Evolutionary medicine: the Progress is coming

Charles Darwin did not discuss the implications of his work for medicine, though biologists quickly appreciated the germ theory of disease and its implications for understanding the evolution of pathogens, as well as an organism’s need to defend against them.

Medicine, in turn, “has modelled itself after a mechanical physics, deriving from Galileo, Newton, and Descartes…. As a result of assuming this model, medicine is mechanistic, materialistic, reductionistic, linear-causal, and deterministic (capable of precise predictions) in its concepts. It seeks explanations for diseases, or their symptoms, signs, and cause in single, materialistic— i.e., anatomical or structural (e.g., in genes and their products)— changes within the body, wrought directly (linearly), for example, by infectious, toxic, or traumatic agents.” (Weiner H ). “Notes on an evolutionary medicine”. 1st July 1998 Psychosom Med. 60 (4): 510–20. PMID 9710299)

This serious underestimation was probably due to the fact that ” The Origin of Species ” by Darwin was drafted in the first half of the nineteenth century and published on 1 July 1858 , while the ‘ melting pot ‘ began only years later , with the so-called Colonialism. Starting from 1860 , the French colonized West Africa , West Africa Saharan Africa , Mauritania , Côte d’ Ivoire , the Belgian Congo , Madagascar , Laos , Cambodia . England, in 1870 , added to its dominion the Bechuanaland (Botswana ) , Rhodesia (Zambia ) , Uganda , Kenya, northern Somalia , Egypt , Sudan , Nigeria , the Gold Coast , Sierra Leone , the Gambia, Yemen , Kuwait , Myanmar , Papua , Brunei , and many Polynesian archipelagos, with large forced commercial facilities in China. At the same time (1870 ) , the German Empire was born and began to expand in Central and South America, (Cameroon , Namibia , Togo and Tanzania ) and the Pacific ( Papua New Guinea and the Bismarck Archipelago ) as on the north coast of China.

After 150 years of mixing of ethnic groups , it has been happening for years a radical change of eating styles and with the Industrialization – also started ‘after Darwin’ – we are all exposed to environmental factors very different from those of 200 years ago. And to think that Westerners and Native Americans had recently (two centuries) faced the shock of the mutual introduction of foods and lifestyles that their grandparents did not even know.

Principal Varieties of Mankind, 3 May 1850.
Portraits by the British artist John Emslie – published by James Reynolds, London, 1850-1860. (Photo by SSPL/Getty Images)

The pioneer was an ethologist, Nikolaas Tinbergen, that in 1963 published “On Aims and Methods in Ethology”, with a high relevance to medicine, if all biological traits need two kinds of explanation, both proximate and evolutionary. The proximate explanation for a disease describes what is wrong in the bodily mechanism of individuals affected by it. An evolutionary explanation is completely different. Instead of explaining why people are different, it explains why we are all the same in ways that leave us vulnerable to disease. Why do we all have wisdom teeth, an appendix, and cells that can divide out of control?” (Randolph Nesse M.D. / University of Michigan – “Evolution: medicine’s most basic science” (Lancet. 372 (Suppl 1): S21–7 December 2008 )  The key developments came with the paper of Paul Ewald in 1980, “Evolutionary Biology and the Treatment of Signs and Symptoms of Infectious Disease”, and that of Williams and Nesse in 1991, “The Dawn of Darwinian Medicine”

Evolutionary medicine or Darwinian medicine is the application of modern evolutionary theory to understanding health and disease. The goal of evolutionary medicine is to understand why people get sick, not simply how they get sick.

Modern medical research and practice has focused on the molecular and physiological mechanisms underlying health and disease, while evolutionary medicine focuses on the question of why evolution has shaped these mechanisms in ways that may leave us susceptible to disease.  The evolutionary approach has driven important advances in our understanding of cancer, autoimmune disease, and anatomy.  Medical schools will have to integrate evolutionary approaches as more standards will be added to the medical curricula.

mitochondrial haplotypes global distribution

Humans evolved to live as simple hunter-gatherers in small tribal bands, a very different way of life and environment compared to that faced by contemporary humans. This change makes present humans vulnerable to a number of health problems, termed “diseases of civilization” and “diseases of affluence”. Humans evolved to live off of the land, and take advantage of the resources that were readily available to them. They evolved for the stone-age, and the environments of today bring about many disease causing ailments, that may or may not be deadly. “Modern environments may cause many diseases-for example, deficiency syndromes such as scurvy and rickets” (Williams, 1991)

In contrast to the diet of early hunter-gatherers, the modern Western diet often contains high quantities of fat, salt, and simple carbohydrates, which include refined sugars and flours. Not to mention the food that is introduced from the Americas. These create health problems. (Eaton SB 2006). “The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition?”. Proc Nutr Soc. 65 (1): 1–6. doi:10.1079/PNS2005471. PMID 16441938)

Adaptations (or persistent mutations) can only occur if they are evolvable. Some adaptations which would prevent ill health are therefore not possible, as DNA cannot be totally prevented from undergoing somatic replication corruption (cancer risk) or humans cannot biosynthesize Vitamin C (scurvy risk , the optic nerve is forced to exit the retina through a point called the optic disc increasing pressure within the eye (glaucoma risk) etcetera.

Many common symptoms and diseases are distributed differently depending on our genome as: fever / vomiting (as functional responses to infection or ingestion of toxins);  Intestinal gas (as product of digestion of fiber); allergies (over-reactive immunological responses); modern diet-related Type 2 Diabetes; Autism (possible malfunctioning of theory of mind module); mild depression or anxiety (as functional responses to mild loss or stress);  gene for malaria resistance that, in homozygous form, causes sickle cell anemia. As it is generally known the genoma dependance of different blood and immune system types, very short or tall height, predisposition to various forms of cancer, skin pigmentation, protection from UV, and the skin synthesis of Vitamin D, hemocromatosis and – precisely – porphyrias.

NYT ADH variants asia

This is a partial list of diseases on which scientists are describing or debating an evolutionary origin, like Adipose tissue in human infants, Arthritis and other chronic inflammatory diseases, Ageing, Alzheimer disease, Childhood, Menarche, Menopause, Menstruation, Morning sickness, Atherosclerosis, Arthritis and other chronic inflammatory diseases, Coug, Cystic fibrosis, Dental occlusion, Diabetes Type II, Diarrhea, Essential hypertension, Fever, Gestational hypertension, Gout, Hemochromatosis, Iron deficiency (paradoxical benefits), Obesity, Phenylketonuria, Placebos, Osteoporosis, Red blood cell polymorphism disorders, Sickle cell anemia, Sickness behavior, Women’s reproductive cancer.

Why not Porphyrias?

Here below, a list of significant studies or articles about the progresses  by evolutionary approach to sickness:

  1. Nesse, RM; et al. (2009). “Making evolutionary biology a basic science for medicine”.Proceedings of the National Academy of Sciences of the United States of America. 107. PNAS. Suppl 1 (suppl_1): 1800–7. doi:10.1073/pnas.0906224106. PMC 2868284free to read.PMID 19918069.
  2. Stearns SC (2005). “Issues in evolutionary medicine”. Am. J. Hum. Biol. 17 (2): 131–40. doi:10.1002/ajhb.20105. PMID 15736177.
  3. Eaton, S. Boyd; Konner, M; Shostak, M (April 1988). “Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective”. American Journal of Medicine. 84 (4): 739–749. doi:10.1016/0002-9343(88)90113-1. PMID 3135745. Retrieved 2010-06-18.
  4. Williams, G. C. (1991). The dawn of darwinian medicine.Europe PubMed Central, 66(1), 1-22. doi:10.1086/417048
  5. Eaton SB, Strassman BI, Nesse RM, Neel JV, Ewald PW, Williams GC, Weder AB, Eaton SB 3rd, Lindeberg S, Konner MJ, Mysterud I, Cordain L (2002). “Evolutionary health promotion” (PDF). Prev Med. 34 (2): 109–18. doi:10.1006/pmed.2001.0876.PMID 11817903.
  6. Eaton SB (2006). “The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition?”. Proc Nutr Soc. 65 (1): 1–6. doi:10.1079/PNS2005471.PMID 16441938.
  7. Abuissa H; O’Keefe JH; Cordain, L (2005). “Realigning our 21st century diet and lifestyle with our hunter-gatherer genetic identity” (PDF). Directions Psych. 25: SR1–SR10.
  8. Eaton, S. Boyd; Cordain, Loren; Sebastian, Anthony (2007). “The Ancestral Biomedical Environment” (PDF). In Aird, William C. Endothelial Biomedicine. Cambridge University Press. pp. 129–34. ISBN 0-521-85376-1.
  9. Eaton SB, Eaton SB (Sep 2003). “An evolutionary perspective on human physical activity: implications for health”. Comp Biochem Physiol a Mol Integr Physiol. 136 (1): 153–9.doi:10.1016/S1095-6433(03)00208-3. PMID 14527637.
  10. Cordain, L., Gotshall, R.W. and Eaton, S.B. (Jul 1998). “Physical activity, energy expenditure and fitness: an evolutionary perspective” (PDF). Int J Sports Med. 19 (5): 328–35. doi:10.1055/s-2007-971926. PMID 9721056.
  11. Cordain, L.; Gotshall, R.W.; Eaton, S.B. (1997). “Evolutionary aspects of exercise”(PDF). World Rev Nutr Diet. World Review of Nutrition and Dietetics (Vol. 81 + 82). 81: 49–60. doi:10.1159/000059601. ISBN 3-8055-6452-X. PMID 9287503.
  12. Williams, George; Nesse, Randolph M. (1996). Why We Get Sick: the new science of Darwinian medicine. New York: Vintage Books. ISBN 0-679-74674-9.
  13. Rotter JI, Diamond JM (1987). “What maintains the frequencies of human genetic diseases?”. Nature. 329 (6137): 289–90. doi:10.1038/329289a0. PMID 3114647.
  14. Williams, George; Nesse, Randolph M. (1996). “Evolution and healing”. Why We Get Sick: the new science of Darwinian medicine. New York: Vintage Books. pp. 37–8. ISBN 0-679-74674-9.
  15. Eaton SB, Eaton SB, Konner MJ (April 1997). “Paleolithic nutrition revisited: a twelve-year retrospective on its nature and implications”. Eur J Clin Nutr. 51 (4): 207–16.doi:10.1038/sj.ejcn.1600389. PMID 9104571.
  16. Eaton SB, Konner M (January 1985). “Paleolithic nutrition. A consideration of its nature and current implications”. N. Engl. J. Med. 312 (5): 283–9.doi:10.1056/NEJM198501313120505. PMID 2981409.
  17. Nesse RM (December 2008). “Evolution: medicine’s most basic science”. Lancet. 372(Suppl 1): S21–7. doi:10.1016/S0140-6736(08)61877-2.
  18.  Ewald PW (September 1980). “Evolutionary biology and the treatment of signs and symptoms of infectious disease”. J. Theor. Biol. 86 (1): 169–76. doi:10.1016/0022-5193(80)90073-9. PMID 7464170.
  19. Williams GC, Nesse RM (March 1991). “The dawn of Darwinian medicine”. Q Rev Biol.66 (1): 1–22. doi:10.1086/417048. PMID 2
  1. Merlo, LMF; et al. (2006). “Cancer as an evolutionary and ecological process”. Nature Reviews Cancer. 6 (12): 924–35. doi:10.1038/nrc2013. PMID 17109012.
  2. Howard RS, Lively CM (November 2004). “Good vs complementary genes for parasite resistance and the evolution of mate choice”. BMC Evol Biol. 4 (1): 48.doi:10.1186/1471-2148-4-48. PMC 543473free to read. PMID 15555062.
  3. Haig D (December 1993). “Genetic conflicts in human pregnancy”. Q Rev Biol. 68 (4): 495–532. doi:10.1086/418300. PMID 8115596.
  4. William, Knowler; Peter Bennett; Richard Hamman; Max Miller (1978). “Diabetes incidence and prevalence in Pima Indians: a 19-fold greater incidence than in Rochester, Minnesota”. American Journal of Epidemiology. 108 (6): 497–505. PMID 736028. Retrieved 2010-06-18.
  5. Milton K (2003). “Micronutrient intakes of non-human primates: are humans different?”(PDF). Comparative Biochemistry and Physiology A. 136 (1): 47–59. doi:10.1016/S1095-6433(03)00084-9. PMID 14527629.
  6. Fox, Molly; Leslie A. Knapp; Paul W. Andrews; Corey L. Fincher (August 11, 2013).“Hygiene and the world distribution of Alzheimer’s disease”. Evolution, Medicine, and Public Health. 2013 (1): 173–186. doi:10.1093/emph/eot015.
  7. Straub, R. H., del Rey, A., Besedovsky, H. O. (2007) “Emerging concepts for the pathogenesis of chronic disabling inflammatory diseases: neuroendocrine-immune interactions and evolutionary biology” In: Ader, R. (2007) “Psychoneuroimmunology”, Volume 1, Academic Press, San Diego, pp.217-232
  8. Wick G, Berger P, Jansen-Dürr P, Grubeck-Loebenstein B (2003). “A Darwinian-evolutionary concept of age-related diseases”. Exp. Gerontol. 38 (1–2): 13–25.doi:10.1016/S0531-5565(02)00161-4. PMID 12543257.
  9. Flaxman SM, Sherman PW (June 2000). “Morning sickness: a mechanism for protecting mother and embryo”. Q Rev Biol. 75 (2): 113–48. doi:10.1086/393377.PMID 10858967.
  10. Jump up^ Flaxman SM, Sherman PW (July 2008). “Morning sickness: adaptive cause or nonadaptive consequence of embryo viability?”. Am. Nat. 172 (1): 54–62.doi:10.1086/588081. PMID 18500939.
  11. Wick G, Perschinka H, Millonig G (December 2001). “Atherosclerosis as an autoimmune disease: an update”. Trends Immunol. 22 (12): 665–9. doi:10.1016/S1471-4906(01)02089-0. PMID 11738996.
  12. Kaifu, Y.; Kasai, K.; Townsend, G. C.; Richards, L. C. (2003). “Tooth wear and the ?design? Of the human dentition: A perspective from evolutionary medicine”. American Journal of Physical Anthropology. 122: 47–61. doi:10.1002/ajpa.10329.PMID 14666533.
  13. NEEL JV (December 1962). “Diabetes Mellitus: A “Thrifty” Genotype Rendered Detrimental by “Progress”?”. American Journal of Human Genetics. 14 (4): 353–62.PMC 1932342free to read. PMID 13937884.
  14. Neel JV, Weder AB, Julius S (1998). “Type II diabetes, essential hypertension, and obesity as “syndromes of impaired genetic homeostasis”: the “thrifty genotype” hypothesis enters the 21st century”. Perspect. Biol. Med. 42 (1): 44–74.doi:10.1353/pbm.1998.0060. PMID 9894356.
  15. Wick G, Jansen-Dürr P, Berger P, Blasko I, Grubeck-Loebenstein B (February 2000).“Diseases of aging”. Vaccine. 18 (16): 1567–83. doi:10.1016/S0264-410X(99)00489-2.PMID 10689131.
  16. Jump up^ Kluger MJ, Ringler DH, Anver MR (April 1975). “Fever and survival”. Science. 188(4184): 166–8. doi:10.1126/science.1114347. PMID 1114347.
  17. Kluger MJ, Rothenburg BA (January 1979). “Fever and reduced iron: their interaction as a host defense response to bacterial infection”. Science. 203 (4378): 374–6.doi:10.1126/science.760197. PMID 760197.
  18. Ames BN, Cathcart R, Schwiers E, Hochstein P (November 1981). “Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis”. Proc. Natl. Acad. Sci. USA. 78 (11): 6858–62.doi:10.1073/pnas.78.11.6858. PMC 349151free to read. PMID 6947260.
  19. Naugler C (2008). “Hemochromatosis: a Neolithic adaptation to cereal grain diets”. Med. Hypotheses. 70 (3): 691–2. doi:10.1016/j.mehy.2007.06.020. PMID 17689879.
  20. Moalem S, Percy ME, Kruck TP, Gelbart RR (September 2002). “Epidemic pathogenic selection: an explanation for hereditary hemochromatosis?”. Med. Hypotheses. 59 (3): 325–9. doi:10.1016/S0306-9877(02)00179-2. PMID 12208162.
  21. Wander K, Shell-Duncan B, McDade TW (October 2008). “Evaluation of iron deficiency as a nutritional adaptation to infectious disease: An evolutionary medicine perspective”.Am. J. Hum. Biol. 21 (2): 172–9. doi:10.1002/ajhb.20839. PMID 18949769.
  22. Woolf LI, McBean MS, Woolf FM, Cahalane SF (May 1975). “Phenylketonuria as a balanced polymorphism: the nature of the heterozygote advantage”. Annals of Human Genetics. 38 (4): 461–9. doi:10.1111/j.1469-1809.1975.tb00635.x. PMID 1190737.
  23. Humphrey, Nicholas (2002). “19. Great Expectations: The Evolutionary Psychology of Faith-Healing and the Placebo Effect” (PDF). The mind made flesh: essays from the frontiers of psychology and evolution. Oxford [Oxfordshire]: Oxford University Press. pp. 255–85. ISBN 0-19-280227-5.
  24. Karasik, D. (Nov 2008). “Osteoporosis: an evolutionary perspective”. Human Genetics.124 (4): 349–356. doi:10.1007/s00439-008-0559-8. ISSN 0340-6717.PMID 18781328.
  25. Williams TN (August 2006). “Human red blood cell polymorphisms and malaria”. Current Opinion in Microbiology. 9 (4): 388–94. doi:10.1016/j.mib.2006.06.009.PMID 16815736.
  26. Ayi K, Turrini F, Piga A, Arese P (November 2004). “Enhanced phagocytosis of ring-parasitized mutant erythrocytes: a common mechanism that may explain protection against falciparum malaria in sickle trait and beta-thalassemia trait”. Blood. 104 (10): 3364–71.doi:10.1182/blood-2003-11-3820. PMID 15280204.
  27. Williams TN; Mwangi TW; Wambua S; et al. (July 2005). “Sickle cell trait and the risk of Plasmodium falciparum malaria and other childhood diseases”. J. Infect. Dis. 192 (1): 178–86. doi:10.1086/430744. PMC 3545189free to read. PMID 15942909.
  28. Eaton SB; Pike MC; Short RV; et al. (September 1994). “Women’s reproductive cancers in evolutionary context”. Q Rev Biol. 69 (3): 353–67. doi:10.1086/418650.PMID 7972680.
  29. Nesse, R., & Williams, G. (1996) Why We Get Sick. NY: Vintage.
  30. Nesse R (1997). “An evolutionary perspective on panic disorder and agoraphobia”. InBaron-Cohen S. The maladapted mind: classic readings in evolutionary psychopathology. East Sussex: Psychology Press. pp. 73–84. ISBN 0-86377-460-1. Retrieved 21 January2011.
  31. Grinde B (June 2005). “An approach to the prevention of anxiety-related disorders based on evolutionary medicine”. Prev Med. 40 (6): 904–9. doi:10.1016/j.ypmed.2004.08.001.PMID 15850894.
  32. Nesse RM (January 2000). “Is depression an adaptation?”. Arch. Gen. Psychiatry. 57(1): 14–20. doi:10.1001/archpsyc.57.1.14. PMID 10632228.
  33. Nesse RM, Berridge KC (October 1997). “Psychoactive drug use in evolutionary perspective”. Science. 278 (5335): 63–6. doi:10.1126/science.278.5335.63.PMID 9311928.
  34. Crow TJ (July 1995). “A Darwinian approach to the origins of psychosis”. Br J Psychiatry.167 (1): 12–25. doi:10.1192/bjp.167.1.12. PMID 7551604.