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Has Statin Therapy Been Oversold?
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2015
Stephen T. Sinatra, Jonny Bowden
In Chapter 1, we discussed what we have colloquially referred to as “The Great Cholesterol Myth,” defined as a belief system based on a collection of deeply intertwined hypotheses about cholesterol, saturated fat, heart disease, and treatment. The origins of this belief system can be found in the “Lipid Hypothesis,” which holds that high cholesterol in the blood leads to heart disease, and the “Diet-Heart Hypothesis,” which further postulates that saturated fat in the diet is the major cause of elevated serum cholesterol and, therefore, by definition, a causal actor in the development of heart disease. Accepting these notions about fat and cholesterol invariably leads to two conclusions: (1) saturated fat has little place in a healthy diet and (2) high cholesterol needs to be treated.
Inflammasomes: a preclinical assessment of targeting in atherosclerosis
Published in Expert Opinion on Therapeutic Targets, 2020
Jeremiah Stitham, Astrid Rodriguez-Velez, Xiangyu Zhang, Se-Jin Jeong, Babak Razani
As we have come to recognize, chronic inflammation and immune dysfunction play different, yet likely integral roles in atherogenesis and cardiovascular disease. Chronic inflammatory and autoimmune disease (e.g. rheumatoid arthritis) carries cardiovascular risk independent of traditional risk factors, such as hyperlipidemia. Thus, the former ‘lipid hypothesis’ and ‘inflammatory hypothesis’ are now best taken together. Successful therapeutic targeting of atherosclerosis will most likely be found at the nexus of aberrant lipid metabolism and inflammation. Identification of pathways and molecular mediators common to both processes is likely to achieve highest efficacy. For instance, aberrant cholesterol handling underlies the development of cholesterol crystals which are pathognomonic of atherosclerotic plaques. Cholesterol crystals are also one of the most important triggers of the NLRP3 inflammasome in atherosclerosis. Selective targeting of this cholesterol/inflammasome nexus brings specificity to an anti-inflammatory therapy that is inherently nonselective.
LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature
Published in Expert Review of Clinical Pharmacology, 2018
Uffe Ravnskov, Michel de Lorgeril, David M Diamond, Rokuro Hama, Tomohito Hamazaki, Björn Hammarskjöld, Niamh Hynes, Malcolm Kendrick, Peter H Langsjoen, Luca Mascitelli, Kilmer S McCully, Harumi Okuyama, Paul J Rosch, Tore Schersten, Sherif Sultan, Ralf Sundberg
The lipid hypothesis has been perpetuated by the authors who have ignored the results from trials with a negative outcome, who have misused statistics, and who have ignored all contradictions documented by independent researchers. The increased risk of CVD in people with FH has been a primary argument in support of the lipid hypothesis. Surprisingly, several studies of untreated people with FH have shown that LDL-C does not differ significantly between those with and without CVD [95–100] and that elderly people with FH live just as long as elderly people from the general population despite their high LDL-C [93,94]. FH individuals with significant CVD may have inherited other, more important risk factors than a high LDL-C.