What Do Statins Deplete in the Body? Unpacking CoQ10, Vitamin D, and Selenium

October 7, 2025 •

4 min read

Millions of people worldwide take statins to lower cholesterol, but a less-known aspect of this treatment is the potential for nutrient depletion. While highly effective at reducing the risk of heart attacks and strokes, statin use can interfere with the body's synthesis of key nutrients. This article explores the answer to the question, "What do statins deplete in the body?" with a focus on Coenzyme Q10 and other potentially affected micronutrients.

Quick Summary

Statins primarily deplete Coenzyme Q10 (CoQ10) by inhibiting the mevalonate pathway, which is crucial for CoQ10 synthesis. This may be linked to common muscle-related side effects. Depletion of other nutrients like Vitamin D is debated but remains a possibility for some individuals.

Key Points

Coenzyme Q10 (CoQ10) Depletion: Statins inhibit the mevalonate pathway, which is essential for both cholesterol and CoQ10 synthesis, leading to lower levels of CoQ10 in the body.
Link to Muscle Pain (Myopathy): Depleted CoQ10 may impair mitochondrial function in muscles, potentially contributing to the muscle pain and fatigue often reported as statin side effects.
Mixed Results for CoQ10 Supplements: While CoQ10 supplementation is often suggested, clinical evidence regarding its effectiveness in relieving statin-associated muscle pain is conflicting.
Vitamin D Connection: The impact of statins on Vitamin D levels is debated, though some research links Vitamin D deficiency to myopathy, suggesting monitoring levels could be beneficial.
Selenium Hypothesis: Some hypotheses propose that statins might affect selenium levels by interfering with the synthesis of selenoproteins, which play a role in muscle health.
Management Strategies: If experiencing side effects, strategies like CoQ10 supplementation, statin type or dose adjustment, and checking for Vitamin D deficiency should be discussed with a doctor.

The Primary Depletion: Coenzyme Q10

The most widely recognized nutrient depleted by statin medication is Coenzyme Q10 (CoQ10), also known as ubiquinone. The mechanism for this is directly related to how statins function. Statins inhibit an enzyme called HMG-CoA reductase, which is the rate-limiting step in the mevalonate pathway. While this effectively reduces cholesterol production, the mevalonate pathway is also a critical manufacturing line for CoQ10. By blocking this pathway, statins inevitably reduce the body's natural production of CoQ10.

The Role of CoQ10 in the Body

CoQ10 is a fat-soluble, vitamin-like substance that plays a vital role in cellular energy production, particularly in the mitochondria, often referred to as the powerhouses of the cell. Because organs like the heart and muscles are highly energy-dependent, they have some of the highest concentrations of CoQ10. It also functions as a powerful antioxidant, protecting cells from damage caused by free radicals.

Symptoms and Supplementation

The link between CoQ10 depletion and statin side effects, especially muscle pain (myalgia) and fatigue, has been a subject of extensive research. The rationale is that reduced CoQ10 could impair mitochondrial function in muscle cells, leading to myopathy. However, the efficacy of CoQ10 supplementation to alleviate these symptoms has produced conflicting results in clinical studies. While some studies show benefit, others find no significant improvement over a placebo. Nonetheless, many healthcare providers may recommend a trial of CoQ10, given its low risk of toxicity and potential for benefit, particularly for patients with debilitating muscle pain.

Potential Secondary Depletions

While CoQ10 is the most established depletion, research suggests statins may have an impact on other nutrients through related biological processes.

Vitamin D: A Controversial Connection

Statins' effect on Vitamin D levels is a more controversial topic, with conflicting evidence in the scientific literature. The primary connection lies in the fact that 7-dehydrocholesterol (7-DHC), a precursor for both cholesterol and Vitamin D, is produced in the mevalonate pathway. Logically, inhibiting this pathway should reduce 7-DHC and thus decrease Vitamin D synthesis. However, some studies have actually reported higher Vitamin D levels in statin users, while others find no correlation. This discrepancy may be due to factors like drug type, patient genetics, and concurrent conditions. Crucially, low Vitamin D levels have been independently associated with muscle weakness and myopathy, suggesting that addressing a pre-existing or statin-induced Vitamin D deficiency could potentially improve statin tolerance.

Selenium: A Hypothesized Impact

Less understood but an area of research is the potential link between statins and selenium levels. A hypothesis suggests that statins may interfere with the synthesis of selenoproteins, which are enzymes containing the trace element selenium. This interference could be related to a reduced availability of isopentenyl pyrophosphate, another product of the mevalonate pathway. Since selenoproteins play a key role in protecting against oxidative stress and maintaining muscle health, their depletion could contribute to statin-induced myopathy. However, more research is needed to validate this hypothesis.

Comparing Nutrient Depletions with Statin Use


Nutrient	Primary Mechanism of Depletion	Evidence for Depletion	Link to Statin Side Effects	Management Approach
Coenzyme Q10 (CoQ10)	Inhibition of the mevalonate pathway, disrupting its synthesis.	Strong, consistently observed decrease in serum levels.	Widely hypothesized to contribute to statin-associated muscle pain (myalgia) and fatigue.	Supplementation may be recommended, though clinical trial results on effectiveness are mixed.
Vitamin D	Interference with the mevalonate pathway and 7-DHC, a Vitamin D precursor.	Conflicting studies; some show depletion, while others show no change or even an increase.	Inadequate Vitamin D levels are an independent risk factor for myopathy, potentially worsening symptoms.	Check Vitamin D levels; address any deficiency with supplementation as recommended by a doctor.
Selenium	Hypothesized interference with selenoprotein synthesis due to reduced isopentenyl pyrophosphate.	Theoretical, based on biochemical pathways; needs further research.	Potential contributor to myopathy and oxidative stress.	Not standard practice to supplement. Dietary intake should be assessed in potentially deficient populations.

Strategies for Managing Potential Depletions

For those concerned about nutrient depletion while on statin therapy, several proactive steps can be taken in consultation with a healthcare provider:

Discuss concerns with your doctor: Before making any changes, it's crucial to talk to your healthcare team. They can help determine if your symptoms are linked to nutrient depletion or other causes.
Consider a CoQ10 supplement: For those experiencing muscle-related side effects, a trial of CoQ10 supplementation may be an option, particularly if other treatment strategies aren't effective.
Adjust dosage or switch statin type: In some cases, a lower dose or a switch to a more hydrophilic statin (like pravastatin or rosuvastatin, which are less associated with muscle symptoms) may help reduce side effects.
Check Vitamin D levels: If muscle-related symptoms persist, a blood test for Vitamin D deficiency is a simple diagnostic step, as correcting a pre-existing deficiency can improve tolerance.
Increase dietary intake: Consuming foods rich in these nutrients, such as fatty fish (CoQ10, Vitamin D), eggs, and whole grains (Selenium), can help support the body's levels, though supplementation is often required for significant deficiencies.
Don't stop statin therapy without guidance: The cardiovascular benefits of statins are substantial. Never discontinue your medication without professional medical guidance, as stopping treatment can significantly increase your risk of heart-related events.

Conclusion

While statins are an essential medication for managing cholesterol and preventing cardiovascular disease, their inhibition of the mevalonate pathway does have consequences beyond lowering cholesterol. The most significant depletion is of Coenzyme Q10, a crucial component for cellular energy and antioxidant defense, which is implicated in the muscle pain and fatigue experienced by some patients. The potential depletion of Vitamin D and Selenium is a subject of ongoing research and may play a role in individual cases. For patients on statin therapy, understanding these potential nutrient depletions and discussing management strategies with a healthcare provider is key to balancing the drug's proven benefits with the potential for side effects.

Mayo Clinic - Statin side effects: Weigh the benefits and risks

Frequently Asked Questions

The main nutrient that statins deplete is Coenzyme Q10 (CoQ10). By blocking the enzyme HMG-CoA reductase, statins interfere with the same metabolic pathway that the body uses to produce both cholesterol and CoQ10.

The research on CoQ10 supplementation for statin side effects, particularly muscle pain, has yielded mixed results. While some studies and anecdotes suggest a benefit, others show no improvement over a placebo. Discussing a trial with a healthcare provider is recommended.

Statins' effect on Vitamin D levels is a controversial and debated topic. While some studies show a link to depletion, others report no change or even increased levels, depending on the patient and statin type. However, low Vitamin D is independently linked to muscle issues, so addressing a deficiency is beneficial.

CoQ10 depletion may be linked to statin-associated side effects such as muscle pain, weakness, and fatigue. Since CoQ10 is vital for energy production in muscle cells, its depletion can impact muscular function.

Statins work by blocking the HMG-CoA reductase enzyme in the mevalonate pathway. This pathway is not exclusive to cholesterol synthesis but also produces other essential compounds, including CoQ10 and precursors for Vitamin D and selenoproteins, leading to potential unintended depletions.

Some hypotheses propose a link between statins and reduced selenium levels due to interference with selenoprotein synthesis. This is less certain than CoQ10 depletion, and more research is needed to fully understand the connection.

If you experience side effects, do not stop your medication. Talk to your healthcare provider about potential solutions, which may include adjusting the dose, switching to a different statin, or testing for and correcting any nutrient deficiencies, like Vitamin D.