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Metabolic programming in early life in humans

Metabolic programming in early life in humans
Metabolic programming in early life in humans
An association of low birth weight with an increased risk of adult cardiovascular disease and diabetes led to the developmental origins of health and disease (DOHaD) hypothesis, which proposes that undernutrition during early development permanently ‘programmes’ organ structure and metabolism, leading to vulnerability to later cardio-metabolic disease. High birth weight caused by maternal gestational diabetes is also associated with later diabetes, suggesting that fetal over-nutrition also has programming effects. Post-natal factors (excess weight gain/obesity, smoking, poor diets and physical inactivity) interact with fetal exposures to increase disease risk. Animal studies have shown permanent metabolic effects in offspring after alterations to maternal or early post-natal diets but evidence in humans is largely limited to observational and quasi-experimental situations such as maternal famine exposure. Randomized trials of maternal nutritional interventions during pregnancy have so far had limited follow-up of the offspring. Moreover, interventions usually started after the first trimester and therefore missed key peri-conceptional or early pregnancy events such as epigenetic changes, placentation and fetal organogenesis. Recent and ongoing trials intervening pre-conceptionally and powered for long-term offspring follow-up will address these issues. While current preventive strategies for cardio-metabolic disease focus on high-risk individuals in mid-life, DOHaD concepts offer a ‘primordial’ preventive strategy to reduce disease in future generations by improving fetal and infant development.
0962-8436
Fall, Caroline
7171a105-34f5-4131-89d7-1aa639893b18
Kumaran, Kalyanaraman
de6f872c-7339-4a52-be84-e3bbae707744
Fall, Caroline
7171a105-34f5-4131-89d7-1aa639893b18
Kumaran, Kalyanaraman
de6f872c-7339-4a52-be84-e3bbae707744

Fall, Caroline and Kumaran, Kalyanaraman (2019) Metabolic programming in early life in humans. Philosophical Transactions of The Royal Society B Biological Sciences, 374 (1770). (doi:10.1098/rstb.2018.0123).

Record type: Article

Abstract

An association of low birth weight with an increased risk of adult cardiovascular disease and diabetes led to the developmental origins of health and disease (DOHaD) hypothesis, which proposes that undernutrition during early development permanently ‘programmes’ organ structure and metabolism, leading to vulnerability to later cardio-metabolic disease. High birth weight caused by maternal gestational diabetes is also associated with later diabetes, suggesting that fetal over-nutrition also has programming effects. Post-natal factors (excess weight gain/obesity, smoking, poor diets and physical inactivity) interact with fetal exposures to increase disease risk. Animal studies have shown permanent metabolic effects in offspring after alterations to maternal or early post-natal diets but evidence in humans is largely limited to observational and quasi-experimental situations such as maternal famine exposure. Randomized trials of maternal nutritional interventions during pregnancy have so far had limited follow-up of the offspring. Moreover, interventions usually started after the first trimester and therefore missed key peri-conceptional or early pregnancy events such as epigenetic changes, placentation and fetal organogenesis. Recent and ongoing trials intervening pre-conceptionally and powered for long-term offspring follow-up will address these issues. While current preventive strategies for cardio-metabolic disease focus on high-risk individuals in mid-life, DOHaD concepts offer a ‘primordial’ preventive strategy to reduce disease in future generations by improving fetal and infant development.

Text
Phil Trans B Review final accepted version - Accepted Manuscript
Restricted to Repository staff only until 25 February 2020.
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More information

Accepted/In Press date: 9 October 2018
e-pub ahead of print date: 25 February 2019
Published date: April 2019

Identifiers

Local EPrints ID: 429957
URI: https://eprints.soton.ac.uk/id/eprint/429957
ISSN: 0962-8436
PURE UUID: dcd1bc7c-f368-4780-b1c3-99dcbed8c522

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Date deposited: 09 Apr 2019 16:30
Last modified: 30 Apr 2019 16:30

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