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High stress during fetal development could cause premature aging, according to a study in chickens, which published today (November 9) in the Proceedings of the Royal Society B. Chickens exposed to high levels of stress hormones in the egg have overactive stress responses, shorter telomeres, and higher levels of oxidative damage—all key markers of aging—suggesting that chicken mothers, and possibly mothers of other species including humans, may unintentionally be shortening the lifespan of their offspring.
“I thought it was really interesting,” said Iowa State University avian physiologist Carol Vleck, who was not involved in the study. “There’s evidence in humans that maternal stress carries over into lots of things in offspring,” she added, and this paper provides a plausible mechanism that could hold true across a wide range of species.
In everything from lizards to bonobos to humans, researchers have shown that animals exposed to higher stress can pass on an overactive stress response that results from high levels of stress hormones such as corticosterone to their young, said Mark Haussmann, a physiologist at Bucknell University in Pennsylvania and lead author of the study. In mammals, “if you have a mom who is stressed out, those hormones are going to cross the placenta, and they’re going to affect the fetus.”
In 2004, researchers showed that mothers facing high stress also had shorter telomeres and high levels of oxidative damage, signs of cellular aging. The length of telomeres, the DNA caps at the ends of chromosomes , is a predictor of how many times a cell can divide before going into senescence, while oxidative damage accumulates as cells age. That study made Haussmann and his colleagues wonder whether stressed mothers would accelerate cellular aging in their young.
To find out, his team injected chicken eggs with higher levels of corticosterone, a stress hormone that helps animals utilize glucose stores in the face of acute stress, and compared the hatchlings to those from unmaniuplated eggs. They used chickens rather than mammals because it allowed them to “take mom completely out of the picture” and expose the chicks to a precise amount of stress hormone, Haussmann said.
Once the chicks hatched and reached adolescence, at about three weeks of age, the researchers measured the levels of corticosterone during and after the birds coped with a stressful environment—being placed inside a breathable, but dark, bag for half an hour.
While birds exposed to higher prenatal stress hormones had similar baseline and peak levels of corticosterone compared to controls, they couldn’t recover as quickly from the experience. Once the hormone spiked, it took longer for it to return to baseline levels.
The group also showed that the exposed birds had higher levels of oxidative damage to lipids and proteins in their cells, and lower antioxidant activity, which normally help mop up oxidative chemicals. Additionally, the stressed out birds had a higher proportion of very short telomeres.
“To show that stress can not only affect the stress axis of the offspring, but that there are these effects on telomeres is really interesting,” said Vleck. The findings suggest that prenatal stress exposure not only makes for hyper-reactive offspring, but may also prime them to age prematurely, she added.
But the study looked at fairly young chicks, so the lifelong effects on telomeres and aging are yet to be determined, Vleck noted. It’s also important to pinpoint the times during development when stress has the greatest effect, she said.
Plus, stress may not be all bad, she added. “Some of these effects might be beneficial to the offspring, too,” Vleck said. “If you have an upregulated stress response you might be able to combat stressful situations better.”
M. Haussmann et al, "Embryonic exposure to corticosterone modifies the juvenile stress response, oxidative stress, and telomere length," Proc. Royal Soc. B, doi:10.1098/rspb.2011.1913, 2011.