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Our bodies respond to our environment // By flicking some genes on, others off // Then, when we reproduce, it seems we don’t just pass on genes // But our on-off patterns too.

The New Heredity

By Rachael Moeller Gorman // Illustrations by David M. Brinley // Fall 2007
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For hundreds of years, people in the tiny parish of Överkalix, in northern Sweden, have endured bad times and celebrated good ones with little connection to the outside world. To the north and west are Lapps, and to the east, Finns. Though they technically speak Swedish, residents of Överkalix use a dialect that makes them virtually unintelligible to fellow Swedes.

But since the sixteenth century, the people of Överkalix have kept impeccable records of their lives. Clergy logged births, causes of deaths, and land ownership; other historical records noted harvests and crop prices. When epidemiologist Gunnar Kaati arrived 20 years ago, he found an extensive set of meticulous data for this isolated, homogeneous population—a perfect foundation for the large, multigenerational study he hoped to conduct. Kaati wanted to use the data to probe a new idea in clinical medicine—that exposure to certain environments during crucial points in development might determine whether a child would suffer disease years later.

We’re familiar with the notion that the environment is linked to disease—that a diet high in saturated fat may clog arteries and cause heart disease or that radiation mutates DNA and can lead to cancer. But in the emerging field of the fetal and developmental origins of adult disease, more subtle factors such as the amount of food a mother ate during pregnancy or the type of mothering she provided directly after birth may determine whether her child will develop cardiovascular disease or be left neurologically susceptible to overstress years later. 

These effects, some researchers believe, have nothing to do with mutations in the DNA code. Rather, they seem to involve what are known as epigenetic changes: structural alterations to the DNA double helix. The notion is that we experience periods in development when our bodies are programmed to collect information about our environment, then readjust our growth depending on what we find. To make this readjustment, our bodies flick genes on or off, sending us on an irreversible trajectory. For example, if a mother doesn’t eat much during pregnancy, that may signal to her fetus that he is about to emerge into a food-poor environment, and he may be born smaller, with a slower metabolism, than if his mother had eaten heartily. Epigenetic changes can lead to, say, type 2 diabetes years later if the world the adult finds—such as a world full of food—is different from that forecast by the fetus.

Kaati took this idea a step further. He wanted to know not just whether a child’s own early environment caused common diseases later in life but whether the environment a child’s parents or even grandparents encountered had an impact. Animal studies suggest that such effects may persist in DNA for generations, and Kaati’s work, still at an early stage, hints that the same thing may happen in humans. Genes might “remember” what our ancestors ate, felt and experienced, altering our own lives generations later.

For many students of biology and evolution, such ideas immediately bring to mind Jean-Baptiste Lamarck, who theorized that traits acquired by an organism during its life can be passed on to its offspring. The classic example is the giraffe that stretches its neck to reach a tree’s top leaves and then gives birth to longer-necked young. Lamarck died 30 years before the 1859 publication of Charles Darwin’s Origin of Species, which detailed evolution as we now know it—a process by which chance differences (later recognized as mutations) improved an individual’s chance of survival and thus ensured the propagation of those traits. Each man proposed a similar result, but by very different mechanisms; in Lamarck’s view, alterations in a species were more immediately driven by environmental change, whereas Darwin saw a longer process of passive natural selection. The subsequent discovery of genes—the primary unit of natural selection— added credence to Darwin’s theory, and Lamarck’s was shelved, seemingly laughable compared with what had been learned about the body’s sophisticated mode of transferring traits.

Yet advances in epigenetic research suggest that Lamarck may have been onto something. As with the giraffe’s tall tree, environmental factors such as lack of food or inattentive mothering appear to alter our epigenomes and sometimes even those of our offspring. (Some researchers think epigenetic changes have helped speed evolution, causing more rapid alterations than could be explained by mutations alone.)

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What’s the Difference?

Mutations and epigenetic changes can make a lasting impact on our genes, but they go about change in distinct ways.


1. “Environmental Epigenomics and Disease Susceptibility,” by Randy L. Jirtle and Michael K. Skinner, Nature Reviews: Genetics, April 2007. A thorough review of the environment’s effects on the epigenome, it uses vivid diagrams and photos to illustrate key points.

2. “Transgenerational Response to Nutrition, Early Life Circumstances and Longevity,” by Gunnar Kaati et al., European Journal of Human Genetics, April 2007. The latest in Kaati’s series of fascinating studies on health in an isolated Swedish village shows that food supply during childhood can alter disease risk generations later.

3. Epigenetics? This European site tackles the tough field of epigenetics for the general public with in-depth feature stories, frequent updates from the laboratory and the latest news.

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