Researchers at Washington State University say the pesticide DDT makes the grandchildren of exposed people more susceptible to weight gain.
While many people have a genetic predisposition to obesity, new research suggests that the use of a controversial pesticide may make us more susceptible to it, as well as other diseases.
Michael Skinner, founder of the Center for Reproductive Biology at Washington State University, says widespread exposure to the pesticide dichlorodiphenyltrichloroethane (DDT) in the 1950s continues to affect the health of humans today.
Previous research has linked DDT to increased rates of diabetes, developmental problems, reproductive harm, miscarriages, and certain cancers. In the 1970s, it was also shown to have impacted bald eagle and peregrine falcon populations.
In a new study published in the journal
“Interestingly, in the first generation, we didn’t see any obesity. We saw many diseases, but not obesity. It took three generations to ramp up,” Skinner said. “What this ancestral exposure does is increase a person’s susceptibility for obesity. This is probably the case with most diseases.”
The process is called transgenerational epigenetic inheritance. While DDT doesn’t mutate genes, exposure to it during key points in development—namely when sex organs are forming in the womb—can affect which genes are expressed.
“This doesn’t promote the disease, but it increases the susceptibility to develop a disease,” Skinner said.
During the 1950s, the U.S. obesity rate was below three percent. Now, more than one third of Americans are considered obese, according to the
Trangenerational epigenetic inheritance essentially means that what our grandparents were exposed to during their lifetimes can affect us today.
Knowing how this mechanism works, Skinner says, means that looking at epigenetic biomarkers early in a person’s life can help determine what diseases they might face later.
“That’s call preventative medicine,” Skinner said. “We’ve never been able to do preventative medicine in the past because we’ve never had these kinds of biomarkers.”
Previously, Skinner’s lab tested the epigenetic effects of other environmental toxins, including plastics, fungicides, and other pesticides besides DDT.
“The reason we did this one was because around four years ago the World Health Organization and the Gates Foundation pushed to remove the ban on DDT so they could use it for malaria treatment, mainly in Africa,” he said.
First synthesized in 1939, DDT was hailed as an effective insecticide to control malaria and typhus, and was used heavily during World War II. It was so highly regarded that Swiss chemist Paul Hermann Müller was awarded the Nobel Prize in 1948 for synthesizing an effective version of DDT.
DDT’s use dropped drastically after the 1962 book Silent Spring was published by biologist Rachel Carson. That book, which discussed the health and environmental impact of DDT, started a movement to get the substance banned.
Before it was banned in 1972, DDT was the most commonly used insecticide in the U.S. While it continues to be banned in many countries, its use in Africa has increased since the WHO backed its use in 2006 to combat malaria and the beginning of the Bill and Melinda Gates Foundation’s program to control malaria.
DDT is a preferred insecticide in developing countries because it is cheap and can typically control malaria outbreaks with a single treatment. Its effectiveness is due to its long half-life, which prevents it from breaking down easily.
Because DDT was such a prominent insecticide in the 1950s and 60s, it is still present in lakes and rivers in the U.S., and continues to affect the ecosystem.
“Literally, DDT is around for hundreds of years,” Skinner said. “This is something that just doesn’t go away.”
Skinner hopes that his research will spur policy makers to reconsider the use of DDT in Africa and other developing countries because other pesticides with a shorter half-life are available.
“Now we need to concern ourselves and reevaluate using DDT,” he said.