Coenzyme Q10 | CoQ10 | ubiquinone
Coenzyme Q10 (CoQ10) is an important fat-soluble nutrient, because it’s essential for cellular energy production (i.e., ATP) and antioxidant defenses, helping protect membranes from oxidative stress. Because of its central role in ATP generation, the highest amounts of CoQ10 are found in organs that use the most energy, like the heart, liver, and kidneys. Meat and fish, especially their organs, are very good food sources. The best vegetarian sources are foods high in fat, including nuts, seeds, avocados, and vegetable oils. A person eating an average diet will get about 3-6 mg of CoQ10 a day.(1–4) Most CoQ10 isn't from diet, it's made in the body (i.e., biosynthesized), with creation requiring at least 12 genes. While the human body can make CoQ10, it may not always be able to make enough to meet its needs.(5) This seems to occur with aging, because CoQ10 gradually declines with age in a number of different tissues.(6, 7)
CoQ10 is most commonly supplemented in its oxidized from, which is called ubiquinone. Most human clinical studies has been the ubiquinone form. It can also be supplemented in its reduced ubiquinol form.
CoQ10 sourcing is focused on ensuring it is non-GMO, gluten-free and vegan.
CoQ10 is dose-dependent (see Neurohacker Dosing Principles) in the range it’s commonly dosed (30 mg to several hundred milligrams a day). Body stores are maintained by a combination of the CoQ10 we consume in foods and supplements, and the CoQ10 made in our body.(7) It’s been suggested that a daily intake ranging from 30–100 mg in otherwise healthy persons is a good range to maintain healthy levels. (7, 8) CoQ10 is additive with other mitochondrial and antioxidant nutrients. This means lower doses of CoQ10 are often needed to support healthy function when it is combined with other nutrients, compared to when it is given as an isolated nutrient.
Mitochondrial biogenesis
Mitochondrial function
Mitochondrial structure
Signaling pathways
Lysosomal function
Antioxidant defenses
Body weight
Cardiovascular function
Brain function
Healthy aging and longevity
Synergies
REFERENCES
[1] C. Weber, A. Bysted, G. Hłlmer, Int. J. Vitam. Nutr. Res. 67, 123–129 (1997).
[2] P. Mattila, J. Kumpulainen, J. Food Compost. Anal. 14, 409–417 (2001).
[3] H. Kubo et al., J. Food Compost. Anal. 21, 199–210 (2008).
[4] I. Pravst, K. Zmitek, J. Zmitek, Crit. Rev. Food Sci. Nutr. 50, 269–280 (2010).
[5] J. D. Hernández-Camacho, M. Bernier, G. López-Lluch, P. Navas, Front. Physiol. 9, 44 (2018).
[6] A. Kalén, E. L. Appelkvist, G. Dallner, Lipids. 24, 579–584 (1989).
[7] L. Ernster, G. Dallner, Biochim. Biophys. Acta. 1271, 195–204 (1995).
[8] R. A. Bonakdar, E. Guarneri, Am. Fam. Physician. 72, 1065–1070 (2005).
[9] Z. Xu et al., Sci. Rep. 7, 8253 (2017).
[10] G. Tian et al., Antioxid. Redox Signal. 20, 2606–2620 (2014).
[11] M. K. Abdulhasan et al., J. Assist. Reprod. Genet. 34, 1595–1607 (2017).
[12] F. L. Crane, J. Am. Coll. Nutr. 20, 591–598 (2001).
[13] J. J. Ochoa, J. L. Quiles, J. R. Huertas, J. Mataix, J. Gerontol. A Biol. Sci. Med. Sci. 60, 970–975 (2005).
[14] J. J. Ochoa, J. L. Quiles, M. López-Frías, J. R. Huertas, J. Mataix, J. Gerontol. A Biol. Sci. Med. Sci. 62, 1211–1218 (2007).
[15] S. K. Lee et al., Cell. Signal. 24, 2329–2336 (2012).
[16] R. I. Bello et al., Exp. Gerontol. 40, 694–706 (2005).
[17] R. Won, K. H. Lee, B. H. Lee, Neuroreport. 22, 721–726 (2011).
[18] H.-Y. Tsai et al., J Diabetes Res. 2016, 6384759 (2016).
[19] K.-L. Tsai et al., Mol. Nutr. Food Res. 55 Suppl 2, S227–40 (2011).
[20] M. Bentinger, K. Brismar, G. Dallner, Mitochondrion. 7 Suppl, S41–50 (2007).
[21] P. Navas, J. M. Villalba, R. de Cabo, Mitochondrion. 7 Suppl, S34–40 (2007).
[22] M. Tomasetti, G. P. Littarru, R. Stocker, R. Alleva, Free Radic. Biol. Med. 27, 1027–1032 (1999).
[23] L. Tiano et al., Eur. Heart J. 28, 2249–2255 (2007).
[24] R. B. Singh et al., Cardiovasc. Drugs Ther. 12, 347–353 (1998).
[25] K. A. Conklin, Integr. Cancer Ther. 4, 110–130 (2005).
[26] E. I. Kalenikova, E. A. Gorodetskaya, E. G. Kolokolchikova, D. A. Shashurin, O. S. Medvedev, Biochemistry . 72, 332–338 (2007).
[27] P. K. Witting, K. Pettersson, J. Letters, R. Stocker, Free Radic. Biol. Med. 29, 295–305 (2000).
[28] K.-L. Tsai et al., J. Nutr. Biochem. 23, 458–468 (2012).
[29] G. F. Watts et al., Diabetologia. 45, 420–426 (2002).
[30] R. Belardinelli et al., Eur. Heart J. 27, 2675–2681 (2006).
[31] L. Gao et al., Atherosclerosis. 221, 311–316 (2012).
[32] R. T. Matthews, L. Yang, S. Browne, M. Baik, M. F. Beal, Proc. Natl. Acad. Sci. U. S. A. 95, 8892–8897 (1998).
[33] J. L. Quiles, J. J. Ochoa, J. R. Huertas, J. Mataix, Exp. Gerontol. 39, 189–194 (2004).
[34] M. C. Rodriguez et al., Muscle Nerve. 35, 235–242 (2007).
[35] M. Sun et al., Scand. J. Med. Sci. Sports. 22, 764–775 (2012).
[36] A. Abadi et al., PLoS One. 8, e60722 (2013).
[37] S. Silvestri et al., J. Clin. Biochem. Nutr. 57, 21–26 (2015).
[38] L. Yang et al., J. Neurochem. 109, 1427–1439 (2009).
[39] M. Shojaei, M. Djalali, M. Khatami, F. Siassi, M. Eshraghian, Iran. J. Kidney Dis. 5, 114 (2011).
[40] V. Badmaev, M. Majeed, L. Prakash, J. Nutr. Biochem. 11, 109–113 (2000).
[41] J. Castro-Marrero et al., Does Oral Coenzyme Q10 Plus NADH Supplementation Improve Fatigue and Biochemical Parameters in Chronic Fatigue Syndrome? Antioxidants & Redox Signaling. 22 (2015), pp. 679–685.