Developmental Origins of Health and Disease: the relevance to developing nations

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Abstract

Low- and middle-income countries (LMICs), particularly those in sub-Saharan Africa, are experiencing rapid increases in the prevalence of non-communicable diseases (NCDs), which may not be fully explained by urbanization and associated traditional risk factors such as tobacco smoking, excessive alcohol consumption, poor diet or physical inactivity. In this commentary, we draw attention to the concept of Developmental Origins of Health and Disease (DOHaD), where environmental insults in early life can contribute to long-term risk of NCDs, the impact of which would be particularly important in LMICs where poverty, malnutrition, poor sanitation and infections are still prevalent.

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Developmental plasticity and human health.

Patrick Bateson, David Barker, Timothy Clutton-Brock … (2004)

Many plants and animals are capable of developing in a variety of ways, forming characteristics that are well adapted to the environments in which they are likely to live. In adverse circumstances, for example, small size and slow metabolism can facilitate survival, whereas larger size and more rapid metabolism have advantages for reproductive success when resources are more abundant. Often these characteristics are induced in early life or are even set by cues to which their parents or grandparents were exposed. Individuals developmentally adapted to one environment may, however, be at risk when exposed to another when they are older. The biological evidence may be relevant to the understanding of human development and susceptibility to disease. As the nutritional state of many human mothers has improved around the world, the characteristics of their offspring--such as body size and metabolism--have also changed. Responsiveness to their mothers' condition before birth may generally prepare individuals so that they are best suited to the environment forecast by cues available in early life. Paradoxically, however, rapid improvements in nutrition and other environmental conditions may have damaging effects on the health of those people whose parents and grandparents lived in impoverished conditions. A fuller understanding of patterns of human plasticity in response to early nutrition and other environmental factors will have implications for the administration of public health.

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Fetal and infant growth and impaired glucose tolerance at age 64.

C N Hales, D. J. Barker, P. M. Clark … (1991)

To discover whether reduced fetal and infant growth is associated with non-insulin dependent diabetes and impaired glucose tolerance in adult life. Follow up study of men born during 1920-30 whose birth weights and weights at 1 year were known. Hertfordshire, England. 468 men born in east Hertfordshire and still living there. Fasting plasma glucose, insulin, proinsulin, and 32-33 split pro-insulin concentrations and plasma glucose and insulin concentrations 30 and 120 minutes after a 75 g glucose drink. 93 men had impaired glucose tolerance or hitherto undiagnosed diabetes. They had had a lower mean birth weight and a lower weight at 1 year. The proportion of men with impaired glucose tolerance fell progressively from 26% (6/23) among those who had weighted 18 lb (8.16 kg) or less at 1 year to 13% (3/24) among those who had weighed 27 lb (12.25 kg) or more. Corresponding figures for diabetes were 17% (4/23) and nil (0/24). Plasma glucose concentrations at 30 and 120 minutes fell with increasing birth weight and weight at 1 year. Plasma 32-33 split proinsulin concentration fell with increasing weight at 1 year. All these trends were significant and independent of current body mass. Blood pressure was inversely related to birth weight and strongly related to plasma glucose and 32-33 split proinsulin concentrations. Reduced growth in early life is strongly linked with impaired glucose tolerance and non-insulin dependent diabetes. Reduced early growth is also related to a raised plasma concentration of 32-33 split proinsulin, which is interpreted as a sign of beta cell dysfunction. Reduced intrauterine growth is linked with high blood pressure, which may explain the association between hypertension and impaired glucose tolerance.

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The thrifty phenotype hypothesis.

C N Hales, D. J. Barker (2001)

The thrifty phenotype hypothesis proposes that the epidemiological associations between poor fetal and infant growth and the subsequent development of type 2 diabetes and the metabolic syndrome result from the effects of poor nutrition in early life, which produces permanent changes in glucose-insulin metabolism. These changes include reduced capacity for insulin secretion and insulin resistance which, combined with effects of obesity, ageing and physical inactivity, are the most important factors in determining type 2 diabetes. Since the hypothesis was proposed, many studies world-wide have confirmed the initial epidemiological evidence, although the strength of the relationships has varied from one study to another. The relationship with insulin resistance is clear at all ages studied. Less clear is the relationship with insulin secretion. The relative contribution of genes and environment to these relationships remains a matter of debate. The contributions of maternal hyperglycaemia and the trajectory of postnatal growth need to be clarified.

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Author and article information

Journal

Journal ID (nlm-ta): Int Health

Journal ID (iso-abbrev): Int Health

Journal ID (publisher-id): inthealth

Title: International Health

Publisher: Oxford University Press

ISSN (Print): 1876-3413

ISSN (Electronic): 1876-3405

Publication date (Print): March 2018

Publication date (Electronic): 08 March 2018

Publication date PMC-release: 08 March 2018

Volume: 10

Issue: 2

Pages: 66-70

Affiliations

[1 ] Medical Research Council/Uganda Virus Research Institute Uganda Research Unit on AIDS, P Box 49, Entebbe, Uganda

[2 ] London School of Hygiene & Tropical Medicine, Keppel Street, London WC1E 7HT, UK

Author notes

Corresponding author: Tel: +256752662773; E-mail: Mandy.Wilja@ 123456mrcuganda.org

Article

Publisher ID: ihy006

DOI: 10.1093/inthealth/ihy006

PMC ID: 5856182

PubMed ID: 29528398

SO-VID: c86a09d4-9f86-4422-a063-07c4028a42de

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 04 January 2018

Date accepted : 22 January 2018

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Pages: 5

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Developmental Origins of Health and Disease: the relevance to developing nations

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Cardiovascular Innovations and Applications

Most cited references 28

Developmental plasticity and human health.

Fetal and infant growth and impaired glucose tolerance at age 64.

The thrifty phenotype hypothesis.

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Cited by 84

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