What is coenzyme Q10?
Coenzyme Q10 (CoQ10) is a lipid-soluble, vitamin-like compound synthesized by the body from mevalonate and tyrosine. CoQ10 plays a crucial role in the production of adenosine triphosphate (ATP) in mitochondria, and serves as a potent endogenous (i.e., produced in the body) antioxidant capable of neutralizing free radicals in lipid structures.[10][11][12]
While the body naturally produces CoQ10, it can also be obtained from supplements or specific foods (refer to the question “What are the main sources of coenzyme Q10?” for more details). CoQ10 exists in either its oxidized form (ubiquinone) or its reduced form (ubiquinol), with the body interchanging the two depending on the cell’s oxidative state.[11][10] The ubiquinol/ubiquinone ratio is often used as an indicator to measure the body’s response to oxidative stress. A low ubiquinol and high ubiquinone ratio may suggest ineffective conversion between the two, potentially indicating decreased antioxidant activity.[13]
What are the main benefits of coenzyme Q10?
CoQ10 is a key endogenous antioxidant; however, its production in the body can be affected by age, underlying medical conditions, and other factors. One meta-analysis, involving healthy participants and those with cardiovascular or metabolic disease, revealed that supplementation with 30–500 mg daily of CoQ10 significantly increased total antioxidant capacity (TAC) scores and decreased malondialdehyde (MDA) levels (an oxidative stress marker) compared to the control group, although it did not significantly affect levels of another endogenous antioxidant, superoxide dismutase (SOD).[11]
Another meta-analysis indicated that supplementation with CoQ10 significantly lowered levels of inflammatory markers such as c-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha), suggesting a potential anti-inflammatory effect.[14]
Additionally, CoQ10 demonstrated potential for reduction of migraine and non-migraine headaches in both adults[6] and children aged 6–12 years.[15]
Furthermore, extensive research has explored the cardiovascular and metabolic benefits of CoQ10, yielding promising results. For detailed information on CoQ10's main benefits on cardiovascular and metabolic health, please refer to the question “What are coenzyme Q10’s main benefits on cardiovascular and metabolic health?”
Finally, preliminary evidence suggests that supplementation with CoQ10 (300 mg) may be effective in reducing symptoms associated with fibromyalgia.[16]
Can coenzyme Q10 reduce statin-related side effects and pathologies?
Does coenzyme Q10 have an impact on fertility?
What is the impact of coenzyme Q10 on skin health?
Can supplementation with coenzyme Q10 improve exercise performance?
What are coenzyme Q10’s main benefits for cardiovascular and metabolic health?
What are the main drawbacks of coenzyme Q10?
Supplementation with CoQ10 is generally considered safe and well-tolerated, even at high dosages (1,200 mg per day)[4] and for durations up to 12 months.[4]
Regarding potential interactions, there is mixed clinical evidence that CoQ10 may interact with warfarin.[17][18][19] Additionally, animal studies suggest a potential interaction between CoQ10 and theophylline (a drug used for asthma and chronic obstructive pulmonary disease).[20]
How does coenzyme Q10 work?
CoQ10 acts as a non-enzymatic endogenous antioxidant,[21] exerting its effects by increasing the production of key antioxidants (e.g., SOD) and by inhibiting lipid peroxyl radicals, thereby reducing lipid peroxidation levels.[4] Additionally, CoQ10 serves as a cofactor in the mitochondrial electron transport chain, transporting electrons from complex I and II to complex III to synthesize ATP, and reducing the production of superoxide (a free radical).[11] Furthermore, CoQ10 appears to regenerate α-tocopherol (vitamin E’s active metabolite) from its radical state back to its antioxidative state.[22][11] Finally, another potential mechanism observed in vitro and in animal studies is the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2), which regulates the cellular response to oxidative stress. However, more research is needed to verify this mechanism of action.[11]
CoQ10 appears to improve glycemic control in individuals affected by type 2 diabetes (characterized by elevated oxidative stress and abnormalities in mitochondrial function), thanks to its antioxidant activity.[5][13]
CoQ10 may improve the lipid profile through several potential mechanisms. In vitro studies showed that exposure of endothelial cells to CoQ10 was linked to downregulation of lectin-like oxLDL receptor (LOX-1), to which oxidized LDL (oxLDL) bind causing an increase in reactive oxygen species (ROS) levels, and stimulation of 5’ adenosine monophosphate-activated protein kinase (AMPK), which regulates mitochondrial ROS production and oxidative stress resistance.[23][24] Furthermore, CoQ10 may increase fatty acid oxidation, therefore reducing the level of free fatty acids in mitochondria,[25] and it may decrease triglyceride levels by increasing lipolysis.[24]
What are other names for Coenzyme Q10
- CoQ10
- Ubiquinone
- Ubiquinol
- 4-benzoquinone
- Vitamin Q
- Idebenone (Synthetic derivative)
Dosage information
The total daily requirement for coenzyme Q10 (CoQ10), encompassing both endogenous synthesis and external sources like food or supplements, is estimated to be approximately 500 mg per day. Notably, only a minimal amount of around 5 mg daily is typically acquired through dietary intake.[1][2]
For supplementation, the recommended dosage usually falls within 100–200 mg per day.[3][4][5] Although some studies have explored doses as high as 1200 mg per day,[4], there is currently no evidence that a higher dosage offers additional benefits.
In the context of migraine prevention, a dosage of 300 mg per day of CoQ10 has been studied with positive outcomes.[6]
CoQ10 is commonly available in capsule form, with oral administration peaking in blood levels 5–10 hours after intake, and an elimination half-life of approximately 33.19 hours.[7]
Due to its lipophilic nature, it’s advised to take CoQ10 with fat-containing foods, and capsules should ideally be formulated with a lipophilic transport (e.g., a carrier oil) for better absorption.[8]
Additionally, grapefruit juice, known to inhibit the transporter P-glycoprotein which mediates CoQ10 efflux in intestinal cells, has been found to enhance CoQ10 absorption when combined in vitro.[9]
Frequently asked questions
Coenzyme Q10 (CoQ10) is a lipid-soluble, vitamin-like compound synthesized by the body from mevalonate and tyrosine. CoQ10 plays a crucial role in the production of adenosine triphosphate (ATP) in mitochondria, and serves as a potent endogenous (i.e., produced in the body) antioxidant capable of neutralizing free radicals in lipid structures.[10][11][12]
While the body naturally produces CoQ10, it can also be obtained from supplements or specific foods (refer to the question “What are the main sources of coenzyme Q10?” for more details). CoQ10 exists in either its oxidized form (ubiquinone) or its reduced form (ubiquinol), with the body interchanging the two depending on the cell’s oxidative state.[11][10] The ubiquinol/ubiquinone ratio is often used as an indicator to measure the body’s response to oxidative stress. A low ubiquinol and high ubiquinone ratio may suggest ineffective conversion between the two, potentially indicating decreased antioxidant activity.[13]
The main dietary sources of coenzyme Q10 include:[47]
| Food category | Food containing CoQ10 | Ubiquinol/Ubiquinone Content (mg/kg) |
|---|---|---|
| Meat (terrestrial) | Pork heart | 118.1–282 |
| Reindeer meat | 157 | |
| Chicken heart | 92.3–192 | |
| Beef heart | 113.3 | |
| Chicken liver | 116.2–132.2 | |
| Chicken breast | 7.8–17.1 | |
| Beef liver | 39.2–50.5 | |
| Chicken thigh | 24.2–25.0 | |
| Beef shoulder | 40.1 | |
| Beef sirloin | 14.0 | |
| Chicken wing | 11.0 | |
| Beef thigh | 30.3 | |
| Beef tenderloin | 26.5 | |
| Meat (aquatic) | Herring heart | 120.0–148.4 |
| Yellowtail | 12.8–20.7 (higher in young fish: 33.4) | |
| Mackerel, general | 43.3 | |
| Mackerel heart | 105.5–109.8 | |
| Mackerel red meat | 67.5–67.7 | |
| Mackerel white meat | 10.6–15.5 | |
| Horse mackerel | 3.6–20.7 (note: one source states 130) | |
| Sardines | 5.1–64.3 | |
| Baltic herring | 10.6–15.9 | |
| Cuttlefish | 4.7–8.2 | |
| Salmon | 4.3–7.6 | |
| Albacore (Tuna) | 6.2 | |
| Tuna general | 4.9 (canned sources: 14.9–15.9) | |
| Pike | 5.4 | |
| Flat fish | 1.8–5.5 | |
| Shrimp | 2.8 | |
| Scallop | 5.0 | |
| Bogue sea bream | 3.7 | |
| Octopus | 3.5 | |
| Annular sea bream | 3.4 | |
| Common pandora | 3.1 | |
| European hake | 2.9 | |
| Red mullet | 2.4 | |
| Striped mullet | 2.4 | |
| Red band fish | 2.4 | |
| Brill | 1.9 | |
| Common mussel | 9.5 | |
| Grooved carpet shell | 6.6 | |
| Dairy and Eggs | Butter | 7.1 |
| Cheeses, general | 1.4–2.1 | |
| Emmental | 1.3 | |
| Edam | 1.2 | |
| Cow’s milk | 0.5–1.9 (lower in UHT milk and lower-fat products) | |
| Yogurt, kefir, cream, curd | 0.3–1.2 (correlated with fat content) | |
| Eggs | 0.7–3.7 (yolk up to 5.2) |
CoQ10 is a key endogenous antioxidant; however, its production in the body can be affected by age, underlying medical conditions, and other factors. One meta-analysis, involving healthy participants and those with cardiovascular or metabolic disease, revealed that supplementation with 30–500 mg daily of CoQ10 significantly increased total antioxidant capacity (TAC) scores and decreased malondialdehyde (MDA) levels (an oxidative stress marker) compared to the control group, although it did not significantly affect levels of another endogenous antioxidant, superoxide dismutase (SOD).[11]
Another meta-analysis indicated that supplementation with CoQ10 significantly lowered levels of inflammatory markers such as c-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha), suggesting a potential anti-inflammatory effect.[14]
Additionally, CoQ10 demonstrated potential for reduction of migraine and non-migraine headaches in both adults[6] and children aged 6–12 years.[15]
Furthermore, extensive research has explored the cardiovascular and metabolic benefits of CoQ10, yielding promising results. For detailed information on CoQ10's main benefits on cardiovascular and metabolic health, please refer to the question “What are coenzyme Q10’s main benefits on cardiovascular and metabolic health?”
Finally, preliminary evidence suggests that supplementation with CoQ10 (300 mg) may be effective in reducing symptoms associated with fibromyalgia.[16]
In one pilot study, CoQ10 supplementation in men with asthenozoospermia (poor seminal motility) appeared to be somewhat effective at improving seminal motility, though not sperm count or sperm morphology,[29] while another study also noted an increase in sperm density with CoQ10 supplementation.[30]
Additionally, one study involving men with a low fertilization rate in an infertility clinic reported an increase in fertility when taking 60 mg of CoQ10 daily for 103 days before in vitro fertilization, suggesting an improvement in sperm function.[31] Moreover, in another study, 200 mg of COQ10 daily for 6 months improved sperm motility in men, leading to increased fertility, with 3 out of 22 couples achieving spontaneous pregnancy within 3 months of the discontinuation of therapy.[29]
Aged skin is strongly correlated with abnormal mitochondrial function, elevated oxidant levels, and a decline in CoQ10 levels. This decline is evident with aging, irrespective of UV radiation exposure, but is exacerbated by excessive UV radiation, leading to oxidative stress. This reduction in CoQ10 is also associated with diminished mitochondrial membrane potential and a shift from lipolysis to glycolysis for sustaining energy metabolism.[32] For these reasons, CoQ10 is believed to offer skin protection due to its role as a mitochondrial factor and antioxidant.[33]
In vitro studies have demonstrated that CoQ10 may improve skin elasticity by increasing elastin expression[34] and preserving collagen.[35] CoQ10 may also have anti-wrinkle effects by protecting against UV damage,[36] and depigmentation potential[34] with more pronounced effects in cells purposely depleted of CoQ10.[37]
Furthermore, the application of a cream containing 0.01% of CoQ10 twice daily for a week, both in older and younger individuals, increased and preserved mitochondrial membrane function, suggesting a potential benefit of using CoQ10 in anti-aging skin care products.[32]
Additionally, a few studies have used combination therapies, usually with vitamin E, retinyl palmitate (highly bioactive form of vitamin A), grape seed extract (as oil), and linseed oil, and found that topical application of these combination therapies protected against UV and reduced wrinkling in aged subjects.[38]
Results to date have been mixed. In one study involving older athletes concurrently taking statin drugs (cholesterol-lowering drugs), supplementation with 200 mg of CoQ10 for 6 weeks improved leg strength, as assessed by leg extensions.[39] On the other hand, another study including younger trained and untrained individuals found that neither a single dose of CoQ10 (200 mg) before exercise nor 2 weeks of continuous supplementation had any significant effect on muscular force production or muscular fatigue.[40]
Regarding anaerobic cardiovascular exercise performance, the evidence of the benefits of CoQ10 supplementation is not conclusive.[39] However, when untrained individuals supplemented with CoQ10 (300 mg) for one week before a 210-minute cycling test, they reported less fatigue rel
CoQ10's impact on the lipid profile in adults varies across studies and depends on the participants' health status, making it challenging to generalize findings. In one meta-analysis that included both healthy individuals and those with cardiovascular and metabolic disorders, supplementation with CoQ10 effectively lowered (improved) total cholesterol (TC), low-density lipoprotein (LDL), and triglyceride (TG) levels.[24] Another meta-analysis involving individuals with chronic kidney disease observed improvements in TC, LDL, MDA, and creatine levels with CoQ10 supplementation, although levels of CRP, TG, high-density lipoprotein HDL, fasting glucose, insulin, and insulin resistance did not vary significantly compared to placebo.[41] Conversely, one meta-analysis of studies whose participants had coronary artery disease, specifically myocardial infarction, coronary heart disease, left ventricular systolic dysfunction, and chronic heart failure, found no significant impact of supplementation with CoQ10 on the lipid profile.[42]
Furthermore, supplementation with CoQ10 appeared to decrease fasting glucose, glycated hemoglobin (HbA1c), fasting insulin levels, and insulin resistance, particularly in individuals with type 2 diabetes, when CoQ10 was taken for 12 weeks or longer, and at a dosage greater than 200 mg daily.[5]
Additionally, for people with heart failure, who often present with CoQ10 deficiencies, supplementation with CoQ10 may be beneficial.[21] One meta-analysis suggested that CoQ10 significantly decreased the risk of mortality and increased the exercise capacity (measured as exercise duration or walking distance) compared to placebo, although it had no significant effect on left ventricular ejection fraction or cardiac function.[43]
Regarding blood pressure, CoQ10 may reduce systolic blood pressure (SBP) in individuals with cardiometabolic disorders (e.g., diabetes, dyslipidemia), particularly when doses of 200 mg per day or higher are taken for longer than 12 weeks. However, more high-quality data is needed to confirm these findings.[3]
Finally, CoQ10 may increase blood flow in people with otherwise-hindered blood flow thanks to its antioxidant properties, which are thought to preserve the actions of nitric oxide (a vasodilating and blood pressure-reducing agent) on the endothelium ( the layer of cells that lines blood vessels).[44]
Supplementation with CoQ10 is generally considered safe and well-tolerated, even at high dosages (1,200 mg per day)[4] and for durations up to 12 months.[4]
Regarding potential interactions, there is mixed clinical evidence that CoQ10 may interact with warfarin.[17][18][19] Additionally, animal studies suggest a potential interaction between CoQ10 and theophylline (a drug used for asthma and chronic obstructive pulmonary disease).[20]
CoQ10 acts as a non-enzymatic endogenous antioxidant,[21] exerting its effects by increasing the production of key antioxidants (e.g., SOD) and by inhibiting lipid peroxyl radicals, thereby reducing lipid peroxidation levels.[4] Additionally, CoQ10 serves as a cofactor in the mitochondrial electron transport chain, transporting electrons from complex I and II to complex III to synthesize ATP, and reducing the production of superoxide (a free radical).[11] Furthermore, CoQ10 appears to regenerate α-tocopherol (vitamin E’s active metabolite) from its radical state back to its antioxidative state.[22][11] Finally, another potential mechanism observed in vitro and in animal studies is the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2), which regulates the cellular response to oxidative stress. However, more research is needed to verify this mechanism of action.[11]
CoQ10 appears to improve glycemic control in individuals affected by type 2 diabetes (characterized by elevated oxidative stress and abnormalities in mitochondrial function), thanks to its antioxidant activity.[5][13]
CoQ10 may improve the lipid profile through several potential mechanisms. In vitro studies showed that exposure of endothelial cells to CoQ10 was linked to downregulation of lectin-like oxLDL receptor (LOX-1), to which oxidized LDL (oxLDL) bind causing an increase in reactive oxygen species (ROS) levels, and stimulation of 5’ adenosine monophosphate-activated protein kinase (AMPK), which regulates mitochondrial ROS production and oxidative stress resistance.[23][24] Furthermore, CoQ10 may increase fatty acid oxidation, therefore reducing the level of free fatty acids in mitochondria,[25] and it may decrease triglyceride levels by increasing lipolysis.[24]
CoQ10 deficiency can be attributed to primary or secondary factors.[2]
A primary deficiency is a result of mutations in genes directly involved in the biosynthesis of CoQ10.[2]
A secondary deficiency can also stem from genetic mutations, but ones that affect genes not directly involved in CoQ10 synthesis, or it can be caused by non-genetic factors. For instance, the production of CoQ10 declines with age, peaking at 25 and decreasing by approximately 50% by the age of 65. Furthermore, certain health conditions, such as mitochondrial DNA depletion syndrome, phenylketonuria, mucopolysaccharidosis, cardiovascular disease, chronic kidney disease, type 2 diabetes[13], and metabolic syndrome, have been associated with lower CoQ10 levels.[2][26]
Finally, medications like statins (cholesterol-lowering drugs), amitriptyline (an antidepressant), and bisphosphonates (used in the treatment of osteoporosis), may interfere with CoQ10 production and reduce its levels when taken long-term.[PM
Ubiquinone is the most common form of CoQ10 found in supplements. After ingestion, ubiquinone is converted into ubiquinol (the reduced form of CoQ10), which has the most antioxidant properties.[45][46] The effectiveness of supplementation with ubiquinol compared to ubiquinone is still unclear. Some studies suggest that ubiquinol may be more effective,[46] while others report no significant difference between the two.[5]
The bioavailability of CoQ10 depends not just on whether it’s taken in the oxidized or reduced form, but also on the supplement formulation. For absorption in the gastrointestinal tract, CoQ10 crystals obtained via synthesis (in a lab or via the yeast fermentation method) must be dissociated into individual CoQ10 molecules, and this dissociation should be maintained throughout the shelf life of the CoQ10 preparation to be effective. This crystal dispersion process appears to play an important role in increasing the bioavailability of CoQ10. Notably, most studies suggesting the superiority of ubiquinol supplementation did not compare it to ubiquinone-dispersed formulations, likely due to their unavailability at the time of the study.[1]
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