The rate of living theory postulates that the faster an organism’s metabolism, the shorter its lifespan. First proposed by Max Rubner in 1908, the theory was based on his observation that smaller animals had faster metabolisms and shorter lifespans compared to larger animals with slower metabolisms.[1] The theory gained further credibility through the work of Raymond Pearl, who conducted experiments on drosophila and cantaloupe seeds, which supported Rubner's initial observation. Pearl's findings were later published in his book, The Rate of Living, in 1928, in which he expounded upon Rubner's theory and demonstrated a causal relationship between the slowing of metabolism and an increase in lifespan.[2]
The theory gained additional credibility with the discovery of Max Kleiber's law in 1932. Kleiber found that an organism's basal metabolic rate could be predicted by taking 3/4 the power of the organism's body weight. This finding was noteworthy because the inversion of the scaling exponent, between 0.2 and 0.33, also demonstrated the scaling for both lifespan and metabolic rate, and was colloquially called the "mouse-to-elephant" curve.[3]
Mechanism
editMechanistic evidence was provided by Denham Harman's free radical theory of aging, created in the 1950s. This theory stated that organisms age over time due to the accumulation of damage from free radicals in the body.[4] It also showed that metabolic processes, specifically the mitochondria, are prominent producers of free radicals.[4] This provided a mechanistic link between Rubner's initial observations of decreased lifespan in conjunction with increased metabolism.
Current state of theory
editSupport for this theory has been bolstered by studies linking a lower basal metabolic rate (evident with a lowered heartbeat) to increased life expectancy.[5][6][7] This has been proposed by some to be the key to why animals like the giant tortoise can live over 150 years.[8]
However, the ratio of resting metabolic rate to total daily energy expenditure can vary between 1.6 and 8.0 between species of mammals. Animals also vary in the degree of coupling between oxidative phosphorylation and ATP production, the amount of saturated fat in mitochondrial membranes, the amount of DNA repair, and many other factors that affect maximum life span.[9] Furthermore, a number of species with high metabolic rate, like bats and birds, are long-lived.[10][11] In a 2007 analysis it was shown that, when modern statistical methods for correcting for the effects of body size and phylogeny are employed, metabolic rate does not correlate with longevity in mammals or birds.[12]
See also
editReferences
edit- ^ Rubner, M. (1908). Das Problem det Lebensdaur und seiner beziehunger zum Wachstum und Ernarnhung. Munich: Oldenberg.
- ^ Raymond Pearl. The Rate of Living. 1928
- ^ Speakman J. R. (2005). "Body size, energy metabolism and lifespan". J Exp Biol. 208 (9): 1717–1730. doi:10.1242/jeb.01556. PMID 15855403.
- ^ a b Harman D (1956). "Aging: a theory based on free radical and radiation chemistry". Journal of Gerontology. 11 (3): 298–300. CiteSeerX 10.1.1.663.3809. doi:10.1093/geronj/11.3.298. PMID 13332224.
- ^ Hulbert, A. J.; Pamplona, Reinald; Buffenstein, Rochelle; Buttemer, W. A. (2007). "Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals". Physiological Reviews. 87 (4): 1175–1213. doi:10.1152/physrev.00047.2006. PMID 17928583.
- ^ Olshansky, S. J.; Rattan, Suresh IS (25 July 2009). "What Determines Longevity: Metabolic Rate or Stability?". Discovery Medicine. 5 (28): 359–362. PMID 20704872.
- ^ Aguilaniu, H.; Durieux, J.; Dillin, A. (2005). "Metabolism, ubiquinone synthesis, and longevity". Genes & Development. 19 (20): 2399–2406. doi:10.1101/gad.1366505. PMID 16230529.
- ^ "The Longevity Secret for Tortoises Is Held In Their Low Metabolism Rate". www.immortalhumans.com. Archived from the original on 2010-07-20.
- ^ Speakman JR, Selman C, McLaren JS, Harper EJ (2002). "Living fast, dying when? The link between aging and energetics". The Journal of Nutrition. 132 (6, Supplement 2): 1583S–1597S. doi:10.1093/jn/132.6.1583S. PMID 12042467.
- ^ Austad, Steven (1997). Why We Age: What Science Is Discovering about the Body's Journey through Life. New York: John Wiley & Sons. ISBN 9780471148036.
- ^ Timmer, John (2019-06-11). "Why do bats have such bizarrely long lifespans?". Ars Technica. Retrieved 2021-08-31.
- ^ de Magalhães JP, Costa J, Church GM (1 February 2007). "An Analysis of the Relationship Between Metabolism, Developmental Schedules, and Longevity Using Phylogenetic Independent Contrasts". The Journals of Gerontology Series A: Biological Sciences and Medical Sciences. 62 (2): 149–60. doi:10.1093/gerona/62.2.149. PMC 2288695. PMID 17339640.[dead link]
- Rubner, M. (1908). Das Problem der Lebensdauer und seiner beziehungen zum Wachstum und Ernährung. Munich: Oldenberg.
- Raymond Pearl. The Rate of Living. 1928
- Speakman J. R. (2005). "Body size, energy metabolism and lifespan". The Journal of Experimental Biology. 208 (Pt 9): 1717–1730. doi:10.1242/jeb.01556. PMID 15855403.
- Harman D (1956). "Aging: a theory based on free radical and radiation chemistry". Journal of Gerontology. 11 (3): 298–300. CiteSeerX 10.1.1.663.3809. doi:10.1093/geronj/11.3.298. PMID 13332224.
- Speakman JR, Selman C, McLaren JS, Harper EJ (June 2002). "Living fast, dying when? The link between aging and energetics". Journal of Nutrition. 132 (6): 1583S–97S. doi:10.1093/jn/132.6.1583S. PMID 12042467.
- Holloszy J. O.; Smith E. K. (1986). "Longevity of cold-exposed rats: A reevaluation of the "rate-of-living theory". Journal of Applied Physiology. 61 (Suppl 2): 1656–1660. doi:10.1152/jappl.1986.61.5.1656. PMID 3781978.