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How We Obtain Sufficient Coenzyme Q
Abstract
Benjamin Dahl
Beloit College, Beloit, Wisconsin
Avoiding Coenzyme Q (CoQ) deficiency is important
because it can help prevent disease. Diet can affect CoQ Figure 1:The function of CoQ is to carry a pair of electrons
levels in multiple ways: a certain amount of CoQ we get
directly from the food we eat, and many of the vitamins
required to synthesize CoQ also come from the food we eat.
My hypothesis was that consuming enough of the necessary
vitamins to allow the body to synthesize CoQ is more
effective in avoiding a deficiency than consuming food with
higher amounts of CoQ. Peer reviewed articles on scientific
research and experiments were used to investigate this
hypothesis. Only ten percent of dietary CoQ is absorbed by
the intestines, and certain vitamin supplements have been
shown to increase CoQ levels. However, the healthy CoQ
level for an average person has not yet been agreed upon.
Since it is synthesized by humans, it is not a vitamin and
may be hazardous when taken as a supplement. Statin
drugs taken to lower cholesterol inhibit the pathway by
which CoQ is made, but the health implications of this have
not been found.
Figure 2: Role of CoQ in the Electron Transport Chain
Introduction
Coenzyme Q (CoQ), also known as ubiquinone, is a
molecule that each cell has in its mitochondria that aids in
multiple steps of ATP production. It is found in every cell in
the body, and so a deficiency in CoQ is serious. Some of
the effects are Parkinson’s disease and heart problems.
The CoQ that we have in our body is a mixture of CoQ that
we synthesize ourselves and CoQ that we get from our diet.
CoQ synthesis is a complicated process that requires a
variety of vitamins. The foods that give the highest amount
of dietary CoQ are animal products, mainly beef and pork.
The average American diet consists of too much meat and
not enough, and a narrow variety, of vegetables. So here
we have a dilemma. On one hand, one could reason that
Americans should be safe from CoQ deficiency because of
all the meat we consume. However, one could also reason
that we are in danger of CoQ deficiency because the lack of
vegetables in our diet would lead to a lack of various
vitamins, which would inhibit our cells from making CoQ. I
intend to use peer-reviewed articles and books to research
this question. My hypothesis is that, in regard to CoQ
deficiency, the problems from lack of vegetables, and
therefore vitamins, will outweigh the benefits from high meat
consumption.
Method
To test my hypothesis I used peer-reviewed articles of
scientific research and experiments.
-Statins block here
Figure 3: Effect of Statin Drugs: To the left
is a simplified diagram of the cholesterol
synthesis process. CoQ is an alternative
product of the same process. Cholesterol
lowering drugs, known as statins, block the
process at the step between HMG CoA
and Mevalonate. It has been shown that
these drugs result in lower CoQ levels.
This is ironic, because lowering cholesterol
is a common way to reduce risk of heart
disease, but lowering CoQ is a very
effective way of increasing risk of heart
disease. (Lovastatin 1)
Results
-Mice fed daily either 0, 93, or 371 mg CoQ/kg body
weight had no effect on lifespan, Electron transport
chain function, or redox functions measured, but did
increase tissue levels with dosage. (Sohal 2006)
-Coenzyme Q deficiency is often a problem based on
genetics (Quinzii 2007)
-CoQ synthesis “requires many enzymes and known
vitamins and minerals for the enzymatic reactions”.
These include vitamins B6, B3, B5, B9, and C.
(Folkers 1974)
-A vitamin E deficiency can decrease CoQ production.
(Folkers 1990)
-Average daily intake of CoQ is between 3-5mg.
(Kagan 2001)
-Total absorption of dietary CoQ is less than 10%.
(Kagan 2001)
-CoQ is predominantly found in animal heart and liver
tissue, but there is also significant amounts found in
beef and pork. (Purchas 2004)
-Lovastatin, a cholesterol lowering drug, lowers CoQ
levels. (Fokkers 1990)
-CoQ from supplements may be hazardous, disturbing
the Electron Transport Chain and producing free
radicals. (Hekimi 2006)
Discussion
It is appropriate to conclude that these results suggest that
my hypothesis was correct. There is not sufficient research
done with regard to the healthy amount of CoQ one should
have, or the healthy daily intake, to come to a concrete
conclusion. Nor is there enough knowledge of the CoQ
biosynthesis process to confidently recommend a list of daily
nutrient intake values that would, without a doubt, help avoid
CoQ deficiency. It has been shown that a lack of Vitamin E,
which is an essential part in CoQ synthesis, leads to lower
levels of CoQ, so sufficient vitamin intake is important to
maintaining CoQ. However, this does not necessarily mean
that it is more important than eating food with lots of CoQ.
References
Folkers, Karl. "Relationships between coenzyme Q and vitamin E." American Journal of
Clinical Nutrition 27(1974): 1026
Folkers, Karl. "Lovastatin decreases coenzyme Q levels in humans." American Journal
of Clinical Nutrition 87(1990):521
Hekimi (2006) in Ordman, http://www.beloit.edu/nutrition/confernotes/ln06AGE.htm
Kagan, Valerian and Quinn, Peter. (editors) Coenzyme Q. Molecular Mechanisms in
Health and Disease. 2001 CRC Press LLC, Boca Ratin, Florida.
Quinzii, Catarina M. “Human Coenzyme Q10 Deficiency.” Neurochemical Research
32(2007): 723
Purchas, RW et al. “Concentrations in beef and lamb of taurine, carnosine, coenzyme
Q10, and creatine.” Meat Science 66 (2004): 629.
Sohal, RS et al. “Effect of coenzyme Q10 intake on endogenous coenzyme Q content,
mitochondrial electron transport chain, antioxidative defenses, and lifespan of mice,”
Free Rad Bio Med 40 (2006): 480.