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Article: A possible explanation for the racial difference in distribution of large-arterial cerebrovascular disease: Ancestral European settlers evolved genetic resistance to atherosclerosis, but confined to the intracranial arteries

TitleA possible explanation for the racial difference in distribution of large-arterial cerebrovascular disease: Ancestral European settlers evolved genetic resistance to atherosclerosis, but confined to the intracranial arteries
Authors
Issue Date2005
PublisherChurchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/mehy
Citation
Medical Hypotheses, 2005, v. 65 n. 4, p. 637-648 How to Cite?
AbstractThe pattern of cerebral atherosclerosis is not the same among different races. White patients rarely have intracranial large arterial steno-occlusive disease even if their systemic arteries are extensively involved, while non-white patients frequently have their intracranial arteries affected. We postulate that during human population diversification, those who settled in Europe had acquired a stroke-suppressor genotype that increases their resistance against atherogenesis, but with protection confined to the intracranial large arteries. The contemporary affluent lifestyle accelerates the development of atherosclerosis. In the whites, it involves the whole arterial bed except the intracranial vessels. People living in non-Western countries used to have a healthier way of living. They did not develop significant atherosclerotic diseases until recently when a westernised lifestyle was adopted. Unlike the whites, their intracranial arteries will not be spared. Atherosclerosis has become a major cause of premature mortality in the modern world, and an anti-atherogenic mechanism would confer a selection advantage. With further adaptive intensification, this protection may extend to the rest of the arterial bed. As a result, future Homo sapiens will be able to tolerate an affluent lifestyle without much adverse sequel such as premature vascular death. Alternatively, if the mediator of this anti-atherogenic mechanism can be identified and applied therapeutically, we will have an ultimate mean to prevent atherosclerosis. © 2005 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78156
ISSN
2015 Impact Factor: 1.136
2015 SCImago Journal Rankings: 0.464
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMak, Wen_HK
dc.contributor.authorCheng, TSen_HK
dc.contributor.authorChan, KHen_HK
dc.contributor.authorCheung, RTFen_HK
dc.contributor.authorHo, SLen_HK
dc.date.accessioned2010-09-06T07:39:47Z-
dc.date.available2010-09-06T07:39:47Z-
dc.date.issued2005en_HK
dc.identifier.citationMedical Hypotheses, 2005, v. 65 n. 4, p. 637-648en_HK
dc.identifier.issn0306-9877en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78156-
dc.description.abstractThe pattern of cerebral atherosclerosis is not the same among different races. White patients rarely have intracranial large arterial steno-occlusive disease even if their systemic arteries are extensively involved, while non-white patients frequently have their intracranial arteries affected. We postulate that during human population diversification, those who settled in Europe had acquired a stroke-suppressor genotype that increases their resistance against atherogenesis, but with protection confined to the intracranial large arteries. The contemporary affluent lifestyle accelerates the development of atherosclerosis. In the whites, it involves the whole arterial bed except the intracranial vessels. People living in non-Western countries used to have a healthier way of living. They did not develop significant atherosclerotic diseases until recently when a westernised lifestyle was adopted. Unlike the whites, their intracranial arteries will not be spared. Atherosclerosis has become a major cause of premature mortality in the modern world, and an anti-atherogenic mechanism would confer a selection advantage. With further adaptive intensification, this protection may extend to the rest of the arterial bed. As a result, future Homo sapiens will be able to tolerate an affluent lifestyle without much adverse sequel such as premature vascular death. Alternatively, if the mediator of this anti-atherogenic mechanism can be identified and applied therapeutically, we will have an ultimate mean to prevent atherosclerosis. © 2005 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherChurchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/mehyen_HK
dc.relation.ispartofMedical Hypothesesen_HK
dc.subject.meshAntioxidants - metabolismen_HK
dc.subject.meshBiological Evolutionen_HK
dc.subject.meshCerebral Arteries - metabolismen_HK
dc.subject.meshEuropean Continental Ancestry Group - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntracranial Arteriosclerosis - geneticsen_HK
dc.subject.meshLife Styleen_HK
dc.subject.meshRisk Factorsen_HK
dc.titleA possible explanation for the racial difference in distribution of large-arterial cerebrovascular disease: Ancestral European settlers evolved genetic resistance to atherosclerosis, but confined to the intracranial arteriesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0306-9877&volume=65&issue=4&spage=637&epage=648&date=2005&atitle=A+possible+explanation+for+the+racial+difference+in+distribution+of+large-arterial+cerebrovascular+disease:+Ancestral+European+settlers+evolved+genetic+resistance+to+atherosclerosis,+but+confined+to+the+intracranial+arteriesen_HK
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_HK
dc.identifier.emailHo, SL:slho@hku.hken_HK
dc.identifier.authorityCheung, RTF=rp00434en_HK
dc.identifier.authorityHo, SL=rp00240en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.mehy.2005.05.017en_HK
dc.identifier.pmid16006051-
dc.identifier.scopuseid_2-s2.0-22544482651en_HK
dc.identifier.hkuros99225en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-22544482651&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume65en_HK
dc.identifier.issue4en_HK
dc.identifier.spage637en_HK
dc.identifier.epage648en_HK
dc.identifier.isiWOS:000231654200001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridMak, W=22948344000en_HK
dc.identifier.scopusauthoridCheng, TS=7404082613en_HK
dc.identifier.scopusauthoridChan, KH=7406034963en_HK
dc.identifier.scopusauthoridCheung, RTF=7202397498en_HK
dc.identifier.scopusauthoridHo, SL=25959633500en_HK

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