Pyrroloquinoline Quinone (PQQ)

Common Names

Pyrroloquinoline Quinone | PQQ | Methoxatin

Top Benefits of PQQ

Supports mitochondrial efficiency*

Supports antioxidant defenses*

Supports brain function and neuroprotection*

Supports healthy gut microbiota*

What is PQQ?

Pyrroloquinoline quinone (PQQ) is thought of as a non-vitamin growth factor, influencing metabolism and the expression of some genes. Although it’s not believed to be a helper molecule (i.e., vitamin cofactor) in any biochemical reactions, It does appear to be essential for healthy growth and function. PQQ is often categorized as a mitochondrial nutrient, supporting mitochondrial efficiency, so they are more capable of converting dietary fats and sugars into cellular energy. PQQ also plays roles in promoting healthy gut microbiome, immune system function, antioxidant defenses, and cognitive function. In the brain, it appears to be especially important in supporting healthy memory and cognition with aging. Some of the best food sources include soy, spinach, parsley, and kiwifruit.*

Qualia PQQ Sourcing

PQQ sourcing is focused on ensuring it is non-GMO, gluten-free and vegan.

PQQ Dosing Principles and Rationale

PQQ is dose-dependent (see Neurohacker Dosing Principles) in the range it’s commonly dosed (up to 20 mg a day). Since we use PQQ in more than one product, and assume some people might take both, our goal was to make sure people taking both products would not be getting too much PQQ. PQQ is additive with other mitochondrial and antioxidant nutrients. This means lower doses of PQQ can be needed to support healthy function when it is combined with other nutrients, compared to when it is given as an isolated nutrient.*

PQQ Key Mechanisms

Supports mitochondrial biogenesis*

Upregulates peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) [1–3]

Upregulates nuclear transcription factors of mitochondrial biogenesis (Nuclear Respiratory Factor 1 [NRF1], NRF2, mitochondrial transcription factor A [TFAM]) [1–3]

Supports mitochondrial size/density/number [1,3]

Supports mitochondrial DNA (mtDNA) amount [1–3]

Supports mitochondrial function and efficiency*

Supports citric acid cycle function [1,2,4]

Supports mitochondrial complex I-V performance [1,2]

Supports the NAD+ pool  [3]

Supports mitochondrial membrane potential [5]

Supports cellular metabolism*

PQQ supports the enzymatic activity of lactate dehydrogenase (LDH) to convert lactate to pyruvate via the oxidation of NADH to NAD+ [6]

By supporting pyruvate levels, PQQ supports ATP production via the mitochondrial citric acid cycle and oxidative phosphorylation [6]

Supports signaling pathways*

Supports AMP-activated protein kinase (AMPK) signaling [3]

Supports liver kinase B1 (LKB1) [3]

Supports SIRT1 [3]

Supports antioxidant defenses*

PQQ is reduced to PQQH2 by reaction with reducing agents such as NADPH or glutathione; PQQH2 has antioxidant properties [7]

Counters oxidative stress and the generation of reactive oxygen species (ROS) [4,5,8,9]

Supports brain function*

Supports neuroprotective functions [8–11]

Supports nerve growth factor (NGF) production [12]

Supports cerebral blood flow [13]

Supports attention and working memory [13]

Supports sleep and resistance to fatigue and stress [14]

Supports a healthy gut microbiota*

Supports a healthy gut microbiota composition [15]

Supports gut barrier function [16]

Counters gut oxidative stress [16]

Supports healthy gut cytokine signaling [15,16]

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

REFERENCES

[1] W. Chowanadisai et al., J. Biol. Chem. 285, 142–152 (2010).
[2] E. Tchaparian et al., Biochem. J. 429, 515–526 (2010).
[3] K. Saihara, R. Kamikubo, K. Ikemoto, K. Uchida, M. Akagawa, Biochemistry. 56, 6615–6625 (2017).
[4] C. B. Harris et al., J. Nutr. Biochem. 24, 2076–2084 (2013).
[5] R. Tao et al., Biochem. Biophys. Res. Commun. 363, 257–262 (2007).
[6] M. Akagawa et al., Sci. Rep. 6, 26723 (2016).
[7] M. Akagawa, M. Nakano, K. Ikemoto, Biosci. Biotechnol. Biochem. 80, 13–22 (2016).
[8] Q. Zhang, M. Shen, M. Ding, D. Shen, F. Ding, Toxicol. Appl. Pharmacol. 252, 62–72 (2011).
[9] J.-J. Zhang, R.-F. Zhang, X.-K. Meng, Neurosci. Lett. 464, 165–169 (2009).
[10] E. Aizenman, K. A. Hartnett, C. Zhong, P. M. Gallop, P. A. Rosenberg, J. Neurosci. 12, 2362–2369 (1992).
[11] J. Kim, R. Harada, M. Kobayashi, N. Kobayashi, K. Sode, Mol. Neurodegener. 5, 20 (2010).
[12] K. Yamaguchi, A. Sasano, T. Urakami, T. Tsuji, K. Kondo, Biosci. Biotechnol. Biochem. 57, 1231–1233 (1993).
[13] Y. Itoh et al., Adv. Exp. Med. Biol. 876, 319–325 (2016).
[14] M. Nakano, T. Yamamoto, H. Okamura, A. Tsuda, Y. Kowatari, Functional Foods in Health and Disease. 2, 307–324 (2012).
[15] J. E. Friedman et al., Hepatol Commun. 2, 313–328 (2018).
[16] X. Yin et al., J. Anim. Sci. (2018), doi:10.1093/jas/sky387.