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Recent paper by Uffe Ravnskov (et al.) - the father of cholesterol "red-pilling"!
"LDL-C Does Not Cause Cardiovascular Disease: a comprehensive review of current literature",
Uffe Ravnskov et al., Taylor & Francis Online, 10 Sep 2018
Key issues (quoted):
- The hypothesis that high TC or LDL-C causes atherosclerosis and CVD has been shown to be false by numerous observations and experiments.
- The fact that high LDL-C is beneficial in terms of overall lifespan has been ignored by researchers who support the lipid hypothesis.
- The assertion that statin treatment is beneficial has been kept alive by individuals who have ignored the results from trials with negative outcomes and by using deceptive statistics.
- That statin treatment has many serious side effects has been minimized by individuals who have used a misleading trial design and have ignored reports from independent researchers.
- That high LDL-C is the cause of CVD in FH is questionable because LDL-C does not differ between untreated FH individuals with and without CVD.
- Millions of people all over the world, including many with no history of heart disease, are taking statins, and PCSK-9 inhibitors to lower LDL-C further are now being promoted, despite unproven benefits and serious side effects.
- We suggest that clinicians should abandon the use of statins and PCSK-9 inhibitors, and instead identify and target the actual causes of CVD.
More Quotes (chapter headlines):
2.1 No association between TC and degree of atherosclerosis
2.2 No exposure-response
3.1 An idea supported by fraudulent reviews of the literature
4. Does high LDL-C cause atherosclerosis? 4.1 An idea based on selected patient groups
5.1 LDL-C of patients with acute myocardial infarction is lower than normal
5.2 Elderly people with high LDL-C live the longest
6.1 No exposure-response in the statin trials
6.2 The benefit of statin treatment is exaggerated
6.3 The benefit from statin treatment has been questioned
6.4 Adverse effects from statin treatment
6.5 Does treatment with PCSK-9 inhibitors improve the outcome?
A new cholesterol-lowering drug has recently been introduced. It is an antibody that inhibits proprotein convertase subtilisin–kexin type 9 (PCSK9), which lowers LDL-C by approximately 60%. In FOURIER, the largest and longest PCSK-9 inhibitor trial, Evolocumab was compared with placebo in more than 27,000 statin-treated patients with CVD [92]. The trial was stopped after 2.2 years because the number of MVE was reduced with statistical significance (9.8% vs. 11.3%). However, both CVD mortality and total mortality had increased, although not with statistical significance. A relevant question is therefore, why the trial, the sponsor of which (Amgen) was responsible for data collection, was ended after only 2.2 years. Furthermore, this trial is yet another proof that there is no exposure-response between LDL-C and total or CVD mortality.
7. Does FH prove that high LDL-C causes CVD?
7.1 A low percent of FH [Familial Hypercholesterolemia] individuals die prematurely
7.2 No LDL-C difference between FH individuals with and without CVD
8. Has CVD mortality decreased after the introduction of statin treatment? ...
American National Health and Nutrition Examination Survey [103] found that during the period 1999-2006 the number of AMI and strokes increased from 3.4 to 3.7%, and from 2.0 to 2.9%, respectively. During the same period mean LDL-C level decreased from 126.1 to 114.8 mg/dL, and the self-reported use of lipid-lowering drugs increased from 8 to 13.4%. Furthermore, statin utilization in 12 European countries between 2000 and 2012 was not associated with reduced CHD mortality or its rate of change over the years [104].
9. Conclusion
The idea that high cholesterol levels in the blood are the main cause of CVD is impossible because people with low levels become just as atherosclerotic as people with high levels and their risk of suffering from CVD is the same or higher. The cholesterol hypothesis has been kept alive for decades by reviewers who have used misleading statistics, excluded the results from unsuccessful trials and ignored numerous contradictory observations.
Quoting the captions for the figures!
Figure 2. The association between degree of LDL-C lowering and the absolute risk reduction of total mortality (per cent per year) in 26 statin trials, where total mortality was recorded and which were included in the study by Silverman et al. and in 11 ignored trials. ARR is weakly associated with degree of LDL-C lowering in the included trials (y = 0.28x + 0.06), but inversely associated in the excluded trials (y = - 0.49x - 0.81). Symbols: see figure 1.
According to Ference et al. [3] the most compelling clinical evidence for causality is provided by “the presence of more than 30 randomized cholesterol-lowering trials that consistently demonstrate that reducing LDL-C reduces the risk of CVD events proportional to the absolute reduction in LDL-C.” As previously noted, this is not true exposure-response. Furthermore, in their figure 5A, that illustrates the association, the authors have only included data from12 of the 30 trials they refer to. If all of the trials in table 1 are included, as we have done in figure 3, there is no association between LDL-C lowering and coronary event rate.
Figure 5. The association between the absolute risk reduction of total mortality in 26 statin trials included in the study by Silverman et al. and in 11 ignored trials; and the year where the trial protocols were published. The vertical line indicates the year where the new trial regulations were introduced. [penalizing publication of false results - the new trials show no risk reduction! commented by S.B.]
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added 5/10/2018
QJM. 2018 May 1;111(5):319-325. doi: 10.1093/qjmed/hcy043.
A longitudinal 20 years of follow up showed a decrease in the survival of heart failure patients who maintained low LDL cholesterol levels.
Charach G1
