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Introduction: If You’re Taking a Statin, Read This Carefully
If you’re currently taking a statin like Lipitor, Crestor, Zocor, or Pravachol to lower your cholesterol, particularly your low-density lipoprotein (LDL) cholesterol, because you’ve been told it will protect you from a heart attack or stroke, this article may leave you feeling confused, surprised, or even angry. That reaction might be a sign that you’re finally getting the full picture.
For starters, most people are unaware that there is growing evidence suggesting statins may shorten lifespan for some individuals. The irony? These same people have been told the drug might be saving their lives. They’ve trusted the system. They’ve followed the guidelines. And in many cases, they’ve been misled.
The science is precise, but it has been buried under decades of marketing, misinterpretation, and misinformation. You’re not alone. Even many well-meaning physicians have been taught the same outdated and distorted narrative. But the time has come to question it. And many already are.
One of the most respected voices calling out this disconnect is Dr. Marty Makary, the 27ᵗʰ Commissioner of Food and Drugs. Before assuming this role, he served as a professor of surgery and public health at Johns Hopkins University. In his book Blind Spots: When Medicine Gets It Wrong, and What It Means for Our Health, Commissioner Makary challenges the deeply entrenched dogmas of modern medicine. Regarding statins and cholesterol, he writes:
“We’ve turned cholesterol into a villain when in fact, for many people, the focus should have been on inflammation and metabolic health, not simply lowering LDL numbers with medication.”
Dr. Makary is one of many experts now pulling back the curtain on how the medical establishment got it wrong when it comes to cholesterol and statins.
You’ve likely been told that high cholesterol is inherently dangerous and that statin drugs like Lipitor, Crestor, and Zocor are your best defense against heart attacks and strokes. Millions of Americans take these drugs based on the belief that lowering LDL cholesterol will save their lives. But what if that belief has been shaped more by flawed science and aggressive marketing than by actual benefit?
If you’re on a statin or considering one, I encourage you to read this article in full and then schedule a conversation with your doctor. Bring this information with you. Ask hard questions. You deserve answers rooted in science, not sales.
Statins: What You’re Not Being Told
For most people, the benefits of statins have been dramatically overstated. When you examine the absolute risk reduction, which reflects your actual chances of avoiding a heart attack or living longer by taking a statin, the benefit is often less than 1%. That means 99 out of 100 people who take a statin will experience no life-extending or heart attack–preventing benefit at all.
Yet pharmaceutical companies don’t advertise that number. Instead, they promote relative risk reductions, such as claiming statins reduce heart attack risk by 30% or more. That sounds impressive, but it’s misleading. What they’re saying is that if your risk of a heart attack is 2% and a statin lowers it to 1.4%, that’s a 30% relative reduction, even though the actual benefit to you is only 0.6%.
When you weigh that tiny benefit against the very real risks, including muscle pain, memory loss, elevated blood sugar, liver damage, increased risk of type 2 diabetes, and even higher all-cause mortality in some groups, the decision becomes clearer. If people truly understood the difference between relative and absolute risk, most in their right minds would never agree to take a statin.
And what about side effects? You might be surprised to learn that many people experience:
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- Muscle pain and weakness
- Fatigue and memory issues
- Elevated blood sugar and increased risk of type 2 diabetes
- Liver damage
- Sexual dysfunction
These side effects are not rare. Research shows they may affect up to 20% or more of users, despite being dismissed or underreported by prescribing physicians.
So how did we get here? How did cholesterol, an essential substance in the body, become enemy number one? Why were statins fast-tracked into widespread use, and why have they remained a cornerstone of “preventative” medicine, even when emerging science paints a different picture?
To answer these questions, we need to revisit the discovery of cholesterol, the controversy surrounding the diet-heart hypothesis, the influence of Ancel Keys, and the aggressive expansion of pharmaceutical marketing.
How Statins Work
To understand statins, it helps to know how the body regulates cholesterol. Your liver produces most of the cholesterol found in your blood. When your body needs more cholesterol, the liver ramps up production. When demand is lower, production slows.
Statins work by blocking an enzyme in the liver called HMG-CoA reductase, which is essential for the body’s internal cholesterol production. By inhibiting this enzyme, statins reduce the liver’s ability to make cholesterol. This forces the liver to remove cholesterol from the bloodstream, effectively lowering circulating LDL cholesterol levels.
However, just because LDL numbers go down doesn’t mean overall health improves. Lowering a number doesn’t always equate to lowering disease risk, especially if the underlying drivers of heart disease, like inflammation and insulin resistance, are not addressed.
The Discovery of Cholesterol and What We Know Today
Cholesterol was first identified in 1789 by French chemist Antoine François Fourcroy. It is a waxy substance found in every cell of the body. It is essential for building cell membranes, synthesizing hormones (such as estrogen and testosterone), producing vitamin D, and aiding in digestion through the production of bile acids.
Today, we understand that cholesterol travels in the blood attached to lipoproteins. Low-density lipoprotein (LDL) has been labeled “bad,” and high-density lipoprotein (HDL) as “good.” But that narrative oversimplifies reality. LDL is essential for transporting cholesterol to cells that need it. Problems arise primarily when inflammation and oxidative stress lead to the damage of LDL particles, especially small, dense LDL.
How Cholesterol Was Blamed for Heart Disease
In the mid-20th century, American physiologist Ancel Keys promoted the diet-heart hypothesis, which suggests that the consumption of saturated fat raises cholesterol levels, leading to arterial clogging and an increased risk of heart disease. His 1950s Seven Countries Study seemed to show a correlation between saturated fat intake and heart disease. Still, critics have since exposed that Keys cherry-picked data, omitting countries that didn’t fit his hypothesis.
Nevertheless, Keys’ research shaped public policy. In 1977, the U.S. government issued dietary guidelines warning against saturated fats, which led to a nationwide shift toward low-fat, high-carbohydrate diets—and, ironically, an increase in the rates of obesity and diabetes.
When Cholesterol Guidelines Changed—And Who Changed Them
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- 1987: The first statin, Mevacor (lovastatin), was approved by the FDA.
- 1988: The National Cholesterol Education Program (NCEP) Adult Treatment Panel I (ATP I) set 240 mg/dL as the threshold for high cholesterol.
- 1993: ATP II promoted even more aggressive LDL lowering.
- 2001: ATP III dropped the “optimal” LDL to below 100 mg/dL, pushing more people into the statin-eligible category. It also redefined total cholesterol levels, labeling 200–239 mg/dL as ‘borderline high’ and ≥240 mg/dL as ‘high,’ effectively lowering the concern threshold to 200 mg/dL.
- 2004: An update recommended targets under 70 mg/dL for high-risk individuals. Eight of nine panel members had ties to statin makers.
- 2013: New guidelines from the American College of Cardiology (ACC) and American Heart Association (AHA) emphasized risk scores over LDL thresholds but still expanded statin use.
The lower the cholesterol threshold fell, the more people qualified for statin prescriptions. These changes often coincided with the expansion or release of new statin medications.
The Most Damning Studies You Probably Haven’t Heard Of
Framingham Heart Study
• Initially supported the cholesterol-heart disease link.
• But later data showed that lowering cholesterol in older adults increased all-cause mortality.
Minnesota Coronary Experiment (1968–1973; re-analyzed 2016)
• Lowering cholesterol with vegetable oil did not reduce mortality.
• Those with the most significant drop in cholesterol had higher death rates.
Sydney Diet Heart Study (1966–1973; re-analyzed 2013)
• Replacing saturated fat with omega-6-rich vegetable oils increased heart disease deaths.
Honolulu Heart Program
• Found that lower cholesterol in older adults was associated with shorter lifespan.
Why Your Doctor Keeps Prescribing Statins
Most physicians rely on medical guidelines shaped by institutions funded by pharmaceutical companies. Medical schools often receive funding from these same corporations. Insurance companies reimburse based on treating lab results, not underlying causes.
Pharmaceutical companies also heavily influence research, fund continuing medical education (CME), and dominate the advertising industry. In 1997, the U.S. Food and Drug Administration (FDA) legalized direct-to-consumer (DTC) pharmaceutical advertising on television. Today, the United States and New Zealand are the only countries in the world that allow this.
This shift opened the floodgates for pharmaceutical marketing, and statins became household names. With slick commercials featuring smiling seniors and dramatized heart attack prevention claims, patients began asking for statins by name, often before a true medical need was established. As a result, the average American now sees statin ads regularly, reinforcing the perception that lowering cholesterol is always the right move.
Relative Risk vs. Absolute Risk: The Marketing Shell Game
If a drug company says a statin reduces your heart attack risk by 50%, they’re using relative risk reduction. Here’s how it works:
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- In a clinical trial, if 2 out of 100 people experience a heart attack without the drug, and 1 out of 100 experience one with the drug, that represents a 50% relative reduction.
- But the absolute reduction is just 1%.
In real-world terms, 99 people out of 100 would not benefit from the drug, but all 100 get exposed to the side effects.
Conclusion: Rethinking Cholesterol and Statins
The idea that lowering cholesterol with a statin automatically leads to better health is deeply flawed.
If the goal of statin therapy is to lower low-density lipoprotein (LDL) cholesterol, it’s important to ask whether that lowering improves health outcomes. While statins do reliably reduce LDL numbers, that doesn’t necessarily translate into longer life or fewer heart attacks for most people.
In low-risk individuals, statins lower LDL but provide no meaningful reduction in death or serious events. Even in high-risk populations, the absolute benefit is often marginal and must be weighed against the side effects. Across many studies, all-cause mortality remains unchanged. In fact, most people who experience heart attacks have “normal” cholesterol levels.
Lowering LDL alone isn’t the answer. The real issues, such as inflammation, oxidative stress, and metabolic dysfunction, are largely overlooked when we focus on cholesterol numbers.
You have the right to question your prescription, review the actual data, and request a thorough discussion of the benefits and risks.
The truth? Cholesterol is not your enemy. Inflammation, oxidative stress, and metabolic dysfunction are far better predictors of heart disease. If you’d like to learn how to naturally reduce inflammation, oxidative stress, and improve your overall health, schedule a free consultation with me. I’ll answer your questions and share available program options.
References
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- Castelli, W.P. (1987). The Framingham Study: Twenty-six-year follow-up of 117,000 persons. American Journal of Cardiology, 60(6), G1-G2.
- Ramsden, C. E., Zamora, D., Leelarthaepin, B., Majchrzak, S. F., Faurot, K. R., Davis, J. M., … & Hibbeln, J. R. (2013). Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ, 346, e8707.
- Ramsden, C. E., Zamora, D., Majchrzak-Hong, S. F., Faurot, K. R., Broste, S. K., Frantz, R. P., … & Hibbeln, J. R. (2016). Re-evaluation of the Minnesota Coronary Experiment. BMJ, 353, i1246.
- Ravnskov, U. (2003). High cholesterol may protect against infections and atherosclerosis. Quarterly Journal of Medicine, 96(11), 927-934.
- Keys, A. (1970). Coronary heart disease in seven countries. Circulation, 41(4 Suppl), 1-211.
- FDA (1997). Guidance for Industry: Consumer-Directed Broadcast Advertisements. U.S. Food and Drug Administration.
- Abramson, J. D., & Wright, J. M. (2007). Are lipid-lowering guidelines evidence-based? Lancet, 369(9557), 168-169.
- Diamond, D. M., & Ravnskov, U. (2015). How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease. Expert Review of Clinical Pharmacology, 8(2), 201-210.
- Makary, M. (2024). Blind Spots: When Medicine Gets It Wrong, and What It Means for Our Health. Penguin Random House.
- Goldstein, J. L., & Brown, M. S. (1985). Regulation of the mevalonate pathway. Nature, 343(6257), 425-430. https://doi.org/10.1038/343425a0
- Abramson, J. D., Rosenberg, H. G., Jewell, N., & Wright, J. M. (2013). Should people at low risk of cardiovascular disease take a statin? BMJ, 347, f6123. https://doi.org/10.1136/bmj.f6123
- Ravnskov, U., Diamond, D. M., Hama, R., Hamazaki, T., Hammarskjöld, B., Hynes, N., … & Okuyama, H. (2018). LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature. Expert Review of Clinical Pharmacology, 11(10), 959–970. https://doi.org/10.1080/17512433.2018.1519391
- Mozaffarian, D., Micha, R., & Wallace, S. (2010). Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Medicine, 7(3), e1000252. https://doi.org/10.1371/journal.pmed.1000252
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Robert Ferguson is a California- and Florida-based single father of two daughters, nutritionist, researcher, best-selling author, speaker, podcast and television host, health advisor, NAACP Image Award Nominee, creator of the Diet Free Life methodology, and Chief Nutrition Officer for iCoura Health. He also serves on the Presidential Task Force on Obesity for the National Medical Association and the Health and Product Advisory Board for Zinzino, Inc.
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