Stearns, et al. Article

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ccrowle1  on February 8, 2012

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Evolution

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Stearns, et al. Article

Stearns et al. Article
"Evolutionary perspectives on health and medicine"
-four general messages
-three classical themes
-three particularly surprising unique insights
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Stearns et al. Article "Evolutionary perspectives on health and medicine"
-four general messages
-three classical themes
-three particularly surprising unique insights
First general message - the view of organisms as machines whose design has been optimized by engineers is as misleading as it is deeply entrenched
- instead, are bundles of compromises shaped by selection to maximize reproduction, not health (thus have unavoidable trade-offs/constraints)
Second general message - biological evolution much slower than cultural change, therefore much disease arises from mismatch of bodies to modern environments
Third general message - pathogens evolve much faster than we do, therefore infection is unavoidable
Fourth general message - many genetic variants interact w/ environments & other genes during development to influence disease phenotypes
- vs. the idea that common heritable diseases are caused by a few defective genes
First classical theme - pathogens rapidly evolve resistance to antibiotics just as cancers rapidly evolve resistance to chemotherapy
second classical theme - pathogens evolve strategies to circumvent host defenses, & virulence levels are shaped by natural selection to maximize transmission
third classical theme -human genetic variations that increase disease resistance often have costs
- some variations that increase vulnerability can have benefits
first surprising insight - humans co-evolved w/ a normal community of symbiotic bacteria & parasitic worms
- when they are eliminated by hygiene or antibiotics, immune systems react to the unnatural situation by producing allergies, asthma, autoimmune disease (e.g. crohn's disease - which can be treated by ingesting parasitic worms)
second surprising insight - widespread use of imperfect vaccines could lead to an increase in the virulence of the pathogen
- particular concern in the case of malaria vaccines
third surprising insight - disruptions of the equilibria achieved in evolutionary coflicts of interest among relatives may be basis of some mental diseases
- particularly autism, schizophrenia
aging & evolution - not an adaptation, but a byproduct of selection for reproductive performance earlier in life
- we have achieved a doubling of lifespan since last common ancester w/ chimpanzees - in part b/c of changes in genes that mediate infection, inflammation, and nutrition
why do humans have cancers more than other species?1. we now have an extended postreproductive life-span relatively invisble to natural selection (not adapted to the new risk factors generated by civilization
2. cancer is virtually inevitable in multicellular organisms that rely on stem cells for tissue maintenance
- mutations occurring in cell lineages during development lead to the cell mosaicism that is a precondition for both cancer & types of neurodegeneration
equilibrium disruption exampleparental conflicts of interest
- when chromosome 15 imprinted gene is expressed w/out normal paternal inhibition, child develops prader-willi syndrome --> high risk of psychosis as an adult
- when paternal interests are solely expressed, (Angelman syndrome) ---> high risk of autism as an adult
- thus, disrupting the equilibrium of an evolutionary conflict of interest appeared to contribute to mental disease
epigenetics- important class of epigenetic change is mediated by methylation of genes
-feinberg and irizarry explor evolutionary consequence of variation across individuals in methylation state:
+genes that increase such variation among individuals can have higher fitness in a varying environment when the epigenetic variation is realized at hte level of the whole organism as phenotypic plasticity, resulting in performance better matched to each state in the varying environment
new genome architecture evidence20 individuals differed on average by 11 copy-number polymorphisms. within sequence entervales they found copy-number variation in 70 different genomic locations which involved genes influencing neurological function, regulation of cell growth, regulation of metabolism, and known to be associated w/ disease

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