Can We Stop the Fiction that Statins Are a Key Heart Disease Prevention Strategy?

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I have been writing for years that government-funded studies showed such small effect sizes for statins that they were no better than buying a lotto ticket. Now a review paper argues that these drugs and the concept that drives them are a myth. So why are we still prescribing them? Let’s dig in.

Telling the Story Two Ways

I’m going to tell the statin heart disease story in two ways. First, I’ll summarize what I have already written on the topic. Then I will translate the recent review paper on why “bad cholesterol” is more Madison avenue than reality.

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My Take

High Cholesterol

Cholesterol is a key molecule that helps to make up the structure of cell membranes. Way back when, a now discredited study that looked at the amount of saturated fat consumed by a country and heart attack risk, claimed that there was an association. Before this could be debunked, the damage was done and a congressional panel put into motion decades of bad health policy as America was launched on a “low fat” craze.

As you’ll see below, eventually this “dietary fat” heart disease link was tied to cholesterol levels. Hence, a new drug class called “statins” was born based on the idea that if we artificially lower cholesterol levels we can reduce heart attacks.

Drug Studies

Drug manufacturers soon began reporting that cholesterol drugs could lower heart attacks by as much as 1/3. However, there was an asterisk beside that number as it was called a “relative risk reduction”. That meant that if the heart attack risk was 3%, using the statin would reduce that risk to 2%. While that was a measly 1% reduction in risk that wasn’t worth taking a drug to capture, it was a 1/3 reduction in “relative risk”. Given that 1/3 sounded far better than 1%, the companies used the relative risk reduction number and fooled a generation of physicians into prescribing these drugs.

That reduction in risk in more recent studies is even worse now. For example, the newer research for a popular cholesterol and blood pressure medication showed a 0.2 – 0.5% reduction in heart attacks, heart failure, and stroke after taking the drug for 5 years. As I have blogged before, the risk reduction from taking statins is so poor, that simply eating blueberries would have a more potent effect. Now a new research review, which I’ll summarize here, adds more fuel to the idea that the Pharma industry has created a craze that wasn’t real.

The New Review

The new review paper is written by a Ph.D. neuroscientist named David Diamond who had to make the decision for himself to take statins or not, so he researched what we knew and was astounded by what he found. He, therefore, placed himself on a low-carb diet instead of popping these pills. He also published what he found. (23)

Intro

The main idea behind statins is that high LDL or “bad cholesterol” is the key driving force behind why arteries in the heart get clogged (1-9). This key “fact” is based on the idea that people with elevated bad cholesterol have more heart disease and conversely that people who take statins to reduce these levels have less heart disease. Or at least that’s the theory. However, is that true or just a pharma sales pitch?

The Research Linking LDL Cholesterol and Heart Disease

The link between “bad cholesterol” (LDL) and heart disease begins with key research linking early premature death to patients with a rare genetic disorder of cholesterol metabolism (Familial Hypercholesterolemia or FH) that is associated with very high LDL cholesterol levels. However, this link is weaker than we have been sold. For example, if high LDL cholesterol causes heart disease, then we would expect that the rate of death among people with FH would increase as they age, as their arteries would be exposed to this toxic substance for longer. In fact, the rate of death declines as FH patients age (10-12). In addition, while more FH patients die young, over the span of their lifetimes, FH patients have an equal to lower risk of death, depending on the study. Hence, so much for the theory that high cholesterol levels cause premature death due to heart disease.

Is LDL or Clogged Arteries Associated with a Heart Attack?

Despite “bad cholesterol” being the number that is primarily tracked by doctors prescribing statins, LDL cholesterol is a poor predictor of who will have a heart attack and/or die from heart disease (13-17). While LDL is a poor predictor of who will get a heart attack, Coronary Calcium Scores (CAC or the degree to which your arteries are clogged as imaged on a CT scan) are a more reliable indicator of heart attack risk (18-21). On that note, 1/3 of individuals with a very high LDL cholesterol level have a zero CAC score! (22) Again, so much for a “bad cholesterol” hypothesis.

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What Does Cause Heart Disease?

The remainder of this review paper is focused on the idea that insulin resistance and metabolic syndrome cause heart disease. That’s too many carbs and not enough exercise. Hence, we would do far better by placing our patients on carb and sugar limited diets and allowing them to eat as much natural saturated fat as they want, In addition, based on my research, the barely there results of statins on preventing death due to heart attack doesn’t warrant taking these medications.

What Should You Do?

If you’re middle-aged or older, chances are you’ve been offered statin treatment. I know I have been offered it many times and I have generally turned it down. Why? This is a side effect laden drug class that can hurt your stem cells. Hence, my advice is to lose weight through a low-carb and calorie-limited diet, exercise more, and control your hormones as I discuss in my ProActive book. That includes taking care of joint, tendon, and ligament problems while they’re small so you can stay active as you age. And one more thing — eat your blueberries!

The upshot? “Bad cholesterol” doesn’t cause heart disease, poor sugar control is more likely the culprit!  In addition, statin drugs are pretty bad at preventing heart attacks. So ditch the statin drugs and get active.

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1. Boren J, Chapman MJ, Krauss RM, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 2020; 41:2313–2330.

2. Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS). Eur Heart J 2020; 41:111–188.

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15. Cromwell WC, Otvos JD, Keyes MJ, et al. LDL particle number and risk of future cardiovascular disease in the Framingham Offspring Study-Implications for LDL management. J Clin Lipidol 2007; 1:583–592.

16. Noakes TD. Hiding unhealthy heart outcomes in a low-fat diet trial: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial finds that postmenopausal women with established coronary heart disease were at increased risk of an adverse outcome if they consumed a low-fat ’heart-healthy’ diet. Open Heart 2021; 8:

17. Steffen BT, Guan WH, Remaley AT, et al. Apolipoprotein B is associated with carotid atherosclerosis progression independent of individual cholesterol measures in a 9-year prospective study of Multi-Ethnic Study of Atherosclerosis participants. J Clin Lipidol 2017; 11:1181–1191.

18. Polonsky TS, McClelland RL, Jorgensen NW, et al. Coronary artery calcium score and risk classification for coronary heart disease prediction. JAMA 2010; 303:1610–1616.

19. Mohlenkamp S, Lehmann N, Moebus S, et al. Quantification of coronary atherosclerosis and inflammation to predict coronary events and all-cause mortality. J Am Coll Cardiol 2011; 57:E886–E1886.

20. Yeboah J, Young R, McClelland RL, et al. Utility of nontraditional risk markers in atherosclerotic cardiovascular disease risk assessment. J Am Coll Cardiol 2016; 67:139–147.

21. Kavousi M, Elias-Smale S, Rutten JH, et al. Evaluation of newer risk markers for coronary heart disease risk classification: a cohort study. Ann Intern Med 2012; 156:438–444.

22. Sandesara PB, Mehta A, O’Neal WT, et al. Clinical significance of zero coronary artery calcium in individuals with LDL cholesterol >/=190 mg/dL: The Multi-Ethnic Study of Atherosclerosis. Atherosclerosis 2020; 292:224–229.

23. Diamond DM, Bikman BT, Mason P. Statin therapy is not warranted for a person with high LDL-cholesterol on a low-carbohydrate diet. Curr Opin Endocrinol Diabetes Obes. 2022 Oct 1;29(5):497-511. doi: 10.1097/MED.0000000000000764. Epub 2022 Aug 4. PMID: 35938780.

Chris Centeno, MD is a specialist in regenerative medicine and the new field of Interventional Orthopedics. Centeno pioneered orthopedic stem cell procedures in 2005 and is responsible for a large amount of the published research on stem cell use for orthopedic applications. View Profile

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NOTE: This blog post provides general information to help the reader better understand regenerative medicine, musculoskeletal health, and related subjects. All content provided in this blog, website, or any linked materials, including text, graphics, images, patient profiles, outcomes, and information, are not intended and should not be considered or used as a substitute for medical advice, diagnosis, or treatment. Please always consult with a professional and certified healthcare provider to discuss if a treatment is right for you.

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