Remember way back in the 1950s when a pesticide called DDT basically blanketed Europe and North America before Rachel Carson’s Silent Spring exposed the fact that DDT is toxic to both humans and the environment?
Even if you don’t remember–and even if you weren’t alive–all that DDT use could still be having an effect on you. In fact, it might be why you’re fat.
Michael K. Skinner, founding director of Washington State University’s Center for Reproductive Biology, has long studied testes and ovary function on the molecular and cellular level. About 10 years ago, he began to experiment with exposing rat fetuses to various environmental toxins and has found surprisingly long-lasting effects. “Most exposures do promote trans-generational disease to the third or fourth generation, but we have gone out to the seventh generation,” he says.
It’s not that these toxins create changes in the DNA. Instead, they generate what are called epigenetic changes in sperm. These are changes in molecular processes that regulate DNA activity but are completely independent of the genome sequence itself.
“We found in the sperm a series of epigenetic changes permanently programmed that appear from generation to generation,” Skinner explains. Those changes caused a variety of trans-generational diseases, including reduced fertility, ovarian disease, kidney disease, prostate disease in the males, and breast tumors in the females.
Then, in 2006, the World Health Organization reversed its ban on DDT so that the Gates Foundation and others could use the insecticide to combat malaria in developing countries. Skinner wondered: what if DDT doesn’t just negatively affect the people who were directly exposed, but impacted other generations as well?
In his latest study, Skinner and a team of researchers examined just that: What happens to future generations of rats if their ancestors are exposed to DDT?
A major effect he found was linked to obesity. “We found in the first generation that there was no incidence of obesity, but we saw a few diseases from direct exposure,” he says. “When we looked at the third generation, the great-grand offspring, we found that over 50% of males and females developed obesity. The frequency was exceedingly high.” The female rats passed on obesity to their male great-grandchildren, while the male rats passed it on to the female great-grandchildren.
DDT doesn’t directly cause obesity, but Skinner’s study shows that it may induce susceptibility to developing obesity. So if there are two different animal on the exact same unhealthy diet–one susceptible, one not–one will become obese, and the other won’t. “How much of this is a component of the current obesity epidemic?” Skinner asks.
In the 1950s, after all, obesity rates were at 3% or less. Now 33% of U.S. adults are obese. As Skinner’s study points out: “Since the primary human exposures to DDT in the U.S. occurred in the 1950s, three generations have developed with a progressively increasing incidence of obesity in the population.”
There are many other factors that public health researchers believe contribute to the rise in obesity–people get less exercise than they used to, Americans eat a lot of junk food, as well as the prevalence of plenty of other environmental toxins that could promote obesity.
But as DDT is used more frequently to control malaria, we need to think about the tradeoffs we’re making. “Alternatives to DDT are more costly and difficult [to implement], but they’re something to consider,” says Skinner. “We need to make sure we’re not going to destroy the future because of our actions today.”