The Fetal Origins of Cardiovascular Disease
Kimona C. Cameron
Advisor: Prof. O’Hara & Dr. Aronson
Depts. of Biology & Chemistry, Amherst College, Amherst, MA 01002
Introduction
Within the last three decades researchers have been interested in
finding correlations between childhood environment and adult health.
Studies across Europe and the United States have shown that
geographical disparities in cardiovascular mortality are linked to past
differences in infant mortality. Studies have also shown that the
differences in the death rates from cardiovascular disease in several
areas throughout England and Wales are closely related to disparities
in neonatal mortality. The results of these findings, among others, have
spurred a new area of interest for researchers to study. They suggest
that the focus should be in-utero rather than from childhood.
Hypertension
In a follow-up study set in Preston, England, the effect of intrauterine
growth and its effect on blood pressure in adult life was examined.
• 449 men and women born and still resided in Preston, ages 4654
• Hypertension or high blood pressure was strongly correlated to
their placental weight and birth weight in both sexes
• Highest blood pressures found in small babies with large
placentas.
• The disparity between these two factors causes the fetus to
adapt its circulatory system, altering its arterial structure as a
child and causing hypertension as an adult.
• It was noted that alcohol consumption and higher body mass
indexes were also associated with hypertension, however the
relationship between blood pressure and placental and birth
weight were independent of these factors.
Fetal Origins Hypothesis
Barker’s fetal origins hypothesis states that fetal under-nutrition in
middle to late gestation, which leads to disproportionate fetal growth,
programs later coronary heart diseases.
• Fetus size at birth reflects its growth and the materno-placental
ability to provide it with enough nutrients.
• If the fetus isn’t provided adequate nutrients it undergoes
developmental adaptations that may be beneficial in short-term
survival (like protecting blood flow to the developing brain) but
detrimental in the long-run causing (decreased blood flow to
the rest of the body) permanent alterations in body structures
and metabolism leading to cardiovascular and metabolic
diseases later in life.
• The mechanism for this is not yet known but the correlation is
very apparent.
Low Birth Weight
• Low birth weight is a global public health issue of which the
general public is most unaware.
• There have been several studies linking low birth weight infants
(<5.5 lb.) to instances of cardiovascular diseases in adult life,
several of which will be discussed in some detail here.
General Cardiovascular Disease
In more recent studies done in Britain and the United States
respectively more evidence was found linking birth weight and
cardiovascular disease . In the British birth cohort study done on over
3000 men and women, babies with higher birth weights had lower rates
of high blood pressure. In the US study it was determined that low birth
weight has a significant role in the onset of disease outside of
childhood socioeconomic concerns. Children with low birth weight had
higher instances of hypertension, stroke, heart attack and heart
disease..
Preventing Low Birth Weight
Low birth weight has long term effects on childhood health and
development as well as adult morbidity and mortality. Its prevention is
crucial in decreasing these pathologies. Some factors associated with the
occurrence of low birth weight include:
Maternal Stress
Poor Nutrition
Smoking
Drug Abuse
Lack of Maternal Role Model and
Love
Depression
Domestic Violence
Poverty
Adverse Living Environments
Social Exclusion
These factors contribute to sustained levels of adrenaline leading to
poor fetal growth and permanent physiological changes
Ischemic Heart Disease
Barker et al. (1989) carried out a study in Hertfordshire, England where
he examined growth and development during early life as it relates to
occurrence of ischemic heart disease–caused by decreased blood
supply to the heart–in later life.
• Increase in cholesterol and plaque in the arteries, which transport
oxygenated blood to the heart, overtime damages the vessels
thus weakening the heart muscle and reducing the amount of
blood the heart pumps to the rest of the body.
• Gathered data on over 5600 men born in Hertfordshire during
1911-1930.
• Men with lowest weights at birth and at 1 year had the highest
instances of death from ischemic heart disease.
• Those who weighed more at birth and were breast-fed had lower
rates of death from the disease.
Birth Weight & Nutrition
Of the studies examined maternal health was cited as a possible
influence on the occurrence of the aforementioned afflictions during
adulthood. Genes determine fetal growth, but growth is limited by the
nutrient and oxygen supply that it receives
• Maternal dietary intake, nutrient stores and the transport of the
nutrients to the placenta influence fetal nutrition.
• Poor nutrition impairs fetal growth during critical periods,
permanently altering the structure and physiology of the fetus’
organs and tissues.
• Rats subjected to low protein diets before and during pregnancy
produced perennial elevated blood pressure and altered glucosemetabolism in the offspring..
References
Agent Orange: Ischemic Heart Disease. (n.d.). Retrieved December 11, 2011, from United States
Department of Veteran Affairs :
http://www.publichealth.va.gov/exposures/agentorange/conditions/ischemicheartdisease.asp
Ashdown-Lambert , J. R. (2005). A review of low birth weight: predictors, precursors, and morbidity
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Barker, D. J. (1995). Fetal Origins of Coronary Heart Disease . British Medical Journal (311).
Barker, D. J. (1997). Maternal Nutrition, Fetal Nutrition and Disease in Later Life. Nutrition (13), 807-813.
Barker, D. J. (1990). The fetal and infant origins of adult disease. British Medical Journal , 301, 1111.
Barker, D. J., Bull, A. R., Osmond, C., & Simmonds, S. J. (1990). Fetal and placental size and risk of
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Johnson, R. C., & Schoeni, R. F. (2011). Early-Life Origins of Adult Disease: National Longitudinal
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