274836 Developmental Origins of Health and Disease (DOHaD): An Overview with Lessons from Hypertension

Wednesday, October 31, 2012 : 8:50 AM - 9:10 AM

Susan Bagby, MD , Heart Research Center, Oregan Health & Science University, Portland, OR
Though initially controversial, studies over the last 20 years show that poor nutrition during early development (especially from conception to age 2, the ‘1st 1000 Days') causes lasting nongenetic changes (‘programming') which alter the offspring's response to postnatal environmental stressors; this increases vulnerability to those chronic non-communicable diseases which are currently overwhelming our healthcare systems: hypertension, obesity/diabetes, and heart disease. We now know that not only classic undernutrition, but also high-calorie/high-fat/low nutrient diets, represent common forms of malnutrition. This introductory presentation will define and review basic concepts of early-life “programming”, including windows of vulnerability/plasticity, indices of abnormal fetal growth, early epidemiologic history from the pioneering work of Professor David Barker, and the capacity for trans-generational transmission of programmed traits. Major pathways of programming – altered organ structure and enhanced regulatory system responses to postnatal stressors - will be illustrated by outlining the pathogenesis of developmental hypertension, emphasizing that interactions between fetally programmed changes (eg reduced nephron number, thrifty phenotype) and the type of postnatal environment encountered (eg diet quantity/quality, socioeconomic stress) will ultimately determine disease manifestation . The age at which disease becomes manifest in offspring is an important difference between maternal under- vs over-nutrition; whereas undernutrition leads to disease in adulthood, overnutrition induces hypertension, obesity, and diabetes in children, thus predating childbearing years and facilitating transgenerational transmission of disease risk. This knowledge mandates that we broaden our public health/preventive focus to encompass robust nutrition and the restoration of nutritional knowledge in our youth, mothers-to-be, and pregnant women and their children.

Learning Areas:
Basic medical science applied in public health
Chronic disease management and prevention
Epidemiology
Program planning

Learning Objectives:
Discuss how poor fetal growth can occur independently of a low birthweight, and thus how fetal programming due to inadequate nutrition can occur across the normal range of birthweight. Describe how reduced nephron number interacts with rapid postnatal growth to increase risk for hypertension and chronic kidney disease. Discuss the threat posed by maternal malnutrition today for health of future populations via transgenerational transmission of programmed chronic disease risk.

Presenting author's disclosure statement:

Qualified on the content I am responsible for because: I have career-long experience as academic internist/Nephrologist, both caring for hypertension and renal disease patients, doing research in the pathogenesis of hypertension, and teaching medical student and postgraduate courses in etiology and treatment of hypertension. Over the past 10 yrs, my NIH-funded research has focused on the developmental origins of hypertension, examining renal and vascular factors in a new model of maternal protein restriction.
Any relevant financial relationships? No

I agree to comply with the American Public Health Association Conflict of Interest and Commercial Support Guidelines, and to disclose to the participants any off-label or experimental uses of a commercial product or service discussed in my presentation.

Back to: 5049.0: The Developmental Origins of Chronic Disease: How Poor Nutrition in the Womb Creates Susceptibility to Hypertension, Diabetes, Obesity, and Coronary Heart Disease