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We all know that what a mother eats, drinks, smokes and does during pregnancy can affect her child’s prenatal development. But can it actually affect the baby’s DNA?
Animal studies have shown that transient environmental exposures of a pregnant female can produce “epigenetic” changes in her offspring — chemical modifications superimposed on the DNA sequence that affect how and when genes are expressed.
It would of course be highly unethical to purposefully subject human mothers to environmental insults for the purpose of studying DNA effects in developing fetuses. But history has provided researchers a unique opportunity to study how one environmental factor, maternal nutrition, can affect an unborn child at the genetic level.
In the winter of 1944-1945, the Germans imposed a food embargo in the western part of the Netherlands, leading to a period of famine known as the Dutch Hunger Winter. Food was so scarce that the average daily caloric intake was cut to about 667 calories. Despite the desperate times, birth registries and the health care system remained operational, allowing researchers today to trace people who were prenatally exposed to the famine.
Higher rates of schizophrenia, addiction, obesity and heart disease have previously been associated with people conceived during the Hunger Winter. But new results, published online last week in the Proceedings of the National Academy of Sciences, offer some of the first evidence that there were also epigenetic effects in these people.
Heijmans and colleagues found that people who were conceived during the Hunger Winter, and thus exposed to famine very early in their development, to this day have fewer epigenetic markers called methyl groups attached to a gene called IGF2 than their unexposed siblings. People who had been in the late stages of gestation during the famine did not show these differences.
The protein encoded by the IGF2 gene is a key factor in human growth and development. A reduction in the number of methyl groups attached to the gene affects whether the maternal copy of the gene is expressed and has been associated with an increased risk of colorectal cancer.
Although people exposed to famine during the earliest days of their development show evidence of epigenetic changes all these years later, their average recorded birth weight was no different than what was seen in children born before the famine. But the people who were late in gestation during the famine and didn’t show epigenetic effects were lighter at birth. This suggests that low birth weight, a commonly used proxy measure for compromised prenatal development, might not be sufficient for understanding the true extent of how a mother’s environment has impacted her child.
The authors of the study suggest that future research should focus on the epigenetic effects of environmental exposures that are more common in modern societies, such as over-nutrition and assisted reproductive technologies.
“Understanding how epigenetic control depends on early exposure may shed light on the link between development and health over the lifespan and ultimately suggest new ways to prevent human disease,” the authors conclude.
Photo: Sander van der Molne