Abstract
This chapter reviews evidence on human aging. Humans are the longestlived primate. Trade-offs modulate human life span. 'Longevity genes' that protect against disease may slow the aging processes in humans and in model organisms, but they are not at high frequency in human populations, probably because they reduce fitness in early life. Insights into their protective mechanisms could yield pharmaceuticals that extend human health, but close attention would have to be paid to side effects, for the effects on humans of genetic alterations that extend life in laboratory mice are not pleasant. Genetic alterations in the GH/IGF-I axis appear at best not to extend life and at worst to shorten it, with many detrimental impacts on health. It would help to have a small, short-lived, primate research model in which anti-aging therapies developed from mouse experiments could be evaluated before testing them on humans.
| Original language | English (US) |
|---|---|
| Title of host publication | Evolution in Health and Disease |
| Publisher | Oxford University Press |
| ISBN (Print) | 9780191728167, 9780199207466 |
| DOIs | |
| State | Published - Apr 1 2010 |
| Externally published | Yes |
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Keywords
- Aging therapies
- Growth hormone
- Human aging
- IGF-1
- Longevity genes
- Mechanisms
ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)
Cite this
The evolutionary context of human aging and degenerative disease. / Austad, Steven N.; Finch, Caleb E.
Evolution in Health and Disease. Oxford University Press, 2010.Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - The evolutionary context of human aging and degenerative disease
AU - Austad, Steven N.
AU - Finch, Caleb E.
PY - 2010/4/1
Y1 - 2010/4/1
N2 - This chapter reviews evidence on human aging. Humans are the longestlived primate. Trade-offs modulate human life span. 'Longevity genes' that protect against disease may slow the aging processes in humans and in model organisms, but they are not at high frequency in human populations, probably because they reduce fitness in early life. Insights into their protective mechanisms could yield pharmaceuticals that extend human health, but close attention would have to be paid to side effects, for the effects on humans of genetic alterations that extend life in laboratory mice are not pleasant. Genetic alterations in the GH/IGF-I axis appear at best not to extend life and at worst to shorten it, with many detrimental impacts on health. It would help to have a small, short-lived, primate research model in which anti-aging therapies developed from mouse experiments could be evaluated before testing them on humans.
AB - This chapter reviews evidence on human aging. Humans are the longestlived primate. Trade-offs modulate human life span. 'Longevity genes' that protect against disease may slow the aging processes in humans and in model organisms, but they are not at high frequency in human populations, probably because they reduce fitness in early life. Insights into their protective mechanisms could yield pharmaceuticals that extend human health, but close attention would have to be paid to side effects, for the effects on humans of genetic alterations that extend life in laboratory mice are not pleasant. Genetic alterations in the GH/IGF-I axis appear at best not to extend life and at worst to shorten it, with many detrimental impacts on health. It would help to have a small, short-lived, primate research model in which anti-aging therapies developed from mouse experiments could be evaluated before testing them on humans.
KW - Aging therapies
KW - Growth hormone
KW - Human aging
KW - IGF-1
KW - Longevity genes
KW - Mechanisms
UR - http://www.scopus.com/inward/record.url?scp=84920090469&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84920090469&partnerID=8YFLogxK
U2 - 10.1093/acprof:oso/9780199207466.003.0023
DO - 10.1093/acprof:oso/9780199207466.003.0023
M3 - Chapter
AN - SCOPUS:84920090469
SN - 9780191728167
SN - 9780199207466
BT - Evolution in Health and Disease
PB - Oxford University Press
ER -