Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women.
Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, hypertension, and noninsulin- dependent diabetes...
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| Format: | Online |
| Language: | English |
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2000
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637808/ |
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pubmed-16378082006-11-17 Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. Osmond, C Barker, D J Research Article Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, hypertension, and noninsulin- dependent diabetes. We review epidemiologic studies in which the incidence of these diseases has been related to the recorded, early growth of individuals, while considering factors in the adult lifestyle, such as obesity and socioeconomic status. We discuss possible mechanisms. For hypertension these mechanisms include placentation, maternal blood pressure, fetal undernutrition; childhood growth, activation of the renin-angiotensin system, renal structure, programming of the hypothalamic-pituitary-adrenal axis, vascular structure, and sympathetic nervous activity. For noninsulin-dependent diabetes we discuss mechanisms concerning both insulin resistance and insulin deficiency. We include a review of evidence for the programming of serum cholesterol and clotting factor concentrations. We address the timing of critical windows for coronary heart disease, reviewing studies that allow assessment of the relative importance of fetal, infant, and childhood growth. We argue for a research strategy that combines clinical, animal, and epidemiological studies. 2000-06 /pmc/articles/PMC1637808/ /pubmed/10852853 Text en |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Osmond, C Barker, D J |
| spellingShingle |
Osmond, C Barker, D J Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. |
| author_facet |
Osmond, C Barker, D J |
| author_sort |
Osmond, C |
| title |
Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. |
| title_short |
Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. |
| title_full |
Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. |
| title_fullStr |
Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. |
| title_full_unstemmed |
Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. |
| title_sort |
fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women. |
| description |
Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, hypertension, and noninsulin- dependent diabetes. We review epidemiologic studies in which the incidence of these diseases has been related to the recorded, early growth of individuals, while considering factors in the adult lifestyle, such as obesity and socioeconomic status. We discuss possible mechanisms. For hypertension these mechanisms include placentation, maternal blood pressure, fetal undernutrition; childhood growth, activation of the renin-angiotensin system, renal structure, programming of the hypothalamic-pituitary-adrenal axis, vascular structure, and sympathetic nervous activity. For noninsulin-dependent diabetes we discuss mechanisms concerning both insulin resistance and insulin deficiency. We include a review of evidence for the programming of serum cholesterol and clotting factor concentrations. We address the timing of critical windows for coronary heart disease, reviewing studies that allow assessment of the relative importance of fetal, infant, and childhood growth. We argue for a research strategy that combines clinical, animal, and epidemiological studies. |
| publishDate |
2000 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1637808/ |
| _version_ |
1611391140296130560 |