Coenzyme Q10 was first isolated from beef heart in 1957 by
Dr. Frederick Crane at the University of Wisconsin. Its structure was
elucidated and it was synthesized only a year later.
The name "coenzyme Q" was chosen
because the molecule was proved to be a quinone (a family of molecules essential
for generating energy in organisms that consume oxygen). The 10 comes from
the number of isoprene units in the tail of the molecule (2). Since its
discovery over forty years ago, much research has been conducted to determine
the role of CoQ10 in human health and disease.
CoQ10 is found in highest
concentrations in the mitochondria of the heart, liver, and kidney; organs whose
cells have the highest energy expenditure. Deficiency of CoQ10 in blood and tissue are known to be
present in a wide variety of human
and animal diseases. Increased
consumption of the coenzyme is seen with excessive exertion,
hypermetabolism, and acute shock states. Additionally,
it has been observed that HMG-CoA reductase inhibitors block
CoQ 10 biosynthesis. Still, the CoQ10 level reduction is not considered
significant enough to require supplementation.
Clinical
application of CoQ10 began in the mid-1960s. Its initial uses
were in the treatment of congestive heart failure (Japan) and as an
antioxidant (Italy), though these uses were largely anecdotal
applications. Scientific progress continued throughout the 1970s
with Italian researchers demonstrating a deficiency of CoQ10 in cases
of human heart disease. In
1978, Peter Michell received the Nobel Prize for contributing to the
understanding of biological energy transfer, for which CoQ 10 is a
part of.
Throughout the 1980s and
1990s, research on this coenzyme continued to receive considerable
attention and support. In 1985, Folkers et al. found that patients with heart failure
had a deficiency of CoQ10 in their myocardial cells and that the degree of
deficiency correlated with the clinical severity of disease (3). In 1998,
Keith et al. published a study demonstrating increased oxidative stress in
patients with congestive heart failure (4). Since then, it has been
postulated that depletion of CoQ10 may contribute to heart failure and that it
may be useful in treating cardiac disease. In fact, it has been proposed
that CoQ10 may be beneficial in a number of different disease, including heart
failure, angina pectoris, cardiac arrhythmias, periodontal disease, immune
disorders, neurologic disease, obesity, diabetes mellitus, and cancers including
breast and prostate (5). Nonetheless, CoQ10 has not been cleared by the
Dietary Supplement Health and Education Act of 1994, despite wide use
in multiple other countries.
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