Deployment cost–benefit selection in physiology

Deployment cost–benefit selection in physiology concerns the costs and benefits of physiological process that can be deployed and selected in regard to whether they will increase or not an animal’s survival and biological fitness. Variably deployable physiological processes relate mostly to processes that defend or clear infections as these are optional while also having high costs and circumstance linked benefits. They include immune system responses, fever, antioxidants and the plasma level of iron. Notable determining factors are life history stage, and resource availability.

Immunity

Activating the immune system has the present and future benefit of clearing infections, but it is also both expensive[1] in regard to present high metabolic energy consumption,[2] and in the risk of resulting in a future immune related disorder. Therefore, an adaptive advantage exists if an animal can control its deployment in regard to actuary-like evaluations of future benefits and costs as to its biological fitness.[3][4] In many circumstances, such trade-off calculations explain why immune responses are suppressed and infections are tolerated.[5][6] Circumstances where immunity is not activated due to lack of an actuarial benefit include:

Fever

Cost benefit trade-off actuary issues apply to the antibacterial and antiviral effects of fever (increased body temperature). Fever has the future benefit of clearing infections since it reduces the replication of bacteria[13] and viruses.[14] But it also has great present metabolic (BMR) cost, and the risk of hyperpyrexia. Where it is achieved internally, each degree raise in blood temperature, raises BMR by 10–15%.[15][16] 90% of the total cost of fighting pneumonia, goes, for example, on energy devoted to raising body temperature.[2] During sepsis, the resulting fever can raise BMR by 55%—and cause a 15% to 30% loss of body mass.[17][18] Circumstances in which fever deployment is not selected or is reduced include:

Antioxidants

Antioxidants such as carotenoids, vitamin C, Vitamin E, and enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) can protect against reactive oxygen species that damage DNA, proteins and lipids, and result in cell senescence and death. A cost exists in creating or obtaining these antioxidants. This creates a conflict between the biological fitness benefits of future survival compared with the use of these antioxidants to advantage present reproductive success. In some birds, antioxidants are diverted from maintaining the body to reproduction for this reason with the result that they have accelerated senescence[22] Related to this, birds can show their biological capacity to afford the cost of diverting antioxidants (such as carotenoids) in the form of pigments into plumage as a costly signal.[23][24]

Hypoferremia

Iron is vital to biological processes, not only of a host, but also to bacteria infecting the host. A biological fitness advantage can exist for hosts to reduce the availability of iron within itself to such bacteria (hypoferremia), even though this happens at a cost of the host impairing itself with anemia.[25][26] The potential benefits of such self impairment is illustrated by the paradoxical effect that providing iron supplements to those with iron deficiency (which interferes with its antibacterial action) can result in an individual being cured of anemia but having increased bacterial illness.[27]

See also

Notes

  1. Lochmiller, R. L.; Deerenberg, C. (2000). "Trade-offs in evolutionary immunology: Just what is the cost of immunity?". Oikos. 88: 87–98. doi:10.1034/j.1600-0706.2000.880110.x.
  2. 1 2 Romanyukha, A. A.; Rudnev, S. G.; Sidorov, I. A. (2006). "Energy cost of infection burden: An approach to understanding the dynamics of host–pathogen interactions". Journal of Theoretical Biology. 241 (1): 1–13. PMID 16378624. doi:10.1016/j.jtbi.2005.11.004.
  3. Read, A. F.; Allen, J. E. (2000). "Evolution and immunology. The economics of immunity". Science. 290 (5494): 1104–1105. PMID 11185007. doi:10.1126/science.290.5494.1104.
  4. Van Boven, M.; Weissing, F. J. (2004). "The Evolutionary Economics of Immunity". The American Naturalist. 163 (2): 277–294. PMID 14970928. doi:10.1086/381407.
  5. Hanssen, S. A.; Hasselquist, D.; Folstad, I.; Erikstad, K. E. (2004). "Costs of immunity: Immune responsiveness reduces survival in a vertebrate". Proceedings of the Royal Society B: Biological Sciences. 271 (1542): 925–930. PMC 1691677Freely accessible. PMID 15255047. doi:10.1098/rspb.2004.2678.
  6. Moret, Y.; Schmid-Hempel, P. (2000). "Survival for immunity: The price of immune system activation for bumblebee workers". Science. 290 (5494): 1166–1168. PMID 11073456. doi:10.1126/science.290.5494.1166.
  7. Lochmiller, R., Vestey, M. Boren, J. (1993). "Relationship between protein nutritional status and immunocompetence in northern Bobwhite chicks". The Auk. Ornithological Societies North America. 110: 503–510. JSTOR 4088414.
  8. Bourée, P. (2003). "Immunity and immunization in elderly". Pathologie-biologie. 51 (10): 581–585. PMID 14622949. doi:10.1016/j.patbio.2003.09.004.
  9. Prendergast, B. J.; Freeman, D. A.; Zucker, I.; Nelson, R. J. (2002). "Periodic arousal from hibernation is necessary for initiation of immune responses in ground squirrels". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 282 (4): R1054–R1062. PMID 11893609. doi:10.1152/ajpregu.00562.2001.
  10. Lindstrom, K. M.; Foufopoulos, J.; Parn, H.; Wikelski, M. (2004). "Immunological investments reflect parasite abundance in island populations of Darwin's finches". Proceedings of the Royal Society B: Biological Sciences. 271 (1547): 1513–1519. PMC 1691748Freely accessible. PMID 15306324. doi:10.1098/rspb.2004.2752.
  11. Nunn, C. L.; Gittleman, J. L.; Antonovics, J. (2000). "Promiscuity and the primate immune system". Science. 290 (5494): 1168–1170. PMID 11073457. doi:10.1126/science.290.5494.1168.
  12. 1 2 Bilbo, S. D.; Drazen, D. L.; Quan, N.; He, L.; Nelson, R. J. (2002). "Short day lengths attenuate the symptoms of infection in Siberian hamsters". Proceedings of the Royal Society B: Biological Sciences. 269 (1490): 447–454. PMC 1690914Freely accessible. PMID 11886635. doi:10.1098/rspb.2001.1915.
  13. Bennett Jr, I. L.; Nicastri, A. (1960). "Fever as a mechanism of resistance". Bacteriological reviews. 24 (1): 16–34. PMC 441034Freely accessible. PMID 13798941.
  14. Herman, P. P.; Yatvin, M. B. (1994). "Effect of heat on viral protein production and budding in cultured mammalian cells". International Journal of Hyperthermia. 10 (5): 627–641. PMID 7806920. doi:10.3109/02656739409022443.
  15. Rodriguez, D. J.; Sandoval, W.; Clevenger, F. W. (1995). "Is Measured Energy Expenditure Correlated to Injury Severity Score in Major Trauma Patients?". Journal of Surgical Research. 59 (4): 455–459. PMID 7564317. doi:10.1006/jsre.1995.1191.
  16. Roe, C. F.; Kinney, J. M. (1965). "The Caloric Equivalent of Fever. Ii. Influence of Major Trauma". Annals of Surgery. 161 (1): 140–147. PMC 1408758Freely accessible. PMID 14252624. doi:10.1097/00000658-196501000-00022.
  17. Kreymann, G.; Grosser, S.; Buggisch, P.; Gottschall, C.; Matthaei, S.; Greten, H. (1993). "Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock". Critical Care Medicine. 21 (7): 1012–1019. PMID 8319458. doi:10.1097/00003246-199307000-00015.
  18. Long, C. L. (1977). "Energy balance and carbohydrate metabolism in infection and sepsis". The American Journal of Clinical Nutrition. 30 (8): 1301–1310. PMID 888781.
  19. Roghmann, M. C.; Warner, J.; MacKowiak, P. A. (2001). "The relationship between age and fever magnitude". The American journal of the medical sciences. 322 (2): 68–70. PMID 11523629. doi:10.1097/00000441-200108000-00003.
  20. Tocco-Bradley, R.; Kluger, M. J.; Kauffman, C. A. (1985). "Effect of age on fever and acute-phase response of rats to endotoxin and Salmonella typhimurium". Infection and immunity. 47 (1): 106–111. PMC 261483Freely accessible. PMID 3880718.
  21. Mouihate, A.; Harré, E. -M.; Martin, S.; Pittman, Q. J. (2008). "Suppression of the Febrile Response in Late Gestation: Evidence, Mechanisms and Outcomes". Journal of Neuroendocrinology. 20 (4): 508–514. PMC 3547979Freely accessible. PMID 18266941. doi:10.1111/j.1365-2826.2008.01666.x.
  22. Wiersma, P.; Selman, C.; Speakman, J. R.; Verhulst, S. (2004). "Birds sacrifice oxidative protection for reproduction". Proceedings of the Royal Society B: Biological Sciences. 271 (Suppl 5): S360–S363. PMC 1810045Freely accessible. PMID 15504018. doi:10.1098/rsbl.2004.0171.
  23. Blount, J. D.; Metcalfe, N. B.; Birkhead, T. R.; Surai, P. F. (2003). "Carotenoid Modulation of Immune Function and Sexual Attractiveness in Zebra Finches". Science. 300 (5616): 125–127. PMID 12677066. doi:10.1126/science.1082142.
  24. Lozano, G (1994). "Carotenoids, parasites, and sexual selection". Oikos. 70: 309–311. doi:10.2307/3545643.
  25. Kluger, M. J.; Rothenburg, B. A. (1979). "Fever and reduced iron: Their interaction as a host defense response to bacterial infection". Science. 203 (4378): 374–376. PMID 760197. doi:10.1126/science.760197.
  26. Weinberg, E. D. (1984). "Iron withholding: A defense against infection and neoplasia". Physiological reviews. 64 (1): 65–102. PMID 6420813.
  27. Murray, M. J.; Murray, A. B.; Murray, M. B.; Murray, C. J. (1978). "The adverse effect of iron repletion on the course of certain infections". British Medical Journal. 2 (6145): 1113–1115. PMC 1608230Freely accessible. PMID 361162. doi:10.1136/bmj.2.6145.1113.
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