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Nutrition, Behavior, and the Developmental Origins of the Metabolic Syndrome

  • Jared Edward Reser
Chapter

Abstract

It is clear that the modern epidemic of obesity, cardiovascular disease, diabetes mellitus, and associated comorbidities is largely a product of our modern environment. Artificially high levels of sugars, fats, and processed foods, along with sedentary behavior constitute an “obesogenic” environment which makes us more susceptible to the metabolic syndrome today than our foraging ancestors were millennia ago. A number of comparative analyses relevant to the influence of behavior, diet, and nutrition on the metabolic syndrome are reviewed here, especially with regard to the developmental origins of the syndrome. It has become clear that early environmental conditions, particularly poor nutrition, have the ability to act as cues that program the phenotype in utero. It is thought that the fetus has an adaptive ability to perceive nutritional deprivation, and reprogram its metabolic systems for energy efficiency, as a predictive response to expected environmental scarcity. These metabolic alterations are thought to be beneficial in times of poor nutritional quality, but unfortunately have consistently been shown to result in adverse health outcomes and metabolic disease, when food is calorie dense and readily available. These early life changes are brought about by alterations in cellular proliferation and differentiation that are ultimately driven by neuroendocrine, cellular, and epigenetic adaptations to undernutrition. Besides the various metabolic changes, animals programmed for thrift have been shown to exhibit neurological changes resulting in hyperphagia, increased sedentariness, and volume reductions in the cerebral cortex. A great deal of evidence, including countless animal studies and a worldwide series of epidemiological investigations, has supported the close relationship between early nutritional status and susceptibility to the major risk factors (increased adiposity, hypertension, and insulin resistance) for the metabolic syndrome in later life. The perspectives originated by James Neel (the thrifty genotype hypothesis), and David Barker (the thrifty phenotype hypothesis) have remained important interpretations through which to view the nature of the genetic, structural, and adaptive facets of the programming of metabolic function. Moreover, these perspectives, and the integrative conceptualizations that they promote, have begun to provide valuable direction for research and health care.

Keywords

Insulin Resistance Metabolic Syndrome Sedentary Behavior Lactase Persistence Nutritional Deprivation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Abbreviations

LDL

Low density lipoprotein

FOAD

Fetal origins of adult disease

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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Psychology DepartmentUniversity of Southern CaliforniaLos AngelesUSA

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