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Josef Neu, Department of Pediatrics, University of Florida, Gainesville, FL,
Amy Mackey, Department of Pediatrics, University of Florida, Gainesville, FL,
Ying Huang, Children’s Hospital of Fudan University, Shanghai, China
It is clear that intrauterine undernutrition and subsequent low birth weight result in significant health problems during adult life. These include obesity, cardiovascular disease, hypertension, and Type 2 diabetes. Evidence for a relationship between early postnatal nutrition and the subsequent development of allergies, immune dysfunction, and autoimmune disorders such as Type 1 diabetes, is beginning to accumulate. Numerous questions about the effects of early postnatal nutrition on subsequent short as well as long-term health have been raised: What happens to infants born prematurely who are subjected to postnatal undernutrition for a “critical period” of rapid growth and development? Are these infants, if born appropriate for gestational age and subjected to nutritional stresses “programmed” for a greater susceptibility to chronic diseases such as obesity, Type 2 diabetes and hypertension, as are undernourished fetuses? Does it matter what infants are fed in terms of development of chronic diseases related to autoimmunity, such as Type 1 diabetes and asthma? Can under or overexposure to certain nutrients such as carbohydrates, lipids or proteins in early life have an effect on the development of chronic disease and can these effects be passed on to subsequent generations? In this chapter, we note that there are several remarkable similarities and differences between the chronic effects of pre- versus postnatal undernutrition. Some of the health consequences of early postnatal malnutrition and hypothetical mechanisms by which early nutrition “programs” the individual for long-term outcomes will be addressed.
As the field of neonatal intensive care began to emerge in the mid-1960s, efforts were made to save prematurely born babies that were previously thought to be nonviable. Many of these infants were considered to be “too unstable” to feed. They were provided neither enteral feedings nor intravenous glucose, essentially being starved for several days after birth. Some investigators recognized that this caused catabolism with subsequent endogenous tissue breakdown and introduced the practice of providing intravenous glucose to sick premature infants, which unsurprisingly reduced catabolism and improved survival. Although we have made progress in the past 40 years, the practice of withholding enteral support to sick infants remains prevalent. The provision of parenteral support with lipids, amino acids, vitamins, minerals, and trace elements likewise, is frequently delayed and/or interrupted for poorly substantiated reasons. As a result, most of these infants experience a significant delay in the growth they would have attained in utero (Figure 24.1). Although many of these individuals catch up in somatic growth to their nonpremature peers over a period of years, it should be recognized that optimum nutrition for the rapidly developing neonate should be aimed at goals beyond simply improved weight gain. The short- and long-term effects of undernutrition during a critical window of susceptibility to several illnesses, as well as the potential for poor neurodevelopment, should not be underestimated.
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