By Duane Graveline MD, MPH
Those of you who have been following my research over the years will know that I consider mitochondrial DNA damage as the ultimate result for many people from taking statins.
Through mevalonate blockade, statins directly inhibit CoQ10 synthesis making mitochondrial damage and mutation all but inevitable. Furthermore, the inhibitory effect of statins on dolichol synthesis makes repair of DNA damage all the more difficult because of the vital role of dolichols in glycoprotein (glycohydrolase) synthesis.
A few years ago I learned of another biochemical substance that also is implicated in this process of mitochondrial maintenance. The name of this biochemical is pyrroloquinoline quinone with the shorthand version being PQQ.
The vital role of PQQ in mitochondrial support has only been documented in the past 15 years. From what I have read of this substance, it is worth considering for those of us who have been damaged by statins, whether by cognitive dysfunction, permanent myopathy, ALS like symptoms, or peripheral neuropathy.
Dietary sources of PQQ include many fruits and vegetables and egg yolk. Natto (fermented soybeans) is a particularly rich source as are celery, parsley, papaya and kiwi fruit. PQQ is also available as a dietary supplement. Human trials and studies will need to be performed to support any claims for the benefits of PQQ supplementation.
One promotion for PQQ begins with, "The more functional mitochondria you have in your cells, the greater your overall health and durability," which is the premise of the upcoming new edition of my book, The Dark Side of Statins, so my interest in this substance is obvious.
The problem is that as we age, our mitochondria degrade and become dysfunctional. Compared with nuclear DNA, mitochondrial DNA is left almost entirely exposed to the ravages of free radicals. It attaches directly to the inner membrane where the mitochondria's furnace rages continuously.
Statin drugs directly hasten this process of mitochondrial DNA degradation by direct inhibition of CoQ10 and dolichol synthesis. The ultimate cause of statin associated adverse reactions is this progressive deterioration of mitochondrial DNA. PQQ is being touted not only for its extra anti-oxidant protection in the fight against free radicals, but also for its potential use for mitochondrial genesis.
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 genesis were calorie restriction or exhaustive physical activity.
You may have heard of the half-starved mice run to exhaustion and most share the opinion that this research, though interesting, is not applicable to humans. However, PQQ research has shown some very interesting results. Experimental animals deprived of PQQ, in addition to stunted growth and development, reveal fewer mitochondria in their tissues. When PQQ is restored, normal growth and development returns and the mitochondrial number is increased.
This has led researchers to the effect of PQQ on certain genes having to do with control of the process of mitochondrial genesis. Their work has led to the promising idea that we now may be able to trigger mitochondrial genesis through the use of this dietary supplement. This seems almost too good to be true, but at this time I cannot fault the research results and feel comfortable in at least bringing it to the attention of statin damage victims and their doctors.
When one compares the boundless energy of a child with the slow shuffle of a senior citizen it is easy to understand the impact of our mitochondria, for mitochondria in the muscles of a child are nearly all burning hot with boundless energy, whereas studies have revealed that in the muscles of seniors, some 95% of their mitochondria is damaged — their once energetic powerhouses now gone cold.
Many things contribute to the maintenance and function of mitochondria. The biochemical processes that we have evolved to derive our energy needs are remarkably tolerant, permitting us to more or less cover this planet of ours despite widely varying diets.
Just as we have recently discovered the adverse effect of statin drugs on mitochondrial DNA, now we have discovered still another substance vital to mitochondrial function. Not only does PQQ appear to bring us enhanced anti-oxidation to help fight the constant war against free radicals, it also offers the possibility of mitochondrial growth.
Research support for this new concept of mitochondrial genesis is rapidly accumulating. In Pflugers Archives, 459(2); 277-89, January 2010, Lanza and Nair of the Mayo Clinic, using liver cells, showed in experimental animals that the influence of PQQ is on the pathways that previous research has shown to regulate mitochondrial biogenesis.
This extraordinary work on mitochondrial function was confirmed by that of Chowanadisai and others at the University of California, Davis, reporting in J Biol Chem. 1;285(1):142-52, January 2010.
Tao and others of the San Francisco VA Medical Center and UCSF used adult rat heart cells to demonstrate the ability of PQQ to preserve mitochondrial function and prevent oxidative injury. Their work was published in Biochem Biophys Res Commun. 16;363(2):257-62. Nov. 2007.
Thus solid evidence exists for the role of PQQ in both liver and heart cells and almost undoubtedly further research will demonstrate a similar effect in any tissue studied, for mitochondrial function is not tissue specific.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
Updated February 2016