Coenzyme Q10, also known as CoQ10, is an essential compound that is commonly known for its role in energy production. The powerhouse complexes within your cells, called the mitochondria, rely on sufficient amounts of CoQ10 to function, where reduced availability of the compound is linked to mitochondrial dysfunction, ageing and a higher risk of disease. 

Mitochondria, while performing their critical function as the battery packs of the cells, generate reactive oxygen species, also known as free radicals. Mitochondria are highly susceptible to damage by these free radicals they produce as well as those produced during other processes happening within the tissues they are located in. They therefore require a great degree of protection from the potential damage, typically through the assistance provided by potent antioxidants. 

CoQ10 effects on ageing

Naturally occuring in the body, CoQ10 is a fat-soluble compound that is made in the inner mitochondrial membrane and is critical for the functioning of these energy cells. Because CoQ10 decreases in production with increase in age it has been extensively studied for its effects on health- and lifespan (1). 

Adequate levels of CoQ10 are needed for protection against oxidative stress (2). There are two important characteristics of CoQ10 that need to be considered, which differentiates the free-radical scavenging mechanisms it uses when compared to other common antioxidants (3,4). 

  1. CoQ10 acts as an electron carrier from complexes I and II to complex III in the mitochondrial electron transport chain, which is critical for the synthesis of the main energy compound of the body, called ATP. Free radicals, or reactive oxygen species (ROS) are byproducts of ATP production and other chemical reactions within the cell. While ROS are involved in multiple cellular functions, such as growth and signalling, chronic high levels damage the proteins, fats and other important compounds that are essential for the cell to function (5). Dysfunction in these cells has been well-studied in its effects on health and disease, which is what gave rise to the 1972 mitochondrial free radical theory of ageing, presented by scientist D. Harman (6).
  2. When the mitochondria are inundated with free radicals and they begin to dysfunction, they shift from creating energy through oxidative phosphorylation (OXPHOS) to the less efficient method called anaerobic glycolysis. CoQ10, however, may mitigate the damage caused by the increase in ROS as it acts as a primary antioxidant and free radical scavenger, removing them before they can cause damage to the cell’s DNA. Additionally, CoQ10 enhances the action of other free radical scavenging antioxidants like vitamin E (7). 

These two mechanisms are the reason CoQ10 has been considered for its role in the prevention and treatment of many chronic diseases. 

Neurological benefits

Due to the heavy reliance of the brain on oxygen and the production of ATP generated by the mitochondria as well as the higher susceptibility of fats to be oxidized by free radicals, dysfunctional OXPHOS and higher ROS increase the risk of neurological disorders. For this reason, CoQ10 has been explored for its role in the prevention and treatment of multiple neurological conditions.

Schizophrenia. Mitochondrial dysfunction has been implicated in the disease pathogenesis of schizophrenia, which is one of the world’s leading causes of disability (8). Despite the mechanisms by which this occurs still requiring further research, it has been suggested that low levels of CoQ10 in patients with this neurological disease may contribute to mitochondrial dysfunction in part due to an increased use of CoQ10 as a result of the shift from OXPHOS to anaerobic glycolosis. In a review of current randomised control trials, researchers investigating the use of CoQ10 to replenish low levels in susceptible patients have found positive effects on cognitive function, energy metabolism as well as affective and motivational difficulties. Research concludes that Coq10 may be a valuable intervention strategy and can be taken as a supplement in schizophrenic patients with minimal side effects (9). 

Parkinson’s disease. Disturbances of the transport of electrons from complex 1 in the mitochondrial ETC as well as increased ROS and reduced levels of CoQ10 have been implicated in the pathogenesis of Parkinson’s disease. Many randomised controlled trials have explored the effects of adding supplemental CoQ10 as a therapy for the treatment of the disease and the effect it has on its progression. Early research showed that when patients in the early stages of Parkinson’s were given 1,200mg of CoQ10 for eight months, their level of decline was significantly slower than those participants given a placebo or a 300mg or 600mg CoQ10 dose (10). Some later studies, however, have not found the same correlation and other studies still, have found that long-term treatment with CoQ10 may not provide meaningful benefit for those with Parkinson’s disease, however, further studies are needed. 

Huntington disease. Mitochondrial impairments have been implicated in the development of this disease where it has been found that as a result of ATP depletion, decreased activity of the ETC and increased levels of oxidation, DNA damage results in the psychiatric, cognitive and clinical decline in genetically susceptible people. In untreated Huntington patients, it has been noted that their CoQ10 levels are significantly lower than those receiving treatment or those without the disease (11). A study conducted in mice allocated the animals to four different groups, where they were either given a control diet, one supplemented with CoQ10, one supplemented with the pharmaceutical drug remacemide, or a combination of both. Results showed that all three of the treatments when compared to the control group, significantly improved their survival, however, the combined therapy of the pharmaceutical and CoQ10 was found to be far more effective than either treatment alone. In fact, the animals were more than twice as likely to have an increase in lifespan when using both compared to each in isolation (12).  A more recent randomized controlled trial to test the hypothesis that high-dose CoQ10 would slow the progression of functional Huntington disease found less positive results, with the conclusion stating that 2,400mg/d of CoQ10 for 60 months was not effective in slowing the decline of HD (13). Notably, however, this high dose was deemed safe and well-tolerated in the subjects for this length of time. 

While preliminary research into the use of CoQ10 in neurological diseases appears promising, it has been suggested that larger clinical trials be conducted to test the effects of various CoQ10 subsets in variable doses. 

Heart health impact

Investigations into the use of CoQ10 in the treatment of cardiovascular disease (CVD) shows that due to its involvement in energy management, it offers great potential as an intervention for both the prevention and treatment of heart ailments. Its mechanisms of action include providing antioxidant properties, which reduces the risk of oxidation of fats and the subsequent reduced collection of cholesterol plaques within the arteries, improved electron transportation and through modulation of the compound B-integrin, offers additional anti-clotting effects. 

Heart failure. Dietary supplements have been well-studied in their effects against heart disease. CoQ10, as an antioxidant is just one of them. It has been suggested that lower levels of CoQ10 are associated with the risk and progression of Cardiovascular Disease (CVD), however, it is not yet known whether this is a cause or an effect. 

Research shows that even short-term supplementation in patients with heart failure, with small doses of 100mg CoQ10 for 12 weeks, was found to improve left ventricular ejection fraction (14). Additionally, 2 years worth of treatment of 300mg of CoQ10 a day as an adjunct therapy in heart failure patients showed a significant reduction in their risk of major cardiovascular events (15). 

A 2014 study following 443 patients aged 70-88 years old for 5 years showed that a supplemental antioxidant combination had positive effects on mortality risk as well as common heart disease risk markers. When combined with another potent antioxidant, selenium, CoQ10 significantly reduced CVD mortality and improved cardiac markers when compared to controls receiving a placebo. The results were not only relevant during the study duration, but also 10 years after the intervention (16). 

Heart and bypass surgery. Prophylactic supplementation of CoQ10 has been implicated in better outcomes for patients undergoing cardiac surgery or cardiopulmonary bypass. While larger studies are needed to improve the quality of the evidence, a review of the current literature including eight clinical trials showed that those who took supplemental CoQ10 prior to surgery were far less likely to require inotropic drugs or develop heart arrhythmias after surgery (17). 

Blood pressure. A 2007 study of 12 clinical trials involving 362 patients showed that at a dose of between 34-225mg/d of CoQ10 for one to 52 weeks reduced systolic blood pressure between 11-17 mmHg and diastolic blood pressure was observed to have fallen 8-10 mmHg on average across the trials (18). 

Cholesterol. In 2015, a European study that included 860 people, looked into the effect of CoQ10 on cholesterol concentrations. A strong correlation between cholesterol levels and serum CoQ10 was noted where an increase in cholesterol was associated with lower CoQ10 and vice versa. In those study participants who were of increased age, not only did they show reduced CoQ10, there was a higher portion of oxidized CoQ10, both of which increase the risk of higher oxidative stress and its related tissue damage (19), which increases the risk of cardiovascular events.  

A 2017 animal study showed positive effects of oral CoQ10 supplementation. Rabbits, divided into groups showed that those who were given additional CoQ10 had lower serum LDL-cholesterol levels when compared to those without intervention (20). 

Statins. It is well-known that certain medications deplete CoQ10, and one of those medications that are commonly taken in our society are statins. Statins impede the body’s ability to make cholesterol by inhibiting an enzyme called HMG-CoA and acting on the mevalonate pathway. Mevalonate is used to synthesize both cholesterol and CoQ10, which is the reason for the depletion. Research has shown that in this way, statins may reduce CoQ10 levels as much as 40% (21). 

One of the common side effects of statin use is muscle cramping, which has been suggested as being as a result of interruption of the mevalonate pathway and reduced CoQ10 availability in the muscle tissue. When supplementing with CoQ10, research showed that in 60 patients with statin-induced myopathy, who took the compound for the three month duration of the trial, they consistently reported improved symptoms which included reduced muscle pain, improved strength in their muscles, and decreased muscle fatigue (22). 

Diabetes management 

Due to its potent antioxidant properties, CoQ10 has also been suggested as a treatment for type 2 diabetes and metabolic syndrome. Due to poor availability of quality studies, there is a lack of evidence to support this hypothesis, however, a number of smaller trials with relevant, albeit less significant outcomes, may provide motivation to do larger trails in this regard. 

For example, type 2 diabetics, who took 260mg of CoQ10 a day for 11 weeks had reduced fasting plasma glucose levels despite no changes noted into their HbA1c or fasting insulin levels (23). 

It is well worth further exploration as it is known that abnormal mitochondrial function plays a role in the development of insulin resistance, which is a precursor condition to type 2 diabetes. One study, which induced insulin resistance in rats by feeding them a high fat high fructose diet for 6 weeks, showed improvements in insulin sensitivity after treating the animals with CoQ10. Rats either received a combination of 20mg/kg CoQ10 and glimepiride or each of the two separately, taken by mouth for 2 weeks. The results showed the greatest effect in the CoQ10 group, with multiple markers of insulin resistance improving following treatment. Lower blood sugar and insulin levels were noted as well as improved insulin indices, cholesterol, glutathione and hormones produced by fatty tissue (24). 

Cancer prevention 

For years, we have known about the effect of CoQ10 supplementation in neurological disorders and cardiovascular disease, however, it is only more recently that its effect has been explored in cancer.  Evidence shows the association between lower concentrations of CoQ10 and a higher risk of several types of cancer where those within the lower percentiles of CoQ10 may have up to 53% higher risk of developing cancer along with a poorer prognosis once diagnosed (25). This association has promoted the use of CoQ10 as a preventative approach to cancer. 

While promising, particularly due to the antioxidant and free radical scavenging effects we know CoQ10 to have, many of the results from studies that use supplementation of CoQ10 as a means to reduce risk of progression of cancer have been contradictory. In breast cancer, the most common form of cancer that affects both women and men, interventions using CoQ10 have produced equally conflicting results. Of importance to note is the combined use of various supplements including CoQ10 as well as other medical and surgical intervention. 

For example, in one early clinical trial, when 90mg of CoQ10 was added to a daily supplements routine of 1.2 g linoleic acid, 3.5 g n-3 fatty acids, 58 mg β-carotene, 2800 mg vitamin C, 2500 IU vitamin E and 385 μg selenium in 32 high-risk patients, it was shown that in a small number, tumor regression was positive. In addition, their need for pain medication was reduced, there were no further metastases and no deaths within the 24 months of follow up. When researchers increased the dose to 300-900mg, there was a further resolution of tumors in two cases. Improvements in the patient’s quality of life were also noted, and improvements in 5- and 10- year survival rate was at 50% and 90% respectively. 

Longevity and anti ageing

Animal models are commonly used to determine how certain nutrients affect different biological pathways that can often be translated in humans. When it comes to CoQ10, in animals, it’s in a form called CoQ. 

In a mouse model, it was found that CoQ supplementation improved mitochondrial activity through activation of the longevity pathway, SIRT1, as well as other known age-related mechanisms. In addition, it slowed the rate of hearing loss and offered protection against the progression of general symptoms of ageing (26).

Fertility offers an understanding of the changes in a woman as a result of ageing, where maternal age has an inverse relationship with mitochondrial function in egg cells. In humans, reduced mitochondrial function and increased reactive oxygen species are associated with lower rates of fertility due to reduced ovulation. To test the theory of CoQ10 in the improvement of ovulation, a rat model was used in a 2015 study. The conclusion of the study suggests that CoQ10 supplementation significantly improved ovulation rates by improving ovarian reserve, in addition, there was an increase in breeding performance of the CoQ10 animals when compared to the matched control (27). 

A mouse model, characterized by premature ageing and increased susceptibility to oxidative stress, offers a unique way to investigate particular interventions and their effect on the pathways involved in longevity, such as CoQ10 supplementation. In testing the effects of CoQ on muscle status, it was observed that CoQ improved overall muscle function alongside the preservation of mitochondrial function (28).

Published in 2015, the conclusion of a 10-year long Swedish study that included over 440 healthy, elderly individuals provided evidence for a significantly reduced risk of cardiovascular mortality in those using a combined intervention of selenium – another potent antioxidant mineral – and CoQ10 for four years. The researchers explained that it’s a small-scale study that provides a hypothesis on which to base other studies, and that the mechanisms through which the intervention worked remains to be expanded on. Cardiovascular incidents are, however, a well-known risk factor of ageing, which is significant, should CoQ10 offer a means of protection (29). 

Another common disease of ageing is sarcopenia. Research suggests that it’s an increasing public health risk due to the expanding population of elderly worldwide. Sarcopenia is characterized by low muscle mass, which gives rise to mobility disorders and it increases the risk of falls and subsequent broken bones, raising the risk of loss of independence and death in the aged. It has long been theorized that sarcopenia is associated with a higher production rate of reactive oxygen species alongside a reduction in available antioxidants.Interestingly, there is also accumulating evidence that suggests mitochondrial dysfunction is part of the disease process of sarcopenia (30). 

CoQ10, being both an antioxidant and a critical factor involved in energy production of the mitochondria, has been suggested to play a role in the prevention of sarcopenia (31).  

Human skin offers valuable information about ageing. In the skin, there are a higher number of reactive oxygen species, and there is a clear correlation between the changes in the skin that arise from internal sources of oxidation (like inflammatory conditions and the normal process of ageing) and external ones (like UV irradiation). While supplemental intake of CoQ10 has been shown to improve free radical production in the mitochondria (32) that are considered internal sources of oxidation, there is little evidence to suggest that it offers protection against external sources, like UV irradiation (33). 


CoQ10 has been shown to have a high safety profile with well-designed randomised placebo-controlled clinical trials suggesting that 1,200,g per day is well-tolerated. Smaller trials have even used 3,000mg for short periods of time, and others 2,400mg for up to 60 months. 

We know that the generation of free radicals is a normal part of cell processing, however, when these levels continue to rise unabated, the tissue and DNA damage they cause is strongly associated with the onset of disease and the overall effects related to ageing. 

CoQ10 is a potent antioxidant compound that plays a critical role in health. Not only does it work in combination with other antioxidants like vitamin E, C and selenium, for example, to reduce free radical destruction, CoQ10 is essential for the health and well-functioning of the mitochondria of the cells.

Mitochondrial dysfunction is well-studied in ageing and is highly implicated in the onset of age-related disease (34). Significant evidence is available to support the use of supplemental CoQ10 to improve the function and offer protection to these important organelles. It’s a natural compound that shows great promise in prevention and treatment of multiple diseases, and not only offers hope for improving lifespan, but healthspan through the ages.


Selection of studies used for this article:

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