Introduction: For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.

Areas covered: The authors of three large reviews recently published by statin advocates have attempted to validate the current dogma. This article delineates the serious errors in these three reviews as well as other obvious falsifications of the cholesterol hypothesis.

Expert commentary: Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality and that the conclusions of the authors of the three reviews are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations.

Full Paper: https://doi.org/10.1080/17512433.2018.1519391

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  • jetOPMAEnglish
    2·
    4 months ago

    This is a very easy to read paper, I highly recommend skimming it at least.

    TLDR: Academic fraud pushing an agenda, unpublished results, and the immense lack of papers since the new trial protocols were required (i.e. must register, must publish, can’t ignore bad results)

    Consistent with that finding is the observation that healthy individuals with low LDL-C have a significantly increased risk of both infectious diseases [23] and cancer [24]; the latter possibly because microorganisms have been linked to almost 20% of all cancer types [25]

    ‘Power, linkage disequilibrium, pleiotropy, canalization and population stratification have all been recognized as potential flaws in the Mendelian randomization approach’

    Using RRR (relative risk reduction) as a measure of benefit is also highly misleading [34], as it inflates the appearance of the rate of event reduction. For instance, in a trial where 2 of 100 participants in the control group die but only 1 of 100 in the treatment group die, the absolute risk reduction (ARR) is only a 1% benefit. However, if one reports the RRR, then a 50% benefit can be reported, because one is 50% of two.

    the authors have only included data from 12 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

    exposing academic fraud and data manipulation

    as calculated recently by Kristensen et al., statin treatment does not prolong lifespan by more than an average of a few days [71].

    Taking a medicine for life to pull down a ldl metric that causes many issues (t2d, insulin resistance)… for a few extra days of life?.. this is why they never report absolute risk reduction

    In 2004–2005, health authorities in Europe and the United States introduced New Clinical Trial Regulations, which specified that all trial data had to be made public. Since 2005, claims of benefit from statin trials have virtually disappeared [72], see Figures 4 and 5

    As most energy is produced in the muscle cells, including those of the heart, the extensive use of statin treatment may explain the epidemics of heart failure that have been observed in many countries [75]

    Shouldn’t this show up in all cause mortality data? or this effect is beyond the study length?

    case–control and cross-sectional studies have shown that statin use is observed significantly more often among patients with cataracts [76], hearing loss [77], suicidal ideation [78], peripheral neuropathy [79], depression [80], Parkinson’s disease [81], interstitial cystitis [82], herpes zoster [83], impotency [84], cognitive impairments [85–88], and diabetes [89,90]. In some of these studies, the side effects disappeared with discontinuation of the statins and worsened with rechallenge

    case–control studies in which the incidence of cancer in statin-treated patients was lower than in controls are invalid because many untreated individuals have low cholesterol, and those on statins have lived most of their lives with high cholesterol that may have provided protection from developing cancer.

    That is interesting, high LDL is protective against cancer, if you only treat people with high LDL you can show a benefit from cancer compared to a general population…

    Key issues

    • ● 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

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