Science

Study says early DDT exposure may set up females for obesity, diabetes

Did the pesticide DDT, used widely in the U.S. for more than two decades, set the stage for an epidemic?
DDT's long-delayed effects in mice may help explain why obesity and diabetes began a steep rise in the 1970s

As they reached adulthood, female mice who were exposed in utero and just after birth to the pesticide DDT showed metabolic changes that put them at greater risk for obesity and type-2 diabetes, a new study says.

The metabolic abnormalities seen in the exposed female mice were dramatically exacerbated when they were fed a high-fat diet for 12 weeks in adulthood. Compared with unexposed mice who also ate a high-fat diet, females exposed to DDT around the time of their birth were more likely to develop high cholesterol, insulin insensitivity, glucose intolerance and metabolic problems that could lead to liver disease.

The study, published Wednesday in the journal PLoS One, helps explain a consistent finding from epidemiological studies: In large populations, exposure to DDT and other persistent organic pollutants, or POPs, is linked to increased rates of type-2 diabetes, obesity and worrisome cholesterol.

Such studies could not establish a cause-and-effect relationship between pesticide exposure and these ills. But the latest study takes a major step in that direction. By directly comparing lab mice deliberately exposed to DDT during gestation and infancy with members of the same breed who were not, researchers set two identical populations on very different tracks, and consistently gathered a wide range of health-related measures from birth to death.

Experimentation on mice has its limits in illuminating physiological processes in humans. But the mammals' compressed lifespan and the broad similarity between the inner workings of mice and human have made the small creatures a useful stand-in for us.

The study confirms that DDT exposure sets in motion circumstances that increase an individual's likelihood over the course of her lifespan of accumulating excess fat, and of metabolizing fats and carbohydrates in ways that increase the risk of developing metabolic syndrome - a precursor to type-2 diabetes.

But the study also underscores that, when it comes to DDT exposure, cause and effect may be separated by a lengthy delay. In lab mice, repeated exposures to DDT "within the range of contemporary human exposures" came during the second of gestation and within the first five days of life.

In young adulthood - around two months - researchers noted that DDT-exposed females had a slightly lower core temperature than their non-exposed sisters, and seemed to expend fewer calories in day-to-day activities. DDT-exposed female mice were slightly heavier and carried a bit more fat as young adults - two to five months after birth.

But it wasn't until they were 6 months old that DDT-exposed females showed clear signs of impaired glucose tolerance, fasting glucose, insulin and lipid levels. And when the two groups of mice were put on a high-fat diet at age 6 months, the trajectories of their weight and their metabolic health diverged even more dramatically.

That delayed response could help place DDT in the pantheon of influences that have contributed to a steady uptick in obesity and type-2 diabetes among Americans during the 1970s, '80s and '90s - and in the later appearance of the same trend throughout the developing world.

From the late 1940s until it was banned in 1972, DDT was widely used in the United States and throughout Europe to control mosquitoes and other insects carrying malaria, polio and typhus. After evidence of its toxic effects on wildlife prompted the U.S. to outlaw its use, DDT continued to be a mainstay of agricultural pest control in many poorer countries for years, and is still used for malaria control in some of the world's poorest countries.

But the study also underscores that DDT exposure may not by itself have set in motion the world's obesity crisis. In order for its effects on basic metabolic function - in females at least - to turn into a public health crisis, a new factor unique to modern human society may also have needed to be in place: the flowering of a vast commercial empire built on offering copious amounts of highly-palatable food to creatures with an evolved drive to consume and store as much energy as could be had.

Another key question is how, when DDT exposure appears primarily to affect females' physiological function, it could possibly explain an obesity crisis that has affected both genders roughly equally. The authors of the latest research found subtle changes in the expression of genes that influence metabolic processes. Only further study will determine whether such changes may be passed on to future generations - and across genders.

Another study may also offer insight:

In a 2013 study published in the journal BMC Medicine, scientists injected pregnant rats with DDT and found no change in their levels of obesity or their offspring. But by the third generation, more than half of the rats (think of them as the great-grandchildren) showed dramatically higher levels of fat and weight gain, even though they were never exposed to the pesticide themselves.

"Here is an ancestral exposure in your great-grandmother, which is passed on to you and you’re going to pass on to your grandchildren," said Michael Skinner, a professor of biological sciences at Washington State University who led the research. At work, Skinner said, is a disease inheritance phenomenon discovered more than 15 years ago.

Watching the nation's weight as well as your own? Follow me on Twitter at https://twitter.com/LATmelissahealy

Copyright © 2014, Los Angeles Times
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