Bad Medicine

Your Diet Affects Your Grandchildren's DNA, Scientists Say

Grandma baking with grandkids.
More and more evidence suggests that what you eat may have a genetic impact on your kids and grandkids. (Image credit: Mat Hayward, Shutterstock)

You are what you eat, the saying goes. And, according to two new genetic studies, you are what your mother, father, grandparents and great-grandparents ate, too.

Diet, be it poor or healthy, can so alter the nature of one's DNA that those changes can be passed on to the progeny. While this much has been speculated for years, researchers in two independent studies have found ways in which this likely is happening.

The findings, which involve epigenetics, may help explain the increased genetic risk that children face compared to their parents for diseases such as obesity and diabetes.

The punch line is that your poor dietary habits may be dooming your progeny, despite how healthy they will try to eat. [10 Worst Hereditary Conditions]


Epigenetics refers to changes in gene expression from outside forces. Different from a mutation, epigenetic changes lie not in the DNA itself but rather in its surroundings — the enzymes and other chemicals that orchestrate how a DNA molecule unwinds its various sections to make proteins or even new cells.

Recent studies have shown how nutrition dramatically alters the health and appearance of otherwise identical mice. A group led by Randy Jirtle of Duke University demonstrated how mouse clones implanted as embryos in separate mothers will have radical differences in fur color, weight, and risk for chronic diseases depending on what that mother was fed during pregnancy.

That is, the nutrients or lack of thereof changed the DNA environment in such a way that the identical DNA in these mouse clones expressed itself in very different ways.

Of mice and humans

Building upon this Duke University work, a new study led by Torsten Plösch of University of Groningen, The Netherlands, delineated the numerous ways in which nutrition alters the epigenome of many animals, including adult humans. The paper has been submitted to the journal Biochimie with lead author Josep C. Jiménez-Chillarón of the Paediatric Hospital Sant Joan de Deu, in Spain.

The researchers said that the diet of human adults induces changes in all cells — even sperm and egg cells — and that these changes can be passed on to offspring.

Such effects on a single generation have been known: Children born to mothers during the Dutch famine at the end of WWII had susceptibilities to various diseases later in life, such as glucose intolerance and cardiovascular disease, depending on the timing and extent of the food shortage during pregnancy.

In 2010, Jiménez-Chillarón and his colleagues took this a step further and found that overfed male mouse pups developed the telltale signs of metabolic syndrome — insulin resistance, obesity and glucose intolerance — and passed some of these traits to their offspring, which then developed elements of metabolic syndrome without overeating.

But what still is missing, Jiménez-Chillarón told LiveScience, is an understanding of how such information is remembered from generation to generation. Unlike a gene mutation, all of the epigenetic inputs to the DNA environment should be forgotten when a newly formed embryo begins to divide.

"The dogma is that during the process of meiosis [cell division], all epigenetic marks are erased," said Jiménez-Chillarón. "But our work, as well as [the work] from many others, suggests that this is not completely true. Although the majority of epigenetic marks is erased, some marks are spared for unknown reasons."

Attack on the DNA

A second study, led in part by Ram B. Singh of the TsimTsoum Institute in Krakow, Poland, published this month in the Canadian Journal of Physiology and Pharmacology, examined nutrients that affect the chromatin. The chromatin is like the chemical soup in which DNA operates.

Aside from creating epigenetic marks, Singh's group speculates that these nutrients also can cause mutations, both good and bad. But the evidence is still inconclusive.

Hints of this were reported in a 2011 paper in Nature by Stanford University scientists who found lingering, positive effects on longevity from nutrition on three generations of the C. elegans worm.

"It is possible that eating more omega-3 fatty acids, choline, betaine, folic acid and vitamin B12, by mothers and fathers, possibly can alter chromatin state and mutations, as well as have beneficial effects…leading to birth of a 'super baby' with long life and [lower risk] of diabetes and metabolic syndrome," Singh told LiveScience. "This is just a possibility, to be proven by more experiments." [10 New Ways to Eat Well]

Both teams of scientists said that cells in an early state of development are more prone to epigenetic changes from nutrition than adult cells, hence the most notable changes are seen fetuses and infants.

Yet it may be only a matter of time, they added, until there is evidence of how we pass along to subsequent generations the consequences of our own nutritional habits.

Christopher Wanjek is the author of a new novel, "Hey, Einstein!", a comical nature-versus-nurture tale about raising clones of Albert Einstein in less-than-ideal settings. His column, Bad Medicine, appears regularly on LiveScience.

Christopher Wanjek
Live Science Contributor

Christopher Wanjek is a Live Science contributor and a health and science writer. He is the author of three science books: Spacefarers (2020), Food at Work (2005) and Bad Medicine (2003). His "Food at Work" book and project, concerning workers' health, safety and productivity, was commissioned by the U.N.'s International Labor Organization. For Live Science, Christopher covers public health, nutrition and biology, and he has written extensively for The Washington Post and Sky & Telescope among others, as well as for the NASA Goddard Space Flight Center, where he was a senior writer. Christopher holds a Master of Health degree from Harvard School of Public Health and a degree in journalism from Temple University.