Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (6)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Ravnskov, U.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ravnskov, U.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Q J Med 2003; 96: 927-934
© Association of Physicians 2003; all rights reserved.

Commentary

High cholesterol may protect against infections and atherosclerosis

U. Ravnskov

Independent researcher

The first 150 words of the full text of this article appear below.


   Introduction
 
Many researchers have suggested that the blood lipids play a key role in the immune defence system.1–21 There is also a growing understanding that an inflammatory response of the arterial intima to injury is a crucial step in the genesis of atherosclerosis. and that infections may be one type of such injury.22 These two concepts are difficult to harmonize with the low-density-lipoprotein (LDL) receptor hypothesis, according to which high LDL cholesterol is the most important cause of atherosclerosis. However, the many observations that conflict with the LDL receptor hypothesis, may be explained by the idea that high serum cholesterol and/or high LDL is protective against infection and atherosclerosis.


   Laboratory evidence
 
Lipopolysaccharide, or endotoxin, the main pathogenic factor of Gram-negative bacteria, binds rapidly to lipoproteins,6 mainly LDL,7 and lipoprotein-bound endotoxin is unable to activate the secretion of various cytokines by monocytes in vitro.6,7,10 Also, Staphylococcus aureus {alpha}-toxin, a toxin produced by most . . . [Full Text of this Article]


   Epidemiological and clinical evidence
 

   Immunoprotective effects of high cholesterol explain observations contradicting the LDL-receptor hypothesis
 

   Contradictions to the hypothesis
 

   Conclusions
 

Address correspondence to Dr U. Ravnskov, Magle Stora Kyrkogata 9, S-22350, Sweden. e-mail: ravnskov@tele2.se


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Infect. Immun.Home page
R. Han, H. Kornfeld, and G. Martens
Is Hypercholesterolemia a Friend or a Foe of Tuberculosis?
Infect. Immun., August 1, 2009; 77(8): 3514 - 3515.
[Full Text] [PDF]

Home page
 ANN INTERN MEDHome page
U. Ravnskov
Lack of Evidence for Recommended Low-Density Lipoprotein Cholesterol Treatment Targets
Ann Intern Med, April 17, 2007; 146(8): 614 - 614.
[Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
M. B Katan
Reply to U Ravnskov
Am. J. Clinical Nutrition, December 1, 2006; 84(6): 1551 - 1552.
[Full Text] [PDF]

Home page
 JAMAHome page
U. Ravnskov
Inflammation, Cholesterol Levels, and Risk of Mortality Among Patients Receiving Dialysis
JAMA, April 21, 2004; 291(15): 1833 - 1834.
[Full Text] [PDF]