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Orthomolecular Medicine News Service, February 16, 2025

Statins: A Band-Aid Solution with Serious Side Effects

Richard Z. Cheng, M.D., Ph.D., Thomas E. Levy, M.D., J.D.

Introduction

Statins are a class of drugs commonly prescribed to lower cholesterol levels, particularly low-density lipoprotein (LDL) cholesterol, which has traditionally been linked to an increased risk of cardiovascular diseases (CVD) such as heart attacks, strokes, and atherosclerosis. Statins work by inhibiting HMG-CoA reductase, an enzyme in the liver responsible for producing cholesterol. By reducing cholesterol production, statins aim to prevent plaque buildup in the arteries, which can lead to blockages and cardiovascular events.

While statins have been shown to lower cholesterol and, in some cases, may reduce the risk of heart attacks and strokes, there are growing concerns about the long-term use of statins, particularly regarding their potential side effects. Furthermore, we and others have demonstrated convincingly that cholesterol is not the root cause of atherosclerotic cardiovascular disease (ASCVD) (1-3). This article explores why statins, despite their wide usage, is not even a reasonable solution for cardiovascular health and why they should not be recommended for the management of ASDVD. Instead, preventing and even reversing ASCVD is readily achieved by the use of a protocol integrating orthomolecular medicine and nutrition (4).

Statin Side Effects: Especially on Mitochondria

Statins, widely used to lower cholesterol, come with several side effects that affect multiple organ systems, including the musculoskeletal, hepatic, digestive, and neurological systems. One of the most concerning, though often overlooked, is their impact on mitochondria, the energy-producing organelles in cells. Statins inhibit the production of Coenzyme Q10 (CoQ10), a crucial antioxidant for mitochondrial function and energy production (5,6). The depletion of CoQ10 impairs mitochondrial energy production, leading to muscle weakness, fatigue, and potentially life-threatening conditions like rhabdomyolysis (7).

This disruption also affects other organs, especially the heart, which relies heavily on mitochondrial energy. As a result, many patients on statins report muscle pain, fatigue, and cognitive issues, symptoms often linked to mitochondrial dysfunction (7). These effects are especially significant in those taking statins long-term, as they can severely impact quality of life. Statins further interfere with respiratory chain complexes, induce mitochondrial apoptosis, and disrupt calcium metabolism (8,9), contributing to statin-induced myopathy, the most common side effect (10-12). Additionally, mitochondrial dysfunction caused by statins may be associated with peripheral insulin resistance and new-onset diabetes (13). While statins can be safe for some, patients with multiple comorbidities are at significant risk of adverse effects, particularly with prolonged use (12).

Mitochondria are the power source of life.

Beyond energy production, mitochondria play a crucial role in cellular health and function, including metabolic regulation, calcium homeostasis, and cell death control (14,15). Their dysfunction is implicated in various age-related diseases, such as neurodegenerative disorders, cardiovascular diseases, metabolic syndrome, and cancer (16,17). The health of our mitochondria is critical, and the last thing we want to do is harm them. Statins are mitochondrial toxins, and should be avoided since other effective and nontoxic treatment approaches are available.

Cholesterol Is Not the Root Cause of ASCVD

Our recent analysis (2) shows that elevated cholesterol is not the root cause of atherosclerotic cardiovascular disease (ASCVD), but rather an intermediary step that can accelerate the process but not initiate it. While cholesterol, particularly LDL, has long been emphasized in ASCVD management, our work highlights that factors such as chronic inflammation, usually from oral cavity infections, oxidative stress, diet, environmental toxins, and nutrient deficiencies are the foundational drivers of ASCVD. This approach challenges the prevailing focus on cholesterol-lowering therapies and underscores the importance of addressing the root causes of ASCVD through Root Cause Analysis (RCA) and holistic treatments. By integrating these strategies, at healthcare can move beyond symptom management and achieve more effective, sustainable outcomes in cardiovascular care.

Reducing Cholesterol Does Not Significantly Improve ASCVD Outcomes

While statins effectively lower LDL cholesterol levels, the question remains: do they significantly improve long-term outcomes in terms of reducing heart attacks, strokes, and cardiovascular mortality? Several large studies have shown that while statins reduce cholesterol, the actual reduction in cardiovascular events is modest at best, and of no consequence for many. For instance, the 2016 ASCOT-LLA trial (18,19) and the JUPITER study (20,21) demonstrated that while statins reduced cholesterol and improved lipid profiles, the effect on heart attack and stroke prevention was limited. A more recent systematic review and meta-analysis of 22 clinical studies evaluated the association between low-density lipoprotein cholesterol (LDL-C) reduction and statin treatment, finding that while statins lower LDL-C, their impact on cardiovascular outcomes is modest and not as significant as often claimed (22). Many patients on statins still experienced heart attacks or strokes, and the overall benefit of statin therapy was relatively small for individuals without pre-existing heart disease (23,24).

Moreover, statins do not address the root causes of atherosclerotic cardiovascular disease (ASCVD), such as inflammation from oral cavity infections, oxidative stress, and insulin resistance, which have a much more significant role in the development and progression of heart disease. Focusing on cholesterol alone is insufficient to reliably improve outcomes for patients at risk for cardiovascular events. Critics argue that the cholesterol hypothesis may distract from other beneficial therapies (25), and some suggest that the benefits of statins have been exaggerated through statistical manipulation (23). Despite guidelines recommending aggressive LDL-C reduction (26), many patients on statins still evolve their coronary atherosclerosis and experience cardiovascular events (24).

Recent studies challenge the effectiveness of cholesterol-lowering therapies in significantly improving ASCVD outcomes. The focus on cholesterol alone is definitely insufficient, as other factors like inflammation and oxidative stress always play crucial roles in ASCVD development (25). However, some experts maintain that more intensive and earlier treatment of ASCVD risk factors, including LDL-C, is necessary for optimal prevention (27,28).

Risks vs Benefits: Statins Are Not Worthwhile

When considering whether to prescribe statins, the risks vs benefits analysis must be carefully weighed. Statins are associated with a range of side effects—from muscle pain and fatigue to more serious risks like liver damage, kidney problems, and memory loss. These side effects can significantly affect a patient's quality of life and may be especially troubling for older adults or those who are already managing multiple health conditions.

On the other hand, the benefit of statins—namely, the reduction in cholesterol and the small reduction in cardiovascular events—may not be worth the potential harm. In patients without significant cardiovascular risk factors, statins may provide little to no benefit, while exposing them to the risks of side effects. Additionally, when considering the long-term use of statins, the cumulative risks over time can outweigh the benefits, especially in light of more effective and natural alternatives for managing heart health (1-4).

The Statin-Centric Approach to ASCVD: A Misguided Strategy Rooted in Oversimplification

The widespread use of statins as the primary treatment for ASCVD, without addressing the root causes of the disease, ignores science, logic, and common sense. Here’s why:

1. Science: Statins target cholesterol, but cholesterol is not the root cause of heart disease. As discussed, factors like inflammation, oxidative stress, and insulin resistance are more significant contributors to ASCVD. Statins do not address these factors, and in many cases, they may even exacerbate underlying health issues (such as insulin resistance or mitochondrial dysfunction). Statins lower levels of many critically important steroids that are produced through the cholesterol pathway. For example, statins can reduce testosterone levels.
2. Logic: Statins work by reducing cholesterol, but the logic behind this approach has been increasingly questioned. If cholesterol is not the root cause of ASCVD, then treating it as though it were the primary factor is a misguided strategy. A more holistic, multifactorial approach that addresses the root causes of cardiovascular disease—such as diet, inflammation, and toxins—makes more sense.
3. Common Sense: Given the side effects of statins and the modest benefit they provide, it simply makes more sense to address cardiovascular health through lifestyle changes, such as a low-carb diet, exercise, and nutritional supplementation. These approaches tackle the root causes of heart disease without the risks and side effects associated with statin medications.

Orthomolecular Medicine Based Integrative Approach to ASCVD

Integrative Orthomolecular Medicine (I-OM) is a science-based, holistic approach that aims to optimize health by addressing the root causes of disease. It combines conventional medicine with micronutrients, lifestyle changes, and natural therapies for long-term well-being. A more comprehensive approach has been previously described (4). Here is a summary:

• Healthy Diet: I-OM promotes a low-carb, anti-inflammatory diet that avoids ultra-processed foods and seed oils to stabilize blood sugar and support metabolic health.
• Avoiding Toxins: Minimizing exposure to environmental pollutants, such as pesticides and heavy metals, helps reduce oxidative stress and inflammation, protecting overall health.
• Addressing Infections: I-OM identifies and treats chronic, hidden infections, usually of the gums and teeth, that contribute to conditions like autoimmune and cardiovascular diseases, reducing chronic inflammation.
• Micronutrient Deficiencies: I-OM focuses on replenishing key nutrients, especially those essential for mitochondrial function (e.g., magnesium, CoQ10, B vitamins), to support energy production and vitality.
• Antioxidant Support: I-OM uses antioxidants (e.g., vitamin C, vitamin E, selenium) to combat oxidative stress, which plays a role in aging and chronic disease.
• Hormonal Balance: I-OM targets imbalances in thyroid, adrenal, and sex hormones, using lifestyle changes and supplementation or bioidentical hormone therapy to restore health.

Through this comprehensive, individualized approach, I-OM aims to restore balance, prevent disease, and promote optimal health.

Summary

As part of our ongoing ASCVD series (1-3), this article examines statin drugs. While statins have been widely prescribed for the prevention of cardiovascular disease, the growing body of evidence and clinical experience demonstrates that they are not the best solution. Statins do not address the root causes of atherosclerotic cardiovascular disease (ASCVD) and come with a range of side effects that can significantly impact quality of life. Furthermore, reducing cholesterol does not substantially improve long-term outcomes for most people.

In the orthomolecular and nutritional approach to cardiovascular health, we emphasize holistic, integrative strategies that target the root causes of heart disease, such as infection-related inflammation, oxidative stress, and metabolic dysfunction. These approaches are safer, more effective, and more in line with the scientific understanding of cardiovascular disease.

For patients seeking to improve their heart health, we recommend exploring an orthomolecular medicine-based integrative approach that includes diet, exercise, nutritional supplementation, and stress management—without relying on statins as the first or only line of defense. In fact, none of the 10 cases of ASCVD that were reversed involved patients taking statin drugs (1).

References:

1. Cheng RZ, Duan L, Levy TE. (2024) A Holistic Approach to ASCVD: Summary of a Novel Framework and Report of 10 Case Studies. Orthomol Med News Serv. 20(20). https://orthomolecular.org/resources/omns/v20n20.shtml

2. Cheng RZ, Levy TE. (2025) The Mismanagement of ASCVD: A Call for Root Cause Solutions Beyond Cholesterol. Orthomol Med News Serv. 21(02) https://orthomolecular.org/resources/omns/v21n02.shtml

3. Cheng RZ (2024) Understanding and Addressing Vitamin D Resistance: A Comprehensive Approach Integrating Genetic, Environmental, and Nutritional Factors. Orthomol Med News Serv. 20(13). https://orthomolecular.org/resources/omns/v20n13.shtml

4. Cheng RZ (2024) Integrative Orthomolecular Medicine Protocol for ASCVD. https://www.drwlc.com/blog/2024/08/01/integrative-orthomolecular-medicine-protocol-for-ascvd

5. Deichmann R, Lavie C, Andrews S (2010) Coenzyme q10 and statin-induced mitochondrial dysfunction. Ochsner J. 10:16-21. https://pubmed.ncbi.nlm.nih.gov/21603349

6. De Pinieux G, Chariot P, Ammi-Saïd M, et al. (1966) Lipid-lowering drugs and mitochondrial function: effects of HMG-CoA reductase inhibitors on serum ubiquinone and blood lactate/pyruvate ratio. Br J Clin Pharmacol. 42:333-337. https://pubmed.ncbi.nlm.nih.gov/8877024

7. Golomb BA, Evans MA (2008) Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism. Am J Cardiovasc Drugs Drugs Devices Interv. 8:373-418. https://pubmed.ncbi.nlm.nih.gov/19159124

8. Mollazadeh H, Tavana E, Fanni G, et al. (2021) Effects of statins on mitochondrial pathways. J Cachexia Sarcopenia Muscle. 12:237-251. https://pubmed.ncbi.nlm.nih.gov/33511728

9. Broniarek I, Jarmuszkiewicz W (2016) [Statins and mitochondria]. Postepy Biochem. 62:77-84. https://postepybiochemii.ptbioch.edu.pl/index.php/PB/article/view/227/332

10. Bell G, Thoma A, Hargreaves IP, Lightfoot AP (2024) The Role of Mitochondria in Statin-Induced Myopathy. Drug Saf. 47:643-653. https://pubmed.ncbi.nlm.nih.gov/38492173

11. Apostolopoulou M, Corsini A, Roden M (2015) The role of mitochondria in statin-induced myopathy. Eur J Clin Invest. 45:745-754. https://pubmed.ncbi.nlm.nih.gov/25991405

12. Ramkumar S, Raghunath A, Raghunath S (2016) Statin Therapy: Review of Safety and Potential Side Effects. Acta Cardiol Sin. 32:631-639. https://pubmed.ncbi.nlm.nih.gov/27899849

13. Abbasi F, Lamendola C, Harris CS, et al. (2021) Statins Are Associated With Increased Insulin Resistance and Secretion. Arterioscler Thromb Vasc Biol. 41:2786-2797. https://pubmed.ncbi.nlm.nih.gov/34433298

14. Meiliana A, Dewi NM, Wijaya A (2019) Mitochondria in Health and Disease. Indones Biomed J. 11:1-15. https://www.inabj.org/index.php/ibj/article/view/779

15. Harrington JS, Ryter SW, Plataki M, et al. (2023) Mitochondria in health, disease, and aging. Physiol Rev. 103:2349-422. https://pubmed.ncbi.nlm.nih.gov/37021870

16. Srivastava S (2017) The Mitochondrial Basis of Aging and Age-Related Disorders. Genes, 8:398. https://pubmed.ncbi.nlm.nih.gov/29257072

17. Wallace DC (2005) A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: a dawn for evolutionary medicine. Annu Rev Genet.39:359-407. https://pubmed.ncbi.nlm.nih.gov/16285865

18. Sever PS, Poulter NR, Dahlof B, et al. (2008) The Anglo-Scandinavian Cardiac Outcomes Trial lipid lowering arm: extended observations 2 years after trial closure. Eur Heart J. 29:499-508. https://pubmed.ncbi.nlm.nih.gov/18175773

19. Sever PS, Dahlöf B, Poulter NR, et al. (2003) Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet(Lond Engl.) 361:1149-1158. https://pubmed.ncbi.nlm.nih.gov/12686036

20. Kostapanos MS, Elisaf MS (2011) JUPITER and satellites: Clinical implications of the JUPITER study and its secondary analyses. World J Cardiol. 3:207-214. https://pubmed.ncbi.nlm.nih.gov/21860701

21. de Lorgeril M, Salen P, Abramson J, et al. (2010) Cholesterol lowering, cardiovascular diseases, and the rosuvastatin-JUPITER controversy: a critical reappraisal. Arch Intern Med. 170:1032-1036. https://pubmed.ncbi.nlm.nih.gov/20585068

22. Byrne P, Demasi M, Jones M, et al. (2022) Evaluating the Association Between Low-Density Lipoprotein Cholesterol Reduction and Relative and Absolute Effects of Statin Treatment: A Systematic Review and Meta-analysis. JAMA Intern Med. 182:474-481. https://pubmed.ncbi.nlm.nih.gov/35285850

23. Diamond DM, Ravnskov U (2015) How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease. Expert Rev Clin Pharmacol. 8:201-10. https://pubmed.ncbi.nlm.nih.gov/25672965

24. Ridker PM (2016) Residual inflammatory risk: addressing the obverse side of the atherosclerosis prevention coin. Eur Heart J. 37:1720-1722. https://pubmed.ncbi.nlm.nih.gov/26908943

25. DuBroff R (2016) Does IMPROVE-IT prove it? Prev Med. 85:32-35. https://pubmed.ncbi.nlm.nih.gov/26791324

26. Stone NJ, Robinson JG, Lichtenstein AH, et al. (2014) Treatment of blood cholesterol to reduce atherosclerotic cardiovascular disease risk in adults: synopsis of the 2013 American College of Cardiology/American Heart Association cholesterol guideline. Ann Intern Med. 160:339-343. https://pubmed.ncbi.nlm.nih.gov/24474185

27. Makover ME, Shapiro MD, Toth PP (2022) There is urgent need to treat atherosclerotic cardiovascular disease risk earlier, more intensively, and with greater precision: A review of current practice and recommendations for improved effectiveness. Am J Prev Cardiol. 12:100371. https://pubmed.ncbi.nlm.nih.gov/36124049

28. Zhou R, Stouffer GA, Smith SC (2021) Targeting the Cholesterol Paradigm in the Risk Reduction for Atherosclerotic Cardiovascular Disease: Does the Mechanism of Action of Pharmacotherapy Matter for Clinical Outcomes? J Cardiovasc Pharmacol Ther. 26:533-549. https://pubmed.ncbi.nlm.nih.gov/34138676

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