by Maryalice Yakutchik
SHE WAS FULL-TERM AT BIRTH. Back in 1962—the Year of the Tiger—preemies simply didn't survive.
Her given name, Fenxi, translates to "Work Toward Hope." It came to her mother in a dream and alludes to a mandate from her parents whose firstborn son had died in infancy. Auspicious though it was for a future physician-scientist, the little girl considered it "too big and not pretty" and dropped it in favor of "Xiaobin." The nickname stuck. In years to come, it would appear on a passport and accumulate a series of academic degrees: MD, MPH, ScD. Most recently, it acquired two new titles that identify her as the Zanvyl Krieger Professor in Children's Health and director of the new Center on the Early Life Origins of Disease at the Bloomberg School.
That her parents were pioneers who raised her in Inner Mongolia, on China's frontier, seems relevant to Xiaobin Wang's future as a clinician doing groundbreaking research. Her aim: to end chronic disease and fundamentally change the practice of public health and medicine in the 21st century. She is focusing on preconception, pregnancy and early childhood as the critical time windows to address diseases where multiple genes and environmental factors contribute to risk. It's a radical notion: preventing adult hypertension or diabetes in infancy or in utero—or perhaps even before that—as opposed to waiting for symptoms to manifest many decades later.
Her work was stimulated by the Barker Hypothesis, which, after being ignored and maligned for a dozen years, has given rise to a burgeoning field known as the developmental origins of health and disease, or DOHaD. Its tenets—that poor fetal growth and small size at birth are followed by increased risk of coronary artery disease, stroke, hypertension, type 2 diabetes and osteoporosis—are now espoused by an enthusiastic cadre of scientists worldwide. Bernard Guyer, for instance, Wang's former doctoral advisor and the inaugural Zanvyl Krieger Professor in the Department of Population, Family and Reproductive Health, cites a Barker study on hypertension that made use of life-course data sets showing that specific increments in blood pressure were related to specific increments in birth weight. Most compelling, Guyer says, was the precision of the quantitative relationship between low-birth-weight babies and obese males.
If the concept of early origins of disease sounds pessimistically deterministic—like we're pretty much doomed by the age of 2—consider this, Guyer says: "One of Xiaobin's brilliant lines is, if we know gene-environment interactions can increase our risk of diseases, then we should be able to find gene-environment interactions that reduce the risk. If there's an interaction, it doesn't have to go always in one direction. We should be able to think about how we can make it go in the other direction."
Worldwide, 15 million of the 135 million babies born in 2010 were premature. —Born Too Soon, a UN report released May 2
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