MitoQ = Targeted CoQ10

CoQ10 plays a crucial role both in energy production and in detox.  Our bodies make less of it as we age, and we function less well for that. For more than 30 years, supplementation with CoQ10 has been identified as a promising anti-aging strategy and preventive for diseases of the heart and the brain.  But in extensive animal studies and dozens of clinical trials, CoQ10 has shown modest benefit, or none at all.  Part of the problem is that, when CoQ10 is taken into the digestive system, very little of it gets to the site where it can work.  Where CoQ10 belongs is in the cellular energy factories, the organelles called mitochondria.  Very recently, a mitochondria-targeted form of CoQ10 has become commercially available.  Preliminary experiments with MitoQ in animals and humans are very promising.


How much is enough?

At the Second SENS conference in 2004, I sidled up to an expert whom I respected and asked, “What’s the optimal dose of CoQ10?”  He laughed and asked, in reply, “How much can you afford?”*

Mitochondria are “organelles”, hundreds of them in every cell, that provide the energy that is used for everything from thinking to fleeing Sabre-tooth tigers.  We have less mitochondria as we age, and the mitochondria we do have function less efficiently.  This fact contribuetes to diverse aspects of aging.  The high-energy redox chemistry of the mitohondria is also the primary source of free radicals that cause oxidative damage associated with age.

Another role played by mitochondria is that they are the designated hit-men when a cell outlives its usefulness, or becomes cancerous or diseased, or needs to be eliminated for any reason.  Apoptosis is the process by which an individual cell is programmed to commit suicide for the sake of the larger organism, and the mitochondria orchestrate the killing, emitting the chemicals that do the dirty work.  In older animals (and people), apoptosis becomes over-active, and we lose perfectly good nerve and muscle cells to cell suicide.

Coenzyme Q, a.k.a. ubiquinone, is a small molecule, a key chemical component in the working of the mitochondria and also the first-line anti-oxidant that prevents the generation of free radicals in the course of energy generation.  As we age, each mitochondrion has less ubiquinone than it needs to function well.  Long-lived species have more CoQ, pound for pound, than short-lived species. Hence CoQ has been recognized as an anti-aging compound for twenty years.  Today it is routinely prescribed by many cardiologists, because statin therapy depletes CoQ.

But eating ubiquinone doesn’t work very well.  It is poorly absorbed in the digestive tract (the molecular variant called ubiquinol is supposed to mitigate this problem), little of it makes it into the blood stream, less into the cells, and a pittance to the mitochondria where it is needed.

This may be one reason CoQ supplementation has failed to live up to its potential.  A Spanish Study (2004) found that CoQ could increase the mean and maximum life spans** of rats on a diet rich in polyunsaturates.  (Polyunsaturated fats are prone to oxidation.)  Doses were modest, equivalent to daily 50mg capsules for humans.  But this result was exceptional.  More typical are these studies (Ref Ref Ref Ref), which begin with great enthusiasm, but report no benefit for life span or mortality in mice and rats.


Provenance of Mito-targeted CoQ

In the 1990s, Michael Murphy and Robin Smith, two New Zealand biochemists, had an idea to get ubiquinone more efficiently into the cells’ mitochondria – the only place where it is useful.  It happens that part of the mitochondria’s electrochemical activity is to continuously pump protons out through their membranes.  Hence they maintain a negative electric potential relative to the rest of the cell.  Anything with a positive charge is drawn into the mitochondria, and if it’s not a proton, it won’t be pumped right back out again.  Murphy and Smith were inspired to create a molecule that combined ubiquinone at one end with a chemical tugboat at the other, a positive ion that is “chelated”, meaning that the positive charge is spread over a large number of atoms so that there is less tendency for it to simply pair up with a negative ion and be permanently neutralized.  The chemical “tugboat”, called TPP for tri-phenyl phosphonium, had been developed 25 years earlier in the Moscow State University lab of Vladimir Skulachev (Grinius et al, 1970).  Connecting the tugboat to the ubiquinone is a simple carbon chain that prevents interference between the chemical properties of the two ends (Smith and Murhpy, 1999)  

The next step was to synthesize this molecule in the lab – a task requiring a lot of ingenuity and lab experience, but Smith was up to it.  Then came years of testing the substance, first in cell cultures, then in animals, with various applications.  Targeting worked amazingly well, with virtually all of the Mito-Q molecules finding their way to the mitochondria. This means that very low doses can result in very high effectiveness.

Skulachev, who had pioneered the early work on the right-hand part of the molecule, picked up this thread early on, and has sponsored much of the research that has demonstrated the rejuvenating potential of the molecule.  The molecular tugboat is known as a “Skulachev ion”, and a similar molecule*** to MitoQ has been dubbed “SkQ” and explored in Russian experiments.

Last year, a New Zealand company completed licensing requirements and created a manufacturing facility, and MitoQ is now available by order on the Internet for delivery worldwide.  The product was first announced at the A4M annual showcase meeting in November.  A year earlier, Skulachev’s company had begun to sell SkQ as eyedrops, available thus far only in Russia.  Skulachev’s group has long-term plans to develop the product for other uses as well, and to obtain licensing in Europe and America.

Some of the reason for enthusiasm about MitoQ is theoretical, and hence tentative.  We know that apoptosis is on a hair trigger as we get older, and not just diseased cells but many useful, healthy cells are eliminating themselves.  Apoptosis has been linked to muscle wasting (sarcopenia) [Ref] and loss of neurons associated dementia [Ref].  It is found in cell cultures that MitoQ strongly inhibits apoptosis, not surprising since peroxides in the mitochondria are a signal that brings on apoptosis, and MitoQ eats peroxide for breakfast.  There are also theoretical reasons to believe MitoQ might be effective in curbing loss of insulin sensitivity [Ref].


Evidence for effectiveness of MitoQ

But the most convincing evidence comes from studies in animals and humans.  Rats were demonstrated to be resistant to a variety of insults, from ischemia (oxygen deprivation) to toxins to carcinogens to high blood pressure, after administering MitoQ to rats in their drinking water.  In a novel experment in mice, MitoQ was shown to protect against insulin resistance.  All these studies were reviewed in a 2011 paper by Smith and Murphy.  Historically, there is a strong correlation of life extension drugs and the ability to enhance stress resistance.  “Together these findings show that MitoQ is protective against pathological changes in a number of animal models of mitochondrial oxidative damage that are relevant to human diseases.”

A lot more animal research was performed in Russia***.  In a rat model of Alzheimer’s disease, SkQ reversed neuronal damage in a few weeks. SkQ fed to rodents led to more rapid healing of skin wounds, especially in old age.  The same paper reports that, applied topically, SkQ was able to reverse scarring.  Most interesting, the Russian team reports small increases in the mean life span of a variety of animals, including mice and fruitflies.  The authors claim without supporting data that there were dramatic life span increases of mice outside of standard (sterile) lab conditions, in which they were exposed to disease and infection.  In another paper by Skulachev (2007) a large number of animal studies are summarized, with impressive benefits for a broad range of aging diseases, including kidney damage and macular degeneration.  Many of the original papers behind this work are available in English through Springer from the journal Biochemistry Moscow.

There is very limited data thus far in humans.  Safety and toxicity tests were concluded with a year-long trial at 80mg/day.  In one study, MitoQ failed to improve the condition of advanced Parkinson’s patients, and in a second study MitoQ showed significant benefit for protecting against liver damage from Hepatitis C.  Dr Skulachev reports that he personally has improved his vision using Sk-Q eye drops.



All this study was carried out under direction of people who have an interest in the success of the compound.  You don’t have to think that scientists are congenitally dishonest to believe it is a good idea to protect them from incentives that might subtly bias their thinking or reporting.  Science Magazine a few weeks ago reported on the failure of mouse studies to translate into human benefit.  Studies conducted by drug companies are notorious.


A Subjective Bottom Line

I’ve known Dr Skulachev as a friend and colleague for more than a decade.  I trust that his work is solid and honest.  I had known that he was planning a campaign to commercialize SkQ, beginning with eye drops that began selling last year in Western Russia.  I was surprised and delighted to see that MitoQ is available as a commercial product, 10 years before I had expected.  It’s my belief that MitoQ is a promising new anti-aging strategy, and I’m signed on to be an early adopter.



* Long-term supplementation with high-dose CoQ10 is being studied as a treatment for and Parkinson’s disease and other neurological diseases of aging.  “High” is up to 3,600 mg/day, though one study found no further increase in bioavailable CoQ above 2,400 mg.  The best price I was able to find for CoQ on line worked out to about $4/g, so 2,400 mg per day would cost over $3,500 /yr.

** For those who follow details of rodent studies, the survival curve of this one stands out.  Most interventions that extend life span work mostly to prevent early deaths (“squaring the curve”).  Often the mean life span is increased, but the max life span in the group benefits much less, or not at all.  In this study, there is no benefit at all until nearly half the rats have already died of old age.  Then the death rate for the remaining rats is much lower.  Max life span is extended 24%, even as average life span is extended only 11%.

*** In the Russian work, Skulachev is using a variant of the Mito-Q molecule based on plastoquinone rather than ubiquinone.  Plastoquinone is the equivalent of ubiquinone in green plants, and Skulachev reports that there is a wider range of effective dosage for plastoquinone compared to ubiquinone.  Scientists at MitoQ disagree that plastoquinone is better.

49 thoughts on “MitoQ = Targeted CoQ10

  1. (1) MitoQ cannot be regarded as a mitochondria-targeted form CoQ or CoQ precursor since it cannot replace CoQ in its master function, i.e. as a respiratory chain electron carrier. MitoQ can be reduced to MitoQH2 by the initial respiratory chain complexes I and II but MitoQH2 is very slowly oxidized by the next respiratory chain complex III. Moreover, MitoQ cannot be decomposed in a way resulting in CoQ release. This is why MitoQ can hardly help when CoQ level is lowered by aging or statin. As to another function of CoQ as an antioxidant, MitoQ is not the best one since the window between anti- and prooxidant concentrations of MitoQ is as small as several times. For SkQ (a MitoQ analog with plastoquinone instead of CoQ), this window is much larger (30 or even 1 000 times, depending on the method of measurement of this parameter). This is why plants use plastoquinone in chloroplasts (the O2-producing organelles) and CoQ in mitochondria (the O2-consuming organelles where the O2 level and hence, the oxidative stress, is always much lower than in chloroplasts).

    (2) P3, para 2: ”The same molecule that is known as MitoQ in the English-speaking word is called SkQ in Russia”. It is not the case. As I already mentioned in (1), MitoQ and SkQ are different molecules. As antioxidant, SkQ is much better.
    [Note – this has been corrected in the text above – JJM]

    (3) P.4, the last para: “Scientists at MitoQ disagree that plastoquinone is better [antioxidants]”. In fact, there is an agreement among organic chemists that plastoquinone is several folds stronger antioxidant than CoQ [1-3].In biological experiments, our group is still the only lab in the world where MitoQ and SkQ were compared in one and the same experiment and it was found that the difference between two compounds is even much larger than in chemical test systems. This may be due to that SkQH2 is oxidized both chemically (by O2) and biochemically (by complex III) slower than MitoQH2, resulting in higher steady state level of reduced form of the antioxidant in the case of SkQ than that of MitoQ.

    (4) P.2, the last para. Our contribution to the field was not limited by the first attempt to use substituted triphenylphosphonium cation (TPP) to target something useful to mitochondria but also by elucidation of the driving force for such a targeting. Using our penetration ions (called by David Green a Skulachev ions or Sk+ [4]) we described “the mitochondrial electricity”, i.e. electric potential difference between mitochondrion and cytosol (mitochondrial interior negative), which is generated by respiration and can be used for electrophoretic accumulation of any penetrating cations or of compounds conjugated with these ions [5-7]. The role of a penetrating cation in such a targeting was defined as that of “electric locomotive” [7] which seems, I am sorry, better that your “tugboat” since it indicates electrical nature of the driving force. The great contribution of M. Murphy and his colleagues [8] consisted in an attempt to use an antioxidant as a cargo.

    (5) P.4, para 1. “The original papers behind this work are available is Russian”. In fact, in Russian and English. Biochemistry (Mosc.) is published in two languages. [Corrected in the text above – JJM]

    (6) P.4, para 2. Dr. Skulachev reports that he personally has improved his vision using SkQ eye props”. These drops are available in Russian drugstore since July 2012. More than 100,000 vials are already sold. Not a single complaint was received by drugstores. In Moscow clinical trials of the drops as a medicine against the Dry eye syndrome, an age-related incurable disease carried out. They proved to be were very positive. Now we obtained FDA permission for clinical trials of SkQ in the U.S.A. The trials will start in February. Our pre-clinical trials on mice were sufficiently repeated by Ora laboratories (Endower, U.S.A.).

    Best regards,

    1. Kruk, J., Jemiola-Rzeminska, M. & Strzalka, K. (1997) Plastoquinol and alpha-tocopherol quinol are more active than ubiquinol and alpha-tocopherol in inhibition of lipid peroxidation, Chemistry and physics of lipids. 87, 73-80.
    2. Roginsky, V., Barsukova, T., Loshadkin, D. & Pliss, E. (2003) Substituted p-hydroquinones as inhibitors of lipid peroxidation, Chemistry and physics of lipids. 125, 49-58.
    3. Antonenko, Y. N., Avetisyan, A. V., Bakeeva, L. E., Chernyak, B. V., Chertkov, V. A., Domnina, L. V., Ivanova, O. Y., Izyumov, D. S., Khailova, L. S., Klishin, S. S., Korshunova, G. A., Lyamzaev, K. G., Muntyan, M. S., Nepryakhina, O. K., Pashkovskaya, A. A., Pletjushkina, O. Y., Pustovidko, A. V., Roginsky, V. A., Rokitskaya, T. I., Ruuge, E. K., Saprunova, V. B., Severina, I. I., Simonyan, R. A., Skulachev, I. V., Skulachev, M. V., Sumbatyan, N. V., Sviryaeva, I. V., Tashlitsky, V. N., Vassiliev, J. M., Vyssokikh, M. Y., Yaguzhinsky, L. S., Zamyatnin, A. A., Jr. & Skulachev, V. P. (2008) Mitochondria-targeted plastoquinone derivatives as tools to interrupt execution of the aging program. 1. Cationic plastoquinone derivatives: synthesis and in vitro studies, Biochemistry (Moscow). 73, 1273-87.
    4. Green, D. E. (1974) The electromechanochemical model for energy coupling in mitochondria, Biochimica et biophysica acta. 346, 27-78.
    5. Liberman, E. A., Topaly, V. P., Tsofina, L. M., Jasaitis, A. A. & Skulachev, V. P. (1969) Mechanism of coupling of oxidative phosphorylation and the membrane potential of mitochondria, Nature. 222, 1076-8.
    6. Liberman, E. A. & Skulachev, V. P. (1970) Conversion of biomembrane-produced energy into electric form. IV. General discussion, Biochimica et biophysica acta. 216, 30-42.
    7. Skulachev, V. P. (1988) Membrane bioenergetics, Springer-Verlag, Berlin ; New York.
    8. Burns, R. J., Smith, R. A. & Murphy, M. P. (1995) Synthesis and characterization of thiobutyltriphenylphosphonium bromide, a novel thiol reagent targeted to the mitochondrial matrix, Archives of biochemistry and biophysics. 322, 60-8.
    9. Skulachev, V. P., Bogachev, A. V. & Kasparinsky, F. O. (2013) Principles of Bioenergetics, Springer, Berlin, Heidelberg.

    • Thank you Josh for putting this together on your site and thank you Vladimir for commenting – and of course for your great work!

      Vladimir, is there any schedule on your side when other forms of SkQ might be available in Europe or Russia (I am from Western Europe but also have access to the Russian market)? I mean forms beyond the eyedrops.

      All the best,

    • Organelles, like every living entity, are constantly adapting to their microenvironments. They respond and react to nutrients, medicines, etc., and simply adapt to the levels/concentrations maintained in that local environment. Moreover, the path that all such responses follow depends upon the entity’s history; variation exists even among the same types of organelle inside the same ‘type’ of cell, etc.

      We see these effects in various chemical therapies in which dosage effects decrease over time and must be increased to sustain effects. Similarly, we see an effect similar in the ‘j’ function of some ambiguously toxic compounds in which, in contrast to large-dose toxic effects, a small dose benefits (hormesis). A related effect is that of the unintentional result of biopsy causing reinvigoration of a tumor.

      Rather than taking a constant dose, it might prove better to vary it over time. I think that Skulachev is exhibiting spurious accuracy in his statement above. We simply don’t know the entire ensemble of effects in these endeavors: those who suggest we are not ignorant are specious.

  2. Thank you for this excellent and informative dialogue on Co-Q10 relatives aiming to solve the mitochondrial utilization problem.

    Just one comment of a general nature. I’m bothered by the current cliche that manufacturer-sponsored research is suspect, while government-sponsored research is above suspicion. Every funded research program I’ve ever known has had built-in biases. Government-funded research institute are notoriously prone to be captured by “in groups” of scientists who all believe in the same set of heuristics. Any kind of monopoly funding for science is therefore a threat to the diversity of approaches we need at the frontier.

    Even as we speak there are Big Science projects afoot that will predictably waste limited resources and suppress heterodox opinions in brain science and other fields. Intellectual monopolies are as bad as economic ones.

    • This is indeed excellent if it holds up.

      I take your point about bias, but I find my scientific friends who are funded by the Feds to be just as biased as those who are not.

      Replication is always essential, including (especially) replication by skeptics.

      I’ll buy this if the data hold up, and if somebody markets it.

  3. Can you tell me where you are able to buy it at that price?

    Only option I can ind is MitoQ from New Zealand and at 5mg/day I question the benefit!

  4. Hi!
    I have a question relating Mito Q, regarding apoptosis. it’s a normal cell control function, that includes marking those deficient cells to kill themselves. If MitoQ somehow reduces this function, will it reduce the body’s ability to kill the cells that really need to be killed? Cancerous cells, for example?
    Best regards

    • This is a good point, and the answer cannot be theoretical – we simply need to do the labwork. The next step is that I’d like to see someone replicate Skulachev’s work extending life span of mice.

  5. Fascinating! Excellent commentary. Good empirical issues are raised. Hope the above dialogue tempts those presently able, to go on to the next research iterations needing study. (For young academicians I see a wealth of publication {and promotion enhancing possibllties in the dozen evident next affordable research steps that beg to be taken, all predicated on work already done to date. This subject clearly involves a topic with both profound and fundamental clinical as well as laboratory implications, and which portends important but low-risk treatment benefits, which along with a promising safety level, and efficacy may well support significant interventions being developed for many now difficult to treat downstream conditions (e.g., Sjogren’s). Like insulin and thyroid this combination molecule (whether SKq or MitoQ) may well come to serve (in time) as a replacement therapy for persons aging rapidly (or even normally beyond 25-30) – as well as in alleviating troublesome symptoms and provide relief where more conventional pharmaceuticals often offer unpleasant side-effects with whatever gains. The only downside in all this will be that to obtain continuing benefit from MitoQ or SKQ, since they will likely serve as a replacement therapies, they likely will have to used chronically, and the relatively high cost per mg. (to produce it) may well limit the numbers who can afford to utilize it over lengthy periods. All replacement therapies reqauire this, so it need not, in the longer term, prove an insurmountable barrier within certain developed societies having more enlightened social insurance systems. All this may or may not be self-evident to some readers and lab folks, but the opportunities for clinical doable, shorter term clinical research are genuinely golden. (Wish I were younger !)

  6. This is indeed something worth being interested on. As much I want this to work I have to be skeptikal so far until future studies and devellopments The question about apoptosis is a very good one, also more info about the side effects and the right dossage will show up in time. Also I am not prepared enough to decide between the NZ version and the Russian version.

  7. Given that no large-scale human trials have been conducted, what would be the scientific pros and cons with regard to safety? Do we know how the molecule is metabolized, and is that process under homeostatic control? Are there any imaginable ways for MitoQ to be toxic, long-term or short-term? Are there any blood tests to do to keep an eye on the effects?

    Thank you very much,


    • I wish I had answers. I can only refer you to the web sites for MitoQ and for SkQ. You can also go to to PubMed and search on SkQ. The bottom line is that you are correct, we don’t have the kind of safety data we’d like to have, and dosage in particular has not been adequately studied.

  8. Although the notion that a biological entity, such as an organism, cell, ecosystem and so on, functions with machine-like precision, the actual dynamics is distinct from machines’. Were nature’s manner of dynamics actually that of machines, “control” would also issue from a central source like a computer’s or any technological device. However, there would be no development from, for example, zygote (fert. egg) to mature adult or cell cycle or ecological succession (colonization) to mature (climax) ecosystem because, as we all know, an extensively changing machine is a failed machine (a developing organism might be likened to a microlight aircraft developing into a jumbo jet while in flight).

    From that perspective we can safely assume that the effect of adding efficiency to a bio system will likely affect only a subelement of the overall system. For example, reintroducing a top predator (wolves) to an ecosystem (Yellowstone Park), allowed more birds to succeed (and avg. coyote size increased) because it shifted the human-constrained food web to one of more natural structure and function. Adapting is what biological systems do.

    Cells perform their ecological function in the body’s larger ecosystem with some thousand different proteins of which only an immeasurable minority might be enhanced or decreased in number. Apoptosis, cell removal, is effected by cells’ milieu — other cells as communicated via their extracellular matrices (ECM). The fact that a given cell, perhaps less functional, survives or dies is determined by such local environments, not by some magical switch within the cellular ‘machine.’

    What we’re doing when we exercise vigorously is stressing our bodily systems, that is, dramatically changing such environments which, in turn, will tend to (the biological legal boilerplate) cause what is known as desaturation in an ecosystem. Desaturation has the effect of returning the system level or “clock” of maturation back to a condition not unlike an earlier stage of development. In ecosystems we see this as a forest meadow being recolonized by successive plant communities that end with trees (secondary succession; primary succession is colonization of the oceanic volcano newly emerged from the sea).

    There’s no magic bullet for health; at best we have only a lucky DNA legacy, fortunate development, and a vigorously active life style.

  9. To Whom It May Concern,

    Currently I am in pretty bad shape. My story is unfortunately similar to many that have taken Cipro, Levaquin, Avelox, and many other Fluoroquinolone antibiotics. All started in June of this year with a kidney stone. Previous to this, I have been an active, healthy individual with virtually no health issues other than a couple bad stomach bugs, over the years. I have not had a flu shot in 20 years. Have not had any major illness ever. I worked 14 hour days in the southern New Mexico oil fields for Halliburton as a Tech. Keep an entire production and stimulation crew running. After that I was managing 40 oil wells for Concho, the largest oil producer in the state. Great job, great friends, had a good life. Little did I know………

    From June to September of 2013 I had 4 kidney stone attacks. The 4th one ended with me getting lithotripsy to remove the stone. Levaquin IV was given preoperative and week followup of cipro 500 mg 2x day. All was fine then had the stent removed during outpatient procedure. Single 500 mg cipro dose given then. After this all was good for about a week. Then started having groin pain for about 3 weeks. Dr did another outpatient cytoscopy and said all was fine. Another single 500 mg dose of cipro. Still had pain. So doc did prostate exam and found elevated white blood cells. No culture was done. Script was 500 mg 2x day of cipro for 6 weeks. No help with pain. Dr added sulindac NSAID to help. 12/7 had another surgery performed to make sure no small stones or strictures were present. None found. More preoperative Levaquin given via IV. About a week later started feeling better. I knew of risk factors with cipro and was paying attention to them. On 12/28. Noticed tight muscles in my calves and by next morning the burning in my legs began. Stopped taking cipro that day. Dr said that cipro could cause the muscle issues but did not know of issues with neuropathy. So now 8 months out I have insomnia, peripheral neuropathy, tinnitus, cognitive dysfunction, suicidal thoughts, depression, some anxiety, and mild depersonalization, chronic fatigue, dye eyes and ears, dry mouth, intolerance to heat and cold. Cold hands and feet, improper sweating. Gi motility dysfunction, lost 30 lbs so far.

    Cannot work, cannot sleep, cannot walk correctly somedays, cannot care for myself. My spouse now does 90 percent of the work for both of us. I spend most of days in bed. This issue has created a lot of stress and depression not only for me, but for my entire family, which now has to help me with many aspects of my life. The uncertainty of recovery also plays a large role in my overall stress/anxiety level.

    Now it’s November of 2014. Been to Mayo, University of Washington, The Peripheral Nerve Clinic, and Anderson Specialty Medical Clinic, and Progressive Medical Center in Atlanta so far. Tried IV Therapy, supplements, vitamins, Physical Therapy, Analgesic Nerve Therapy, etc. Had almost every test imaginable. MRI, CT Scans, Blood tests, autonomic tests. Have more tests coming. So far, not much of any improvement. Some better with sleep, but still have to take all kinds of drugs to get sleep. Anxiety is not bad, tendinopathy is better, and some slow improvements in GI function, but have bad relapses every couple weeks. Have spend 10’s of thousands of dollars, not including insurance paid costs, for treatments, supplements, travel, etc.

    There are reports that many of the symptoms are tied to mitochondrial dysfunction and autonomic system dysfunction. I have added a file outlining the new request to the FDA about the dangers of Mitochondrial toxicity caused by fluoroquinolones. Mito dysfunction causes an entire cascade effect and creates a vicious circle of ROS and cell apoptosis. I could kill you with the technical details regarding NO/OONO cycles, Electron Transport Chain, oxidative phosphorylation, anerobic cell respiration, etc, but I have posted some references at this end of this email.
    I have tried PQQ and coq10 and both times seems to drastically worsen my symptoms. Please advise as to why one of these compounds could do this?

    Here are some links that further describe what has happened to me, and thousands of others.

    All the Best,
    Charles Tooraen

    • Thanks for referring me to the literature on fluoroquinolones. I agree that they are being irresponsibly prescribed, and that until we have a means of determining which individuals will suffer devastating reactions, these drugs should be prescribed only when all else fails.

      I don’t have medical advice for you, both because I don’t have the background to give that kind of advice, and, even if I did, I would not presume to diagnose you from a distance. However, I encourage you to seek advice from a variety of medical professionals with different backgrounds and specialties, and to remain optimistic as you experiment. You have learned the hard way that individual responses to the same treatment can be very different. Begin with treatments that are very unlikely to hurt you, even if they seem dubious or far-flung. (You may be tempted to begin with what your insurance will cover, and this is seldom a good guide.) Take charge of your own medical treatment. Experiment patiently on yourself. Don’t give up until you find something that works for you.

      • Thanks John, I appreciate it. There are a lot of theories out there that are tossed around. Mitochondrial issues, toxic poison/metabolite issues, gut flora eradication issues, etc. Collagen production issues, GABA receptor blockage issues. A whole host of ideas and none completely fit, but all overlap and could be concurrent. I keep trying, small things, a little at a time now to watch and see. Too much to risk some of the setbacks I have had. Some though have appeared to have good success with MitoQ. I was wondering if Vladimir Skulachev may have some insight as to why some would have a bad reaction to a quinolone type compound. How closely related is something like mitoq/PQQ/C0q10 to a Fluoroquinolone? We are just searching for common threads.


        Charles Tooraen

    • I took levaquin for pneumonia. Just one pill made my mind so messed up I couldn’t even drive my car.
      Nasty stuff

      I just ordered a bottle of MitoQ as I have fibromyalgia, IBS and Interstitial cystitis (a bladder condition).
      Ubiquinol doesn’t seem to do much for energy levels, though PQQ helps a little. I also tried Shilajit.
      I want to see if the MitoQ makes a difference

      • MitoQ should be taken as a prophylaxis during fluoroquinolone treatment. It protects tendon cells from oxidative stress during treatement :

        Unless your mtDNA has been damaged and lacks the ability to produce sufficient Q10, MitoQ probably won’t give you extra energy. But worth a try, I guess.

        • I tried a bottle of the MitoQ. It definitely gave me more sustained energy but for some reason made me feel strange.
          I’m now back to CoQ10 and PQQ.
          I may try the MitoQ again during the summer (busy time at work)

          • MitoQ also made me feel extremely strange.

            I’m starting to take the view that there is precious little evidence that any vitamins or mineral supplementation does anything for life extension. I think most of us take these things based on scant research that is suggestive but does not really prove anything.

          • If you cannot establish a benefit in double blind studies, then how do you establish that supplements “prevent” any specific condition?

            I think they are just as likely to cause extensive harm as they are to prevent any harm, and people take these substances based on little more than hope, desperation for immortality, and extremely sparse and inconclusive research.

            In my own case, I used to take about 40 supplements a day, and all I succeeded in doing was turning up my metabolism in a very bad way and sending all of my pituitary hormones sky high. I didn’t feel better; I felt worse.

            I think the vast majority of these substances prevent nothing, and probably do as much harm as good, given that we have very poor mechanisms for measuring the effects and regulating the dose based on responses.

          • Yes – we are experimenting on ourselves. On my web site I list a few supplements for which there is life extension evidence we can have confidence in.

          • They can definitely be overdone but I trust supplements more than prescription drugs.
            It’s prudent to do a lot of research before experimenting on ourselves

          • Josh, I did a quick review of your antiaging site, and some of those like Vitamin D and melatonin are no brainers. I always try to explain to people that melatonin release in sleep is a critical restorative hormone, but for some reason people resist the idea. I am always confused why the common dose for supplements is 3 mg when the appropriate dose is more like 300 mcg.

            There are a handful of supplements like these for which there is clear evidence. Most of the rest look to me like wishful thinking and no clear call to action.

          • steve, to me most prescription drugs are poisons, and most supplements are placebos or poisons too (at least without very careful biochemical analysis which no one taking supplements does and which is not cost effective to do).

            I no longer trust supplements simply because they are supplements.

  10. Does anyone have a link to the information for the US trial of the SkQ eye drops to treat dry eyes? I understood they were recruiting for an FDA trial.

  11. I’m confused. Per Vladi’s statement above, MitoQ does not work… “Moreover, MitoQ cannot be decomposed in a way resulting in CoQ release. This is why MitoQ can hardly help when CoQ level is lowered by aging or statin.” Looks like I’m cancelling my order.

    • Skulachev is in the habit of downtalking MItoQ (even in his published papers) because it is the only commercially available competitor to his compounds. Also, MitoQ can be “decomposed in a way resulting in CoQ release” and there are several studies showing this.

  12. I read a piece on the benefits of PQQ and mitoQ . I am one of hundreds of thousands who is suffering from fluoroquinolone toxicity (I was given Cipro). I am almost a year out in my struggle to recover and I was wondering about the “quinolone” in PQQ. Is it the same quinolone in fluoroquinolones? I want to take the supplement but am nervous about making my situation worse.

  13. There is one important question asked in the article … how much is enough? It would be very interesting for me to get a hint on how much on a daily basis of MitoQ is considered enough (and no too much) to show the wanted results. As long as SkQ1 isn’t available we have to stick to MitoQ … As mentioned before MitoQ ist marketed as 5 mg pills and the recommended daily dosage is 10 mg.

  14. The problem with MitoQ is that the window between anti- and prooxidant activity is very small, making it ineffcient at low doses and harmfull at larger doses. I once asked the manufacturer of MitoQ, if I could up the dose to 20 or 40 mg a day, since I didn’t feel any increase in energy levels and they answered that, if I didn’t feel any positive effect, I could take 20 or even 40 mg a day. This trial and error approach isn’t very appealing. I’m betting on SKQ1 instead.

    • People were administered up to 80mg/day for a year with minimal to no side effects in the Parkinson’s trial of MitoQ. Other cohorts in trials have received 10, 20 and 40 mg daily doses with an excellent tolerability profile. Cost is the issue…

  15. Just because 80mg didn’t kill them, it doesn’t necessarily mean that it didn’t cause them any harm. It is a well established fact that mitoquinone acts as a pro-oxidant at larger doses. I haven’t been able to get the manufacturer to tell me, what the maximum dose (mg/kg) should be. As long as they just say “up the dose, if you don’t notice any benefits”, I err on the side of caution.

    • Well looking at the full text of that paper, the only significant AE was nausea and vomiting and only an issue in the 80mg group. Those on 40 had the same rate of AEs and discontinuation as the placebo group. Like I said, cost will limit almost everyone going over 40mg/day. If you don’t get any benefit from a dose that high I wouldn’t bother continuing. It doesn’t help everyone but it does help a lot of people

  16. Comments on this new study?

    Age-related loss of skeletal muscle mass and function is a major contributor to morbidity and has a profound effect on the quality of life of older people. The potential role of age-dependent mitochondrial dysfunction and cumulative oxidative stress as the underlying cause of muscle aging remains a controversial topic. Here we show that the pharmacological attenuation of age-related mitochondrial redox changes in muscle with SS31 is associated with some improvements in oxidative damage and mitophagy in muscles of old mice. However, this treatment failed to rescue the age-related muscle fiber atrophy associated with muscle atrophy and weakness. Collectively, these data imply that the muscle mitochondrial redox environment is not a key regulator of muscle fiber atrophy during sarcopenia but may play a key role in the decline of mitochondrial organelle integrity that occurs with muscle aging.

  17. coming from a purely non scientific person who has purchased and used mitoQ for almost 2 months now, at the sustained 2 capsule daily dose i can say that the long term sustained energy and drive to actually initiate work/exercise has increased. Sustained sleep has increased however this may be a side effect of the increased physical activity.
    As for negative side effects i have noticed a tendancy to heightened mood/uncharacteristic behavior, and strangely less appetite.
    There are a few other effects i will not mention at this stage as it would be too early to tell if this was the mitoq. I will update at 6 month intervals on my status and other postive/negative changes.
    Oh and i have not noticed any skin/anti aging effects 😉

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