Disease — it all starts in the womb
The foetus was once thought to be a perfect parasite.
Hidden and shielded in the safe uterus and receiving sufficient nutrients through a perfect filter, the placenta or after birth.
No harmful substances would be let thought and the correct amount of helpful ones were selected to pass through and nourish the vulnerable little passenger.
Things like smoking and drinking were even permitted, which is not too strange for a time when doctors were even used to advertise cigarette brands.
The first evidence that the placenta was an imperfect filter presented with the Thalidomide episode in the late 1950s.
This drug was licensed for the treatment of morning sickness from 1957 to 1961 until it was identified as the cause of foetal birth defects such as the absence of limbs.
In 1973 foetal alcohol syndrome was described, not as a previously thought of as a hereditary condition but as a direct consequence of foetal in utero exposure to alcohol.
Both these adverse effects are evident early in neonatal and childhood life but what about more subtle exposures that may have latent effects that only present in later adult life?
These would present as significantly troublesome as it would take decades to correlate potential exposure to outcome.
David Barker, a British physician was the most famous proponent of the foetal origin hypothesis.
He proposed that inadequate nutrition in utero programmes a foetus to later develop all the characteristics of metabolic syndrome, including, obesity, hypertension, diabetes and high cholesterol.
This leads to a very high risk of adult cardiovascular disease, one of the largest and most expensive public health concerns.
He postulated that these effects are persistent, latent and cause genetic programming changes that may even be transmitted to future generations.
This is called transgenerational epigenetic inheritance.
Interestingly, these malnourished neonates with low birth weights were worse off after rapid “catch-up” weight gain during early childhood.
Crucial metabolic organs like the liver, kidneys and pancreas that have starved in utero cannot handle the subsequent high energy diet post-partum.
The Dutch famine of 1944 was used to test this hypothesis.
As the Nazis occupied the Netherlands, food imports were blocked and many starving mothers were reduced to surviving on tulip bulbs.
Because nutrition had been adequate just before the famine the adults born just before and during the famine could be compared.
Interestingly the long-term effects were not only physical (higher obesity and metabolic syndrome rates) but there was also an increase in schizophrenia and abnormal cognition rates among those affected by the famine.
The focus of the research was also moved to other regions where war and famine had occurred and results were replicated.
The major difficulty with research in this field is the time delay that is involved in the presentation of these latent effects as well as the propensity to rather look at large events or major potential exposure.
What about more subtle in utero exposure such as pollution or stress?
More recently, economists and health economists have become interested in this theory.
They devise health policies that implement cost-effective interventions to secure the wellbeing of future generations.
They have access to huge databases including health outcomes and potential exposures.
They started looking at the non-health endpoint and have revealed more concerns.
Low birth weight children were less likely to finish high school or be employed by age 33.
Marital status is negatively affected and welfare dependency is increased.
Economists studied the effects of children born to mothers who were infected by the 1918 “Spanish flu” epidemic.
These children were 20% more likely to be disabled, experienced lower wages than their peers and had reduced educational attainment.
Even the effects of diurnal fasting in early pregnancy during Ramadan increased the risk of learning disabilities in two studied populations.
There are multiple similar examples that I will not go into.
Studies into foetal exposure to pollution and its effects have many limitations and proving damage will be difficult and likely controversial.
Extrapolating from smoking and passive smoking effects may be a stretch but it gives reason for concern.
Interventions to improve public health in large populations have focused on early childhood intervention and support.
Future policies may move towards a focus on maternal health as this could be a more effective way to achieve the goals of a healthy future generation.
Interventions like folic acid fortification and iodine supplementation have already shown great success.
Our main challenges remain in identifying less obvious, softer insults or exposures in utero.
Finding markers for long-term adverse effects will speed up research to provide evidence and thus changes to health policy.
The ideal scenario would be to have all at-risk women receive proper prenatal counselling by a health-care worker with thorough, up-to-date knowledge of all factors that may negatively affect her pregnancy.
In the developing world, this is far from the reality.
• Dr T is a registered medical practitioner working in Nelson Mandela Bay
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