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The human obesity epidemic, the mismatch paradigm, and our modern "captive" environment

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dc.contributor.author Power, Michael L. en
dc.date.accessioned 2013-06-20T18:45:02Z
dc.date.available 2013-06-20T18:45:02Z
dc.date.issued 2012
dc.identifier.citation Power, Michael L. 2012. "<a href="https%3A%2F%2Frepository.si.edu%2Fhandle%2F10088%2F20988">The human obesity epidemic, the mismatch paradigm, and our modern 'captive' environment</a>." <em>American Journal of Human Biology</em>. 24 (2):116&ndash;122. <a href="https://doi.org/10.1002/ajhb.22236">https://doi.org/10.1002/ajhb.22236</a> en
dc.identifier.issn 1042-0533
dc.identifier.uri http://hdl.handle.net/10088/20988
dc.description.abstract In the distant past obesity in humans was rare and likely caused by metabolic dysregulation due to genetic or disease-related pathology. External factors precluded the ability of most people to overeat or under exert. Socio-cultural obesity came about due to the rareness of obesity and its difficulty to achieve. What is rare becomes valuable and what is difficult to achieve becomes a badge of prestige. The modern human obesity epidemic would appear to represent a third class of obesity: environmental obesity. Much like the captive environments which humans construct for the captive/companion animals in our care, the modern human environment has greatly decreased the challenges of life that would restrict food intake and enforce exertion. And like us, our captive/companion animal populations are also experiencing obesity epidemics. A further concern is that maternal obesity alters maternal signaling to offspring, in utero through the placenta and after birth through breast milk, in ways that perpetuate an enhanced vulnerability to obesity. Molecules such as leptin, produced by adipose tissue and placenta, have significant developmental effects on brain areas associated with feeding behavior. Leptin and other cytokines and growth factors are found in breast milk. These molecules have positive effects on gut maturation; their effects on metabolism and brain development are unclear. Placenta and brain also are hotspots for epigenetic regulation, and epigenetic changes may play significant roles in the later vulnerability to obesity and to the development of a diverse array of diseases, including heart disease, hypertension, and noninsulin-dependent diabetes. Am. J. Hum. Biol., 2012. (C) 2012 Wiley Periodicals, Inc. en
dc.relation.ispartof American Journal of Human Biology en
dc.title The human obesity epidemic, the mismatch paradigm, and our modern &quot;captive&quot; environment en
dc.type Journal Article en
dc.identifier.srbnumber 110178
dc.identifier.doi 10.1002/ajhb.22236
rft.jtitle American Journal of Human Biology
rft.volume 24
rft.issue 2
rft.spage 116
rft.epage 122
dc.description.SIUnit Peer-Reviewed en
dc.description.SIUnit NZP en
dc.citation.spage 116
dc.citation.epage 122


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