Coenzyme Q10

Coenzyme Q10
is featured in:

Learn More

Learn More
Related Content

CoQ10 Common Names

Coenzyme Q10 | CoQ10 | ubiquinone

Top Benefits of CoQ10

  • Supports mitochondrial health*
  • Supports antioxidant defenses*
  • Support cardiovascular function*
  • Supports brain function*
  • Supports healthy aging*

What is CoQ10?

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)

Neurohacker’s CoQ10 Sourcing

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  Dosing Principles and Rationale

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. 

CoQ10 Key Mechanisms

Mitochondrial biogenesis

  • Upregulates peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC1α) (9, 10)
  • Upregulates nuclear transcription factors of mitochondrial biogenesis (nuclear respiratory factor 2 [NRF2], mitochondrial transcription factor A [TFAM]) (10)
  • Upregulates mitochondrial DNA (mtDNA) (10)
  • Upregulates mitochondrial number (10, 11)

Mitochondrial function

  • CoQ10 is part of the electron transport chain of the inner mitochondrial membrane (12)
  • CoQ10 transfers electrons from complexes I and II to complex III by undergoing redox cycles between its three redox states (ubiquinone [fully oxidized], ubisemiquinone, and ubiquinol [fully reduced]) (12)
  • CoQ10 is critical in ATP generation via the electron transfer chain (12)
  • Supports mitochondrial complex I-V performance (10, 13, 14)
  • Promotes ATP production (11)
  • Upregulates the NAD+ pool (NAD/NADH ratio) (10)
  • Supports β-oxidation (15)
  • Downregulates NAD(P)H:quinone oxidoreductase 1 (NQO1) (16, 17) (upregulated in response to mitochondrial impairment to protect the cells against oxidative stress)

Mitochondrial structure

  • Supports mitochondrial membrane potential (11, 18)

Signaling pathways

  • Upregulates AMP-activated protein kinase (AMPK) activity (9, 10, 15, 18, 19)
  • Upregulates peroxisome proliferator-activated receptor alpha (PPARα) (9, 10, 15)
  • Upregulates liver kinase B1 (LKB1) (10)
  • Upregulates cAMP (9, 10)

Lysosomal function

  • Supports the transport of protons across lysosomal membranes to maintain the optimal pH (12)
  • Supports the activity of digestive enzymes within lysosomes (12)
  • Supports the lysosomal digestion of cellular debris (12)

Antioxidant defenses

  • Coenzyme Q10 (as ubiquinol) is a potent lipid soluble antioxidant (12, 20, 21)
  • Protects from the peroxidation of cell membrane lipids and of lipoproteins in the blood(7, 20)
  • Protects from oxidative damage of proteins, lipids, and DNA (10, 20, 22)
  • Downregulates the production of reactive oxygen species (ROS) (10, 17, 18)
  • Upregulates antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPx]) (13, 14, 23)
  • Replenishes glutathione (GSH) levels (10)
  • Regenerates the lipophilic antioxidant alpha-tocopherol (vitamin E) (12, 21)

Body weight

  • Downregulates fat accumulation and blood/liver lipid levels (9)
  • Inhibits adipocyte differentiation and lipid accumulation (9)
  • Downregulates peroxisome proliferator-activated receptor gamma (PPARγ) (9)
  • Promotes the thermogenic function of brown adipose tissue (BAT) (9)
  • Upregulates uncoupling protein 1 (UCP1) (9)

Cardiovascular function

  • Cardioprotective effects (24–26)
  • Protects vascular function (27)
  • Protects endothelial cells against oxidative damage (19, 28)
  • Protects endothelial progenitor cells (18)
  • Supports endothelial function and blood flow (29–31)

Brain function

  • Neuroprotective against neurotoxic agents (17, 32)
  • Upregulates the number of mitochondria in the brain (32)

Healthy aging and longevity

  • Upregulates SIRT1 and SIRT3 (9, 10)
  • Protects from DNA double-strand breaks (33)
  • Extends lifespan (rats fed on a PUFA-rich diet) (33)

Synergies

  • Lipoic acid — support of mitochondrial function (34–37)
  • Creatine — neuroprotection and support of mitochondrial function (34, 35, 38)
  • L-carnitine  — support of mitochondrial function (39)
  • Piperine — increases bioavailability of CoQ10 (40)
  • Vitamin B3 (NAD+ precursors)  — supports improved mitochondrial performance (41)
  • Vitamin E — support of mitochondrial function (36)

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.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.