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Nutrition and ageing

Published online by Cambridge University Press:  01 April 2001

Jaime Miquel*
Affiliation:
Department of Biotechnology, University of Alicante, C. Marqués de Campo 66, E-03700 Denia (Alicante), Spain
*
*Corresponding author: Email [email protected]
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Abstract

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The reviewed literature indicates that, even in industrialised countries, the nutrition of mature and aged subjects is often inadequate (because of deficiency or excess), which may lead to premature or pathological senescence.

Recent nutritional research on ageing laboratory animals shows that dietary restriction may be the most effective procedure to achieve along and disease-free life span, probably owing to a better protection against mitochondria-linked oxygen stress. Likewise, the experimental and clinical work from many laboratories, including our own, indicates that age-dependent changes in the cardiovascular and immune systems are linked to oxygen stress and that an adequate intake of dietary antioxidants may protect those systems against chronic degenerative syndromes in the physiopathology of which reactive oxygen species (ROS) play a key role.

The extant data indicate that the antioxidant vitamins C and E are centrally involved in defending the above two systems against ROS attack. Moreover, recent research suggests that the glutathione-related thiolic antioxidants, thiazolidine carboxylic acid (thioproline) and N-acetylcysteine, as well as the phenolic liposoluble ‘co-antioxidants’ of Curcuma longa, may have a significant protective effect against age-related atherogenesis and immune dysfunction.

Key messages from this paper are the following. (1) It is generally accepted that oxygen free radicals released in metabolic reactions play a key role in the physiopathology of ‘normal ageing’ and of many age-related degenerative diseases. (2) Consumption of adequate levels of antioxidants in the diet is essential in order to preserve health in old age. (3) A certain degree of protection against atherogenesis and immune dysfunction may be achieved by preventing vitamin E deficiency and an excessive oxidation of the glutathione-supported thiol pool.

Type
Research Article
Copyright
Copyright © CABI Publishing 2001

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