Abstract
Impairment of intrauterine environment during critical periods may result in perturbations in growth and development of the fetus. Barker et al. have originally proposed the hypothesis that several chronic adult diseases can be programmed in early life. These authors examined the mortality records of 5,654 men who were born during 1911–1930 in Hertfordshire (UK). In this report was found that the men with the lowest weights at birth subsequently had the highest death rates from ischemic heart disease. In addition, a retrospective study of babies born during the Dutch famine of 1945 has demonstrated a significant association between cardiovascular disease (CVD) and early nutritional impairment during gestation. In this programming concept, stimulus or injury during the critical period of development can result in the permanent changes in physiology and the metabolism and produces persistent effects throughout life. Afterward, Hales and Barker suggested the “Thrifty Phenotype Hypothesis” or “Economic Phenotype” to explain the biological basis of the fetal origin hypothesis. In this context, impairment of fetal environment can result in a physiological adaptive response that promotes early survival at the detrimental of later health. In fact, poor nutritional conditions during pregnancy can alter the development of a fetus to prepare him or her to survive in an environment with low nutritional resources. The main basis of this hypothesis is that the deleterious effects are more pronounced when there is a significant difference between the early nutritional deficiency and later nutritional intake. Reduced growth, represented mainly by low birth weight, is the major result of a suboptimal intrauterine environment and is associated with chronic conditions in adulthood, such as type 2 diabetes, hypertension, and CVD.
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Franco, M. (2015). Perinatal Programming of Cardiovascular Disease. In: Berbari, A., Mancia, G. (eds) Arterial Disorders. Springer, Cham. https://doi.org/10.1007/978-3-319-14556-3_6
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DOI: https://doi.org/10.1007/978-3-319-14556-3_6
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