Johannes Veldhuis

University of Virginia Health System, NIH General Clinical Research Center, Department of Internal Medicine, Divisioon of Endocrinology and Metabolism, PO Box 800202, Charlottesville, Virginia 22908-0202, USA

Abraham Lincoln once said that it is better to remain silent and appear ignorant than to speak freely and remove all doubt! Thus, I will attempt brie£y to highlight some of the discussions we have had over the last few days. Ageing can be viewed as an array of sequelae, some of which we interpret as undesirable, ranging from decreased bone mass to atrophic skin and hair greying; and from relative sarcopenia and variable cognitive defects to increased visceral fat and heightened risk of cardiovascular disease. This panoply is somehow directed by an ensemble of cellular and systemic factors. The resultant complexity ofthe ageing process is thus challenging. Causal endocrine and non-endocrine factors undoubtedly overlap, even in ways beyond those we recognize. From an endocrine perspective, there is a substantial decline of GH and sex-steroid input to target cells. A gradual reciprocal increase in integrated cortisol receptor drive throughout age seems to contribute to catabolic changes, particularly in a waning anabolic context of attenuated GH/IGF1 and sex-steroid production. Concomitantly, alterations in the insulin pathway condition cellular signalling in ageing, which strongly in£uences epidemiological risk. Operating on this fourfold hormonal background is the genetic endowment and any number of environmental factors. Only the thyroidal axis seems to be spared substantially. This symposium has tried to unravel some of the intersecting causes and consequences of these neurohormonal changes in ageing.

Endocrine Facets of Ageing.

Novartis 242

Copyright © 2002 John Wiley & Sons Ltd Print ISBN 0-471-48636-1 Online ISBN 0-470-84 6 54-2

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