The evolutionary context of human aging and degenerative disease

Steven N. Austad, Caleb E. Finch

Research output: Chapter in Book/Report/Conference proceedingChapter

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 languageEnglish (US)
Title of host publicationEvolution in Health and Disease
PublisherOxford University Press
ISBN (Print)9780191728167, 9780199207466
DOIs
StatePublished - Apr 1 2010
Externally publishedYes

Fingerprint

Primates
mice
insulin-like growth factor I
human population
human health
Health
Medical Genetics
adverse effects
Insulin-Like Growth Factor I
drugs
therapeutics
organisms
genes
testing
Research
Pharmaceutical Preparations
Population
Genes
Therapeutics

Keywords

  • Aging therapies
  • Growth hormone
  • Human aging
  • IGF-1
  • Longevity genes
  • Mechanisms

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)

Cite this

Austad, S. N., & Finch, C. E. (2010). The evolutionary context of human aging and degenerative disease. In Evolution in Health and Disease Oxford University Press. https://doi.org/10.1093/acprof:oso/9780199207466.003.0023

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 proceedingChapter

Austad, SN & Finch, CE 2010, The evolutionary context of human aging and degenerative disease. in Evolution in Health and Disease. Oxford University Press. https://doi.org/10.1093/acprof:oso/9780199207466.003.0023
Austad SN, Finch CE. The evolutionary context of human aging and degenerative disease. In Evolution in Health and Disease. Oxford University Press. 2010 https://doi.org/10.1093/acprof:oso/9780199207466.003.0023
Austad, Steven N. ; Finch, Caleb E. / The evolutionary context of human aging and degenerative disease. Evolution in Health and Disease. Oxford University Press, 2010.
@inbook{ca5c6b3044884dcba3f65ce96f93f506,
title = "The evolutionary context of human aging and degenerative disease",
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.",
keywords = "Aging therapies, Growth hormone, Human aging, IGF-1, Longevity genes, Mechanisms",
author = "Austad, {Steven N.} and Finch, {Caleb E.}",
year = "2010",
month = "4",
day = "1",
doi = "10.1093/acprof:oso/9780199207466.003.0023",
language = "English (US)",
isbn = "9780191728167",
booktitle = "Evolution in Health and Disease",
publisher = "Oxford University Press",

}

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

SN - 9780191728167

SN - 9780199207466

BT - Evolution in Health and Disease

PB - Oxford University Press

ER -