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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.