Pharmacology
Pharmacology of coenzyme Q10:
Relevance to cardiovascular
and other disorders
Abstract
Coenzyme Q10 (CoQ10) is a vitamin-like substance that plays a
key role in the metabolic process that supplies all cells with energy.
Tissues with a high energy requirement, such as the heart, are
particularly dependent on maintaining an adequate supply of CoQ10
for normal functioning. Deficiency of CoQ10 has been identified
as a risk factor for a variety of disorders, including cardiovascular
and neurological diseases. The objective of this article is, therefore,
to provide a brief overview of the pharmacology of CoQ10, with
particular emphasis on its role in the prevention and treatment of
cardiovascular disorders.
C oenzyme Q10 (CoQ10) is a naturally occurring
vitamin-like substance, first characterised in 1957
by Professor Fred Crane at the University of Wisconsin.
CoQ10 is also known as ubiquinone, because of its
ubiquitous distribution in all body tissues. Coenzyme
quinones occur in several chemical forms, with CoQ10
being the only form found in human tissues. CoQ10
plays a key role in the biochemical mechanism involved
in supplying cells with energy, acting in conjunction
with enzymes (hence the name CoQ10) to convert
sugars and fat into energy. The action of CoQ10 is of
particular importance in tissues with a high energy
requirement, such as cardiac muscle. CoQ10 is also
important as an antioxidant within the body. The
objective of this article is, therefore, to provide an
overview of the pharmacology of CoQ10, and its role
in the prevention and treatment of disease, particularly
cardiovascular disorders.
Functions of CoQ10
CoQ10 is an essential cofactor of the enzymes
involved in the process that supplies all cells with
Dr David Mantle is a Medical Adviser at Pharma Nord UK
Ltd.
Email: dmantle@pharmanord.co.uk
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David Mantle
energy (cellular respiration). CoQ10 is stored in
mitochondria, the specialised structures found
within cells responsible for the generation of energy.
Specifically, CoQ10 is an intermediate in the electron
transport system that generates energy in the chemical
form of adenosine triphosphate (ATP), shuttling
electrons from complexes I and II to complex III of the
mitochondrial respiratory chain. Tissues with a high
energy requirement, especially the heart and skeletal
muscles, contain higher numbers of mitochondria
within their cells, and are particularly reliant on
maintaining adequate tissue CoQ10 levels for their
normal functioning. For example, the heart and skeletal
muscles typically contain about 1000 mg of CoQ10, out
of a total body pool of 1500–2000 mg.
CoQ10 is also important within the body as a major
fat-soluble antioxidant, protecting cell membranes (and
particularly the membranes of the mitochondria) from
the damaging effects of free radicals. Free radicals are
generated continually within the body as an unwanted
by-product of normal cellular metabolism, particularly
cellular respiration. CoQ10 is the only lipid soluble
antioxidant produced within the body.
Most recently, gene expression profiling has shown
that CoQ10 influences the expression of several
hundred genes. In particular, studies in cell culture,
animal models and human subjects have shown that
CoQ10 can directly regulate gene expression relevant
to inflammation and fat metabolism (Schmelzer et al,
2008; Yubero-Serrano et al, 2012). In addition, CoQ10
supplementation has been reported to decrease levels of
inflammatory markers in patients with coronary artery
disease (Lee et al, 2012).
CoQ10 occurs in cells in two closely related forms,
oxidised (ubiquinone) and reduced (ubiquinol). The
inter-conversion between these two forms is essential
for the normal functioning of CoQ10.
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Synthesis and deficiency of CoQ10
Although some CoQ10 (approximately 25% of
requirement) is obtained from the normal diet, most is
manufactured within the body, particularly by the liver.
It has been estimated that the population of Denmark,
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 Pharmacology
for example, obtain only 3–5 mg of CoQ10 per day
from their normal dietary sources (Weber et al, 1997).
The synthesis of CoQ10 is a complex process requiring
a number of amino acids, vitamins and trace element
precursors and cofactors; a deficiency in any of these
can adversely affect the normal production of CoQ10.
It is of note that CoQ10 shares a common synthetic
pathway with cholesterol.
As people age, the capacity of the body to produce
CoQ10 decreases; optimal production occurs around
the mid-twenties, with a continual decrease thereafter.
CoQ10 levels can also be depleted by intense exercise,
certain types of prescription medicines, and by illness.
Dietary supplementation with coenzyme CoQ10
therefore provides a mechanism to maintain adequate
levels within the body. However, it is important to note
that the pharmaceutical quality and bioavailability of
coenzyme supplements from different manufacturers
may vary widely.
Deficiency of CoQ10 has been linked with the
increased risk of a number of disorders, including
cardiovascular disease, neurodegenerative disease,
immune disorders, periodontal disease and male
infertility. Tissues that are metabolically most active,
and have the highest energy/CoQ10 requirements are
the most susceptible to deficiency, for example:
■■ Cardiac and skeletal muscles
■■ Immune response cells
■■ Gingiva.
Most cases of deficiency result from factors such as
aging or the effects of drugs such as statins, and this
is known as secondary deficiency. Primary deficiency
results from defects in the genes responsible for the
various steps in the body’s synthesis of CoQ10; these are
rare and can be successfully treated by supplementation
if identified in infancy.
Bioavailability of supplemental
CoQ10
Bioavailability is defined as the proportion of an orally
administered substance that reaches the systemic
circulation. CoQ10 is a fat-soluble substance. Following
emulsification and micelle formation, CoQ10 is absorbed
by mucosal cells of the small intestine, as occurs for
any other dietary fat. CoQ10 is then transported via
chylomicrons by the lymphatic system to the liver, where it
is released into the blood in association with lipoproteins
(very-low-density lipoprotein (VLDL), low-density
lipoprotein (LDL), high-density lipoprotein (HDL)).
Because of its hydrophobicity and large molecular weight,
intestinal absorption of CoQ10 is in general slow and
somewhat limited; as much as 50% of a typical oral dose
may be excreted in the faeces.
For dietary supplements, oil-based formulations
show enhanced bioavailability (Weis et al, 1994). There
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is a correlation between supplemental CoQ10 intake
and plasma level, up to approximately 300 mg/day.
Absorption of CoQ10 is non-linear, with increasing
doses absorbed to a decreasing degree. Higher daily
doses of CoQ10 are therefore best taken in split doses.
For ubiquinone, maximum plasma concentration
(Cmax) is reached after approximately 6 hours (Tmax),
and the half life (T(1/2)) is approximately 33 hours,
resulting in the time to pharmacological steady
state being rather prolonged (1-2 weeks). Normal
plasma levels are in the range of 0.5 to 1.5 mcg/ml.
Supplementation with 100 mg CoQ10 twice daily
has been reported to raise blood levels from 0.90 to
3.25 mcg/ml (Weiss et al, 1994).
Cardiovascular disease and CoQ10
Early studies on cardiovascular disease were hampered
by a shortage of supply of CoQ10, poor absorption of
CoQ10 in its original crystalline form, and insufficient
daily dosage (30–60 mg). However, following the
successful treatment of congestive heart failure in
the 1970s (for which CoQ10 received approved drug
status in Japan), CoQ10 was subsequently shown to
benefit patients with atherosclerosis, hypertension,
hyperlipidaemia, coronary artery disease and heart
failure, as well as those treated with lipid-lowering
statin drugs (reviewed by Langsjoen and Langsjoen,
1999; Mortensen, 1993; Mortensen, 2003). Langsjoen
and Langsjoen (1999) state that optimum improvement
in heart function requires a plasma CoQ10 level of at
least 3.5 mcg/ml.
CoQ10 protects against atherosclerosis by inhibiting
the oxidation of LDL cholesterol. The role of CoQ10 in
protecting LDL cholesterol from free radical-induced
oxidative damage has been described by Alleva et al
(1995) and Tomasetti et al (1999). A meta-analysis
(comprising 5 randomised controlled trials and 200
patients) carried out by Gao et al (2012) reported that
supplementation with CoQ10 resulted in a significant
improvement in arterial endothelial function in patients
with and without cardiovascular disease.
In hypertensive patients, supplementation with CoQ10
may represent an alternative treatment strategy for those
who need to avoid adverse effects associated with some
types of prescription anti-hypertensive drugs. A number
of clinical trial studies have reported that supplementation
with CoQ10 can significantly reduce blood pressure in
hypertensive patients, without adverse effects; these studies
include randomised controlled double blind trials (e.g.
Burke et al, 2001), as well as observational studies (e.g.
Langsjoen et al, 1994). A meta-analysis by Rosenfeldt
et al (2007) concluded that CoQ10 could lower systolic
© 2013 MA Healthcare Ltd
blood pressure by up to 17 mm of mercury, and diastolic
pressure by 10 mm, without significant adverse effects in
hypertensive patients. Whilst this meta-analysis (of 12
clinical trial studies comprising some 350 patients) was
limited by the heterogeneity of study populations and
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overall patient numbers, the authors concluded ‘until
the results of a large scale trial are available, it would
seem acceptable to add CoQ10 to conventional anti-
hypertensive therapy.’
Singh et al (1998; 2003) reported that oral
administration of CoQ10 can have a significant
protective effect from further adverse events in
patients with acute myocardial infarction. A number
of randomized controlled clinical trial studies have
suggested that perioperative oral supplementation with
CoQ10 can improve outcomes in patients undergoing
cardiac surgery (Makhija et al, 2008; Leong et al, 2010).
Patients with congestive heart failure have low blood
levels of CoQ10. Meta-analyses by Soja and Mortensen
(1997), Molyneux et al (2009) and Fotino et al (2013) have
demonstrated the benefits of CoQ10 supplementation for
congestive heart failure, with significant improvements in
ejection fraction (increased by 4-8%) and cardiac output
(increased by 300 ml/min) reported. The authors consider
these data to be clinically relevant. The potential benefits
of CoQ10 supplementation in paediatric cardiomyopathy
have been reviewed by Bhagavan and Chopra (2005).
There have been two recent important clinical
trial studies of CoQ10 of relevance to cardiovascular
function. Firstly, the KiSel-10 study was carried out
on the elderly population of the Kinda region of
Stockholm, who were given supplemental selenium
and CoQ10 (hence KiSel-10). In a 5-year prospective
randomised double-blind placebo-controlled trial
in 440 individuals aged 70-88 years, participants
were assigned 200 mcg selenium (SelenoPrecise) and
200 mg CoQ10 (Bio-Quinone Q10) daily, or placebo.
Assessment included clinical examination, ECG
and the biochemical marker of heart tissue stress,
NT‑proBNP (brain natriuretic peptide) status. There
was a greater than 50% reduction in cardiovascular
mortality in the treatment group versus placebo group
(5.9% vs 12.6%). In addition, cardiac function assessed
by ECG and NT-proBNP levels was significantly
improved in the treatment group compared to placebo
(Alehagen et al, 2012). It is of note that this study also
highlights the importance of adequate dietary intake of
selenium for normal cardiovascular function. Dietary
deficiency of selenium is the cause of Keshan disease,
a cardiomyopathy endemic to regions of China with
selenium-depleted soils.
Secondly, the results of the Q-Symbio study were
recently reported at the European Society of Cardiology
Heart Failure Congress in Lisbon (July 2013). Q-Symbio is
a multi-national clinical trial study headed by Professor S
Mortensen of Copenhagen University Hospital, Denmark.
The study was carried out in patients with chronic
© 2013 MA Healthcare Ltd
heart failure over 18 years of age; the effects of CoQ10
supplementation on symptoms and biomarker status
(hence Q-Symbio) were assessed. This was a long-term
randomised double-blind placebo-controlled multi-centre
trial in 420 patients with chronic heart failure (New York
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Pharmacology
Heart Association class III or IV). Patients were assigned
300 mg CoQ10 (Bio-Quinone Q10) daily, or placebo.
Assessment included clinical examination, ECG and pro-
BNP biochemical marker status. There was a reduction
in mortality of 52% in the treatment group compared to
the placebo group (18 vs 37). In addition, cardiac function
was improved, and hospital admissions reduced, in the
treatment group compared to placebo. The mortality
outcomes reported in this study, whilst promising, need to
be approached with caution pending the results of a larger
scale, suitably powered study.
Most clinical trial studies to determine the efficacy
and safety of CoQ10 have used the ubiquinone form.
Patients with severe congestive heart failure are least able
to benefit from oral supplementation with conventional
ubiquinone CoQ10 supplements (up to 900 mg/day)
because of their difficulty in adequately assimilating the
latter due to intestinal and hepatic oedema. In the first
reported clinical trial of CoQ10 in the reduced (ubiquinol)
form in such patients (Langsjoen and Langsjoen, 2008),
critically ill individuals orally supplemented with 450 mg/
day ubiquinol for 3 months showed a threefold increase
in plasma CoQ10 level, and a 25-50% improvement in
heart function (quantified via echocardiography ejection
fraction).
Statins and CoQ10
Statins are drugs that reduce circulatory cholesterol
levels, and are used primarily to protect at-risk patients
from adverse cardiovascular events. Statins are potent
inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A
(HMGCoA) reductase, the rate-limiting enzyme in
cholesterol biosynthesis. Whilst the safety record of these
drugs is generally considered to be acceptable (particularly
in limited time-frame usage), adverse effects do occur in a
significant number of patients. These include:
■■ Myopathy
■■ Gastrointestinal disturbance
■■ Liver dysfunction
■■ Initiation or acceleration of cataracts
■■ Cognitive dysfunction and increased risk of
polyneuropathy.
The severity of muscle-related symptoms can range
from relatively mild myalgia to myopathy (myalgia plus
elevated creatine kinase), which can lead to potentially
life-threatening rhabdomyolysis and renal failure in rare
extreme cases.
The inhibitory effect of statins on cholesterol
biosynthesis is not selective, resulting in the inhibition
of several nonsterol isoprenoid end products, including
CoQ10. The statin-induced reduction in CoQ10 levels
has been well documented in both animal models and
clinical studies (reviewed by Langsjoen and Langsjoen,
2003). Many of the adverse effects resulting from statin
use can be rationalized in terms of concomitant CoQ10
depletion. Rundek et al (2004) have reported that even
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 Pharmacology
brief exposure to atorvastatin reduces CoQ10 levels, with
adverse effects on heart function (Silver et al, 2004). It is
possible that the true therapeutic potential of statin drugs
is being partially negated by reduced CoQ10 levels, and
that co-administration of both substances would lead to
an even greater reduction in cardiovascular morbidity
and mortality. Oral supplementation of CoQ10 would
be necessary, as the latter is not available from the diet in
sufficient amounts (100-200 mg/day) to compensate for
the depletion in levels induced by statins. Randomised
controlled trials by Caso et al (2007) and Marcoff and
Thompson (2007) reported that supplementation with
CoQ10 (100 mg/day for 30 days) significantly reduced
muscle pain associated with statin treatment. Whilst
these two relatively small studies are not conclusive, in
the absence of larger scale clinical trials, DiNicolantonio
(2012) states that it is a reasonable strategy to supplement
CoQ10 in patients with statin-induced myalgia.
In Canada, the packaging of statin drugs is required to
include a so-called ‘black box warning’, recommending the
drugs be taken in conjunction with CoQ10.
Other disorders and CoQ10
Neurodegenerative and neuromuscular disorders
Depletion of CoQ10, mitochondrial dysfunction and
impaired cellular energy supply have been implicated
as common factors in a number of neurodegenerative
disorders, including Parkinson’s disease, Huntington’s
disease and Friedreich’s ataxia (Mancuso et al, 2010;
Chaturvedi and Beal, 2013; Salama et al, 2013).
Supplementation with CoQ10 improves quality of life
in patients with Parkinson’s disease, and may play a
role in delaying the progression of this disorder (Shults
et al, 2002; Muller et al, 2003). Supplementation with
CoQ10 improves fatigue, hyperalgesia and quality
of life in patients with fibromyalgia (Cordero et al,
2013; Miyamae et al, 2013). There is also evidence
for mitochondrial dysfunction in migraine, and
Key Points
■■ CoQ10 is a naturally occurring vitamin-like substance that
plays a key role in the metabolic process supplying cells with
energy
■■ CoQ10 is of particular importance in tissues with a high
energy requirement, such as the heart
■■ CoQ10 levels are reduced by aging, illness and certain drug
types, such as statins
■■ Deficiency of CoQ10 has been linked with a number of
disorders, including cardiovascular disease
■■ Clinical studies have demonstrated that oral supplementation
with CoQ10 can be of benefit in the prevention or treatment
of a variety of cardiovascular and other disorders
■■ None of the clinical trial studies using CoQ10 have reported
significant adverse effects.
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npre_2013_11_12_602.indd 606
symptomatic benefit following CoQ10 supplementation
(Markley, 2012).
Reproductive disorders
Supplementation with CoQ10 in infertile men with
idiopathic asthenozoospermia improved semen quality,
in terms of sperm count, normal morphology and
motility (Balercia et al, 2009; Safarinejad, 2009). CoQ10
supplementation improved symptoms in patients with
Peyronie’s disease (Safarinejad, 2010), and reduced the
risk of developing pre-eclampsia during pregnancy
(Teran et al, 2009).
Safety of CoQ10
CoQ10 is generally well tolerated, with no serious
adverse effects reported in long term use. Very rarely,
individuals may experience mild gastrointestinal
disturbance. There are no known toxic effects, and
CoQ10 cannot be overdosed. CoQ10 is well tolerated
in healthy adults at an intake of 900 mg/day, and in
rats at a dose of up to 1200 mg/kg/day. CoQ10 is not
recommended for pregnant or lactating women, in
whom the effects of CoQ10 have not been extensively
studied. Several case studies have suggested that CoQ10
may interfere with the action of warfarin; however, a
randomised controlled clinical trial showed CoQ10
supplementation at 100 mg/day had no effect on the
clinical action of warfarin (Engelsen et al, 2003).
It should be noted that CoQ10 is not available in
the UK as a licensed medicinal product; there is a
version licensed elsewhere in the EC (Myoquinone)
as an adjuvant for treatment of cardiovascular disease,
available in the UK as an unlicensed medicine.
Otherwise, CoQ10 is available in the UK as a
nutritional supplement.
Conclusions
To date there are more than 600 articles published in
the peer-reviewed medical literature (including some
60 randomised controlled clinical trial studies) relating
to CoQ10 and cardiovascular disease listed on Medline
(the database of the US National Library of Medicine).
However, many health professionals remain unfamiliar
with the potential role of CoQ10 in the prevention or
management of cardiovascular disease. Of course not
every one of the above articles has reported positive
findings with regard to CoQ10 and cardiovascular
disease, however the balance of published evidence
supports a beneficial role for CoQ10 in the prevention
and management of cardiovascular disease, as outlined
in the article above. None of the clinical trial studies
have reported any significant adverse effects following
© 2013 MA Healthcare Ltd
oral supplementation with CoQ10.
Conflict of interest: Dr David Mantle is a medical
adviser for Pharma Nord (UK) Ltd., a manufacturer of
CoQ10 supplements.
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