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Published on: June 29, 2013
[Intrauterine growth retardation and vascular changes in neonates]
Hege Svangtun1, Gottfried Greve, Elisabeth Leirgul
1Institutt for klinisk medisin, Universitetet i Bergen, 5021 Bergen. hege.svangtun@student.uib.no
Insights
Low birth weight is linked to early vessel changes, increasing the risk of arteriosclerosis (cardiovascular disease) and adult mortality. This supports the fetal programming hypothesis for cardiovascular disease development.
Area of Science:
- Vascular biology and developmental origins of health and disease.
- Epidemiology of cardiovascular diseases.
Context:
- Cardiovascular disease (arteriosclerosis) is a leading cause of premature death in industrialized nations.
- Established risk factors include dyslipidemia, hypertension, diabetes, family history, and smoking.
- The fetal programming hypothesis suggests prenatal conditions influence adult cardiovascular health.
Purpose:
- To review the literature on the connection between low birth weight and arteriosclerosis.
- To explore the fetal programming hypothesis in relation to cardiovascular disease development.
Summary:
- Arteriosclerosis is a lifelong process influenced by known risk factors.
- Recent evidence links low birth weight to early vascular changes.
- Low birth weight is associated with increased risk of arteriosclerosis and cardiovascular mortality in adulthood.
Impact:
- Provides evidence supporting the fetal programming hypothesis for cardiovascular disease.
- Highlights low birth weight as a significant factor in long-term cardiovascular health.
- Offers insights into early life origins of adult arteriosclerosis.
Background:
Cardiovascular disease (arteriosclerosis) is one of the most common causes of premature illness and death in industrialized countries. The established risk factors for its development are dyslipidemia, hypertension, diabetes mellitus, positive family history and smoking. The fetal programming hypothesis (i.e. that prenatal conditions are important for the development of cardiovascular diseases) has been used to explain causal mechanisms of arteriosclerosis, such as biological disturbances in the blood vessels of growth-retarded neonates. This hypothesis differs from the more traditional explanation that health in adulthood is more or less determined by accumulated incidents throughout life.
Material And Methods:
The article is based on a review of relevant literature retrieved from PubMed (from 1980-2007), including all references in the English articles, and own research.
Results And Interpretations:
Arteriosclerosis is a lifelong process, with a number of wellknown risk factors. The last 10-15 years have provided sound evidence for the connection between low birth weight and early morphological and physiological changes in vessels. This may explain why individuals with low birth weight have an increased risk of developing arteriosclerosis and provide a link between low birth weight and an increased mortality rate due to cardiovascular diseases in adult life.
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