Predicting Later-Life Outcomes of Early-Life Exposures

Boekelheide, Kim; Blumberg, Bruce; Chapin, Robert E.; Cote, Ila; Graziano, Joseph H.; Janesick, Amanda; Lane, Robert H.; Lillycrop, Karen A.; Myatt, Leslie; States, J. Christopher; Thayer, Kristina A.; Waalkes, Michael P.; Rogers, John M.

doi:10.1289/ehp.1204934

Cited by 164 publications

(109 citation statements)

References 135 publications

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“…Surprisingly, we know little about how early-life exposure to stressors affects the risk of infectious diseases later in life. Indeed, a review on later-life outcomes of early-life exposures [4] provides several examples of stress early in life having enduring effects on non-infectious disease outcomes, but offers no examples of early-life exposures affecting infectious diseases later in life (but see [5]). …”

Section: Introductionmentioning

confidence: 99%

Early-life exposure to a herbicide has enduring effects on pathogen-induced mortality

et al. 2013

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Exposure to stressors at formative stages in the development of wildlife and humans can have enduring effects on health. Understanding which, when and how stressors cause enduring health effects is crucial because these stressors might then be avoided or mitigated during formative stages to prevent lasting increases in disease susceptibility. Nevertheless, the impact of earlylife exposure to stressors on the ability of hosts to resist and tolerate infections has yet to be thoroughly investigated. Here, we show that early-life, 6-day exposure to the herbicide atrazine (mean + s.e.: 65.9+3.48 mg l 21) increased frog mortality 46 days after atrazine exposure (post-metamorphosis), but only when frogs were challenged with a chytrid fungus implicated in global amphibian declines. Previous atrazine exposure did not affect resistance of infection (fungal load). Rather, early-life exposure to atrazine altered growth and development, which resulted in exposure to chytrid at more susceptible developmental stages and sizes, and reduced tolerance of infection, elevating mortality risk at an equivalent fungal burden to frogs unexposed to atrazine. Moreover, there was no evidence of recovery from atrazine exposure. Hence, reducing early-life exposure of amphibians to atrazine could reduce lasting increases in the risk of mortality from a disease associated with worldwide amphibian declines. More generally, these findings highlight that a better understanding of how stressors cause enduring effects on disease susceptibility could facilitate disease prevention in wildlife and humans, an approach that is often more cost-effective and efficient than reactive medicine.

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Section: Introductionmentioning

confidence: 99%

Early-life exposure to a herbicide has enduring effects on pathogen-induced mortality

et al. 2013

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“…The notion of biological embedding is now widely accepted, even though the mechanisms are not completely understood (Tarry-Adkins and Ozanne 2011). Maternal nutritional status, gestational diabetes, high levels of maternal stress, hypoxia/placental insufficiency, and environmental toxins have been associated with the development of T2DM in children and adolescents (Warner and Ozanne 2010;Boekelheide et al 2012). Furthermore, the relationship of these high-risk maternal factors to intrauterine growth restriction (IUGR) and small-for-gestational-age (SGA) newborns with their predisposition for obesity, insulin resistance, and T2DM later in life has been established as well.…”

Section: Preconception and Intrauterine Lifementioning

confidence: 99%

Pediatric Type 2 Diabetes: Prevention and Treatment Through a Life Course Health Development Framework

Salsberry

Tanda

Anderson

et al. 2017

Handbook of Life Course Health Development

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Estimates project that one in three US adults may have diabetes in 2050. Until very recently, type 2 diabetes mellitus (T2DM) was a disease diagnosed in adults, but as the childhood obesity epidemic has spread, the diagnosis of T2DM in adolescents has become more common. Early indicators suggest that the disease may be more severe and more difficult to manage when diagnosed in adolescents. It is projected that adolescents with T2DM will lose approximately 15 years of life. The economic burden of T2DM rises significantly as the years with disease increase. This grim forecast highlights that not only will the disease burden be significant but the economic burden will be high. The risk for developing T2DM begins in utero. Individual health development trajectories build from this starting point, the result of multiple factors that accumulate across time and are the result of biological conditioning during sensitive developmental periods. A major aim of this chapter is to demonstrate that a life course health development approach to pediatric T2DM is critical to a sound national strategy to prevent and treat pediatric T2DM. We review major factors known to influence the development of pediatric T2DM and track these across childhood. While these factors will likely change over the next decade, what will not change is the importance of placing these factors into context and recognizing that T2DM development is highly sensitive to the timing and social structures of multiple environmental exposures. Research recommendations are discussed through a life course lens.

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“…However, it is most vulnerable to environmental factors during embryogenesis when the DNA synthesis rate is high, and the elaborate DNA methylation patterning required for normal tissue development is established [9]. In-utero and early-life events can significantly modulate the epigenome and lead to altered phenotypes and disease susceptibility throughout the life course [10].…”

Section: Genetic-epigenetic-environmental Interactionsmentioning

confidence: 99%

A Complex Adaptive System in Which Environmental Stress Affects Gene Expression During Development

KOH

TOH

O’DONNELL

et al. 2017

WIT Transactions on State-of-the-Art in Science and Engineering

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Dental development is a complex adaptive system influenced by genetic-epigenetic-environmental factors. The mature dentition is a paradigm for general development and is an accessible, permanent record of interactions affecting development from 6 weeks in-utero to 20 years of age. Published research on the dentition of a large group of Romano-Britons has indicated that three major environmental insults acting throughout the developmental period are associated with high frequencies of dental variations. Based on those studies and the literature, the aetiological network incorporates the effects of excessive lead ingestion, poor nutrition and infections on the endocrine and immune systems, epigenome and gene expression. The environmental insults act independently and synergistically on both the endocrine and immune systems, which in turn have reciprocal interactions with each other, as well as on the epigenome. Thus, a complex subnetwork influences the epigenome and modifies one or more of three mechanisms by which it controls gene expression, that is, DNA methylation, post-translational histone modification and microRNA expression. The environmental-epigeneticgenetic interactions behave as a complex adaptive system that can be illustrated in a network diagram. The epigenetic modifications can have long-term health effects in the individual and some may also be heritable.

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Predicting Later-Life Outcomes of Early-Life Exposures

Cited by 164 publications

References 135 publications

Early-life exposure to a herbicide has enduring effects on pathogen-induced mortality

Early-life exposure to a herbicide has enduring effects on pathogen-induced mortality

Pediatric Type 2 Diabetes: Prevention and Treatment Through a Life Course Health Development Framework

A Complex Adaptive System in Which Environmental Stress Affects Gene Expression During Development

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