Rejuvenate Your Cells by Growing New Mitochondria

Mitochondrial dysfunction is a primary cause of age-related decline. [1-7] In a revealing study, a team of researchers showed that muscle tissue of a 90-year-old man contained 95% damaged mitochondria compared to almost no damage in that of a 5-year-old. [8]  When one looks at the boundless energy of a child compared to an elderly person, the devastating impact of mitochondrial degradation become instantly apparent.  A myriad of recent scientific reports link defective and deficient mitochondria to virtually all degenerative diseases, including Alzheimer’s, type 2 diabetes, heart failure, and cancer. [9-13]  Up until now, the best we could do was protect and improve the function of existing mitochondria using nutrients like L-carnitine, lipoic acid, and coenzyme Q10.

In an unprecedented breakthrough, a compound has been discovered that promotes the growth of new mitochondria structures within aging cells. [14]  In this article, you will discover how this novel compound can help reverse cellular aging by activating genes that stimulate mitochondrial biogenesis, which means the generation of new mitochondria.

Mitochondria are the only cell components (other than the nucleus) to possess their own DNA. This means mitochondria have the ability to replicate and increase their number within a single human cell.  Human cells may house anywhere from 2 to 2,500 mitochondria, [15-17] depending on tissue type, antioxidant status, and other factors.  A growing number of biologists espouse the theory that mitochondrial number and function determine human longevity. [18-20]

To put it simply, the more functional mitochondria you have in your cells, the greater your overall health and durability.  The problem is that as we age, our mitochondria degrade and become dysfunctional. Age-related destruction of the mitochondria occurs more rapidly than in other cell components, meaning that for most people, it is loss of functional mitochondria that ultimately leads to personal extinction.  The challenge aging humans face is that methods to increase the generation of new mitochondria are difficult to adhere to. Up until recently, the only natural ways to stimulate mitochondrial biogenesis were calorie restriction or exhaustive physical activity.

A natural agent with the power to safely induce mitochondrial biogenesis would mark an extraordinary advance in the quest to halt and reverse cellular aging. A compound called pyrroloquinoline quinone or PQQ is rapidly emerging as that nutrient.

PQQ: A Quantum Leap That May Reverse Cellular Aging

PQQ (pyrroloquinoline quinone) plays a critical role across a range of basic life functions. As an ultra potent antioxidant, it provides extraordinary defense against mitochondrial decay: PQQ’s chemical structure enables it to withstand exposure to oxidation up to 5,000 times greater than vitamin C. [21]  When combined with CoQ10, research shows just 20 mg per day of PQQ can significantly preserve and enhance memory, attention, and cognition in aging humans. [22]  But the most exciting revelation on PQQ emerged early in 2010, when researchers found it not only protected mitochondria from oxidative damage—it also stimulated growth of new mitochondria!

PQQ (pyrroloquinoline quinone) plays a critical role across a range of basic life functions. As an ultra potent antioxidant, it provides extraordinary defense against mitochondrial decay: PQQ’s chemical structure enables it to withstand exposure to oxidation up to 5,000 times greater than vitamin C. [21]  When combined with CoQ10, research shows just 20 mg per day of PQQ can significantly preserve and enhance memory, attention, and cognition in aging humans. [22]

But the most exciting revelation on PQQ emerged early in 2010, when researchers found it not only protected mitochondria from oxidative damage—it also stimulated growth of new mitochondria! [14]

PQQ Is an Essential Micronutrient

PQQ is ubiquitous in the natural world. It has been found in all plant species tested and is present in human milk. Humans, however, are not capable of synthesizing it. [23] This has led researchers to classify PQQ as an essential micronutrient.  PQQ’s potential to stimulate mitochondrial biogenesis was foreshadowed by early findings indicating its central role in growth and development across multiple forms of life.

PQQ has been shown to be a potent growth factor in plants, bacteria, and higher organisms. [21,24,25] Pre-clinical studies reveal that when deprived of dietary PQQ, animals exhibit stunted growth, compromised immunity, impaired reproductive capability, and most importantly, fewer mitochondria in their tissue. Rates of conception, the number of offspring, and survival rates in juvenile animals are also significantly reduced in the absence of PQQ. [26-28]  When PQQ is introduced back into the diet, it reverses these effects, restoring systemic function while simultaneously increasing mitochondrial number and energy efficiency.

These compelling data prompted a team of researchers at the University of California- Davis to specifically analyze PQQ’s influence on cell signaling pathways involved in the formation of new mitochondria. [14] Their work, published last year, led to several extraordinary discoveries. They found that PQQ’s critical biological roles stem from its ability to activate genes directly involved in cellular energy metabolism, development, and function. [14]

Their findings shed light on results from favorable prior studies. For example, PQQ deficiency in juvenile mice results in a 20-30% reduction in the number of mitochondria in the liver, elevated blood glucose, and impairment in oxygen metabolism. [26]  These are hallmark indicators of mitochondrial dysfunction. Yet when PQQ was put back into the diet, these pathological effects were reversed, along with an increase observed of new mitochondria.  This and additional animal model data [28] taken together confirm PQQ’s ability to significantly boost mitochondrial number and function—a key to cellular anti-aging and longevity.

How PQQ Generates New Mitochondria

Mitochondrial biogenesis can be defined as the growth and division of pre-existing mitochondria. This phenomenon is not only accompanied by increased mitochondria numbers, but also their size and mass.

Mitochondrial biogenesis requires the coordinated synthesis and import of 1,000- 1,500 proteins where they facilitate the production of healthy new mitochondria.

Mitochondrial biogenesis occurs through the combined effects of genes activated by PQQ via the following three mechanisms:

  • PQQ increases expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha or PGC-1a. pGC-1a is a “master regulator” gene that mobilizes your cells’ response to various external triggers. It directly activates genes that boost mitochondrial and cellular respiration, growth, and reproduction. Its capacity to modulate cellular metabolism at the genetic level favorably affects blood pressure, cholesterol and triglyceride breakdown, and the onset of obesity. [29]
  • PQQ activates a signaling protein known as caMp-response element-binding protein or CReb. The CreB gene plays a pivotal role in embryonic development and growth. It also beneficially interacts with histones, molecular compounds shown to protect and repair cellular DNa. CreB also stimulates the growth of new mitochondria. [30]
  • PQQ regulates a recently discovered gene called dj-1. as with pGC-1a and CreB, DJ-1 is intrinsically involved in cell function and survival. It has been shown to prevent cell death by combating intensive antioxidant stress and is of particular importance to brain health and function. DJ-1 damage and mutation have been conclusively linked to the onset of Parkinson’s disease and other neurological disorders. [31-34]

Protecting Against Mitochondria- generated Free Radicals

As the primary energy engines of our cells, the mitochondria rank among the structures most vulnerable to destruction from oxidative damage.  The formidable free radical-scavenging capacity of PPQ furnishes the mitochondria considerable antioxidant protection.  At the core of this capacity is an extraordinary molecular stability. [35] As a bioactive coenzyme, PQQ actively participates in the energy transfer within the mitochondria that supplies the body with most of its bioenergy (like CoQ10).

Unlike other antioxidant compounds, the stability of PQQ allows it to carry out thou- sands of electron transfers without undergoing molecular breakdown. It has been proven especially effective in neutralizing the ubiquitous superoxide and hydroxyl radicals. [36]  According to the most recent research, “PQQ is 30 to 5,000 times more efficient in sustaining redox cycling . . . than other common [antioxidant compounds], e.g. ascorbic acid.” [37]

Protection Against Brain Aging

PQQ has been shown to optimize function of the entire central nervous system. It reverses cognitive impairment caused by chronic oxidative stress in pre-clinical models, improving performance on memory tests. [40] It has also been shown to safeguard a gene involved in the development of Parkinson’s disease (called DJ-1) from self-oxidation—an early step in the onset of Parkinson’s. [41]

Reactive nitrogen species (RNS), like reactive oxygen species, impose severe stresses on damaged neurons. [42] They arise spontaneously following stroke and spinal cord injuries, and have been shown to account for a substantial proportion of subsequent long- term neurological damage. PQQ directly suppresses RNS in experimentally induced strokes. [43] It also provides additional protection by blocking gene expression of inducible nitric oxide synthase, a major source of RNS, following spinal cord injury. [44]

PQQ protects brain cells against damage following ischemia-reperfusion injury— the inflammation and oxidative damage that result from the sudden return of blood and nutrients tissues deprived of them by stroke. [45] Given immediately before induction of stroke in animal models, PQQ significantly reduces the size of the damaged brain area. [46]  This finding implies that if a person were to suffer a temporary loss of cerebral blood flow due to cardiac arrest, stroke, or trauma, that having PQQ in their body would afford considerable protection against permanent brain damage.

PQQ also beneficially interacts with brain neurotransmitter systems. In particular, PQQ protects neurons by modifying the important NMDA receptor site. [47,48] NMDA is a powerful mediator of “excitotoxicity,” a response to long-term overstimulation of neurons that is associated with many neurodegenerative diseases and seizures. [49-51] PQQ protects against neurotoxicity induced by other toxins, including mercury. [52,53]

A mounting body of evidence points to PQQ as a potent intervention in Alzheimer’s and Parkinson’s disease. Both are triggered by accumulation of abnormal proteins that initiate a cascade of oxidative events resulting in brain cell death.  PQQ prevents development of alpha-synuclein, the protein responsible for Parkinson’s disease. [54] It also protects nerve cells from the oxidizing ravages of the Alzheimer’s- causing amyloid-beta protein. [55] A 2010 study revealed that PQQ could prevent formation of amyloid-beta molecular structures. [56]  These effects were traced to three distinct biochemical mechanisms described earlier.

PQQ has also been shown to protect memory and cognition in aging animals and humans. [22,57] It stimulates production and release of nerve growth factor in cells that support neurons in the brain. [58] This may partially explain why PQQ supplementation of aging rats resulted in marked retention of their maximum memory function. [57]  In humans, supplementation with 20 mg per day of PQQ resulted in improvements on tests of higher cognitive function in a group of middle-aged and elderly people. [22]

PQQ has also been shown to protect memory and cognition in both aging animals and humans.

These effects were significantly amplified when the subjects also took 300 mg per day of CoQ10. Presumably a lower dose of the more absorbable ubiquinol form of CoQ10 would provide the same benefit as 300 mg of ubiquinone.

Cardiovascular Defense

As with strokes, damage in heart attacks is inflicted via ischemia-reperfusion injury. Ischemia-reperfusion means loss of blood flow (ischemia) to part of the body and the subsequent re-flow (reperfusion) when blood flow is restored. Cells are injured when blood flow is interrupted and often sustain even greater damage when blood flow is suddenly restored.  Supplementation with PQQ reduces the size of ischemia-reperfusion damaged areas in animal models of acute myocardial infarction (heart attack). [5] This occurs whether the supplement is given before or after the ischemic event itself.

To further investigate this potential, researchers at the VA Medical Center at UC-San Francisco compared PQQ with metoprolol, a commonly prescribed beta blocker that is standard post-heart attack clinical treatment. [60] Given alone, both treatments reduced the damaged areas’ size and protected against heart muscle dysfunction. When they were given together, the left ventricle’s pumping pressure was enhanced. The combination also increased mitochondrial energy-producing functions—but the effect was small compared with the better response seen with PQQ alone. [60] And only PQQ favorably reduced lipid peroxidation. The remarkable conclusion: “PQQ is superior to metoprolol in protecting mitochondria from ischemia/reperfusion oxidative damage.” [60]

Subsequent research from the same team has demonstrated that PQQ helps heart muscle cells resist acute oxidative stress. [61]  The mechanism? Preserving and enhancing mitochondrial function.

Why Mitochondria are so Vulnerable to Free Radical damage

The death spiral of our mitochondria is accelerated by the very physiological function they must perform, i.e. energy production. As the cell’s power generators, mitochondria are the site of enormous and constant oxidative activity that spews out toxic free radicals. To make matters worse, relative to nuclear DNA, mitochondrial DNA possesses few defenses against free radical damage. [38,39]

DNA in the cell’s nucleus is protected by numerous “guardian” proteins that blunt the impact of free radicals. No such repair systems exist to protect mitochondrial DNA.

Nuclear DNA also enjoys superior structural defenses. It is housed within a protective double-membrane that separates it from the rest of the cell. This double-membrane is complemented by a dense matrix of filament proteins called the nuclear lamina, a kind of hard shell casing to further buffer DNA from external impacts.

By comparison, mitochondrial DNA is left almost entirely exposed: it attaches directly to the inner membrane where the mitochondria’s electrochemical furnace rages continuously, generating an enormous volume of toxic reactive oxygen species. This is why supplementation with lipoic acid, carnosine, and other mitochondrial-protecting antioxidants is so important.

The extraordinary antioxidant capacity of PQQ represents a powerful new intervention that may effectively reinforce the mitochondria’s meager defenses.


Cellular aging is intimately associated with the decline in mitochondrial number and functionality. Nutrients that provide pro- tection to existing mitochondria include resveratrol, carnosine, lipoic acid, L-carnitine, and CoQ10. During the course of normal aging, however, the number of functional mitochondria pathologically diminishes, leading to a host of debilitating disorders followed by death of the organism.  For the first time in scientific history, a natural compound called PQQ is available to increase the functionality of existing mitochondria while promoting the generation of new mitochondria inside aging cells.

This article is copyright 2010 by Life Extension Magazine (R), a sponsor of H+ Magazine, and is reprinted with permission.

To order PQQ, please call Life Extension at 1-866-748-7538, or visit


1. Bliznakov EG. Aging, mitochondria, and coenzyme Q(10): the neglected relationship. Biochimie. 1999 Dec;81(12):1131-2.

2. Linnane AW, Marzuki S, Ozawa T, Tanaka M. Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases. Lancet. 1989 Mar 25;1(8639):642-5

3. Lanza IR, Nair KS. Mitochondrial metabolic function assessed in vivo and in vitro. Curr Opin Clin Nutr Metab Care. 2010 Jul 7.

4. Mota MP, Peixoto FM, Soares JF, et al. Influence of aerobic fitness on age-related lymphocyte DNA damage in humans: relationship with mitochondria respiratory chain and hydrogen peroxide production. Age (Dordr). 2010 Mar 20.

5. Tranah G. Mitochondrial-nuclear epistasis: Implications for human aging and longevity. Ageing Res Rev. 2010 Jun 25.

6. Cho DH, Nakamura T, Lipton SA. Mitochondrial dynamics in cell death and neurodegeneration. Cell Mol Life Sci. 2010 Jun 25.

7. Wei YH, Ma YS, Lee HC, Lee CF, Lu CY. Mitochondrial theory of aging matures—roles of mtDNA mutation and oxidative stress in human aging. Zhonghua Yi Xue Za Zhi (Taipei). 2001 May;64(5):259-70.

8. Linnane AW, Kovalenko S, Gingold EB. The universality of bioenergetic disease: age-associated cellular bioenergetic degradation and amelioration therapy. Ann N Y Acad Sci. 1998 Nov 20;854:202-13.

9. Bugger H, Abel ED. Mitochondria in the diabetic heart. Cardiovasc Res. 2010 Jul 16.

10. Conley KE, Amara CE, Jubrias SA, Marcinek DJ. Mitochondrial function, fibre types and ageing: new insights from human muscle in vivo. Exp Physiol. 2007 Mar;92(2):333-9.

11. Lesnefsky EJ, Moghaddas S, Tandler B, Kerner J, Hoppel CL. Mitochondrial dysfunction in cardiac disease: ischemia—reperfusion, aging, and heart failure. J Mol Cell Cardiol. 2001 Jun;33(6):1065-89.

12. Maruszak A, Zekanowski C. Mitochondrial dysfunction and Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry. 2010 Jul 15.

13. Singh KK. Mitochondria damage checkpoint, aging, and cancer. Ann N Y Acad Sci. 2006 May;1067:182-90.

14. Chowanadisai W, Bauerly KA, Tchaparian E, Wong A, Cortopassi GA, Rucker RB. Pyrroloquinoline quinone stimulates mitochondrial biogenesis through cAMP response element-binding protein phosphorylation and increased PGC-1 alpha expression. J Biol Chem. 2010 Jan 1;285:142-52.

15. Bruce A, Johnson A, Lewis J, Raff M, Roberts K, Walter P. Molecular Biology of the Cell. New York, NY: Garland Publishing, Inc.;1994.

16. Voet D, Voet JG, Pratt CW. Fundamentals of Biochemistry: Life at the Molecular Level. 2nd ed. New Jersey: John Wiley and Sons, Inc.; 2006:547.

17. Pike RL, Brown M. Nutrition: An Integrated Approach. New York, NY: Prentice-Hall; 1984:450-84.

18. Lanza IR, Nair KS. Mitochondrial function as a determinant of life span. Pflugers Arch. 2010 Jan;459(2):277-89.

19. Robb EL, Page MM, Stuart JA. Mitochondria, cellular stress resistance, somatic cell depletion, and life span. Curr Aging Sci. 2009 Mar;2(1):12-27.

20. Alexeyev MF, LeDoux SP, Wilson GL. Mitochondrial DNA and aging. Clin Sci. 2004;107:355-364.

21. Rucker R, Chowanadisai W, Nakano M. Potential physiological importance of pyrroloquinoline quinone. Altern Med Rev. 2009 Sep;14(3):268-77.

22. Nakano M, Ubukata K, Yamamoto T, Yamaguchi H. Effect of pyrroloquinoline quinone (PQQ) on mental status of middle-aged and elderly persons. FOOD Style. 2009;21:13(7):50-3.

23. Smidt CR, Bean-Knudsen D, Kirsch DG, Rucker RB. Does the intestinal microflora synthesize pyrroloquinoline quinone? Biofactors.1991 Jan;3(1):53-9.

24. Stites TE, Mitchell AE, Rucker RB. Physiological importance of quinoenzymes and the O-quinone family of cofactors. J Nutr. 2000 Apr;130(4):719-27.

25. Choi O, Kim J, Kim JG, et al. Pyrroloquinoline quinone is a plant growth promotion factor produced by Pseudomonas fluorescens B16. Plant Physiol. 2008 Feb;146(2):657-68.

26. Stites T, Storms D, Bauerly K, et al. Pyrroloquinoline quinone modulates mitochondrial quantity and function in mice. J Nutr. 2006 Feb;136(2):390-6.

27. Steinberg F, Stites TE, Anderson P, et al. Pyrroloquinoline quinone improves growth and reproductive performance in mice fed chemically defined diets. Exp Biol Med (Maywood). 2003 Feb;228(2):160-6.

28. Bauerly KA, Storms DH, Harris CB, et al. Pyrroloquinoline quinone nutritional status alters lysine metabolism and modulates mitochondrial DNA content in the mouse and rat. Biochim Biophys Acta. 2006 Nov;1760(11):1741-8.

29. Entrez Gene: PPARGC1A peroxisome proliferator- activated receptor gamma, coactivator 1 alpha [ Homo sapiens ] GeneID: 10891.

30. Entrez Gene: CREBBP CREB binding protein [ Homo sapiens ] GeneID: 1387.

31. Zhong N, Xu J. Synergistic activation of the human MnSOD promoter by DJ-1 and PGC-1alpha: regulation by SUMOylation and oxidation. Hum Mol Genet. 2008 Nov 1;17(21):3357-67.

32. Mitsumoto A, Nakagawa Y. DJ-1 is an indicator for endogenous reactive oxygen species elicited by endotoxin. Free Rad Res. 2001; 35(6):885-93.

33. Nunome K, Miyazaki S, Nakano M, Iguchi-Ariga S, Ariga H. Pyrroloquinoline quinone prevents oxidative stress-induced neuronal death probably through changes in oxidative status of DJ-1. Biol Pharm Bull. 2008 Jul;31(7):1321-6.

34. Taira T, Saito Y, Niki T, Iguchi-Ariga SM, Takahashi K, Ariga H. DJ-1 has a role in antioxidative stress to prevent cell death. EMBO Rep. 2004 Feb;5(2):213-8.

35. Paz MA, Martin P, Fluckiger R, Mah J, Gallop PM. The catalysis of redox cycling by pyrroloquinoline quinone (PQQ), PQQ derivatives, and isomers and the specificity of inhibitors. Anal Biochem. 1996;238:145-9.

36. Urakami T, Yoshida C, Akaike T, Maeda H, Nishigori H, Niki E. Synthesis of monoesters of pyrroloquinoline quinone and imidazopyrroloquinoline, and radical scavenging activities using electron spin resonance in vitro and pharmacological activity in vivo. J Nutr Sci Vitaminol (Tokyo). 1997 Feb;43(1):19-33.

37. Stites TE, Mitchell AE, Rucker RB. Physiological importance of quinoenzymes and the O-quinone family of cofactors. J Nutr. 2000 Apr;130(4):719-27.

38. Richter C. Oxidative damage to mitochondrial DNA and its relationship to ageing. Int J Biochem Cell Biol. 1995;27:647-53.

39. Miquel J. An update on the mitochondrial-DNA mutation hypothesis of cell aging. Mutat Res. 1992 Sep;275(3-6):209-16.

40. Ohwada K, Takeda H, Yamazaki M, et al. Pyrroloquinoline quinone (PQQ) prevents cognitive deficit caused by oxidative stress in rats. J Clin Biochem Nutr. 2008 Jan;42:29-34.

41. Nunome K, Miyazaki S, Nakano M, Iguchi-Ariga S, Ariga H. Pyrroloquinoline quinone prevents oxidative stress-induced neuronal death probably through changes in oxidative status of DJ-1. Biol Pharm Bull. 2008 Jul;31(7):1321-6.

42. Ono K, Suzuki H, Sawada M. Delayed neural damage is induced by iNOS-expressing microglia in a brain injury model. Neurosci Lett. 2010 Apr 5;473(2):146-50.

43. Zhang Y, Rosenberg PA. The essential nutrient pyrroloquinoline quinone may act as a neuroprotectant by suppressing peroxynitrite formation. Eur J Neurosci. 2002 Sep;16(6):1015-24.

44. Hirakawa A, Shimizu K, Fukumitsu H, Furukawa S. Pyrroloquinoline quinone attenuates iNOS gene expression in the injured spinal cord. Biochem Biophys Res Commun. 2009 Jan 9;378(2):308-12.

45. Jensen FE, Gardner GJ, Williams AP, Gallop PM, Aizenman E, Rosenberg PA. The putative essential nutrient pyrroloquinoline quinone is neuroprotective in a rodent model of hypoxic/ischemic brain injury. Neuroscience. 1994 Sep;62(2):399-406.

46. Zhang Y, Feustel PJ, Kimelberg HK. Neuroprotection by pyrroloquinoline quinone (PQQ) in reversible middle cerebral artery occlusion in the adult rat. Brain Res. 2006 Jun 13;1094(1):200-6.

47. Aizenman E, Hartnett KA, Zhong C, Gallop PM, Rosenberg PA. Interaction of the putative essential nutrient pyrroloquinoline quinone with the N-methyl- D-aspartate receptor redox modulatory site. J Neurosci. 1992 Jun;12(6):2362-9.

48. Aizenman E, Jensen FE, Gallop PM, Rosenberg PA, Tang LH. Further evidence that pyrroloquinoline quinone interacts with the N-methyl-D-aspartate receptor redox site in rat cortical neurons in vitro. Neurosci Lett. 1994 Feb 28;168(1-2):189-92.

49. Hossain MA. Molecular mediators of hypoxic-ischemic injury and implications for epilepsy in the developing brain. Epilepsy Behav. 2005 Sep;7(2):204-13.

50. Dong XX, Wang Y, Qin ZH. Molecular mechanisms of excitotoxicity and their relevance to pathogenesis of neurodegenerative diseases. Acta Pharmacol Sin. 2009 Apr;30(4):379-87.

51. Foran E, Trotti D. Glutamate transporters and the excitotoxic path to motor neuron degeneration in amyotrophic lateral sclerosis. Antioxid Redox Signal. 2009 Jul;11(7):1587-602.

52. Hara H, Hiramatsu H, Adachi T. Pyrroloquinoline quinone is a potent neuroprotective nutrient against 6-hydroxydopamine-induced neurotoxicity. Neurochem Res. 2007 Mar;32(3):489-95.

53. Zhang P, Xu Y, Sun J, Li X, Wang L, Jin L. Protection of pyrroloquinoline quinone against methylmercury- induced neurotoxicity via reducing oxidative stress. Free Radic Res. 2009 Mar;43(3):224-33.

54. Kobayashi M, Kim J, Kobayashi N, et al. Pyrroloquinoline quinone (PQQ) prevents fibril formation of alpha-synuclein. Biochem Biophys Res Commun. 2006 Oct 27;349(3):1139-44.

55. Zhang JJ, Zhang RF, Meng XK. Protective effect of pyrroloquinoline quinone against Abeta-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. Neurosci Lett. 2009 Oct 30;464(3):165-9.

56. Kim J, Kobayashi M, Fukuda M, et al. Pyrroloquinoline quinone inhibits the fibrillation of amyloid proteins. Prion. 2010 Jan;4(1):26-31.

57. Takatsu H, Owada K, Abe K, Nakano M, Urano S. Effect of vitamin E on learning and memory deficit in aged rats. J Nutr Sci Vitaminol (Tokyo). 2009;55(5):389-93.

58. Murase K, Hattori A, Kohno M, Hayashi K. Stimulation of nerve growth factor synthesis/secretion in mouse astroglial cells by coenzymes. Biochem Mol Biol Int. 1993 Jul;30(4):615-21.

59. Zhu BQ, Zhou HZ, Teerlink JR, Karliner JS. Pyrroloquinoline quinone (PQQ) decreases myocardial infarct size and improves cardiac function in rat models of ischemia and ischemia/reperfusion. Cardiovasc Drugs Ther. 2004 Nov;18(6):421-31.

60. Zhu BQ, Simonis U, Cecchini G, et al. Comparison of pyrroloquinoline quinone and/or metoprolol on myocardial infarct size and mitochondrial damage in a rat model of ischemia/reperfusion injury. J Cardiovasc Pharmacol Ther. 2006 Jun;11(2):119-28.

61. Tao R, Karliner JS, Simonis U, et al. Pyrroloquinoline quinone preserves mitochondrial function and prevents oxidative injury in adult rat cardiac myocytes. Biochem Biophys Res Commun. 2007 Nov 16;363(2):257-62.


  1. I’ve read a few books suggesting taking PQQ to help mitochondrial function but I’ve still not tried it. Some even claim you will be bouncing with energy after a few months on the supplement…very enticing promise but somehow it still concerns me to take things without conclusive proof….

  2. sorry I meant BUY

  3. the ad at the end where it says where you can bye the stuff is a bit of a give away.

  4. Reading the above comments,especially those wanting, “scientific proof,” we have over 300 scientist lying and cheating to secure grants. We have big pharma. whose drugs bring about thousands of deaths every year. We have the FDA that punishes whistle blowers in their agency. We have FDA officials who leave the agency and work for big pharma. I told a group of doctors who look on nutrients with disdain that if the PDR contained any thing that would sustain life I would eat it or drink it.

  5. Before making your negative comments, all you nay sayers should actually try the product.
    I am 76 years old and have been using the Mitochondrial Energy Optimizer from Life Extension Foundation for just three weeks. I am beginning to feel like a young man again. Yesterday I rode 39 miles on my bicycle on a hot afternoon. Now this may sound impressive in itself for a 76 year old man, but what is even more impressive is that I did the bike ride after spending 2 hours in the YMCA doing light weight training. I truthfully cannot remember when I had such high levels of youthful energy.

  6. Give the man a break – he works free on the magazine, listens to your opinions has the decency to answer with great humility about a mistake in style he has made and people STILL hammer him. Ben I for one thank you for your time and effort

  7. So which foods should I get for this miraculous PPQ to kick in. 🙂

  8. I agree, lay off Ben. He thought it was interesting and linked it in here for us. So Ben has extraordinary focus to see past the hokum to the bare scientific facts, it may be a good vitamin. It doesn’t mean he’s trying to get you to buy in to the stuff, just to look at it. So look, and use your own judgment on the stuff. Ben shouldn’t have to predigest the content, especially if he’s not getting paid, and you should have the prominent intellect to make your own decisions. Also, Ben, don’t feed the trolls – it only makes them more vicious. Thank you for all that you do.

  9. Regarding the whole “this article should be fair and balanced” thing: I have yet to see any opposing opinion to this, despite looking very hard (as I said earlier, I was initially very skeptical of this article). You don’t have to teach both sides if there only exists one, and, as far as I can tell, the propositions in this article are as well established as any other.

    Also, with regards to the “advert” format of this article: I agree that I found it annoying. You don’t, however, have to leave twenty comments informing Ben of that; I think he got the message with the first five.

    Finally, I must admit that I was also slightly surprised at the “injection of religion” that appeared in earlier articles, e.g. the one on the Mormon Transhumanist Association. Although I agree that this is not very objective, you also have to realize that there were probably Christian Transhumanists reading that article, who then said “Oh, this sounds interesting!” While a nonbeliever, I also investigated the MTA and made a few friends there.


  10. It’s good that people are busting your balls a bit, Ben. It means they care. 🙂

  11. Seriously, this is an advertisement.

    You can put all the spin on it you want. If I paid for this magazine and I discovered such an article, I’d cancel the subscription.

    I was very happy with the original more OBJECTIVE H+ magazine. If you do not have the time to edit the magazine, move on. This kind of editing along with all that religion injected earlier in other work simply identifies the device as suspect.

    I am very happy NOT to be paying at the moment.

  12. Reads like a (bad) sales pitch. Considering this is the third article I read from hplus, I really – *really* – hope this isn’t indicative of the general quality of your articles…

    That the first article (i read) was basically just magical thinking about all the things that’ll fall into place when we get AGI doesn’t help either…

    Quality over quantity might be something to strive for, in a magazine that purports to be the voice of transhumanism.

    • Goodness you Internet commentators are heartless!!!

      I help edit this magazine for free, and I have a lot of other things to do with my time….

      The style of this article may not be quite right for H+ magazine, but the contents are actually interesting and relevant, let’s not forget that, OK?

      And the article you refer to as “magical thinking” is presumably the one I recently wrote on AGI and nuclear power (as a Forbes commentator accused that article of being “magical thinking”). I addressed that complaint in a P.S. to the article; it’s really not valid, since I do have a detailed scientific path written down for working toward the goals described there. Perhaps that wasn’t my best article, but hey, nobody hits a home run every time.

      Fortunately I don’t have the personality to give up when a bunch of people whine at me for doing something imperfectly; I just try to learn from it and keep on going…

      But .. jeez…

  13. Is that an affiliate link? You may want to look into the new FTC guidance on disclosure for blogs.

    I went through that whole article waiting for the “how to incorporate PQQ in your life” section .. and it was a link to a single specific reseller’s affilate link despite this stuff supposedly being “ubiquitous in the natural world”.

    This smacks of a sales pitch not a balanced/journalist examination of the substance’s worth. you could have at least marked it as such.

  14. Journalism needs to present multiple sides. Since this is a one-sided exposition, there’s no help for the unsophisticated reader (me) in weighing the claims presented.

    • Actually I don’t accept the idea that every article should present multiple sides. That is one valid journalistic style, but there are others — e.g. Hunter Thompson style gonzo embedded journalism, and so forth…. I find it frustrating when journalists go out of their way to give the appearance of presenting a balanced opinion…. Personally I found this article interesting which I why I approved it for publication, but after reading these comments I can see we should have chosen a different way of presenting the content…

  15. I’ve been doing some research since the article went up (since it wouldn’t have been the first time a transhumanist advocated something that turned out to be pseudomedicine), and it seems that this is valid; PPQ does indeed improve health by increasing mitochondrial biogenesis. The main study on the subject is , though there are a couple others. It’s also used in some supplements for this exact reason. So it looks like this does in fact increase rejuvenation, though side effects don’t seem to have been investigated at this point.

    • . . . crap; I fail at HTML. The link at the end links to a study in the Journal of Biochemistry, but it looks like I forgot to put in the closing tag.

      • Hey don’t get down on yourself, people make mistakes sometimes. It’s only code.

    • Yes, it’s valid… I checked out the references myself before deciding to publish it. But based on all these comments it’s obvious that just re-posting LEF content on hplusmagazine wasn’t a good idea; we should have undertaken the work to write an ordinary H+ mag article on the same content…. The LEF style is too different and doesn’t fit into the H+ mag well, although the content is actually solid…

      Actually these comments have been somewhat educational for me, so thanks for posting them…. I realize that when I read something, I tend to go right for the content and ignore the style, but apparently many others have a different approach, and are turned off by certain styles more than I would be…

      • Forgive us our crude crap-detection heuristics. There’s much bunk and marketing on the interwebs, if you haven’t noticed.

  16. It seems like most of the commenter’s complaints about it being an ad are based on how it upholds a very specific compound as a kind of “miracle drug”, sold through the Life Extension company. Sometimes it seems we’re too cynical to really accept that something so simple and seemingly good would be true. To those of you who would like to see the “analysis” of the article, I would suggest that you read the studies cited and decide for yourself if they hold up to scrutiny. The font changes look more like the work of an over-excited editor than a salesman, there seem to be too few hyperlinks to the store for that to be true. Or if it is a salesman, they’re pretty lousy at their job, and should consider looking for work somewhere else.

  17. I was going to say this looks like an ad, but everyone else seems to have beat me to it. it’s almost like reading Life Extension magazine; that one’s free guys.

    • Sorry Ben, didn’t read your comment before I posted. My bad. The numerous references are solid, but like I said you can kind of tell it’s an article from Life Extension- they have a way of “plugging” their products in scientific articles. I don’t know about everyone else, but I’d prefer solid science- the more detailed the better (correlation coefficients, types of statistical tests used in analysis, etc.)- over “scientific marketing” any day.

  18. Aging is the product of a lot processes. This article completely omits this fact, thus it is misleading.
    For example, aging is also partially caused by telomere shortening and several other forms of DNA damage, including mutations.

  19. Hmmm … OK, in hindsight the negative comments on this article are not wholly surprising!! But let me try to clarify a few things.

    Firstly, it’s not an “ad” — although Life Extension Foundation is a donor to Humanity+, they didn’t buy advertising space in which to run “ads as articles.” Rather, they gave us permission to choose some of their more scientifically interesting (in our opinion) articles from Life Extension Magazine to re-run in H+ Magazine. I thought this was a cool opportunity to get some interesting information out to our audience…. But based on some the comments on the article, I can see that it may have come across the wrong way…. (Hey, I’m a scientist, not a marketeer ;p)

    I chose to run this article because the scientific grounding seemed pretty strong to me. I think it’s an interesting article, even if different from ordinary H+ fare. Actually I’ve done some work on the relation between mitochondrial function and aging myself, and the science in the article seems pretty solid to me. (Although of course, that doesn’t imply taking the supplement is necessarily a great idea — I’m not a doctor or a nutritionist, blah blah….)

    Anyway, we’ll take your critiques under consideration in determining our future content! Perhaps we can figure out a different way to bring this sort of info to H+ mag readers without raising anybody’s ire, or giving any untoward appearances…

    Thanks for your tolerance as we experiment with our magazine!

    Ben Goertzel
    Chair, Humanity+
    Co-Editor, H+ Magazine

    • It has some interesting info, but it’s pretty obvious it was written by a marketing copy writer and not a writer commenting on the achievement.

      removal of the overused boldface and italics would have been a good start, and editing down some of the boilerplate sales talk would have helped too. It reads like a snake oil sales pitch, when it should read like a report on the development and potential promises of PQQ

      • Sure … good points, Valkyrie…

  20. I Hope H+ gt bank for this ad. does anyone have unbiased info about this miracle vitimin?

  21. Please don’t mix up ads and articles! This is a piece of advertising that has NOTHING to do among articles by Ben Goertzel and Extropia daSilva. Who is monitoring this magazine????

  22. Vitamins…yummy…I must be the only one here that enjoyed reading this.

    This is not just an ad. Look at all the references and the work that went into it.

  23. oh look, more vitamins.

  24. If you’re trying to pass a stealth ad off as an article, don’t bold so much and have so many stock “doctor/lab” photos.

    Or if you do, call it an ad.

  25. This is just an ad and the next time you make an ad, I would suggest leaving out the pics. It makes you look like a journalist rather than a pseudoscientist…

    Also, “overall health and durability” is not a verifiable statement. I don’t doubt mitochondria are important to health but I would need more specific claims to even judge you right or wrong.

    So you are not even wrong.


  26. This article is just a product placement and it should be marked as an ad from the front page!

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