Prenatal exposure to famine and health in later life

Ravelli, A.C.; Meulen, Jhp van der

doi:10.1016/s0140-6736(05)79096-6

Cited by 3 publications

(1 citation statement)

References 2 publications

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“…A well-documented period providing epidemiological evidence linking early-life adversity and health outcomes is the 1944–1945 Dutch Famine (see Table 1). A cohort of 741 subjects exposed to the Dutch Famine prenatally had a reduced birth weight, yet at adulthood these subjects had increased body weight, BMI, fasting proinsulin levels, and glucose intolerance (63). A report of 7557 women exposed to the Dutch famine showed increased risk for T2DM development in their offspring (64).…”

Section: Does Early-life Stress Affect Risk For Later Life Metabolic mentioning

confidence: 99%

Early-Life Stress, HPA Axis Adaptation, and Mechanisms Contributing to Later Health Outcomes

2014

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Stress activates the hypothalamic–pituitary–adrenal (HPA) axis, which then modulates the degree of adaptation and response to a later stressor. It is known that early-life stress can impact on later health but less is known about how early-life stress impairs HPA axis activity, contributing to maladaptation of the stress–response system. Early-life stress exposure (either prenatally or in the early postnatal period) can impact developmental pathways resulting in lasting structural and regulatory changes that predispose to adulthood disease. Epidemiological, clinical, and experimental studies have demonstrated that early-life stress produces long term hyper-responsiveness to stress with exaggerated circulating glucocorticoids, and enhanced anxiety and depression-like behaviors. Recently, evidence has emerged on early-life stress-induced metabolic derangements, for example hyperinsulinemia and altered insulin sensitivity on exposure to a high energy diet later in life. This draws our attention to the contribution of later environment to disease vulnerability. Early-life stress can alter the expression of genes in peripheral tissues, such as the glucocorticoid receptor and 11-beta hydroxysteroid dehydrogenase (11β-HSD1). We propose that interactions between altered HPA axis activity and liver 11β-HSD1 modulates both tissue and circulating glucocorticoid availability, with adverse metabolic consequences. This review discusses the potential mechanisms underlying early-life stress-induced maladaptation of the HPA axis, and its subsequent effects on energy utilization and expenditure. The effects of positive later environments as a means of ameliorating early-life stress-induced health deficits, and proposed mechanisms underpinning the interaction between early-life stress and subsequent detrimental environmental exposures on metabolic risk will be outlined. Limitations in current methodology linking early-life stress and later health outcomes will also be addressed.

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Section: Does Early-life Stress Affect Risk For Later Life Metabolic mentioning

confidence: 99%

Early-Life Stress, HPA Axis Adaptation, and Mechanisms Contributing to Later Health Outcomes

2014

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Long-term effects on offspring of intrauterine exposure to deficits in nutrition

Petry

Hales²

2000

Human Reproduction Update

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The number of cell divisions during embryonic and fetal life makes the embryo/fetus particularly vulnerable to effects resulting from exposure to an adverse intrauterine environment. Exposure to drugs and irradiation at this stage of development are able to cause congenital malformations and various cancers in later life. In-utero exposure to hyperglycaemia is able to lead to future diabetes that is heritable, but not genetic in origin. Fetal malnutrition causing growth restriction is able to lead to an increased risk of developing type 2 diabetes, hypertension and ischaemic heart disease in later life, especially if the growth restriction is followed by catch-up growth postnatally. This review discusses the various mechanisms by which these effects may occur, and presents the difficulties that will have to be faced if their world-wide health burdens are to be reduced.

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The Potential Use of DNA Methylation Biomarkers to Identify Risk and Progression of Type 2 Diabetes

Gillberg

Ling

2015

Front. Endocrinol.

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Type 2 diabetes mellitus (T2D) is a slowly progressive disease that can be postponed or even avoided through lifestyle changes. Recent data demonstrate highly significant correlations between DNA methylation and the most important risk factors of T2D, including age and body mass index, in blood and human tissues relevant to insulin resistance and T2D. Also, T2D patients and individuals with increased risk of the disease display differential DNA methylation profiles and plasticity compared to controls. Accordingly, the novel clues to DNA methylation fingerprints in blood and tissues with deteriorated metabolic capacity indicate that blood-borne epigenetic biomarkers of T2D progression might become a reality. This Review will address the most recent associations between DNA methylation and diabetes-related traits in human tissues and blood. The overall focus is on the potential of future epigenome-wide studies, carried out across tissues and populations with correlations to pre-diabetes and T2D risk factors, to build up a library of epigenetic markers of risk and early progression of T2D. These markers may, tentatively in combination with other predictors of T2D development, increase the possibility of individual-based lifestyle prevention of T2D and associated metabolic diseases.

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Prenatal exposure to famine and health in later life

Cited by 3 publications

References 2 publications

Early-Life Stress, HPA Axis Adaptation, and Mechanisms Contributing to Later Health Outcomes

Early-Life Stress, HPA Axis Adaptation, and Mechanisms Contributing to Later Health Outcomes

Long-term effects on offspring of intrauterine exposure to deficits in nutrition

The Potential Use of DNA Methylation Biomarkers to Identify Risk and Progression of Type 2 Diabetes

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