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Updated: Aug 15, 2026

Assessment of Maternal Vascular Remodeling During Pregnancy in the Mouse Uterus
Published on: December 5, 2015
Intrauterine growth, the vascular system, and the metabolic syndrome
Richard I G Holt1, Christopher D Byrne
1Endocrinology and Metabolism Sub-Division, Fetal Origins of Adult Disease Division, School of Medicine, Southampton University, Southampton General Hospital, Southampton, England. righ@soton.ac.uk
Insights
Low birth weight is linked to adult cardiovascular disease risk due to fetal adaptations to undernutrition. Preventing growth imbalances may reduce disease risk.
Area of Science:
- Developmental biology
- Epidemiology
- Cardiovascular medicine
Background:
- Substantial evidence links birth size to adult cardiovascular disease (CVD) and its risk factors.
- The fetal origins hypothesis suggests CVD originates from fetal adaptations to undernutrition.
- These adaptations can be cardiovascular, metabolic, or endocrine, permanently altering body structure and function.
Purpose of the Study:
- To examine recent epidemiological associations between low birth weight and adult atherosclerotic vascular disease.
- To discuss potential mechanisms underlying these associations.
Main Methods:
- Epidemiological studies examining birth weight and adult cardiovascular disease risk factors.
- Review of proposed biological mechanisms linking fetal development to adult disease.
Main Results:
- Low birth weight is associated with increased risk of adult atherosclerotic vascular disease.
- Fetal adaptations to undernutrition, including cardiovascular, metabolic, and endocrine changes, are implicated.
- Imbalances in fetal growth or nutrient supply may contribute to disease development.
Conclusions:
- Birth size is a significant determinant of adult cardiovascular health.
- Preventing prenatal and postnatal growth imbalances is crucial for CVD prevention.
- Understanding fetal adaptations is key to mitigating lifelong disease risk.
Abstract:
There is substantial evidence linking birth size with the risk of developing cardiovascular disease and its major biological risk factors in adulthood. The fetal origins hypothesis proposes that these diseases originate through adaptations, which the fetus makes when it is undernourished. These adaptations may be cardiovascular, metabolic, or endocrine. They permanently change the structure and function of the body. Prevention of the diseases may depend on prevention of imbalances in fetal growth or imbalances between prenatal and postnatal growth, or imbalances in nutrient supply to the fetus. The purpose of this article is to examine some of the more recent epidemiological associations between low birth weight and adult atherosclerotic vascular disease and its risk factors. We will also discuss mechanisms that might explain these associations.
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