Ubiquinol
1. Identity: Chemical Names, Structure, Natural Sources, and Common Forms
Chemical Identity and Nomenclature
Ubiquinol is the fully reduced form of coenzyme Q10 (CoQ10). CoQ10 is a lipophilic endogenous compound with a benzoquinone ring and 10 isoprene side-chain units in its structure, and it is present in two redox forms in the human body: the oxidized form, ubiquinone, and the reduced form, ubiquinol. The 1,4-benzoquinone head group of CoQ is its redox active moiety and undergoes reversible one- or two-electron reduction to the semiquinone and ubiquinol, respectively.
The compound is known under several systematic and trade names, including: ubiquinol, coenzyme Q10 (reduced form), CoQ10 (reduced), ubichinol, reduced coenzyme Q10, and the trade ingredient name Kaneka QH®. Its systematic chemical name is 10-[(2R)-6,10,14,18,22,26,30,34-octamethyl-2,6,10,14,18,22,26,30-tetracontanonaenyl]-3,4-dimethoxy-2-methyl-5,6-dihydro-1,4-benzoquinol.
At the molecular level, ubiquinol has a substituted benzenediol nucleus (2,3-dimethoxy-5-methyl) with a decaprenyl (10 isoprene units) lipophilic side chain. Reduction of the quinone to the hydroquinone converts carbonyls to phenolic hydroxyls, creating the ubiquinol structure. CoQ10, which is present in humans, has a side chain of 10 isoprenoid units comprising 50 carbon atoms.
Endogenous Synthesis and Biochemical Classification
Unlike vitamins, CoQ10 is not classified as an essential nutrient because healthy cells can synthesize it de novo from the amino acid tyrosine via the mevalonate pathway, the same biosynthetic route used to produce cholesterol. The CoQ10 biosynthesis pathway is initiated in the cytosol where the isoprene tail is made from the conversion of mevalonate, a key intermediate involved in the synthesis of cholesterol, dolichol, and protein prenylation adducts. The end of the isoprene tail is formed by a cytosolic heterotetrameric protein complex encoded by PDSS1 and PDSS2 genes. The quinone ring unit is also produced in the cytosol from tyrosine or phenylalanine and attached to the isoprene tail inside mitochondria. The benzoquinone ring is then modified in the inner mitochondrial membrane and this process involves at least 12 nuclear-encoded proteins, which are required for the formation of a multiprotein complex known as the "synthome."
CoQ10 is the major species of coenzyme Q found in humans and contains 10 isoprenyl side chains. Reduced CoQ10 (ubiquinol-10) is the predominant form in the human body, accounting for over 90% of circulating CoQ10.
Natural Dietary Sources
CoQ10 is most abundant in fish, chicken, pork, beef, and other muscle meats, liver and other animal organs, and some bee pollens. Plant foods contain less of this vital nutrient than animal foods, with avocado, broccoli, spinach, peanuts, pistachios, and dates providing the most. Being heat-sensitive, CoQ10 is vulnerable to cooking. Total dietary CoQ10 intake is approximately 5 mg/day. Ubiquinol can be provided by dietary sources — typically egg yolks, oily fish, organ meats, and in smaller amounts in nuts and seeds and leafy green vegetables.
Commercial Forms and Preparations
CoQ10 is mainly used as a dietary supplement. It is also available as eye drops and for other topical applications. Supplements offer CoQ10 in either the oxidized form (ubiquinone) or the reduced form (ubiquinol). Oral delivery vehicles include softgel capsules (which are considered superior vehicles due to the lipophilic nature of the molecule), hard-shell capsules, chewable tablets, liquids, and powders mixed into beverages. Various formulations such as liposomes, nanocapsules, and nanoemulsions are being explored to improve bioavailability. Ubiquinol has an important stability problem that hampers its storage and formulation, as it can be easily transformed into its oxidized form — ubiquinone — even at low temperature.
2. Historical and Traditional Context
Discovery and Scientific History
Ubiquinone or coenzyme Q was discovered in the mid-to-late 1950s and identified soon after as an intermediate carrier in the electron transport chain. Moore and colleagues identified coenzyme Q10 in 1940. In 1957, coenzyme Q10 was isolated from beef heart by Dr. Frederick Crane. Karl Folkers, a scientist at Merck Sharpe and Dohme, elucidated its chemical formula. It was not until 1958 that Dr. Karl Folkers identified the precise chemical structure.
CoQ10 has no classical "traditional" or ethnobotanical use, because it is an endogenous mammalian molecule rather than a plant or herbal extract. Historically, it was not used as a traditional remedy; its therapeutic use arises from modern biochemical discovery and clinical research into mitochondrial dysfunction and oxidative stress.
Traditionally, CoQ10 clinical use was based on its antioxidant properties; however, a wide range of highly interesting alternative functions have recently been discovered. In this line, CoQ10 has shown pain-alleviating properties in fibromyalgia patients, a membrane-stabilizing function, immune system enhancing ability, and a fundamental role for insulin sensitivity, apart from potentially beneficial properties for familial hypercholesterolemia patients.
In most countries, CoQ10 has been widely used as a dietary supplement for more than 20 years. The development of commercially available ubiquinol (the reduced form) as a distinct supplement product came later than ubiquinone-based supplements, driven by research demonstrating that ubiquinol is the biologically active, circulating form in human plasma.
3. Key Constituents, Active Compounds, and Mechanisms of Action
The Redox Couple: Ubiquinol and Ubiquinone
Within cells, CoQ10 molecules are continually being switched between two forms. One form, called ubiquinone, is an oxidized state. The other, ubiquinol, is a reduced state. This back-and-forth "cycling" process is the basis of CoQ10's vital roles in human health.
Mitochondrial Bioenergetics
CoQ harvests electrons from two major electron transport chain complexes — NADH:ubiquinone oxidoreductase (complex I) and succinate dehydrogenase (complex II) — and funnels them to ubiquinol:cytochrome c oxidoreductase (complex III). CoQ10 is involved in adenosine triphosphate (ATP) production by transferring electrons from complexes I and II to complex III. The Q cycle within the matrix membrane allows proton transfer from the mitochondrial matrix to the intermembrane space, helping to generate the electrochemical gradient for ATP production.
Antioxidant Function
Ubiquinol is a lipid-soluble electron carrier in the respiratory chain and an electron acceptor for various enzymes in metabolic pathways that intersect at this cofactor hub in the mitochondrial inner membrane. The reduced form of CoQ is an antioxidant which protects against lipid peroxidation. In its reduced form, ubiquinol is a potent lipophilic antioxidant or free radical scavenger. Other relevant functions of CoQ10, such as cell signaling, gene expression, and membrane stabilization, have also been described.
CoQ10 can potentially increase the production of vital antioxidants, such as superoxide dismutase, an enzyme that effectively mitigates vascular oxidative stress in individuals with hypertension. In addition, CoQ10 lowers lipid peroxidation levels by diminishing pro-oxidative compounds. Furthermore, CoQ10 can improve blood flow and safeguard blood vessels by preserving nitric oxide.
Biosynthetic Pathway and Statin Inhibition
Besides the physiological age-related decrease, CoQ10 biosynthesis may also be affected by treatment with hypocholesterolemic drugs that target the mevalonate pathway. Statins are selective inhibitors of β-hydroxy β-methylglutaryl-CoA reductase (HMG-CoA), a key enzyme in this pathway that leads to the synthesis of cholesterol as well as dolichol, ubiquinone, and prenylated proteins.
Age-Related Decline
CoQ levels decline in some tissues in humans and rodents during aging, and coenzyme Q10 supplementation has shown benefits as an anti-aging agent, especially under certain conditions associated with increased oxidative stress. For a 70-year-old patient, tissue CoQ10 may be 40–50% below the levels present at peak synthesis.
Absorption and Pharmacokinetics
As a lipophilic substance, CoQ10 is absorbed in the small intestines with the aid of secretions from the pancreas and bile. After absorption, CoQ10 is reduced to ubiquinol, incorporated into chylomicrons, and transported via lymphatics to the circulation. In the liver, it is incorporated into very low density lipoprotein (VLDL)/low-density lipoprotein (LDL) particles and again released into the circulation. After oral ingestion, the maximum plasma concentration occurs in 6 to 8 hours and has an elimination half-life of more than 30 hours. The primary route of elimination is biliary and fecal. A small fraction is eliminated in the urine.
CoQ10 is a hydrophobic (lipophilic) molecule with a high molecular weight; absorption of dietary CoQ10 is slow but is improved in the presence of fatty meals. Solubilized CoQ10 formulations provide improved bioavailability, with peak plasma concentrations typically ranging from 5.80 to 8.10 hours, depending on the specific formulation. Evidence from pharmacokinetic studies suggests that exogenous CoQ10 does not influence the biosynthesis of endogenous CoQ9/CoQ10, nor does it accumulate into plasma or tissues after cessation of supplementation.
4. Ubiquinol vs. Ubiquinone: Bioavailability Comparison
For ubiquinone to work in the body, it needs to be converted into ubiquinol, the active form of the antioxidant, in the blood or intestines. This conversion process can differ considerably, particularly among older adults and individuals with specific chronic conditions. This phenomenon may be linked to the varying efficiency of the enzymatic system responsible for converting ubiquinone to ubiquinol.
The bioavailability of the reduced form (ubiquinol) was compared to oxidized ubiquinone with identical soft gel capsule excipients by measuring steady-state plasma CoQ10 levels in 12 healthy volunteers. After baseline levels were obtained, follow-up lab work was performed after 4 weeks of 200 mg/day of ubiquinone, after 4 weeks washout, and after 4 weeks of 200 mg/day of ubiquinol. Plasma total CoQ10 increased from 0.9 to 2.5 µg/mL (P < 0.001) after 4 weeks of ubiquinone and increased from 0.9 to 4.3 µg/mL (P < 0.001) after 4 weeks of ubiquinol. Both the increase in plasma CoQ10 and the increase in CoQ10/cholesterol ratio were significantly greater after ubiquinol than after ubiquinone supplementation.
Pharmacokinetic analyses indicated that a test ubiquinol formulation demonstrated substantially higher relative systemic bioavailability compared with a ubiquinone reference product. However, the evidence on bioavailability superiority is not uniformly consistent across studies. Although some studies suggest ubiquinol may be slightly more bioavailable, some research shows no significant difference in bioavailability between the two forms when the ubiquinone is delivered in an optimized, solubilized softgel.
An important caveat regarding the clinical evidence base is that the major clinical trials for heart failure (Q-SYMBIO), migraine prevention, and statin myopathy all used ubiquinone — standard CoQ10 — not ubiquinol. The ubiquinol evidence base consists primarily of absorption studies and fertility research.
5. Scientific Evidence by Area of Use
5.1 Cardiovascular Disease and Heart Failure
CoQ10 acts as a potent antioxidant, membrane stabilizer, and cofactor in the production of adenosine triphosphate by oxidative phosphorylation, inhibiting the oxidation of proteins and DNA. Patients with heart failure have shown CoQ10 deficiency; therefore, a number of clinical trials investigating the effects of CoQ10 supplementation in heart failure have been conducted. CoQ10 supplementation may confer potential prognostic advantages in heart failure patients with no adverse hemodynamic profile or safety issues.
Robust evidence, including data from the Q-SYMBIO trial, demonstrates that CoQ10 supplementation can improve functional capacity, ejection fraction, and reduce major cardiovascular events in heart failure with reduced ejection fraction. The Q-SYMBIO trial was a multi-center, randomized, double-blind, placebo-controlled trial. This landmark randomized controlled trial of 420 patients with chronic heart failure found that 300 mg/day of CoQ10 for 2 years reduced major adverse cardiovascular events by 43%.
A 2024 systematic review and meta-analysis specifically examining CoQ10 efficacy in heart failure was published in Future Cardiology. This review aimed to analyze past literature to evaluate the efficacy of CoQ10 in the population with heart failure. A systematic literature search was conducted through MEDLINE (via PubMed) and Cochrane Library. The outcomes analyzed were reduction in HF-related mortality, improvement in exercise capacity, and left ventricular ejection fraction (LVEF). Among 16 studies, CoQ10 significantly reduced HF-related mortality by 40% and improved exercise capacity in patients with HF, but demonstrated no significant difference in LVEF. CoQ10 significantly enhances exercise capacity and reduces HF-related mortality; however, its impact on patients with reduced LVEF requires further investigation.
Ubiquinol specifically has also been studied in heart failure. Ubiquinol supplementation has high bioavailability and has been demonstrated to improve clinical recovery in patients with severe heart failure. The evidence for CoQ10 in heart failure is among the strongest of any application, supported by multiple randomized controlled trials and meta-analyses, though limitations include heterogeneity in study populations and outcome measures.
5.2 Endothelial Function and Dyslipidemia
A randomized clinical trial published in PMC examined ubiquinol specifically in subjects with mild-to-moderate dyslipidemia. Analysis of data from 48 participants who completed the study demonstrated a significantly increased flow-mediated dilation (FMD) in both treated groups compared with the placebo group (200 mg/day, +1.28% ± 0.90%; 100 mg/day, +1.34% ± 1.44%; p < 0.001) and a marked increase in plasma CoQ10, both total and reduced. Serum nitric oxide metabolites (NOx) increased significantly and dose-dependently in all treated subjects, while LDL oxidation lag time improved significantly in those receiving 200 mg/day. Ubiquinol significantly ameliorated dyslipidemia-related endothelial dysfunction. This effect was strongly related to increased nitric oxide bioavailability and was partly mediated by enhanced LDL antioxidant protection.
5.3 Statin-Associated Myopathy
Studies on CoQ10's efficacy for statin myopathy have yielded inconsistent results, with some reporting symptom relief and others showing no significant benefit. Plasma CoQ10 decreases of 25–50% have been documented in multiple studies of standard statin doses within 2–4 weeks of initiation. The underlying rationale is biochemically established: statins are inhibitors of the synthesis of mevalonate, an intermediate molecule acting as a precursor for both cholesterol and CoQ10.
It should be stressed that research has focused on the treatment, rather than prevention, of statin-induced myopathies, and that there is no evidence from adequate clinical trials whether CoQ10 may be beneficial for prevention. The evidence for CoQ10 in statin-associated muscle symptoms is therefore characterized as mixed and inconclusive, and no definitive recommendation can be made based on currently available data.
5.4 Male and Female Fertility and Reproduction
From a mechanistic standpoint, CoQ10 appears to improve mitochondrial energetics, attenuate oxidative stress, and reduce modifications to DNA, proteins, and lipids. Such mechanisms appear to underpin improvements in oocyte quality and fertilization, markers of sperm quality, and more broadly PCOS symptoms and hormone levels which can impact fertility.
Male fertility: Oxidative stress is one factor that can underpin idiopathic male infertility and CoQ10 is thought to reduce this. Meta-analytical evidence implies that sperm motility, morphology, and sperm counts could potentially be favorably modulated by CoQ10 supplementation.
One published study specifically examining ubiquinol in male subfertility enrolled 62 patients with idiopathic astheno-teratozoospermia. In this retrospective study, 62 patients received 100 mg ubiquinol twice a day for six months due to idiopathic infertility. A separate non-randomized study examining the effects of ubiquinol on men with oligoasthenozoospermia supplemented 60 men with 150 mg/day of ubiquinol for six months. The total sperm count increased by 53% (p < 0.05) and total sperm motility was observed to be 26% higher (p < 0.05) after supplementation.
The evidence is strong in favor of CoQ10 in male subfertility and the most commonly used dose was 200 mg per day, although one study compared a daily dose of 200 mg with 400 mg and found better results with the higher dose. As it takes 3 months for sperm cells to mature, duration of supplementation should be a minimum of 3 months.
Female fertility: Female fertility is influenced by a wide range of factors, with oocyte quality and ovarian reserve representing major limiting determinants. Even before conception, research shows that hormonal contraception use reduces plasma CoQ10 and serum total antioxidant capacity levels. Some evidence from animal studies suggests that ubiquinol plays a role in rescuing oocyte quality beyond the effects of oxidative stress alone. Research advancements suggest that when physiological demands rise during certain life stages such as the reproductive years, the amount of ubiquinol produced internally may not be enough to meet heightened needs, particularly with advanced maternal or paternal age. This places a heavier reliance on obtaining ubiquinol from the diet, presenting it as a conditionally essential nutrient during certain life stages. Overall, ubiquinol appears to enhance mitochondrial energy production and antioxidant defense in gametes, a process that appears to aid sperm function, oocyte quality, and early embryo development.
It should be noted that the majority of fertility research uses CoQ10 broadly (often as ubiquinone); head-to-head clinical trials specifically powered on ubiquinol versus ubiquinone for fertility outcomes are ongoing rather than fully reported.
5.5 Aging and Mitochondrial Function
CoQ levels decline in some tissues in humans and rodents during aging, and CoQ10 supplementation has shown benefits as an anti-aging agent, especially under certain conditions associated with increased oxidative stress. CoQ10 has also shown therapeutic benefits in aging-related disorders, particularly in cardiovascular and metabolic diseases.
CoQ10 is an endogenous lipophilic quinone found in equilibrium between its oxidized (ubiquinone) and reduced (ubiquinol) form, ubiquitous in biological membranes and endowed with antioxidant and bioenergetic properties, both crucial to the aging process. While mechanistic rationale is well-established, the clinical evidence specifically linking ubiquinol supplementation to measurable anti-aging endpoints in healthy humans remains limited and largely preliminary.
5.6 Neurological Conditions
Numerous age-related metabolic and physiological changes, such as increased inflammation and oxidative stress, decreased ATP production, poorer cardiovascular function, and reduced cerebral blood flow, have been implicated in cognitive decline, prompting research into interventions. Among these, CoQ10, an antioxidant and metabolic stimulant, has shown promise in improving some of the underlying biological mechanisms of cognitive decline. Not much is currently known about the efficacy of CoQ10 supplementation on cognition in the elderly.
Regarding neurodegenerative diseases, in adults, CoQ10 at 2,400 mg/day for 5 years has been reported safe and well tolerated, as is ubiquinol (CoQH2) at 1,500 mg/day for 48 weeks, the latter studied in a multicenter, randomized, double-blind, placebo-controlled phase 2 trial in multiple system atrophy. Evidence from completed trials in Parkinson's disease and Huntington's disease using CoQ10 has not demonstrated significant disease modification; findings from these larger trials have been generally negative or inconclusive with respect to slowing disease progression.
5.7 Glycemic Control and Metabolic Function
An open-label pilot study referenced in the clinical literature found that the reduced form of coenzyme Q10 (ubiquinol) may improve glycemic control in patients with type 2 diabetes. CoQ10 has shown a fundamental role for insulin sensitivity, though the evidence base for ubiquinol specifically in metabolic disease consists primarily of pilot studies and mechanistic investigations. Larger, well-powered randomized controlled trials are needed before conclusions can be drawn.
5.8 Sepsis and Critical Illness
Mitochondrial dysfunction has been implicated in the pathogenesis of inflammation and multi-organ dysfunction in major trauma, including burn injury. A randomized, double-blind, placebo-controlled study of ubiquinol in burn patients used 1,800 mg/day administered in divided doses. CoQ10 supplementation increased plasma concentrations of total and reduced CoQ10 and total CoQ10 content in peripheral blood mononuclear cells in burn patients compared with the placebo group. CoQ10 supplementation did not significantly change circulating levels of mitochondrial DNA, inflammatory markers (e.g., interleukins, TNF-α, IFN-γ), or Sequential Organ Failure Assessment (SOFA) scores compared with the placebo group. This study showed that a relatively high dose of reduced CoQ10 supplementation increased the intracellular CoQ10 content as well as plasma concentrations in burn patients. Clinical evidence in sepsis and critical illness remains at early stages, with ubiquinol demonstrating bioavailability but not yet confirmed clinical benefit in these settings.
6. Body Systems and Health Areas Associated with Ubiquinol
- Cardiovascular system: Heart failure, cardiomyopathy, endothelial function, blood pressure regulation, and lipid protection via antioxidant activity on LDL particles.
- Mitochondrial bioenergetics: ATP synthesis across all high-energy tissues; particularly relevant to heart, liver, skeletal muscle, kidney, and brain.
- Reproductive system: Sperm quality, motility and morphology; oocyte mitochondrial function and fertilization; embryo development.
- Neuromuscular system: Muscle function in the context of statin-associated myopathy; neurological disease research in Parkinson's, Huntington's, and multiple system atrophy.
- Metabolic system: Emerging evidence in glycemic regulation and insulin sensitivity.
- Immune and systemic: CoQ10 can potentially increase the production of vital antioxidants such as superoxide dismutase. Antioxidant protection of cellular membranes and circulating lipoproteins from oxidative damage.
- Integumentary: CoQ10 is present in skin; declining levels with age have been associated with reduced antioxidant protection in dermal fibroblasts.
7. Dosage Forms and Dosages Reported in Studies
The human supplementation dose of CoQ10 is generally 100 to 300 mg/d. Toxicity is unlikely up to a daily intake of 1200 mg/d, although typical dosages have been 100 to 200 mg/d.
Specific dosages reported in identified clinical studies and trials include:
- Bioavailability comparison (Langsjoen 2014): 200 mg/day of ubiquinol or ubiquinone for 4 weeks each in a crossover design in 12 healthy volunteers.
- Endothelial function/dyslipidemia RCT: Both 100 mg/day and 200 mg/day of ubiquinol for 8 weeks were studied in 48 participants with mild-to-moderate dyslipidemia.
- Heart failure (Q-SYMBIO trial): 300 mg/day of CoQ10 for 2 years in 420 patients with chronic heart failure.
- Male subfertility (retrospective): 100 mg ubiquinol twice a day (200 mg/day) for six months in 62 patients with idiopathic infertility.
- Male subfertility (ubiquinol): 150 mg/day ubiquinol was supplemented to 60 men with oligoasthenozoospermia, age 20–40 years, for six months.
- Male subfertility (ubiquinol, placebo-controlled): A more recent placebo-controlled prospective study investigated 300 mg of oral ubiquinol for 26 weeks (approximately two spermatogenesis cycles) in 106 patients.
- Burn patient study (RCT): 1,800 mg/day of reduced CoQ10 (ubiquinol-10) administered in three divided doses.
- Multiple system atrophy (phase 2 trial): Ubiquinol (CoQH2) at 1,500 mg/day for 48 weeks in a multicenter, randomized, double-blind, placebo-controlled phase 2 trial.
- Diastolic heart failure protocol: 600 mg/day ubiquinol has been described as well within the clinically recommended range.
- Bioavailability in older adults (crossover RCT): 200 mg/day of ubiquinol or ubiquinone for 2 weeks with 2-week washout between crossover.
Absorption of dietary CoQ10 is slow but is improved in the presence of fatty meals. The acceptable daily intake (ADI) of CoQ10 has been set at 12 mg/kg/day.
8. Safety Considerations and Drug Interactions
General Safety Profile
Published reports concerning safety studies indicate that CoQ10 has low toxicity and does not induce serious adverse effects in humans. The acceptable daily intake (ADI) is 12 mg/kg/day, calculated from the no-observed-adverse-effect level (NOAEL) of 1,200 mg/kg/day derived from a 52-week chronic toxicity study in rats. Risk assessment for CoQ10 based on various clinical trial data indicates that the observed safety level (OSL) for CoQ10 is 1,200 mg/day/person.
In preclinical studies, ubiquinol's No-Observed-Adverse-Effect Level (NOAEL) is 300 to 600 mg/kg in Sprague-Dawley rats.
The side effects reported in human studies are generally limited to mild gastrointestinal symptoms such as nausea and stomach upset seen in a small number of subjects. No side effects were noted in the 12-person crossover bioavailability study comparing 200 mg/day ubiquinol and ubiquinone.
High-Dose and Long-Term Safety
For genetic CoQ10 deficiencies in children, supplementation with CoQ at 4 mg/kg body weight per day for four years is confirmed safe. In adults, CoQ at 2,400 mg/day for 5 years has been reported safe and well tolerated.
Interaction with Anticoagulants (Warfarin)
From a chemistry perspective, CoQ10 is an analogue of vitamin K. Through this analogy, it — in particular, the R-enantiomer — may interact with warfarin through cytochrome P450. There are several case reports on the interaction between coenzyme Q10 and warfarin. Nevertheless, a randomized, double-blind, placebo-controlled, cross-over trial found no clinical significance of interaction in the coenzyme Q10 supplement at 100 mg daily with warfarin therapy. Because of its structural similarity to vitamin K, CoQ10 has been suggested to have procoagulant activity; this indicates that patients on anticoagulant therapy may need to have their INR monitored and anticoagulant dosage adjusted accordingly.
Interaction with Antihypertensive Medications
Polypharmacy should be considered when examining the effects of CoQ10, as negative interactions with medications such as warfarin and antihypertensive medications may increase the risk of negative health outcomes. CoQ10 has documented blood-pressure-lowering effects in clinical trials, and concurrent use with antihypertensive drugs may require monitoring.
Statin Interaction (Mechanistic)
Statins are inhibitors of the synthesis of mevalonate, an intermediate molecule acting as a precursor for both cholesterol and CoQ10. In an in vitro skin model, statin addition resulted in CoQ10 deprivation and signs of aging, but upon addition of CoQ10 to the medium, the tissue levels could be restored and markers of aging were reduced. The shared biosynthetic pathway means that statins reduce endogenous CoQ10 levels, providing a mechanistic rationale for supplementation in patients taking these drugs, though clinical benefit in alleviating statin myopathy has not been definitively established.
Stability and Storage Considerations
Ubiquinol has an important stability problem which hampers its storage and formulation. It can be easily transformed into its oxidized form — ubiquinone — even at low temperature. Ubiquinol needs to be protected from extreme heat and light, and should be stored in a cool and dry place.
Regulatory Status
Although CoQ10 lacks approval from the United States Food and Drug Administration (FDA) for treating any medical condition, it is readily accessible as an over-the-counter dietary supplement. In the U.S., CoQ10 (ubiquinol/ubiquinone) is regulated as a dietary supplement under DSHEA. The FDA does not evaluate dietary supplements for safety or effectiveness prior to marketing, but manufacturers must ensure safety and truthful labeling.
References
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