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The AHA’s cholesterol guideline cites a large review of trials from 2012 as the principal evidence for treating cholesterol in healthy people.

The following table is from that review, webfigure 9, in the supplement. It’s okay for your eyes to glaze over, I’ll summarize the important parts.

People in statin trials were assessed for their 5-year risk of having a heart problem. The table, which shows deaths in statin and placebo groups, divides people by this risk. The first two rows are the lowest risk, at <5% and 5-10%.

Note the ‘box-and-whisker’ in these first two rows. It crosses the solid vertical line. Meaning, no detectable difference in deaths between statin and placebo.

The last column shows relative risks and confidence intervals that include 1. Confirmed: Statins and placebo were the same.

We can therefore make the following statement, and it is undisputed: For people at <10% risk, there was no survival benefit.

For higher risk people mortality benefits accrued over time to 2% or more. At the highest risk levels, therefore, about 1 in 50 people who took statins lived longer.

Now check yourself.

Plug in your numbers for ‘ASCVD’ risk on the AHA calculator website. If you are less than 20% (in 10 years) then the first two rows are the most relevant to you.

Case closed.

Most people who take statins are in the first two rows. Rows 3 to 5 are mostly for people with known vascular disease, in which case reducing cholesterol is reasonable and uncontroversial.

For everyone else, however, statins did not prolong life. Yet that is precisely the benefit people are led to believe they are getting from their daily statin drugs.

Incidentally, the authors of the 2012 review claimed that the benefits of statins for the lowest risk groups “greatly exceed any known hazards.”

Huh. What benefits, and what hazards?

Certainly not mortality, which they refuse to acknowledge, saying: “There were too few deaths in the lower risk participants to allow reliable direct assessment of the effects of statin therapy.”

Did they see their own data?

The numbers (53K low risk people, 1,800+ deaths) are unprecedented and allowed them to potentially detect a mortality benefit as small as 1 in every 250 people. They didn’t.

So if not mortality, what benefits DO they mean?

The 2012 review headlined a custom-made composite, “major vascular events.” This was a combination of strokes, nonfatal MIs, ‘coronary deaths’, and revascularization procedures. A combo for which the authors report a 1.1% overall benefit in low risk people. Or, as they say it, 11 people per 1,000.

Let us break that benefit into its parts. (Then we’ll talk hazards). Using the trial figures, the 11 events break down roughly as follows.

About 30-35% of it is ‘revascularizations’, 30-35% is nonfatal MI, 15% is coronary deaths, and 20% is nonfatal stroke.

On revascularizations, we now know procedures like stents for stable disease don’t save lives or prevent heart attacks or strokes. Cardiologists did not know this when designing the statin trials, so we can politely recognize the error and remove it from the calculation.

On ‘nonfatal MI’, see part 2. In short, nonfatal MI in trials is not a condition that represents, or is even associated with, death or disability. It is a false surrogate, a historical bait-and-switch that used to be critically important (when it was defined differently), and now mostly constitutes a lab test derangement.

The next part, at about 15%, is ‘coronary deaths’. But deaths are not prevented in this risk group—see table above. ‘Coronary deaths’ is therefore a red herring. Death re-labeled, then placed under a shell, then moved. It is a ghost in the data that disappears when using the patient-centered version—all-cause mortality.

Finally, let us accept nonfatal stroke as a benefit, at about 2-3 strokes per 1000, or about 1 in every 300 people.

Now let’s compare this to statin harms. And for readers who are sad because we removed nonfatal MI, let’s toss them back in, at 3 per 1000.

It turns out the CTT group, responsible for the most pro-statin paper in history, also had the data on statin-induced diabetes. In 2024, twelve years after their review that put statins in the mouths of millions, they showed it to us. Whereupon we learned that the lowest dose of statins cause diabetes in 6 per 1000 people. At higher doses it’s 60 (or 1 in every 17 people taking a statin).

Even at the lowest statin dose this harm eclipses the stroke and MI benefit.

Moreover, the one randomized trial of statin muscle effects found that 5% experienced statin-induced chronic muscle pains. That is 48 per 1000. Add this to the 6 diabetes cases and we have now eclipsed the stroke and nonfatal MI benefit by ten times over.

One might say that the hazards of statins greatly exceed any known benefits.

There is an old adage in medicine: Doctors are trained to seek pathology and diagnose disease. But patients just want to feel better and live longer.

In cholesterol management, that tension is the problem. We began by trying to prevent death. We ended by counting events most people would never have known occurred.

The result is an approach to cholesterol that serves the system—but not the patient.

That is the Big Mistake.

Next week, in part 4 we’ll talk about how this all happened, and what was lost in translation.



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