Metabolic Health

Okay, I've been happily ignoring your little idee fixee on LDL aside from one gentle comment but I feel the need to comment here again.

This article is utterly disingenuous and sets up a complete strawman to knock down. It sets out to disprove a notion of cholesterol that was last current decades ago. Right in the first paragraph and throughout the article LDL is referred to as “the” major cause of atherosclerosis which to my knowledge even the Framingham authors wouldn't have been comfortable with, it is however a significant contributing factor.

It is well known that some people with elevated LDL or total cholesterol are at low risk(this is the reason for weak or negative results in whole population studies), atherosclerosis is a complex disease with multifactorial causes, no practising doctor I know thinks it is “the” major cause, or even the most important contributing factor.

That being said it is thoroughly established that statin use in select patients reduces the risk of MI and CVA, especially in those with established atherosclerosis, but also those with other substantial risk factors (high BP, family history, smoking, diabetes etc.). This is totally uncontroversial and the pathogenic mechanisms, while complex, are increasingly well understood.

I have been a doctor for over a decade and I consider myself diligent in keeping up with research, and although the selection of patients for statin therapy is an ongoing and regularly changing area of research on which experts can disagree, the fact that select patients will have substantially lower risk of coronary events due to statin therapy is uncontroversial.

Here is an article written by people who payed attention in stats class and have bothered to make their case with evidence rather than knocking down strawmen

Efficacy and safety of long-term treatment with statins for coronary heart disease: A Bayesian network meta-analysis (2016)

Or for a more succinct and easy to read summary here is the Cochrane conclusion

"Of 1000 people treated with a statin for five years, 18 would avoid a major CVD event which compares well with other treatments used for preventing cardiovascular disease."

Statins for the primary prevention of cardiovascular disease

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TLDR: Academic fraud pushing an agenda, unpublished results, and the immense lack of papers since the new trial protocols were required (i.e. must register, must publish, can't ignore bad results)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