Losing body fat before pregnancy could help break the obesity cycle and improve the lifelong health of babies born to obese mothers, according to US researchers who are studying what happens across generations that could be contributing to the obesity crisis.
Obesity is a growing problem worldwide, and more and more women are obese when they fall pregnant.
Babies born to obese mothers are themselves more likely to become obese children and adults, another factor that drives the obesity and overweight epidemic.
However, a collaborative study between the Center for Pregnancy and Newborn Research at the University of Texas Health Science Center (UTHSC) at San Antonio and the National Institute of Nutrition in Mexico City, suggests that if obese mothers lose body fat before they fall pregnant, they can pass on health benefits to their children.
Dr Peter Nathanielsz, a professor in UTHSC’s Center for Pregnancy and Newborn Research, and colleagues studied female rats raised on high-fat diets, comparing one obese group that continued eating the same diet through mating, pregnancy and lactation with another group that was switched to a healthier lower fat diet one month before mating.
They then studied the male offspring of both groups and found those born to mothers who remained obese and stayed on the high-fat diets through pregnancy to lactation, had higher levels of triglycerides, leptin, insulin and insulin resistance at the weaning stage, whereas in babies born to mothers who were put on low fat diets before pregnancy so they lost body fat, these levels were normal.
They also found the babies born to obese mothers had increased fat mass and fat cell size, whereas these changes were significantly reversed, although not totally, in babies born to mothers in the group that switched to a low fat diet before pregnancy.
The researchers told the press that, although the extent of reversibility depended on the tissue affected, this was the first time research had shown it was possible to reverse metabolic effects in offspring born to obese mothers by changing the mothers’ diets before pregnancy.
Nathanielsz said it was interesting that the offspring born to obese mothers had high levels of leptin, a hormone that tells the brain to reduce appetite.
Perhaps this means the offspring developed a brain that was resistant to the signal that tells them they are getting fat and they just go on eating and getting fat, like their mothers.
“That is what we mean when we say that the effects are transgenerational,” said Nathanielsz.
“Leptin levels were normal in the offspring of the intervention group, showing that we can break this cycle,” he added.
Nathanielsz explained they were able to achieve at least 50 to 60 per cent return to normal levels, which he regards as a first step.
Perhaps the next stage is to try a no-fat diet or add micronutrients to the diet, but this has to be done carefully because there could be unwanted consequences in trying to restore levels to normal too quickly.
“We believe this sort of information is necessary to provide guidelines as to the type of dietary intervention for women during pregnancy. Much remains to be done,” he cautioned.
The role of leptin is not straightforward. It is natural for it to peak after birth in newborn rodents, and it seems this peak is an important feature in the development of the brain’s hypothalamic appetite control centers.
But from this and other experiments with rodents, Nathanielsz and colleagues showed that newborn offspring of obese mothers have larger and longer-lasting leptin peaks.
In another recent study published online on 24 January in the Journal of Physiology, Nathanielsz and colleagues from the University of Wyoming, describe a similar experiment with sheep, which suggests that the presence of higher levels of cortisol in lambs born to obese ewes could be disrupting the normal peaking of leptin in the lambs’ first few days of life, thereby “predisposing them to increased appetite and weight gain in later life”.
“Maternal obesity eliminates the neonatal lamb plasma leptin peak.”
Nathan M. Long, Stephen P Ford, and Peter W Nathanielsz.
The Journal of Physiology, published online before print, 24 January 2011.
DOI: 10.1113/jphysiol.2010.201681
Additional source: University of Texas Health Science Center at San Antonio (2 Feb 2011 press release), Wikipedia.
Written by: Catharine Paddock, PhD