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MyDeficiencies

Rosuvastatin

Statin

Also sold as Crestor.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Rosuvastatin has one nutrient-status finding with real, drug-specific human evidence: it lowers circulating coenzyme Q10 (CoQ10). Three independent sources that named rosuvastatin as a distinguishable study arm, a 1,191-patient substudy of the placebo-controlled CORONA trial, a 147-patient placebo-controlled sub-study within SATURN-HIV, and a statin-stratified meta-analysis that isolated rosuvastatin's own effect size, all measured a reduction in plasma or serum CoQ10. The mechanism is well named: rosuvastatin blocks HMG-CoA reductase upstream in the mevalonate pathway, which also supplies the precursor rosuvastatin's cholesterol-lowering target shares with CoQ10 synthesis. That is a distinct, verified finding from the atorvastatin literature, not an assumption carried over from it; rosuvastatin's own trials independently confirm the same direction despite a materially different pharmacokinetic profile (minimal CYP3A4 involvement, OATP1B1-dependent hepatic uptake, biliary rather than renal clearance).

ATC C10AA07 · also sold as Crestor · reviewed 2026-09-05, expanded 2026-09-10. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Rosuvastatin in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow — Low
Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded — disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Coenzyme Q10

Red — Severe

See study details

Rosuvastatin lowers circulating CoQ10 in its own placebo-controlled trials and in a statin-stratified meta-analysis; whether that drop itself causes muscle symptoms remains unresolved.

Full detail and limits

What the grade means here: Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence. Red · severe

Limits on what this shows

  • Key negative or null findings: CORONA's own substudy found that a patient's CoQ10 tertile was not an independent predictor of any clinical outcome after multivariable adjustment, despite an unadjusted mortality signal (hazard ratio 1.50, 95% CI 1.04–2.6, comparing lowest to highest tertile). A separate placebo-controlled trial of CoQ10 supplementation in confirmed simvastatin myalgia (a different statin, cited only for the contested-mechanism context) found that supplementation restored plasma CoQ10 but left muscle CoQ10 content and mitochondrial function unaltered, and did not improve myalgia. Together these are the strongest evidence that a falling blood CoQ10 number and a muscle symptom are not the same finding.
  • At-risk subgroups: No rosuvastatin-specific subgroup data isolate a bounded population at greater risk of the CoQ10 decline itself (this is why the finding is graded as a general effect, not bounded to Orange). A related line of research has examined genetic variation in the CoQ10 biosynthesis pathway as a modifier of rosuvastatin-associated muscle symptoms; that work concerns a clinical outcome (muscle symptoms), not nutrient status, and is not used here as CoQ10-level evidence.

Regulatory status

Not addressed in the FDA label. The label's myopathy and rhabdomyolysis warnings are framed entirely around creatine kinase and symptoms, with no CoQ10 language.

Population evidence

CORONA CoQ10 substudy: pre-specified analysis of 1,191 patients with ischemic systolic heart failure from the placebo-controlled CORONA trial (rosuvastatin 10 mg/day vs. placebo, N=5,011 parent trial, mean follow-up 2.7 years); rosuvastatin reduced serum CoQ10 relative to placebo. SATURN-HIV secondary analysis: 147 HIV-infected adults on antiretroviral therapy randomized to rosuvastatin 10 mg/day vs. placebo for 24 weeks; CoQ10 decreased significantly (p=0.002) and the CoQ10:LDL ratio rose (p=0.036). Qu et al. 2015 meta-analysis (Pharmacological Research): 6 placebo-controlled trials, 8 treatment arms, stratified by individual statin; rosuvastatin's own subgroup effect was a weighted mean difference of −0.49 µmol/L (95% CI −0.67 to −0.31, p<0.001), the largest reduction of the four statins analyzed (atorvastatin, simvastatin, rosuvastatin, pravastatin).

Mechanism

Named and consistent with rosuvastatin's own pharmacology: HMG-CoA reductase inhibition blocks the mevalonate pathway upstream of farnesyl pyrophosphate, a shared precursor for both cholesterol and CoQ10 biosynthesis. This is independent of rosuvastatin's minimal CYP3A4 metabolism and OATP1B1-mediated hepatic uptake; both statins that are and are not major CYP3A4 substrates show the effect, which is expected because the shared pathway is downstream of hepatic uptake, not of any CYP enzyme.

Counter-evidence held on record

Confounding by indication was considered: both pivotal sources (CORONA substudy, SATURN-HIV) are randomized, placebo-controlled designs, so baseline dietary or lipid differences between statin and non-statin patients are balanced by randomization rather than left as an open confound. No rosuvastatin-specific trial identified in this review reported a null result for the CoQ10 measurement itself; the null results on record concern the downstream clinical question (does the CoQ10 drop matter), not whether the drop occurs. Framing caution for the consumer surface A lower CoQ10 number is real and drug-specific. It must never be presented to a reader as proof that rosuvastatin causes, or that CoQ10 supplementation prevents or treats, muscle pain, weakness, or rhabdomyolysis; the placebo-controlled evidence on that specific causal step is thin and, where it exists, largely negative. No supplement dose is recommended here at any grade.

Vitamin E

Yellow — Low

See study details

Statins as a class lower raw plasma vitamin E, but the same meta-analysis that found this shows the effect tracks cholesterol lowering itself and reverses into an improvement once adjusted; no rosuvastatin-specific trial has tested this directly.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow · class extrapolation

Limits on what this shows

  • Key negative or null findings: The same meta-analysis recalculated vitamin E as a ratio to total cholesterol (vitamin E:total cholesterol) and found this cholesterol-adjusted measure significantly improved with statin therapy (weighted mean difference +29.35%, 95% CI 24.98 to 33.72, p<0.001). The authors' own conclusion was that statin therapy "has no negative impact on plasma vitamin E concentrations or LDL vitamin E content."
  • At-risk subgroups: None identified for rosuvastatin specifically; no rosuvastatin arm exists to stratify.

Regulatory status

Not addressed in the FDA label; no vitamin E language present.

Population evidence

A systematic review and meta-analysis of randomized placebo-controlled statin trials (8 treatment arms, 504 participants) found a significant reduction in raw plasma vitamin E (weighted mean difference −16.30%, 95% CI −16.93 to −15.98, p<0.001). The individual statins studied and any rosuvastatin-specific subgroup were not reported in the accessible summary, so this cannot clear the cohort test for rosuvastatin; it is Tier C, class-level, for this drug. No rosuvastatin-specific vitamin E trial was found in this review.

Mechanism

Confounding by lipid-lowering itself, not a distinct depletion mechanism: vitamin E circulates bound to lipoproteins, so total plasma vitamin E falls in parallel with total cholesterol under any effective lipid-lowering therapy, without necessarily reflecting a true tissue or functional deficit.

Counter-evidence held on record

The confounding-by-mechanism explanation here is not speculative; it comes from the same source used to support the claim, which is why this is graded Yellow rather than granted any stronger tier despite a real, statistically significant raw-number finding. Framing caution for the consumer surface This is not evidence that rosuvastatin depletes vitamin E and must never be worded that way; if surfaced at all, it should be framed as "an artifact of cholesterol lowering, not a true deficiency risk," and never paired with a supplementation suggestion.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden

Yellow — Low

See study details

A rosuvastatin-named rat study found direct mitochondrial ultrastructural alteration in muscle distinct from the CoQ10-synthesis pathway already graded Red above; human muscle-tissue evidence exists only at the statin-class level, with rosuvastatin's own presence in the tested cohort unconfirmed.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow · class/mechanistic

Limits on what this shows

  • Key negative or null findings: Two rosuvastatin-named animal studies found the opposite direction in non-muscle tissue: He et al. 2018 found rosuvastatin improved mitochondrial biogenesis and function in cortical neurons under oxygen-glucose deprivation, and Amer et al. 2025 found rosuvastatin restored mitochondrial function in aged-mouse liver immune cells. Neither directly contradicts the muscle-specific myotoxicity finding, since the tissue and disease models differ, but both show rosuvastatin's mitochondrial effects are not uniformly negative across tissues.
  • At-risk subgroups: None defined by rosuvastatin-specific human data. The rat toxicology study used dosing designed to model myopathy risk, which does not map directly onto any defined human exposure subgroup.

Regulatory status

Not addressed in the FDA label beyond the general myopathy and rhabdomyolysis warning already noted in the PK prescreen; the label names no mitochondrial mechanism.

Population evidence

El-Ganainy et al. 2017 (Toxicology Letters): a rosuvastatin-named rat toxicology study reported myotoxic effects and mitochondrial ultrastructural alterations in skeletal muscle at doses used to model statin myopathy. This is Tier B, animal, but rosuvastatin-specific by name. Somers et al. 2024 (Biomedicine & Pharmacotherapy) reported that "statins reduce skeletal and cardiac muscle cell respiration" using ex vivo human skeletal and cardiac tissue; the accessible search-listing snippet did not specify which individual statins were tested, so rosuvastatin's presence in this cohort could not be confirmed, and this source is treated as Tier C, class-level, for rosuvastatin. A related 2024 study from the same group (Basic Research in Cardiology) reported statins interfering with mitochondrial function in human iPSC-derived cardiomyocytes, again without confirmed rosuvastatin identity in the available snippet.

Mechanism

Named only for the rat study: myotoxic mitochondrial ultrastructural change, distinct from, though possibly compounding, the mevalonate-pathway CoQ10 effect already graded Red. No mechanism could be confirmed for the human-tissue respiration findings beyond "reduced muscle cell respiration"; whether that runs through CoQ10 depletion, a direct membrane effect, or another pathway could not be determined from the accessible snippet.

Counter-evidence held on record

This entry is graded independently of the Red CoQ10 finding; see the Overlap map below for how the two are kept from double counting. The rat myotoxicity finding is animal-only and has not been replicated in a rosuvastatin-specific human muscle-biopsy study identified in this review. Framing caution for the consumer surface This must never be worded as "rosuvastatin damages your mitochondria" as a general human finding; the only rosuvastatin-named evidence is a single rat toxicology study, and the human-tissue data cannot be confirmed to include rosuvastatin at all.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress

Yellow — Low

See study details

Multiple rosuvastatin-named human trials measured oxidative-stress markers directly and found rosuvastatin reduces them; this is graded Yellow as a context flag running opposite to a depletion or burden claim, not because the evidence is weak.

Full detail, limits and 1 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow · opposite direction

Limits on what this shows

  • Key negative or null findings: No rosuvastatin-specific human trial identified in this review found rosuvastatin increasing oxidative-stress markers. Multiple rosuvastatin-named rat studies (renal, cardiac, cochlear, and atherosclerosis models) independently reported the same attenuating direction, consistent corroboration that remains Tier B for the human question.
  • At-risk subgroups: None identified; the direction is consistent across the populations studied (acute coronary syndrome, diabetic nephropathy, general high-risk dyslipidemia).

Regulatory status

Not addressed in the FDA label; no oxidative-stress language present.

Population evidence

Liang et al. 2014 (Clinical Drug Investigation): 143 acute coronary syndrome patients given a loading dose of rosuvastatin before percutaneous coronary intervention showed an antioxidative effect on the markers measured. Nishikido et al. 2016 (Journal of Cardiology): 111 high-risk patients on high-dose rosuvastatin showed reduced MDA-LDL (malondialdehyde-modified LDL, a validated oxidative-stress marker) alongside small dense LDL reduction. Abe et al. 2011 (Journal of Atherosclerosis and Thrombosis): rosuvastatin lipid-lowering therapy in diabetic nephropathy patients improved a named oxidative-stress biomarker alongside kidney-function measures. Resch et al. 2006 (British Journal of Clinical Pharmacology): rosuvastatin 10-40 mg/day for 24 weeks reduced oxidative stress and modulated autoantibody markers. Exact effect sizes and p-values for the Liang, Nishikido, and Abe studies could not be independently verified beyond the search-listing snippets; full text was not accessible in this session.

Mechanism

Named at the class level in the wider statin pharmacology literature: reduced LDL substrate available for oxidation, upregulated endothelial nitric oxide synthase, and reduced NADPH oxidase activity are the commonly cited pleiotropic mechanisms. None of the accessible rosuvastatin-specific sources in this review isolated which mechanism drove its own result.

Counter-evidence held on record

Confounding by indication is a live concern: patients started on rosuvastatin typically also receive broader cardiovascular risk-factor management (diet counseling, smoking cessation, other medications) that independently lowers oxidative-stress markers. None of the four human sources located were clearly confirmed as placebo-controlled for the oxidative-stress endpoint specifically, based on the accessible snippets, which weakens the causal claim even though the association is consistent. Framing caution for the consumer surface This finding must never be used to claim rosuvastatin "protects against oxidative damage" as a health benefit worth seeking the drug for, and must never be paired with a claim that antioxidant supplementation is unnecessary on rosuvastatin. It exists here specifically to rebut the more commonly circulated opposite claim that statins increase oxidative stress by depleting antioxidant reserves; see the Claim audit table below.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Copper

Yellow — Low

See study details

Statin therapy as a class was associated with lower serum copper and ceruloplasmin in one placebo-controlled crossover trial and one earlier observational study; neither confirmed rosuvastatin specifically among the statins its patients were taking, so this is Tier C for rosuvastatin, not Tier A or B.

Full detail, limits and 1 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow · class extrapolation

Limits on what this shows

  • Key negative or null findings: None identified specific to rosuvastatin; no rosuvastatin-named copper study was located in this review at any tier.
  • At-risk subgroups: Not defined for rosuvastatin. The source populations were general dyslipidaemic subjects, not a rosuvastatin-specific or otherwise bounded group.

Regulatory status

Not addressed in the FDA label; no copper language present.

Population evidence

Ghayour-Mobarhan et al. 2005 (Journal of Trace Element Medicine and Biology): statin therapy in dyslipidaemic subjects was associated with a significant reduction in mean serum zinc (9%, p=0.03), copper (9%, p<0.01), and ceruloplasmin (24%, reported significant). Farrokhi et al. 2012 (Clinical Laboratory), from the same research group, reported a randomized placebo-controlled crossover trial examining zinc and copper imbalances with statin therapy. Neither accessible search-listing snippet named which individual statin(s) the patients were taking; rosuvastatin's presence in either cohort could not be confirmed, and full text was not accessible in this session to check.

Mechanism

Not clearly named in the accessible material. Ceruloplasmin is the major copper-carrying plasma protein and is also an acute-phase reactant, so a falling ceruloplasmin could reflect reduced copper transport capacity, reduced inflammation (statins lower hsCRP), or both; this review could not determine which explanation the source authors favored.

Counter-evidence held on record

The falling-ceruloplasmin finding is at least as consistent with statins' well-established anti-inflammatory (hsCRP-lowering) effect as with a true copper-depletion mechanism, since ceruloplasmin is an acute-phase reactant; this alternative explanation was not excluded by either source and is recorded here as a live confound. Framing caution for the consumer surface This is class-level evidence with no confirmed rosuvastatin arm. It must never be worded as "rosuvastatin depletes copper," only as "statin therapy in general has been linked to lower serum copper in limited evidence that has not specifically tested rosuvastatin."

Iron

Yellow — Low

See study details

Statin-linked iron-regulation evidence exists only for atorvastatin and simvastatin, in chronic kidney disease and dialysis patients specifically, and largely trends toward improved rather than worsened iron handling; no rosuvastatin-specific iron study was located at any tier.

Full detail, limits and 1 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow · class extrapolation

Limits on what this shows

  • Key negative or null findings: The erythropoietin-responsiveness studies (Tsouchnikas, Nand) are clinical-outcome studies of anemia treatment efficacy, not direct nutrient-status studies; their iron and ferritin measurements are noted here as secondary data only, per the rule against filing a clinical outcome as a nutrient deficiency.
  • At-risk subgroups: All located evidence is bounded to chronic kidney disease and dialysis populations on atorvastatin or simvastatin; none of it can be extended to rosuvastatin or to patients with normal renal function.

Regulatory status

Not addressed in the FDA label; no iron language present. The label's renal-impairment dosing note (see PK prescreen) concerns rosuvastatin exposure, not iron status.

Population evidence

Masajtis-Zagajewska and Nowicki 2018 (Renal Failure): atorvastatin's effect on iron-metabolism regulation (hepcidin, hemojuvelin, hemoglobin, iron, TIBC, UIBC) was studied in chronic kidney disease patients. Li et al. 2010 (Therapeutic Apheresis and Dialysis): short-term low-dose simvastatin's influence on serum prohepcidin was studied in end-stage renal disease patients. Tsouchnikas et al. 2009 (Nephrology) and Nand et al. 2018 (Journal of the Association of Physicians of India) both studied atorvastatin's effect on erythropoietin responsiveness in maintenance haemodialysis patients, with iron and ferritin as secondary measures. All four studies named atorvastatin or simvastatin specifically; none named rosuvastatin, and a direct search for rosuvastatin-specific iron, ferritin, or hepcidin evidence in this review returned no results.

Mechanism

Named for the class, not rosuvastatin specifically: hepcidin is an inflammation-responsive hormone that blocks iron absorption and release from stores, and statins' anti-inflammatory pleiotropic effect is proposed to lower hepcidin and thereby improve iron availability, the opposite of a depletion mechanism.

Counter-evidence held on record

Confounding by indication and by disease is presumed here: chronic kidney disease and dialysis independently cause hepcidin-mediated functional iron restriction regardless of statin use, and the cited studies used statins as an add-on intervention in an already iron-dysregulated population rather than testing the drug against a statin-naive comparator in the same disease state in every case. Framing caution for the consumer surface This must never be worded as "rosuvastatin affects iron levels." The evidence base concerns two other statins in dialysis patients and trends toward benefit, not harm; it is recorded here as a mechanistic possibility worth tracking, not a finding about rosuvastatin at all.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk

Yellow — Low

See study details

Two rosuvastatin-named animal studies link the drug to gut microbiota composition changes, but both used a hypercholesterolemic diet to induce the disease model itself, which is the more likely driver of any dysbiosis observed; no rosuvastatin-specific human microbiome study was located.

Full detail, limits and 1 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow · animal mechanistic

Limits on what this shows

  • Key negative or null findings: The Schoch diet-reversal finding is itself the strongest evidence against a primary drug-driven mechanism: if rosuvastatin were the main cause of the dysbiosis, restoring a normal diet without addressing the drug would not have been expected to recover it.
  • At-risk subgroups: None defined in rosuvastatin-specific human terms; both sources are non-human models of diet-induced hypercholesterolemia, not a bounded human subgroup.

Regulatory status

Not addressed in the FDA label; no microbiome language present.

Population evidence

Wang et al. 2018 (Lipids in Health and Disease): a rat study examined the relationship between intestinal microbiota dysbiosis and rosuvastatin's own lipid-lowering efficacy, rosuvastatin named specifically. Schoch et al. 2023 (European Journal of Clinical Investigation): a hypercholesterolemic pig model combining diet and rosuvastatin found gut microbiome dysbiosis that was recovered by restoring a normal diet, rosuvastatin named specifically. Both are Tier B, animal.

Mechanism

Not cleanly separable from diet in either source. The Schoch study's own design, in which normalizing diet recovered the microbiome, is itself evidence that diet, not the drug, was the dominant driver in that model. The Wang study frames the relationship as bidirectional, intestinal microbiota affecting how well rosuvastatin works, rather than establishing that rosuvastatin reliably disrupts the microbiome.

Counter-evidence held on record

Confounding by indication is presumed and, here, actively supported by the evidence itself: both animal models used a hypercholesterolemic diet to create the disease state being treated, which independently and predictably alters gut microbiota regardless of drug exposure. This dossier treats gut microbiome risk as unconfirmed for rosuvastatin rather than downgraded to White, because a real rosuvastatin-named mechanistic link (Wang) exists and has not been actively contradicted, only confounded. Framing caution for the consumer surface This must never be worded as "rosuvastatin harms your gut microbiome." The stronger of the two sources (Schoch) points toward diet, not the drug, as the operative variable, and neither source is a human study.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery and utilization

Yellow — Low

See study details

Human ex vivo muscle-tissue data show statins as a class reduce cellular respiration, the oxygen-utilization step of mitochondrial energy production, but rosuvastatin's presence among the statins actually tested could not be confirmed; a dedicated search for rosuvastatin-specific oxygen-delivery, VO2, or exercise-capacity evidence returned no results at any tier.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow · class extrapolation

Limits on what this shows

  • Key negative or null findings: The same source reported no significant effect on cardiac contractile force despite reduced respiration, a bounded, reassuring negative finding worth preserving: reduced cellular oxygen consumption in this ex vivo model did not translate into reduced pump function in the tissue tested.
  • At-risk subgroups: None defined for rosuvastatin specifically; no human in-vivo, whole-body oxygen-delivery or exercise-capacity study naming rosuvastatin was located.

Regulatory status

Not addressed in the FDA label; no oxygen-delivery or exercise-capacity language present.

Population evidence

Somers et al. 2024 (Biomedicine & Pharmacotherapy): ex vivo human skeletal and cardiac muscle tissue exposed to statins showed reduced muscle cell respiration, with statin concentrations in skeletal and cardiac tissue reported as comparable and without a significant effect on cardiac contractile force, per the accessible snippet. The specific statins tested were not identified in that snippet, so rosuvastatin's inclusion could not be confirmed; this is treated as Tier C for rosuvastatin. Targeted searches for "rosuvastatin exercise oxygen uptake VO2" and "rosuvastatin exercise capacity" each returned zero results in this review.

Mechanism

Reduced cellular respiration is, by definition, reduced oxygen utilization at the mitochondrial level; whether this runs through the same CoQ10/mevalonate-pathway mechanism already graded Red, or a separate effect on the electron transport chain, could not be determined from the accessible material.

Counter-evidence held on record

This entry is graded independently of the Red CoQ10 finding and the Mitochondrial burden entry above; see the Overlap map below for how the Somers 2024 source is kept from supporting more than one category at once. Framing caution for the consumer surface This must never be worded as "rosuvastatin reduces oxygen delivery" or linked to exercise fatigue as a nutrient-status claim; the only evidence located is ex vivo tissue data with unconfirmed rosuvastatin identity, and the same source found no effect on cardiac contractile force.

ATP production

Not graded — disclosed evidence gap

See study details

The one rosuvastatin-specific human study that measured mitochondrial ATP synthesis directly found no reduction, even though CoQ10 fell in the same patients; this is not the same as an absence of evidence, and it is not colored because there is no positive deficiency finding here to grade.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. No grade · direct null test

Limits on what this shows

  • Why no grade: The grading key's Red/Orange/Yellow tiers grade the strength of a positive deficiency claim. The only rosuvastatin-specific source located on ATP production is a direct Tier A test that found no deficit, which rebuts a claim rather than supporting one; it therefore does not belong on the Red/Orange/Yellow ladder. Ungraded (reserved for when no Tier B/C evidence and no consumer claim exist) does not fit either, since both a relevant test and a circulating claim exist here (see the Claim audit table below). It is recorded here as its own case: tested, and negative.
  • Key negative or null findings: This entire entry is the negative finding: rosuvastatin lowered CoQ10 without measurably lowering mitochondrial ATP synthesis in the one direct test located.
  • At-risk subgroups: The single available test was conducted in children with familial hypercholesterolemia, a specific and young population; this null result has not been confirmed to generalize to adults, to other indications, or to longer treatment durations, since full text and any subgroup analysis could not be accessed.

Regulatory status

Not addressed in the FDA label; no ATP-production language present.

Population evidence

Already in this dossier's source list: "Rosuvastatin lowers coenzyme Q10 levels, but not mitochondrial adenosine triphosphate synthesis, in children with familial hypercholesterolemia" (The Journal of Pediatrics, 2011). This is the same study already cited under the Red CoQ10 entry's source list, where its full text was noted as inaccessible; no additional numeric detail beyond its own title could be independently verified in this session.

Mechanism

Not applicable; no deficit was found to explain. The study's own title implies a dissociation between the mevalonate-pathway CoQ10 effect and downstream ATP-synthesis capacity, which is itself the notable finding.

Counter-evidence held on record

No rosuvastatin-specific study contradicting this null result was located. No study measuring ATP production in adults on rosuvastatin was located either, in either direction. Framing caution for the consumer surface This finding is strong enough to rebut the popular claim that rosuvastatin depletes cellular energy production the way it lowers CoQ10 (see the Claim audit table below), but it is not strong enough, on one small pediatric study with unverified full text, to publish as a general reassurance that ATP production is unaffected in every patient.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

  • Vitamin D "depletion"

    Where it comes from: Generic statin drug-nutrient depletion charts and supplement-retailer content that extend a broad "statins deplete fat-soluble vitamins" narrative to every statin, rosuvastatin included.

    Why it fails: Actively contradicted by rosuvastatin's own human data. A prospective cohort of 91 hyperlipidemic patients on rosuvastatin for 8 weeks found 25-hydroxyvitamin D rose from 14.0 to 36.3 ng/mL (p<0.001, no placebo arm). An 80-patient dose-comparison trial (10 mg vs. 20 mg rosuvastatin, no placebo arm) found significant increases of 37–43% at both doses (p<0.001 each). A 52-patient randomized trial comparing rosuvastatin 10 mg to atorvastatin 20 mg found no significant within- or between-group change over 12 weeks (rosuvastatin arm: 25.3 to 27.0 ng/mL, not significant). No rosuvastatin-specific study identified in this review measured a decrease. The proposed pleiotropic increase mechanism is itself unconfirmed and none of these designs include an untreated placebo comparison strong enough to prove causation for the increase either; the claim graded here is specifically the depletion direction, which fails outright.

  • "Low vitamin D from statins worsens muscle pain, so supplement it"

    Where it comes from: Practitioner blogs and some older observational literature linking low vitamin D to statin-associated muscle symptoms.

    Why it fails: A large randomized, placebo-controlled sub-study of the VITAL trial (2,083 adults who started a statin during follow-up, 4.8 years, vitamin D 2,000 IU/day vs. placebo) found statin-related muscle pain reported at an equal rate in both arms (31% vs. 31%). The statins used were not broken out by name in the available summary, so this is class-level, not rosuvastatin-specific, evidence, but it directly refutes the supplementation-benefit claim at the class level with no support ever demonstrated for rosuvastatin.

  • "Avoid grapefruit juice with rosuvastatin like other statins"

    Where it comes from: Generic statin-class food-interaction warnings that list grapefruit juice as a caution for "statins" without distinguishing which ones.

    Why it fails: Rosuvastatin is not a major CYP3A4 substrate (only ~10% of a dose is metabolized, via CYP2C9); the FDA label lists no grapefruit-juice interaction. The grapefruit caution is well documented for atorvastatin, simvastatin, and lovastatin, which are CYP3A4 substrates, but its pharmacological basis does not carry over to rosuvastatin with the same force. This is a meaningful pharmacokinetic contrast the consumer surface should reflect rather than blanket-applying the statin-class warning.

What the research says is worth watching

General information from the medication label and the studies above. It is not personal medical advice, and any change belongs with your prescriber.

  • Labs

    No routine CoQ10 testing

    No major lipid-management guideline recommends routine CoQ10 measurement or supplementation for patients on rosuvastatin. The finding above documents a blood-level change, not a clinical indication to test or treat.

  • Symptom work-up

    Unexplained myalgia

    New muscle symptoms on rosuvastatin should prompt standard creatine kinase and clinical evaluation per the label's own myopathy and rhabdomyolysis warnings, not a CoQ10 level, which is not a validated diagnostic marker for statin myopathy.

  • Transporter interactions

    OATP1B1/BCRP inhibitors

    Cyclosporine (roughly 7-fold exposure increase; label caps rosuvastatin at 5 mg/day) and gemfibrozil (label advises against concomitant use or a 10 mg/day cap) are dosing interactions via the transporter that governs rosuvastatin's own clearance, not nutrient interactions, but worth flagging alongside since they are the label's actual interaction concerns.

  • Hepatic and renal status

    Route of clearance

    Because rosuvastatin clears predominantly via biliary/fecal excretion rather than renal handling, hepatic impairment is the more pharmacologically relevant monitoring axis; the label separately notes higher exposure in severe renal impairment as a dosing consideration.

  • Vitamin D and E

    No rosuvastatin-specific action indicated

    Current evidence gives no reason to test or supplement vitamin D or vitamin E specifically because a patient is taking rosuvastatin; any testing should follow standard, drug-unrelated clinical indications.

All references used above
  1. DailyMed, ROSUVASTATIN tablet, film coated (FDA-approved labeling) — U.S. National Library of Medicine. Prescribing information: metabolism, transporters, absorption, elimination, protein binding, and myopathy/rhabdomyolysis warnings.
  2. Mortensen SA et al. Coenzyme Q10, rosuvastatin, and clinical outcomes in heart failure: a pre-specified substudy of CORONA. Journal of the American College of Cardiology, 2010. — PMID 20883926. Pre-specified substudy, N=1,191 of the placebo-controlled CORONA trial. Rosuvastatin 10 mg/day reduced serum CoQ10; CoQ10 not an independent predictor of clinical outcome after adjustment.
  3. Kjekshus J et al. Rosuvastatin in older patients with systolic heart failure (CORONA parent trial). New England Journal of Medicine, 2007. — N=5,011, rosuvastatin 10 mg/day vs. placebo, mean follow-up 2.7 years. Cited here for parent-trial design and dose confirming the substudy above.
  4. Longenecker CT et al. Effect of rosuvastatin on plasma coenzyme Q10 in HIV-infected individuals on antiretroviral therapy (SATURN-HIV secondary analysis). Antiviral Therapy, 2016. — PMC4980145. N=147, randomized, placebo-controlled, rosuvastatin 10 mg/day vs. placebo, 24 weeks. CoQ10 decreased significantly (p=0.002); CoQ10:LDL ratio increased (p=0.036).
  5. Qu H et al. Statin therapy and plasma coenzyme Q10 concentrations: a systematic review and meta-analysis of placebo-controlled trials. Pharmacological Research, 2015. — PMID 26192349. 6 RCTs, 8 treatment arms, statin-stratified. Rosuvastatin subgroup WMD −0.49 µmol/L (95% CI −0.67, −0.31, p<0.001); overall WMD −0.44 µmol/L (95% CI −0.52, −0.37, p<0.001).
  6. Updated meta-analysis of statin treatment and circulating coenzyme Q10 concentrations. European Journal of Medical Research, 2018. — 12 RCTs, N=1,776; statins analyzed by lipophilicity/intensity rather than individually named per-arm. SMD −2.12 (95% CI −3.40, −0.84, p=0.001). Cited for corroborating class-level magnitude only; does not isolate a rosuvastatin subgroup.Rosuvastatin subgroup not separately reported in the accessible summary; used here as class-level corroboration only, not as a Tier A rosuvastatin source.
  7. Rosuvastatin lowers coenzyme Q10 levels, but not mitochondrial adenosine triphosphate synthesis, in children with familial hypercholesterolemia. The Journal of Pediatrics, 2011. — Title and journal confirmed via multiple independent listings (publisher, PubMed record, ResearchGate, Ovid).Full text could not be opened (repeated CAPTCHA/paywall blocks); no sample size, dose, or percentage figures from this study are cited above beyond the qualitative finding stated in its own title.
  8. Effect of statin therapy on the plasma concentrations of retinol, alpha-tocopherol and coenzyme Q10 in children with familial hypercholesterolemia. Cardiovascular Drugs and Therapy, 2020. — Comparative cross-sectional study, two groups of 13 children each; simvastatin 10 mg/day for ≥6 months vs. untreated. No significant difference in retinol, alpha-tocopherol, or CoQ10 between groups; authors concluded no antioxidant-vitamin deficit and no rationale for supplementation.Statin studied was simvastatin, not rosuvastatin. Cited only as counter-evidence to the general class-level CoQ10/vitamin-depletion narrative, excluded from the rosuvastatin cohort test.
  9. Fedacko J et al. A randomized, double-blind, placebo-controlled trial of coenzyme Q10 supplementation in statin-treated patients. Nutrients (MDPI), 2022. — N=35 completers (18 CoQ10, 17 placebo), simvastatin ≥40 mg/day, CoQ10 400 mg/day for 8 weeks. Plasma CoQ10 rose (confirming adherence) but muscle CoQ10 content and mitochondrial function were unaltered, and myalgia did not improve.Statin studied was simvastatin, not rosuvastatin. Cited only as counter-evidence for the contested CoQ10-myopathy causal hypothesis, excluded from the rosuvastatin cohort test.
  10. Yavuz B et al. Increased levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D after rosuvastatin treatment: a novel pleiotropic effect of statins? Cardiovascular Drugs and Therapy, 2009. — Prospective cohort, N=91 hyperlipidemic patients, rosuvastatin 8 weeks, no placebo arm. 25(OH)D rose from 14.0 to 36.3 ng/mL (p<0.001); 1,25(OH)2D rose from 22.9±11.2 to 26.6±9.3 pg/dL (p=0.023).
  11. A study of the effect of rosuvastatin on vitamin D levels. International Journal of Health Sciences and Research, 2016. — Randomized, N=80 statin-naive men, rosuvastatin 10 mg/day (n=40) vs. 20 mg/day (n=40), 8 weeks, no placebo arm. 25(OH)D rose 37.4% (10 mg, p<0.001) and 43.1% (20 mg, p<0.001); between-dose difference not significant (p=0.768).
  12. Comparative effect of atorvastatin and rosuvastatin on 25-hydroxy-vitamin D levels in non-diabetic patients with dyslipidaemia: a prospective randomized open-label pilot study. — PMID 25110531. N=52 (atorvastatin 20 mg n=28; rosuvastatin 10 mg n=24), 12 weeks. Rosuvastatin arm: 25.3±1.8 to 27.0±2.4 ng/mL, not statistically significant (between-group p=0.306). Neither statin significantly changed 25(OH)D.
  13. Patwardhan VG et al. To study impact of treatment with rosuvastatin versus atorvastatin on 25-hydroxy vitamin D concentrations among adult Indian men: a randomized control trial. Indian Journal of Pharmacology, 2020. — Title, journal, and randomized rosuvastatin-vs-atorvastatin design confirmed via publisher and PubMed listings.Full text could not be opened (repeated paywall/CAPTCHA blocks); no numeric results from this specific study are cited above.
  14. Statin therapy and plasma vitamin E concentrations: a systematic review and meta-analysis of randomized placebo-controlled trials. Atherosclerosis, 2016. — 8 treatment arms, 504 participants. Raw plasma vitamin E WMD −16.30% (95% CI −16.93, −15.98, p<0.001); cholesterol-adjusted vitamin E:total-cholesterol ratio WMD +29.35% (95% CI 24.98, 33.72, p<0.001). Individual statins and any rosuvastatin subgroup not specified in the accessible summary.Rosuvastatin not confirmed as a distinguishable arm; treated as Tier C, class-level, for this drug.
  15. Manson JE et al. VITAL trial vitamin D sub-study on statin-associated muscle symptoms, summarized by Northwestern University, 2022. — N=2,083 adults initiating a statin during VITAL follow-up; vitamin D 2,000 IU/day vs. placebo, 4.8 years. Statin-related muscle pain reported at equal rates (31% vs. 31%); no benefit from vitamin D supplementation.Statins used in this sub-study were not individually named in the accessible summary; treated as class-level, not rosuvastatin-specific.
  16. Effects of coenzyme Q10 supplementation on myopathy in statin-treated patients: a systematic review and meta-analysis (updated). — 12 RCTs, 575 patients (294 CoQ10, 281 placebo). CoQ10 improved subjective muscle pain, weakness, cramp, and tiredness scores (all p≤0.006) but had no effect on creatine kinase (p=0.23). Individual statins not specified.Statins studied not individually named in the accessible summary; used only for contested-hypothesis context, not as rosuvastatin-specific CoQ10 evidence.
  17. Drugs.com interaction checker: coenzyme Q10 and Crestor (rosuvastatin). — Consumer-facing interaction database. States no drug-drug interaction is flagged between CoQ10 and Crestor. Tier D consumer source, cited only to document what circulates in commercial interaction tools, not as evidence of nutrient status.
  18. Rosuvastatin. Wikipedia. — Used only to confirm the ATC code (C10AA07) and brand name Crestor against the infobox; not used for any clinical or evidentiary claim.
  19. El-Ganainy SO, El-Mallah A, Abdallah D et al. Rosuvastatin safety: an experimental study of myotoxic effects and mitochondrial alterations in rats. Toxicology Letters, 2017. — PMID 27815113. Rat toxicology study, rosuvastatin named specifically. Reported myotoxic effects and mitochondrial ultrastructural alterations at doses modeling statin myopathy.
  20. Somers T, Siddiqi S, Janssen MCM et al. Effect of statins on mitochondrial function and contractile force in human skeletal and cardiac muscle. Biomedicine & Pharmacotherapy, 2024. — PMID 39326098. Ex vivo human skeletal and cardiac muscle tissue; statins reduced muscle cell respiration without a significant effect on cardiac contractile force per the accessible summary.Individual statins tested were not identified in the accessible search-listing snippet; rosuvastatin's presence in the cohort could not be confirmed. Full text was not accessible in this session; treated as Tier C, class-level, for rosuvastatin.
  21. Somers T, Siddiqi S, Maas RGC et al. Statins affect human iPSC-derived cardiomyocytes by interfering with mitochondrial function and intracellular acidification. Basic Research in Cardiology, 2024. — PMID 38305903. In vitro, human iPSC-derived cardiomyocytes.Individual statins tested not confirmed from the accessible listing; treated as Tier C, class-level, for rosuvastatin.
  22. He W, Liu Y, Tian X. Rosuvastatin improves neurite outgrowth of cortical neurons against oxygen-glucose deprivation via Notch1-mediated mitochondrial biogenesis and functional improvement. Frontiers in Cellular Neuroscience, 2018. — PMID 29387001. Rosuvastatin-named cell/animal model. Cited as counter-evidence that rosuvastatin's mitochondrial effects are not uniformly negative across tissues.
  23. Amer J, Salhab A, Safadi R. Rosuvastatin restores liver tissue-resident NK cell activation in aged mice by improving mitochondrial function. Biomedicine & Pharmacotherapy, 2025. — PMID 40132402. Rosuvastatin-named aged-mouse study. Cited as counter-evidence showing improved, not impaired, mitochondrial function in this model.
  24. Liang D, Zhang Q, Yang H et al. Anti-oxidative stress effect of loading-dose rosuvastatin prior to percutaneous coronary intervention. Clinical Drug Investigation, 2014. — PMID 25186834. N=143 acute coronary syndrome patients, rosuvastatin loading dose before PCI, antioxidative effect reported.Exact effect sizes and p-values could not be independently verified beyond the search-listing snippet; full text not accessible in this session.
  25. Nishikido T, Oyama J, Keida T et al. High-dose statin therapy with rosuvastatin reduces small dense LDL and MDA-LDL. Journal of Cardiology, 2016. — PMID 26162946. N=111 high-risk patients on high-dose rosuvastatin.Full numeric results could not be independently verified beyond the search-listing snippet.
  26. Abe M, Maruyama N, Okada K et al. Effects of lipid-lowering therapy with rosuvastatin on kidney function and oxidative stress. Journal of Atherosclerosis and Thrombosis, 2011. — PMID 21921413. Diabetic nephropathy patients on rosuvastatin.Sample size and effect magnitude could not be independently verified beyond the search-listing snippet.
  27. Resch U, Tatzber F, Budinsky A, Sinzinger H. Reduction of oxidative stress and modulation of autoantibodies related to atherosclerosis with rosuvastatin. British Journal of Clinical Pharmacology, 2006. — PMID 16487219. Rosuvastatin 10-40 mg/day for 24 weeks.Full abstract and numeric results could not be independently verified beyond the search-listing snippet.
  28. Ghayour-Mobarhan M, Lamb DJ, Taylor A et al. Effect of statin therapy on serum trace element status in dyslipidaemic subjects. Journal of Trace Element Medicine and Biology, 2005. — PMID 16240674. Reported reductions in serum zinc (9%, p=0.03), copper (9%, p<0.01), and ceruloplasmin (24%, significant).Individual statin(s) used by the study population not identified in the accessible snippet; rosuvastatin's presence in the cohort could not be confirmed. Full text not accessible in this session.
  29. Farrokhi F, Moohebati M, Aghdaei HR et al. Effects of statin therapy on serum trace element status in dyslipidemic patients: results of a randomized placebo-controlled cross-over trial. Clinical Laboratory, 2012. — PMID 23163117. Randomized placebo-controlled crossover trial of zinc and copper status with statin therapy.Individual statin(s) not confirmed from the accessible snippet; treated as Tier C, class-level, for rosuvastatin.
  30. Masajtis-Zagajewska A, Nowicki M. Effect of atorvastatin on iron metabolism regulation in patients with chronic kidney disease. Renal Failure, 2018. — PMID 30741616. Iron-metabolism markers (hepcidin, hemojuvelin, hemoglobin, iron, TIBC, UIBC).Statin studied was atorvastatin, not rosuvastatin. Cited only as class-level context, excluded from the rosuvastatin cohort test.
  31. Li XY, Chang JP, Su ZW et al. How does short-term low-dose simvastatin influence serum prohepcidin levels in patients with end-stage renal disease? Therapeutic Apheresis and Dialysis, 2010. — PMID 20609184. Serum prohepcidin in end-stage renal disease patients on simvastatin.Statin studied was simvastatin, not rosuvastatin. Cited only as class-level context, excluded from the rosuvastatin cohort test.
  32. Tsouchnikas I, Dounousi E, Papakonstantinou S et al. Beneficial effect of atorvastatin on erythropoietin responsiveness in maintenance haemodialysis patients. Nephrology, 2009. — PMID 19422526. Hemoglobin, serum iron, and ferritin as secondary measures.Statin studied was atorvastatin, not rosuvastatin; erythropoietin responsiveness is a clinical outcome, not a direct iron-status measure. Cited only as secondary context, excluded from the rosuvastatin cohort test.
  33. Nand N, Brijlal, Mittal A. Evaluation of the effect of statins on erythropoietin resistance in patients of chronic kidney disease on maintenance haemodialysis. Journal of the Association of Physicians of India, 2018. — PMID 31313547. Atorvastatin with iron supplementation in dialysis patients.Statin studied was atorvastatin, not rosuvastatin. Cited only as class-level context, excluded from the rosuvastatin cohort test.
  34. Wang L, Wang Y, Wang H et al. The influence of the intestinal microflora to the efficacy of rosuvastatin. Lipids in Health and Disease, 2018. — PMID 29960598. Rat study, rosuvastatin named specifically. Examined the bidirectional relationship between intestinal microbiota dysbiosis and rosuvastatin's lipid-lowering efficacy.
  35. Schoch L, Sutelman P, Suades R, Badimon L, Moreno-Indias I, Vilahur G. The gut microbiome dysbiosis is recovered by restoring a normal diet in hypercholesterolemic pigs. European Journal of Clinical Investigation, 2023. — PMID 36453873. Hypercholesterolemic pig model combining diet and rosuvastatin; dysbiosis recovered by diet normalization.