Maternal diet can reduce future cancer risk in offspring, OSU biochemist David Williams has found in studies with mice. In humans, cancer is second only to accidents as a cause of childhood deaths.
Cancer may begin, and could be won or lost, well before we are born. The battle may, in fact, have started with what our mothers ate. By shedding new light on the power of diet to influence the health of offspring, David Williams and a research team at OSU’s Linus Pauling Institute may offer new ways to protect future generations.
Williams and colleagues in the institute’s Cancer Chemoprotection Program have specialized in natural dietary compounds. For example, they have shown that chlorophyllin, a derivative of chlorophyll, can cut the rate of liver and other cancers in humans. In recent years, they have turned to chemicals that can cross the placental barrier and affect the health of children. Last fall, they reported that a chemical found in cruciferous vegetables (broccoli, cabbage, kale and their relatives) and fed to pregnant mice cut the rate of some cancers in their offspring.
It was the first demonstration that the compound (indole–3–carbinol) can confer such protection. And the benefit was long–lasting. Reductions in the cancer rate lasted well into the rodents’ middle age.
"Cancer is second only to accidents as the leading cause of death of children in the U.S.," says Williams, who also directs OSU’s Marine and Freshwater Biomedical Sciences Center. "If we can find ways to affect childhood cancer through maternal diet, it could be enormously important."
How is it possible that a mother’s diet during gestation could have such long–term effects? What it suggests, says Williams — even though he can’t yet prove it — is that the "imprinting" of certain genes was permanently changed so that they provided more resistance to carcinogens and cancer.
If confirmed, these findings could contribute to a growing body of evidence that links environmental and dietary factors to health in ways that can be passed from one generation to another. The field is known as "epigenetics" and focuses on chemicals that exert control over genes — turning them on or off or changing the way they operate — instead of the genes themselves.
In their studies, Williams and his team exposed pregnant mice to a single high dose of dibenzopyrene, a potent carcinogen. About 80 percent of 100 mouse offspring died early in life from an aggressive T–cell lymphoma. Of those that survived to the mouse–equivalent of middle age, all had lung tumors.
For comparison, a group of pregnant mice given the same carcinogen also received indole–3–carbinol. Deaths among off–spring from lymphoma were cut in half, and the number of lung tumors later in life was significantly reduced. The protection in adulthood remained, even though the only change had been the mother’s diet during pregnancy and nursing.
"When we first started looking at indole–3–carbinol, I expected it might be a blocking agent that detoxified carcinogens," Williams adds. "Turned out that wasn’t it. And we had to scramble a little bit to figure out what was going on."
That work is ongoing. OSU scientists want to learn how these protective nutrients work, whether they are in fact turning genes on or off and whether the lab results will translate to humans.
"There’s a lot still to learn, but it’s an extremely exciting model for research," Williams says. "A best–case scenario would be a diet or supplements we could recommend to pregnant women that would help protect their children against cancer and possibly birth defects. If this is an epigenetic phenomenon, that may be possible.
"This could be a dream come true."