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home:pathogenesis:evolution [08.21.2017] – [Read more] sallieqhome:pathogenesis:evolution [09.14.2022] (current) – external edit 127.0.0.1
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 ====== Evolutionary perspective on chronic disease ====== ====== Evolutionary perspective on chronic disease ======
  
-One useful way to determine if a disease is caused by faulty human genes is look towards the central principle of evolutionary biology: evolutionary fitness. [[http://en.wikipedia.org/wiki/Fitness_(biology)|Evolutionary fitness]] is defined as the extent to which an organism is adapted to or able to produce offspring in a particular environment. The fitness concept can be applied to the problem of disease causation to distinguish evolutionarily feasible hypotheses of causation from marginally feasible or untenable ones.(({{pubmed>long:10893730}})) (({{pubmed>long:10839723}}))+One useful way to determine if a disease is caused by faulty human genes is look towards the central principle of evolutionary biology: evolutionary fitness. [[https://en.wikipedia.org/wiki/Fitness_(biology)|Evolutionary fitness]] is defined as the extent to which an organism is adapted to or able to produce offspring in a particular environment. The fitness concept can be applied to the problem of disease causation to distinguish evolutionarily feasible hypotheses of causation from marginally feasible or untenable ones.(({{pmid>long:10893730}})) (({{pmid>long:10839723}}))
  
 Generally speaking, diseases have three major causes: genetic, environmental, and infectious. Each disease affects, to some degree, an organism's ability to reproduce, that is, their reproductive fitness. As a general rule, infectious disease confers no reproductive benefit but genetic diseases do, either currently or historically.  Generally speaking, diseases have three major causes: genetic, environmental, and infectious. Each disease affects, to some degree, an organism's ability to reproduce, that is, their reproductive fitness. As a general rule, infectious disease confers no reproductive benefit but genetic diseases do, either currently or historically. 
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 ===== Genetic diseases confer a benefit ===== ===== Genetic diseases confer a benefit =====
  
-Major diseases known to be genetic in origin offer some characteristic which confers a reproductive edge, and almost always that edge involves resistance to infection.(({{pubmed>long:10893730}})) When a group of people having that trait migrates and that advantage is lost or starts being harmful, the gene is weeded out of the population.+Major diseases known to be genetic in origin offer some characteristic which confers a reproductive edge, and almost always that edge involves resistance to infection.(({{pmid>long:10893730}})) When a group of people having that trait migrates and that advantage is lost or starts being harmful, the gene is weeded out of the population.
 ==== Sickle-cell anemia ==== ==== Sickle-cell anemia ====
  
-Although [[http://en.wikipedia.org/wiki/Cystic_fibrosis|cystic fibrosis]], [[http://en.wikipedia.org/wiki/Thalassemia|thalassemias]], and [[http://en.wikipedia.org/wiki/Polycystic_kidney_disease|polycystic kidney disease]] are genetic disorders all known to prevent genetic damage caused by infection, the genetic disorder sickle-cell anemia is a [[http://en.wikipedia.org/wiki/Malaria#Evolutionary_pressure_of_malaria_on_human_genes|prototypical example]]. In sickle-cell disease, there is a mutation in the HBB gene which confers resistance to malaria, providing a benefit in some regions of the world but doing harm in others. Groups of people who move from areas of the world infested with malaria to areas which are not, quickly lose the trait for sickle-cell within generations:+Although [[https://en.wikipedia.org/wiki/Cystic_fibrosis|cystic fibrosis]], [[https://en.wikipedia.org/wiki/Thalassemia|thalassemias]], and [[https://en.wikipedia.org/wiki/Polycystic_kidney_disease|polycystic kidney disease]] are genetic disorders all known to prevent genetic damage caused by infection, the genetic disorder sickle-cell anemia is a [[https://en.wikipedia.org/wiki/Malaria#Evolutionary_pressure_of_malaria_on_human_genes|prototypical example]]. In sickle-cell disease, there is a mutation in the HBB gene which confers resistance to malaria, providing a benefit in some regions of the world but doing harm in others. Groups of people who move from areas of the world infested with malaria to areas which are not, quickly lose the trait for sickle-cell within generations:
  
 <blockquote>Recorded history spans about 5,000 years, and the frequencies of deleterious alleles can change substantially in a small fraction of that time. Consider the sickle-cell allele [one of many competing versions of a gene], which protects heterozygotes from malaria and causes a lethal anemia in homozygotes. If a population with a sickle-cell allele frequency of 20 percent were transferred to an environment without malaria, the negative effects of sickle-cell anemia should cause the frequency of the sickle-cell allele to decrease by a factor of about three within about 10 generations. This estimate accords with geographic differences. In the United States, the sickle-cell allele frequency is about half of what would be expected from African source populations after accounting for admixture [the act of mixing or mingling]. A geographic comparison within the Caribbean between malaria-free and malaria-endemic areas is also consistent: the frequency of the sickle-cell allele is low in Curaçao, where malaria has not been endemic, but not in Surinam, where malaria has been endemic.((Vogel, F., and A. G. Motulsky. Human Genetics, 3rd ed. Berlin: Springer Verlag, 1997.)) <blockquote>Recorded history spans about 5,000 years, and the frequencies of deleterious alleles can change substantially in a small fraction of that time. Consider the sickle-cell allele [one of many competing versions of a gene], which protects heterozygotes from malaria and causes a lethal anemia in homozygotes. If a population with a sickle-cell allele frequency of 20 percent were transferred to an environment without malaria, the negative effects of sickle-cell anemia should cause the frequency of the sickle-cell allele to decrease by a factor of about three within about 10 generations. This estimate accords with geographic differences. In the United States, the sickle-cell allele frequency is about half of what would be expected from African source populations after accounting for admixture [the act of mixing or mingling]. A geographic comparison within the Caribbean between malaria-free and malaria-endemic areas is also consistent: the frequency of the sickle-cell allele is low in Curaçao, where malaria has not been endemic, but not in Surinam, where malaria has been endemic.((Vogel, F., and A. G. Motulsky. Human Genetics, 3rd ed. Berlin: Springer Verlag, 1997.))
  
- //**Gregory Cochran,** et al.//  (({{pubmed>long:10893730}}))+ //**Gregory Cochran,** et al.//  (({{pmid>long:10893730}}))
 </blockquote> </blockquote>
  
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 If the common inflammatory diseases (including autoimmune diseases) were genetic, the only way they would manage not to be weeded out of the population would be if they conferred some sort of beneficial survival trait not related to the disease.   If the common inflammatory diseases (including autoimmune diseases) were genetic, the only way they would manage not to be weeded out of the population would be if they conferred some sort of beneficial survival trait not related to the disease.  
  
-To date, no such benefits have been identified in any disease, schizophrenia being a good example.(({{pubmed>long:12878806}})) Schizophrenics have a high suicide rate, few children, and a high rate of abnormality in their children.(({{pubmed>long:10978869}})) (({{pubmed>long:8885043}})) Schizophrenic mothers are more likely than non-schizophrenics to have stillborn babies and children with congenital malformations.(({{pubmed>long:11448375}})) +To date, no such benefits have been identified in any disease, schizophrenia being a good example.(({{pmid>long:12878806}})) Schizophrenics have a high suicide rate, few children, and a high rate of abnormality in their children.(({{pmid>long:10978869}})) (({{pmid>long:8885043}})) Schizophrenic mothers are more likely than non-schizophrenics to have stillborn babies and children with congenital malformations.(({{pmid>long:11448375}})) 
  
 Among chronic diseases, as opposed to genetic illnesses, there has certainly been no documented increased resistance to infection. Crohn's disease is typical in that patients who suffer from the disease are known for getting [[home:diseases#evidence_of_infectious_cause|substantially more co-infections]]. Among chronic diseases, as opposed to genetic illnesses, there has certainly been no documented increased resistance to infection. Crohn's disease is typical in that patients who suffer from the disease are known for getting [[home:diseases#evidence_of_infectious_cause|substantially more co-infections]].
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 <blockquote>Therefore, I argue that the biological function of humans is basically over with at 20–25 years, and that is what nature is used to as well.  <blockquote>Therefore, I argue that the biological function of humans is basically over with at 20–25 years, and that is what nature is used to as well. 
  
-//**Rolf Zinkernagel**// (({{pubmed>long:18311378}}))</blockquote>+//**Rolf Zinkernagel**// (({{pmid>long:18311378}}))</blockquote>
  
 The problem with this argument is that many chronic diseases do strike before reproductive age. Consider, once again, schizophrenia, a disease which is not at all unique in this regard. Schizophrenia drastically reduces reproductive fitness. Epidemiological data clearly show that people with schizophrenia are much more likely die before reproductive age.  The problem with this argument is that many chronic diseases do strike before reproductive age. Consider, once again, schizophrenia, a disease which is not at all unique in this regard. Schizophrenia drastically reduces reproductive fitness. Epidemiological data clearly show that people with schizophrenia are much more likely die before reproductive age. 
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 ===== Persistence of chronic diseases ===== ===== Persistence of chronic diseases =====
  
-Further evidence against the genetic hypothesis for inflammatory disease is that a number of diseases - diseases like Crohn's, atherosclerosis, autism, breast cancer, schizophrenia and multiple sclerosis - tend to strike around or before reproductive age. These are diseases which have been around for at least thousands of years, allowing for plenty of time for harmful traits to be weeded out of the population. Manifestations of both arteriosclerosis(({{pubmed>long:10495769}})) ((Ackerknecht, E. H. (1955). //A Short History of Medicine//. New York: Ronald Press)) and cardiac disease(({{pubmed>long:10938170}})) can be observed in mummies of ancient Egypt. [[http://en.wikipedia.org/wiki/Ötzi_the_Iceman|Ötzi the Neolithic Iceman]] who lived around 3300 BC was found to have arthritis.(({{pubmed>long:12701332}})) There is currently no evidence that any of the supposedly genetic chronic diseases haven't been around for at least millenia. +Further evidence against the genetic hypothesis for inflammatory disease is that a number of diseases - diseases like Crohn's, atherosclerosis, autism, breast cancer, schizophrenia and multiple sclerosis - tend to strike around or before reproductive age. These are diseases which have been around for at least thousands of years, allowing for plenty of time for harmful traits to be weeded out of the population. Manifestations of both arteriosclerosis(({{pmid>long:10495769}})) ((Ackerknecht, E. H. (1955). //A Short History of Medicine//. New York: Ronald Press)) and cardiac disease(({{pmid>long:10938170}})) can be observed in mummies of ancient Egypt. [[https://en.wikipedia.org/wiki/Ötzi_the_Iceman|Ötzi the Neolithic Iceman]] who lived around 3300 BC was found to have arthritis.(({{pmid>long:12701332}})) There is currently no evidence that any of the supposedly genetic chronic diseases haven't been around for at least millenia. 
  
 ===== Interplay between environmental factors and genes ===== ===== Interplay between environmental factors and genes =====
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 ===== Read more ===== ===== Read more =====
  
-  * [[http://bacteriality.com/2008/02/11/ewald/|Interview with evolutionary biologist Paul Ewald]] <html>&nbsp;</html> [[http://bacteriality.com|{{:home:bacteriality.gif}}]] +  * [[https://bacteriality.com/2008/02/11/ewald/|Interview with evolutionary biologist Paul Ewald]] <html>&nbsp;</html> [[https://bacteriality.com|{{:home:bacteriality.gif}}]] 
-  * [[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841832/?tool=pubmed/|Article by Paul Ewald on chronic diseases and immunopathology]]+  * [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841832/?tool=pubmed/|Article by Paul Ewald on chronic diseases and immunopathology]]
  
 {{tag> Pathogenesis}} {{tag> Pathogenesis}}
 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
-removed groken link --- //Sallie Q 08.21.2017// http://vetmed.illinois.edu/courses/path516/Cochran%20et%20al%5b1%5d.pdf|Infectious causation of disease: an evolutionary persepctive+broken link --- https://vetmed.illinois.edu/courses/path516/Cochran%20et%20al%5b1%5d.pdf|Infectious causation of disease: an evolutionary persepctive
  
   *  Legacy content   *  Legacy content
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-===== References =====+===== References =====</nodisp> 
home/pathogenesis/evolution.1503302366.txt.gz · Last modified: 08.21.2017 by sallieq
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