In addition to physical activity and caloric intake, other non-chemical stressors that may influence weight include personal habits (e.g., smoking); psychosocial stress (e.g., parental divorce, domestic violence, exercising poor judgement, depression); access to health care; and/or aspects of the built and natural environments. [24][25][26][27] There is also increasing evidence that obesogens (i.e., chemical stressors) may influence obesity by affecting metabolic activities in the body. Finally, genetic predisposition plays a large role, accounting for 440% of the population variation in body mass index (BMI), suggesting that genes factor into how the body captures, stores, and uses energy from food consumption.…”

Section: Introductionmentioning

confidence: 99%

Chemical and non-chemical stressors affecting childhood obesity: a systematic scoping review

Lichtveld

Thomas

Tulve

2017

J Expo Sci Environ Epidemiol

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Childhood obesity in the United States has doubled over the last three decades and currently affects 17% of children and adolescents. While much research has focused on individual behaviors impacting obesity, little research has emphasized the complex interactions of numerous chemical and non-chemical stressors found in a child's environment and how these interactions affect a child's health and well-being. The objectives of this systematic scoping review were to (1) identify potential chemical stressors in the context of non-chemical stressors that impact childhood obesity; and, (2) summarize our observations for chemical and non-chemical stressors in regards to child-specific environments within a community setting. A review was conducted to identify chemical and non-chemical stressors related to childhood obesity for the childhood life stages ranging from prenatal to adolescence. Stressors were identified and grouped into domains: individual behaviors, family/household behaviors, community stressors, and chemical exposures. Stressors were related to the child and the child's everyday environments and used to characterize child health and well-being. This review suggests that the interactions of chemical and non-chemical stressors are important for understanding a child's overall health and well-being. By considering these relationships, the exposure science research community can better design and implement strategies to reduce childhood obesity.

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“…Apart from nutritional challenges, maternal stress that increases circulating glucocorticoids during pregnancy is also known to program the offspring for metabolic diseases (12,37,38). In humans, prenatal stress in the form of maternal bereavement or natural disasters during pregnancy has been shown to increase the risk for obesity in childhood (6,27). Numerous studies in rodents and primates suggest that prenatal stress or dexamethasone administration reduces birth weight and predisposes the offspring to glucose intolerance, insulin resistance, and reduced ␤-cell mass, especially when they are exposed to a high-fat (HF) diet (7,29,33,42).…”

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confidence: 99%

Differential effects of prenatal stress on metabolic programming in diet-induced obese and dietary-resistant rats

Balasubramanian¹,

Varde²,

Abdallah

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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Balasubramanian P, Varde PA, Abdallah SL, Najjar SM, MohanKumar PS, MohanKumar SM. Differential effects of prenatal stress on metabolic programming in diet-induced obese and dietaryresistant rats. Am J Physiol Endocrinol Metab 309: E582-E588, 2015. First published July 28, 2015; doi:10.1152/ajpendo.00167.2015.-Stress during pregnancy is a known contributing factor for the development of obesity in the offspring. Since maternal obesity is on the rise, we wanted to identify the effects of prenatal stress in the offspring of diet-induced obese (DIO) rats and compare them with the offspring of dietaryresistant (DR) rats. We hypothesized that prenatal stress would make both DIO and DR offspring susceptible to obesity, but the effect would be more pronounced in DIO rats. Pregnant DIO and DR rats were divided into two groups: nonstressed controls (control) and prenatal stress (subjected to restraint stress, three times/day from days 14 to 21 of gestation). After recording birth weight and weaning weight, male offspring were weaned onto a chow diet for 9 wk and shifted to a high-fat (HF) diet for 1 wk. At the end of the 10th wk the animals were euthanized, and visceral adipose mass, blood glucose, serum insulin, and C-peptide levels were measured. Prenatal stress resulted in hyperinsulinemia and higher C-peptide levels without altering caloric intake, body weight gain, or fat mass in the DIO offspring after 1 wk of HF intake, but not in DR offspring. To determine the mechanism underlying the hyperinsulinemia, we measured the levels of CEACAM1 that are responsible for insulin clearance. CEACAM1 levels in the liver were reduced in prenatally stressed DIO offspring after the HF challenge, suggesting that preexisting genetic predisposition in combination with prenatal stress increases the risk for obesity in adulthood, especially when offspring are fed a HF diet. diet-induced obese; dietary resistant; hyperinsulinemia; fetal programming; carcinoembryonic antigen-related cell adhesion molecule 1 OBESITY IS ONE OF THE MAJOR HEALTH ISSUES that has worldwide prevalence (1). In addition to genetic and lifestyle factors, growing evidence suggests that prenatal conditions could also contribute to the development of obesity in the offspring. According to Barker's hypothesis, compromised in utero conditions can induce permanent alterations in tissue structure and function of the developing fetus and increase their susceptibility to diseases like obesity and diabetes in adult life (2,17).Several studies have shown that offspring of dams placed on low-protein diets or subjected to caloric restriction have low birth weight. These offspring subsequently undergo catchup growth that places them at higher risk for obesity, hypertension, and diabetes in adulthood (18,24,32). Apart from nutritional challenges, maternal stress that increases circulating glucocorticoids during pregnancy is also known to program the offspring for metabolic diseases (12,37,38). In humans, prenatal stress in the form of maternal bereavement or natural disasters d...

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Prenatal exposure to a natural disaster increases risk for obesity in 5½-year-old children

Cited by 97 publications

References 43 publications

The effect of genotype and in utero environment on interindividual variation in neonate DNA methylomes

The effect of genotype and in utero environment on interindividual variation in neonate DNA methylomes

Chemical and non-chemical stressors affecting childhood obesity: a systematic scoping review

Differential effects of prenatal stress on metabolic programming in diet-induced obese and dietary-resistant rats

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