The Explanation for Why Statins Do Not Lead to Fewer Cardiovascular Events

Executive Summary

• Statins are ineffective at improving any health outcomes.
• This article covers how this is the case for a widely prescribed drug.

Introduction

Statins are presented as improving health; however, while they reduce cholesterol, they do not impact health outcomes.

The Problem With the Conventional Cholesterol and Statin Argument

The logic for prescribing statins makes absolutely no sense. This is explained in the following quotation from the book Metabolica.

Cholesterol (and more specifically LDL-C) emerged as a risk factor from the Framingham Heart Study, an observational study in Massachusetts that started after World War II and continues today. The takeaway was that if you had very high LDL-C you were more likely to suffer a heart attack.

But when the data were analyzed, unless LDL-C was very high (over 200), it wasn’t a risk factor. In fact, patients with really high LDL-C levels often have a genetic disorder (I’m one of the lucky carriers).

LDL-C Is Primarily Genetically Determined — Not Related to Diet

Your LDL-C level is for the most part genetically determined.

Conversely, those with LDL-C levels less than 70 develop relatively little heart disease.

LDL-C Is Not an Indicator of Heart Attack Risk

Yes, there seems to be a genetic protection at the low end, and risk at the high end. But for the rest of the population, LDL-C is not a great predictor of who will suffer a heart attack. It’s true that the HR ratio (hazard risk ratio; a measure of difference in risk versus the general population) of LDL-C is 1.3, which means that if your LDL-C is high, you have a 30 percent increase in risk for a heart attack. But correlation doesn’t mean causation.

And there is another problem, which is that while a high LDL-C level increases risk — it is still primarily genetic. As we will see, while it’s easy to get drugs to reduce LDL-C, that does not correlate to reduced heart attack risk, making those drugs, or statins, useless for heart attack and giving highly adverse side effects for cellular metabolism.

A Confounding Aspect of LDL-C

For example, if LDL-C is truly the bad boy of heart disease, as the Medical Establishment says, then why, when you remove younger people from the analysis and just look at older people (greater than sixty years), do high LDL-C levels correlate with longevity?

That is a significant problem because most heart attacks occur after 60; most occur after 70. 80% of heart disease deaths occur after 70, and heart disease deaths before 70 are rare.

Maybe, once you factor out the people with genetic reasons for high LDL-C (like those with genetic disorders), then LDL-C isn’t really so bad. Or maybe we’re measuring the wrong biomarker. Let’s say you go see your provider, who tells you that you have high LDL-C. Nine times out of ten you’re going to walk out of that office with a prescription for a statin, which inhibits cholesterol synthesis.

Again, it inhibits the body from doing what it thinks it should do regarding cholesterol synthesis and replacing it with what the pharmaceutical companies believe the correct cholesterol level should be.

The current mindset among clinicians is to downshift everyone’s LDL-C through low-fat diet and drugs.

What Are the Actual Benefits of Statins?

The only benefit to statins is that they reduce cholesterol or LDL-C, which is only helpful if you look at the data incorrectly. So, there are no benefits to statins because the side effects must be included in the analysis, so the net benefit of statins is negative.

This is explained additionally in the following quotation.

Despite governmental recommendations to eat low-fat and despite a high prescription rate of statins, at a population level LDL-C levels haven’t change appreciably. It isn’t just the pill that’s the problem. The recommendation of a low-fat diet is just as bad. But the real story is that more people are suffering heart attacks with lower LDL-Cs than before, because the standard fasting lipid profile—the blood test ordered by your practitioner to test your cholesterol—assumes that all LDL particles are the same. There are two different LDLs, but the lipid profile test measures them together. The majority (80 percent) of circulating LDL species are called large buoyant or type A LDL, which are increased by dietary fat consumption.

This is the species reduced by eating low-fat or by taking statins. However, large buoyant LDL is cardiovascularly neutral—meaning it’s not the particle driving the accumulation of plaque in the arteries leading to heart disease.

So, to sum up, statins reduce the wrong type of LDL, the LDL-C.

How Medicine Focused on the Wrong LDL and Introducing LDL B

Then there’s a second, less common (only 20 percent) LDL species called small dense or type B LDL. There is some debate as to whether or not it’s the actual perpetrator of the plaque, but it doesn’t matter; small dense LDL is predictive of risk for a heart attack. The problem is that statins will lower your LDL-C because they’re lowering the type A LDL, which is 80 percent of the total; but they’re not doing anything to the type B LDL, which is the problematic particle. Over the years, medical guidelines have continually expanded the number of individuals for whom statin therapy is recommended.

But again, this information will never impact the prescriptions for statins because the US medical system focuses on making revenues for pharma and health service providers.

This is why the term “evidence-based medicine” is precisely what medicine does not do.

Lowering LDL-C Without Impacting Adverse Heart Events?

Without a doubt they lower LDL-C. No argument, if the goal is reducing LDL-C, statins are a simple way to do it. And if you have a genetic disorder, they’re a necessary way to do it. But do they reduce the risk of heart attack across the board? Without a doubt they don’t!

This gets back to the primary point. Statins reduce the value of an item, in this case, LDL-C, but it is not at all relevant to health. This is increasingly common among pharma companies, where they market against the item controlled without any other concern.

The absolute numbers themselves mean very little, and total cholesterol means less than nothing. In fact, it’s actually detrimental—and the FDA knows it, which is why they’ve removed dietary cholesterol from the Nutrition Facts label.

The FDA knows it and has removed the dietary cholesterol from the Nutrition Facts label — however, they have not recalled all of the statins that were approved based on faulty studies.

The LDL particle number (LDL-P), rather than the LDL cholesterol level (LDL-C), is what we care about, because it factors out the dilution of the large buoyant LDLs that aren’t important. But LDL-P is still considered a research test and done in only a few specialized labs around the country.

The Importance of HDL

The second thing to look at is the HDL. If it’s over 60, it almost doesn’t matter what the other fractions are, as this is a sign of good cardiovascular health. If the HDL is under 40 (men) or under 50 (women), then your predisposition for heart disease is much higher.

About Small Dense LDL

Almost assuredly, statins are reducing the large buoyant LDL but not doing anything about the small dense LDL—therefore the risk of a first heart attack remains unchanged. Conversely, up to 20 percent of statin users demonstrate some form of side effect, often quite serious.

Yes, this is standard — statins are not beneficial to health but have side effects, and that means statins are not worth the side effects. One side effect is interfering with cellular metabolism within the mitochondria; therefore, statins promote metabolic disease.

This is explained in the following quotation from the article Highlighting The Substantial Body Of Evidence Confirming The Importance Of Vitamin K₂ As A Cardio-Support Nutrient, And How The Right K₂ Makes All The Difference.

Statins are a common recommendation for lowering LDL-C levels (cholesterol), and their use has been on the rise over the last few decades. However, a 2015 paper stated statins may act as “mitochondrial toxins” with negative effects on the heart and blood vessels via the depletion of coenzyme Q₁₀ (CoQ₁₀) and by inhibiting Vitamin K₂ synthesis.

But that is only one of many side effects, which I also cover in the article The Side Effects fo Statins Like Lipitor. Anything that reduces mitochondrial metabolism will naturally lead to the issues listed in the following quotation.

Increasing Glucose Intolerance, Diabetes, and Weight Gain

There’s now a burgeoning literature that statins increase glucose intolerance and risk for both diabetes and weight gain.

Is it that, by acting on the liver, statins worsen insulin resistance? Or could it be the inverse—that statin use makes people think they can eat whatever they want because they are now impervious to any cardiovascular risk? It could be both.

And it does not matter which is which — at least practically, as statins are a promoter of mitochondrial dysfunction.

The Evidence-Free Push to Sell Statins

This quote is from the article What Can Statins Teach Us About The COVID-19 Vaccines?

For decades, researchers have looked for ways to lower cholesterol levels reliably. Once statins (the first drugs which could reliably do this) were discovered, the cholesterol hypothesis took off, and reasons were created to create more and more urgency for lowering cholesterol levels.

This has gone to the point prominent doctors have called for statins to be added to the water supply, a degree of fanaticism not that different from what we saw from many of the advocates for mass COVID vaccination.

Similarly, since cholesterol is essential for life, many issues result from eliminating it. Nonetheless, statin sales are now over 15 billions dollars a year, and hundreds of millions of people have been placed on them.

Before COVID vaccines, I considered statin medications to have one of the worst benefit-to-harm ratios of any drug on the market. I would argue this is because the statins played a pivotal role in creating the playbook that was reused throughout the pandemic. Similarly, many of those who dissented from the narrative could immediately recognize what was happening because they had already gone through it with previous pharmaceuticals (e.g., what was done with the SSRIs).

Pushed Onto Statins

Statins are pushed onto patients — as is explained in the following quotation.

In the case of statins, a relatively simple pattern has emerged. As time goes forward, “research” keeps appearing that suggests more people need to be placed on statins. The experts on the guideline panels then conclude that even more people need to be given statins, and clinical practice guidelines are published requiring this, which doctors are sanctioned for failing to follow (e.g., Medicare gives them less money).

Controlling Medicine Through Guidelines

As time has gone forward, a great deal of effort has been made to transform the practice of medicine from doctors independently utilizing their best judgment on how to treat patients to doctors following treatment algorithms that committees of experts create. This arrangement creates a creative way to skirt the law since these committees do not require a legislative process to be enacted. In turn, a few times, they have been sued for the absurd guidelines they put forward.

In each case (e.g., the recent one against the FDA for it preventing ivermectin from being used to treat COVID-19), those promoting the guidelines successfully argue their guidelines are only ‘suggestions’ and thus cannot be legally challenged. This is important to remember since, in one ruling against Lyme patient advocates, the federal judge specified that guidelines are voluntary (which means they cannot be treated as law). Nonetheless, once these “voluntary” guidelines are created (and hence cannot be challenged through any legal process), everyone treats them as law.

One of the best examples of this was shared by Dr. Malcolm Kendrick in chapter 7 of Doctoring Data:

The National Cholesterol Education Programme (NCEP) has been tasked by the NIH to develop [legally enforceable] guidelines for treating cholesterol levels. Excluding the chair (who was by law prohibited from having financial conflicts of interest), the other 8 members on average were on the payroll of 6 statin manufacturers. In 2004, NCEP reviewed 5 large statin trials and recommended: “Aggressive LDL lowering for high-risk patients [primary prevention] with lifestyle changes and statins.” [these recommendations in turn were adopted around the world]

In 2005 a Canadian division of the Cochrane Collaboration reviewed 5 large statin trials (3 were the same as NCEP’s, while the other 2 had also reached a positive conclusion for statin therapy). That assessment instead concluded: “Statins have not been shown to provide an overall health benefit in primary prevention trials.”

In addition to doctors being forced to follow these guidelines, patients often are too. Doctors often retaliate against patients who do not take statins (similar to how many unvaccinated patients were denied essential medical care during COVID-19). Employers sometimes require cholesterol numbers to meet a certain threshold for employment (although they never did anything on the scale of the COVID vaccine mandates placed on workers around America). Similarly, life insurance policies often penalize those with “unsafe” cholesterol numbers.

How The ACC / AHA Heart Disease Calculator (Statin Promoter) is Rigged by Pharmaceutical Companies

This is explained in the quote from the article 25 years of evidence based medicine part ii: what we can learn about ebm from the cholesterol / statin debate / debacle.

Based on advice from his panel of “experts” who were from the ACC / AHA, Mitchell suggested using a “calculator” to figure your own personal risk of developing cardiovascular disease.  Take a guess who invented the “Risk Calculator” (also known as the ACC / AHA Heart Calculator)? The name being a dead giveaway; it was invented two of the most corrupt organizations in all of medicine; the American Heart Association and the American College of Cardiology.

What did a May 2016 study (Accuracy of the Atherosclerotic Cardiovascular Risk Equation in a Large Contemporary, Multiethnic Real-World Population) say about the accuracy of this calculator? Only that it “substantially overestimated actual 5-year risk in adults without diabetes, overall and across sociodemographic subgroups.” Overestimation of risk means more statin prescriptions — way more statin prescriptions.

Buying Off Medical Journals to Not Publish Negative Statin Studies

Many academic experts have been bought off to produce studies arguing for more and more statin usage. Simultaneously, many medical journals have also been bought out and will only publish studies that favor the use of statins. This results in an overwhelming amount of evidence in favor of the drugs, despite their benefits being almost non-existent and their harms quite frequent.

Time For Eight Years Olds to be Prescribed Statins?

Even the American Academy of Pediatrics says that eight-year-olds with high LDL-C need to be treated with statin therapy.

This is similar to what many health authorities said about young children getting the covid vaccines, even though their risk from covid was unmeasurable. There is no logic; the medical authorities then pretend that this is “following the science” when they have been bought off.

Focusing on the Wrong Thing

Further, the main reason for high triglycerides has nothing to do with LDL-C; rather, it’s the refined carbohydrates and sugars in your diet. Again, the #1 risk factor for heart disease isn’t LDL-C; it’s the insulin resistance of metabolic syndrome, of which triglyceride is a much better biomarker than LDL-C.

However, the medical establishment was not interested in focusing on metabolic syndrome because that would have led to discussions of a diet of ultra-processed foods, which does not lead to maximizing revenues.

The Confusion on the Role of Cholesterol on Heart Disease

This quote is from the article What Causes Alzheimer’s Disease?

Cardiovascular disease, in most cases is due to damage to the arterial system, which often occurs as a result of lack of vitamin C (which humans and guinea pigs lost the gene to synthesize).

•This damage primarily consists of atherosclerotic plaques in those blood vessels.

•Although atherosclerotic plaques are believed to result from excessive cholesterol deposition on those blood vessels, there is a large body of scientific evidence that disproves cholesterol’s role in forming atherosclerotic plaques.

•Kendrick instead argues that these plaques are a result of successive blood clots forming at the site of a blood vessel injury, and the cholesterol found there is either from blood cells or the body using cholesterol to repair the damage because vitamin C is not available [vitamin C is also very important in the treatment of COVID-19 and to a lesser extent vaccine injuries including those from spike protein vaccines). Initially, this process is life-saving (otherwise you would inevitably bleed to death), but over time, it becomes maladaptive because successive healed blood clots interfere with the normal circulatory functions of the blood vessel.

That is the medical establishment jumped on a correlation — cholesterol deposited within plaques — and then assumed that these plaques were because of cholesterol. Hence the desire to reduce cholesterol. This entirely misunderstands atherosclerotic plaques.

How Lowered Cholesterol Became a False Surrogate Marker or Intermediate Endpoint for Cardiovascular Health

Surrogate markers are explained in the following quote rom the article Why Do Vaccines Consistently Fail?

The idea behind surrogate markers is that if it is known that something is “good” for you, such as lowering blood pressure, then it can be assumed that if a pharmaceutical is observed to create that “good” effect, it can also be assumed that the pharmaceutical will improve the health of the participants. This idea often does not hold up, and pharmaceuticals that are proven to improve a surrogate marker often end up having negative rather than a positive effects on recipients. For those interested in learning more about the problems with surrogate markers, Malcolm Kendrick has extensively detailed in Doctoring Data how surrogate markers ruin clinical research.

The reason for surrogate markers, or as I like to call them intermediate endpoints as I think this is more descriptive, is that the final endpoint does not improve with the surrogate marker/intermediate endpoint. I cover in the article How The Endpoint of the Covid Vaccine FDA Studies Was Rigged by Pharma Companies.

Other Examples of Optimizing Around Surrogate Markers

Pharmaceutical companies always prefer intermediate endpoints because they are so much easier and such a lower bar to meet. A major factor for why we have so many drugs that are ineffective against the final objective — is the allowance by drug regulators of intermediate endpoints.

Furthermore, with a focus on intermediate endpoints, the drug or vaccine can be made to only affect the endpoint — to the detriment of the final endpoint. 

This is explained in the following quotation.

For example, with the HPV vaccine, Merck discovered that it was quite difficult to produce sufficient antibodies there, so to solve the problem, they used a very strong adjuvant that also has a side effect of creating a variety of autoimmune conditions and has resulted in their vaccine being much more likely to harm than benefit the recipients.

Yes — the objective of creating antibodies — is put ahead of creating a safe vaccine. The negative affect on the patient is irrelvant to Merck as they only need to get FDA approval. A more ethical solution would be to create a vaccine that uses powerful adjuvants to get FDA approval — but then make sure the vaccine only includes a saline solution once the vaccine is put into general use. If everyone given a covid vaccine was given a saline solution, global health would be far better.

This same optimization around an intermediate endpoint to the detriment of the final endpoint and to safety was done with the covid vaccines.

The Covid vaccinations were designed to maximize the production of antibodies to the virus, and from what I have been able to piece together from reading the literature, antibodies to the spike proteins were found to be the easiest to produce which likely influenced spike protein producing vaccines being decided upon (more cynical parties will argue it was either due to their toxicity or tendency to produce variants requiring an endless stream of new boosters).

Unfortunately, there are many components to the immune system beyond antibodies to a specific antigen, and in many cases when production of a specific antibody is prioritized, the net result is impaired rather than improved immunity.

Rigging the Risk Reduction From Statins

The following quote is from the article 25 years of evidence based medicine part ii: what we can learn about ebm from the cholesterol / statin debate / debacle.

“For years, I’ve been an ardent critic of the Madison avenue message that we all desperately need to lower our serum cholesterol by taking cholesterol drugs (statins). First, we have observed that these drugs tend to hurt adult stem cells. Second, I’ve had to research them for my own use. In that research, I was appalled at the paltry benefits of the drugs versus the hyped benefits out of the Madison avenue pharma machine.

To add insult to injury, major Cardiology meetings these past few years have consistently revealed that the main cholesterol number that the commercials told you was critical is largely meaningless….. You might be wondering why I didn’t quote the number thrown around by Pfizer for how much the cholesterol miracle cure Lipitor reduces heart attack risk (36%).

This is because it’s not a 36% reduction in heart attack risk, but “relative risk”. You get to 36% only after a little creative math quoting that the difference between the percentage of heart attacks in the Lipitor versus the placebo group (2% versus 3%).

How Do Statins Compare to Blueberries?

Risk reduction for heart attack; eating blueberries, 32% over 18 years; taking statins, 1% over 3.5 years.”

This is exactly what a growing number of scientists and cardiologists have been pointing out for a very long time, and it has to do with surrogate markers / surrogate endpoints.

Conclusion

The fact that statins not only do nothing for health but reduce the efficiency of cellular metabolism has zero to do with whether statins will continue to be prescribed and taken. On the essential criteria of the pharmaceutical companies and the FDA, which is producing revenue streams for many companies and MDs, statins are a very successful drug by this measurement.

For more information on the problems with statins, see the article The Side Effects of Statins Like Lipitor.