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Neuroendocrine and Pharmacological Manipulations to Assess How Caloric Restriction Increases Life Span

^a Departments of Neurobiology and Geriatrics, Mt. Sinai School of Medicine, New York City
^b Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana
^c Department of Nutritional Sciences, University of Wisconsin Medical School, Madison
^d Department of Physiology, Southern Illinois University School of Medicine, Carbondale, Illinois
^e Andrus Gerontology Center, University of Southern California, Los Angeles
^f Joslin Diabetes Center, Harvard Medical School, Cambridge, Massachusetts
^g Section on Behavioral Neuropharmacology, National Institute of Mental Health, Bethesda, Maryland
^h Department of Physiology, University of Texas Health Science Center at San Antonio

Charles V. Mobbs, Associate Professor, Neurobiology of Aging Laboratory, Box 1639, Mt. Sinai School of Medicine, New York, NY 10029 E-mail: mobbsc{at}alum.mit.edu.

As part of an effort to review current understanding of the mechanisms by which caloric restriction (CR) extends maximum life span, the authors of the present review were requested to develop a list of key issues concerning the potential role of neuroendocrine systems in mediating these effects. It has long been hypothesized that failure of specific neuroendocrine functions during aging leads to key age-related systemic and physiological failures, and more recently it has been postulated that physiological neuroendocrine responses to CR may increase life span. However, although the acute neuroendocrine responses to fasting have been well studied, it is not clear that these responses are necessarily identical to those observed in response to the chronic moderate (30% to 50% reduction) CR that increases maximum life span. Therefore the recommendations of this panel fall into two categories. First, further characterization of neuroendocrine responses to CR over the entire life span is needed. Second, rigorous interventional studies are needed to test the extent to which neuroendocrine responses to CR mediate the effects of CR on life span, or alternatively if CR protects the function of essential neuroendocrine cells whose impairment reduces life span. Complementary studies using rodent models, nonhuman primates, and humans will be essential to assess the generality of elucidated mechanisms, and to determine if such mechanisms might apply to humans.

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