Please use this identifier to cite or link to this item: https://repositorio.udes.edu.co/handle/001/3689
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dc.contributor.authorLópez Jaramillo, Patriciospa
dc.contributor.authorSilva, Sandra Y.spa
dc.contributor.authorRodríguez Salamanca, Narellaspa
dc.contributor.authorDurán Hernández, Álvaro-Hernánspa
dc.contributor.authorMosquera, Walterspa
dc.contributor.authorCastillo, Victor R.spa
dc.date.accessioned2019-08-29T16:11:06Zspa
dc.date.available2019-08-29T16:11:06Zspa
dc.date.issued2008-07spa
dc.identifier.isbn1536-3686spa
dc.identifier.issn1075-2765spa
dc.identifier.urihttps://repositorio.udes.edu.co/handle/001/3689spa
dc.description11 p.spa
dc.description.abstractThe prevalence of cardiovascular diseases (CVD) and diabetes mellitus type 2 (DM 2) is decreasing in developed countries despite the increase in the percentage of subjects with obesity and other wellrecognized cardiovascular risk factors. In contrast, the recent transition of the economic model experienced by developing countries, characterized by the adoption of a Western lifestyle, that we have named ‘‘socioeconomic pathology,’’ has led to an increase in the burden of CVD. It has been demonstrated that conventional cardiovascular risk factors in developed and developing countries are the same. Why then does the population of developing countries currently have a higher incidence of CVD than that of developed countries if they share the same risk factors? We have proposed the existence of a higher susceptibility to the development of systemic inflammation at low levels of abdominal obesity in the population of developing countries and the consequent endothelial dysfunction, insulin resistance, DM 2, and CVD. In contrast, an important percentage of obese people living in developed countries have a healthy phenotype and low risk of developing CVD and DM 2. Human epidemiologic studies and experimental dietary interventions in animal models have provided considerable evidence to suggest that nutritional imbalance and metabolic disturbances early in life may later have a persistent effect on an adult’s health that may even be transmitted to the next generations. Epigenetic changes dependent on nutrition could be key in this evolutionary health behavior, acting as a buffering system, permitting the adaptation to environmental conditions by silencing or increasing the expression of certain genes.eng
dc.format.mimetypeapplication/pdfspa
dc.language.isoengspa
dc.relation.ispartofAmerican Journal of Therapeuticseng
dc.relation.ispartofseriesAmerican Journal of Therapeutics;Vol. 15 (4), pp. 362-372. 2008eng
dc.rightsDerechos Reservados - American Journal of Therapeutics, 2008spa
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/spa
dc.sourcehttps://journals.lww.com/americantherapeutics/fulltext/2008/07000/Are_Nutrition_Induced_Epigenetic_Changes_the_Link.14.aspx#pdf-linkeng
dc.titleAre nutrition-induced epigenetic changes the link between socioeconomic pathology and cardiovascular diseases?eng
dc.typeArtículo de revistaspa
dc.identifier.doi10.1097/MJT.0b013e318164bf9cspa
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessspa
dc.rights.creativecommonsAtribución-NoComercial 4.0 Internacional (CC BY-NC 4.0)spa
dc.subject.proposalObesityeng
dc.subject.proposalMetabolic syndromeeng
dc.subject.proposalEpigeneticeng
dc.subject.proposalAdaptive responseeng
dc.subject.proposalSocioeconomic pathologyeng
dc.type.coarhttp://purl.org/coar/resource_type/c_6501spa
dc.type.driverinfo:eu-repo/semantics/articlespa
dc.type.versioninfo:eu-repo/semantics/draftspa
dc.type.contentTextspa
dc.type.redcolhttp://purl.org/redcol/resource_type/ARTspa
oaire.accessrightshttp://purl.org/coar/access_right/c_abf2spa
oaire.versionhttp://purl.org/coar/version/c_b1a7d7d4d402bccespa
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