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- Publisher Website: 10.1016/j.mehy.2005.05.017
- Scopus: eid_2-s2.0-22544482651
- PMID: 16006051
- WOS: WOS:000231654200001
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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
Title | 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 |
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Authors | |
Issue Date | 2005 |
Publisher | Churchill 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/78156 |
ISSN | 2023 Impact Factor: 2.1 2023 SCImago Journal Rankings: 0.587 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Mak, W | en_HK |
dc.contributor.author | Cheng, TS | en_HK |
dc.contributor.author | Chan, KH | en_HK |
dc.contributor.author | Cheung, RTF | en_HK |
dc.contributor.author | Ho, SL | en_HK |
dc.date.accessioned | 2010-09-06T07:39:47Z | - |
dc.date.available | 2010-09-06T07:39:47Z | - |
dc.date.issued | 2005 | en_HK |
dc.identifier.citation | Medical Hypotheses, 2005, v. 65 n. 4, p. 637-648 | en_HK |
dc.identifier.issn | 0306-9877 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/78156 | - |
dc.description.abstract | The 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.language | eng | en_HK |
dc.publisher | Churchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/mehy | en_HK |
dc.relation.ispartof | Medical Hypotheses | en_HK |
dc.subject.mesh | Antioxidants - metabolism | en_HK |
dc.subject.mesh | Biological Evolution | en_HK |
dc.subject.mesh | Cerebral Arteries - metabolism | en_HK |
dc.subject.mesh | European Continental Ancestry Group - genetics | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Intracranial Arteriosclerosis - genetics | en_HK |
dc.subject.mesh | Life Style | en_HK |
dc.subject.mesh | Risk Factors | en_HK |
dc.title | 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 | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+arteries | en_HK |
dc.identifier.email | Cheung, RTF:rtcheung@hku.hk | en_HK |
dc.identifier.email | Ho, SL:slho@hku.hk | en_HK |
dc.identifier.authority | Cheung, RTF=rp00434 | en_HK |
dc.identifier.authority | Ho, SL=rp00240 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.mehy.2005.05.017 | en_HK |
dc.identifier.pmid | 16006051 | - |
dc.identifier.scopus | eid_2-s2.0-22544482651 | en_HK |
dc.identifier.hkuros | 99225 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-22544482651&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 65 | en_HK |
dc.identifier.issue | 4 | en_HK |
dc.identifier.spage | 637 | en_HK |
dc.identifier.epage | 648 | en_HK |
dc.identifier.isi | WOS:000231654200001 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Mak, W=22948344000 | en_HK |
dc.identifier.scopusauthorid | Cheng, TS=7404082613 | en_HK |
dc.identifier.scopusauthorid | Chan, KH=7406034963 | en_HK |
dc.identifier.scopusauthorid | Cheung, RTF=7202397498 | en_HK |
dc.identifier.scopusauthorid | Ho, SL=25959633500 | en_HK |
dc.identifier.issnl | 0306-9877 | - |