351 replies to this topic

[agram]

 

gregmacpherson

 

Are you aware of MitoQ being used for Mito dysfunction caused by adverse drug reactions such as statins or fluoroquinolones?

 

thanks

Hi Agram, 

 

Yes, we have quite a few customers using MitoQ for both issues.   Those with Statins are best to combine a low dose CoQ10 (30-50mg) with MitoQ as there is still a need for CoQ10 in cell compartments other than the mitochondria. 

 

Thanks

 

Thanks for the quick reply Greg,

 

What I'm worried about is the MitoQ having a pro-oxidant effect in Mito that's been damaged by the drug. Have you heard of any ADRs from MitoQ with people damaged by fluorquinolones or statins? Finally if I buy it, is it safe for me to open the capsule and take half a dose? I like to start low on supplements to see how I react.

 

Many thanks

[gregmacpherson]

 

 

gregmacpherson

 

Are you aware of MitoQ being used for Mito dysfunction caused by adverse drug reactions such as statins or fluoroquinolones?

 

thanks

Hi Agram, 

 

Yes, we have quite a few customers using MitoQ for both issues.   Those with Statins are best to combine a low dose CoQ10 (30-50mg) with MitoQ as there is still a need for CoQ10 in cell compartments other than the mitochondria. 

 

Thanks

 

Thanks for the quick reply Greg,

 

What I'm worried about is the MitoQ having a pro-oxidant effect in Mito that's been damaged by the drug. Have you heard of any ADRs from MitoQ with people damaged by fluorquinolones or statins? Finally if I buy it, is it safe for me to open the capsule and take half a dose? I like to start low on supplements to see how I react.

 

Many thanks

 

 

A good question.  Right at the beginning of our journey with MitoQ there was some conjecture about the theoretical risk of pro-oxidant effects of MitoQ but in all of in vivo research it has not come to pass.   

 

I am not aware of any ADR's with people on fluoroquinolones or statins.  We work with an independent vigilance company called Safety Call based in the States and nothing has come through to date on that front.  

 

It is perfectly fine for you to split a capsule to see how you respond.  Please keep me posted!

 

Thank you. 

[Razor444]

 

 

Greg, could you comment on this study?

 

Cell Rep. 2017 May 9;19(6):1202-1213.

Mitochondrial ROS Production Protects the Intestine from Inflammation through Functional M2 Macrophage Polarization.

Formentini L1, Santacatterina F1, Núñez de Arenas C1, et al.

Mitochondria are signaling hubs in cellular physiology that play a role in inflammatory diseases. We found that partial inhibition of the mitochondrial ATP synthase in the intestine of transgenic mice triggers an anti-inflammatory response through NFκB activation mediated by mitochondrial mtROS. This shielding phenotype is revealed when mice are challenged by DSS-induced colitis, which, in control animals, triggers inflammation, recruitment of M1 pro-inflammatory macrophages, and the activation of the pro-oncogenic STAT3 and Akt/mTOR pathways. In contrast, transgenic mice can polarize macrophages to the M2 anti-inflammatory phenotype. Using the mitochondria-targeted antioxidant MitoQ to quench mtROS in vivo, we observe decreased NFκB activation, preventing its cellular protective effects. These findings stress the relevance of mitochondrial signaling to the innate immune system and emphasize the potential role of the ATP synthase as a therapeutic target in inflammatory and other related diseases.

PMID: 28494869

 

 

Hi Ta5,

 

I don't think this is a concern. This study used a very interesting - but obscure - TG mouse model to explore mito ROS signalling pathways. The situation in colitis/Crohn's/IFB is quite different. More importantly, if you look at the two papers in the links below you will see that there is strong evidence in mouse models that MitoQ prevents the damage in colitis.

 

https://www.ncbi.nlm...pubmed/25034594

 

https://www.ncbi.nlm...pubmed/23915129

 

Thanks.

 

 

I take MQ for ulcerative colitis and find it helpful.

[gregmacpherson]

Some news out today that is relevant to those with IBD

 

http://www.dailymail...ohn-s-cure.html

 

The abstract is here .. https://www.ncbi.nlm...pubmed/28401939

[gregmacpherson]

Hi All, 

 

For those that are interested we are having a special on MitoQ 5mg and MitoQ + Curcumin for the balance of the week (Expires June 3) for those that are interested. 

 

Enter LONG20 at check out.  Max of 3 bottles per order. 

 

Thanks! 

[Puppalupacus]

For the Longecity code, is there a max limit for purchase?  For example, when I used to enter the SUBSCRIBE20 code, I was limited to a max of $400 (if I remember correctly).  Also, can anyone confirm the Longecity code is worth 15% off?  Just trying to crunch numbers before buying membership.

Edited by Call of the Void, 07 June 2017 - 10:37 PM.

[gregmacpherson]

Hi - You can use the coupon 10 times and you get 15% discount.

 

 

Hi, the code is valid for 10 uses and is 15% discount. Thanks.

[ta5]

I wonder if Greg or anyone can comment on this study. The link below is to the full text.

 

Physiol Rep. 2018 Apr;6(7):e13667. doi: 10.14814/phy2.13667.

The targeted anti-oxidant MitoQ causes mitochondrial swelling and depolarization in kidney tissue.

Gottwald EM1, Duss M2, Bugarski M1, Haenni D1,3, Schuh CD1, Landau EM2, Hall AM1,4.

Kidney proximal tubules (PTs) contain a high density of mitochondria, which are required to generate ATP to power solute transport. Mitochondrial dysfunction is implicated in the pathogenesis of numerous kidney diseases. Damaged mitochondria are thought to produce excess reactive oxygen species (ROS), which can lead to oxidative stress and activation of cell death pathways. MitoQ is a mitochondrial targeted anti-oxidant that has shown promise in preclinical models of renal diseases. However, recent studies in nonkidney cells have suggested that MitoQ might also have adverse effects. Here, using a live imaging approach, and both in vitro and ex vivo models, we show that MitoQ induces rapid swelling and depolarization of mitochondria in PT cells, but these effects were not observed with SS-31, another targeted anti-oxidant. MitoQ consists of a lipophilic cation (Tetraphenylphosphonium [TPP]) joined to an anti-oxidant component (quinone) by a 10-carbon alkyl chain, which is thought to insert into the inner mitochondrial membrane (IMM). We found that mitochondrial swelling and depolarization was also induced by dodecyltriphenylphosphomium (DTPP), which consists of TPP and the alkyl chain, but not by TPP alone. Surprisingly, MitoQ-induced mitochondrial swelling occurred in the absence of a decrease in oxygen consumption rate. We also found that DTPP directly increased the permeability of artificial liposomes with a cardiolipin content similar to that of the IMM. In summary, MitoQ causes mitochondrial swelling and depolarization in PT cells by a mechanism unrelated to anti-oxidant activity, most likely because of increased IMM permeability due to insertion of the alkyl chain.

PMID: 29611340

 

[APBT]

 

I wonder if Greg or anyone can comment on this study. The link below is to the full text.

 

Physiol Rep. 2018 Apr;6(7):e13667. doi: 10.14814/phy2.13667.

The targeted anti-oxidant MitoQ causes mitochondrial swelling and depolarization in kidney tissue.

Gottwald EM1, Duss M2, Bugarski M1, Haenni D1,3, Schuh CD1, Landau EM2, Hall AM1,4.

Kidney proximal tubules (PTs) contain a high density of mitochondria, which are required to generate ATP to power solute transport. Mitochondrial dysfunction is implicated in the pathogenesis of numerous kidney diseases. Damaged mitochondria are thought to produce excess reactive oxygen species (ROS), which can lead to oxidative stress and activation of cell death pathways. MitoQ is a mitochondrial targeted anti-oxidant that has shown promise in preclinical models of renal diseases. However, recent studies in nonkidney cells have suggested that MitoQ might also have adverse effects. Here, using a live imaging approach, and both in vitro and ex vivo models, we show that MitoQ induces rapid swelling and depolarization of mitochondria in PT cells, but these effects were not observed with SS-31, another targeted anti-oxidant. MitoQ consists of a lipophilic cation (Tetraphenylphosphonium [TPP]) joined to an anti-oxidant component (quinone) by a 10-carbon alkyl chain, which is thought to insert into the inner mitochondrial membrane (IMM). We found that mitochondrial swelling and depolarization was also induced by dodecyltriphenylphosphomium (DTPP), which consists of TPP and the alkyl chain, but not by TPP alone. Surprisingly, MitoQ-induced mitochondrial swelling occurred in the absence of a decrease in oxygen consumption rate. We also found that DTPP directly increased the permeability of artificial liposomes with a cardiolipin content similar to that of the IMM. In summary, MitoQ causes mitochondrial swelling and depolarization in PT cells by a mechanism unrelated to anti-oxidant activity, most likely because of increased IMM permeability due to insertion of the alkyl chain.

PMID: 29611340

 

You may want to cross-post this in the supplement forum to gain more views.

[bosharpe]

Is anyone still using Mitoq - if so any benefits?

[gregmacpherson]

Hi All, 

 

Apologies for the long silence - we have been flat out.  We have an exciting new human clinical trial that will be published soon evaluating the effect of MitoQ on cardiovascular aging. The results are very positive.  

 

The study you refer to is very flawed/poor quality it just shows that high concentrations of hydrophobic TPP cations in vitro are accumulated and can cause swelling. The in vitro experiments were done with high vol of buffer - neglecting accumulation. We know that mitoq is protective against the kidney in several studies in vivo and also during organ storage. We also have a clinical trial that has been underway for the last few years evaluating MitoQ in CKD.

 

BTW - If you incubated the cells with 500 mM sucrose they'd die as well but that doesn't mean anything.

 

This sort of issue would have come to the fore early in our research and clinical trials if it was a real problem. 

 

 

 

 

I wonder if Greg or anyone can comment on this study. The link below is to the full text.

 

Physiol Rep. 2018 Apr;6(7):e13667. doi: 10.14814/phy2.13667.

The targeted anti-oxidant MitoQ causes mitochondrial swelling and depolarization in kidney tissue.

Gottwald EM1, Duss M2, Bugarski M1, Haenni D1,3, Schuh CD1, Landau EM2, Hall AM1,4.

Kidney proximal tubules (PTs) contain a high density of mitochondria, which are required to generate ATP to power solute transport. Mitochondrial dysfunction is implicated in the pathogenesis of numerous kidney diseases. Damaged mitochondria are thought to produce excess reactive oxygen species (ROS), which can lead to oxidative stress and activation of cell death pathways. MitoQ is a mitochondrial targeted anti-oxidant that has shown promise in preclinical models of renal diseases. However, recent studies in nonkidney cells have suggested that MitoQ might also have adverse effects. Here, using a live imaging approach, and both in vitro and ex vivo models, we show that MitoQ induces rapid swelling and depolarization of mitochondria in PT cells, but these effects were not observed with SS-31, another targeted anti-oxidant. MitoQ consists of a lipophilic cation (Tetraphenylphosphonium [TPP]) joined to an anti-oxidant component (quinone) by a 10-carbon alkyl chain, which is thought to insert into the inner mitochondrial membrane (IMM). We found that mitochondrial swelling and depolarization was also induced by dodecyltriphenylphosphomium (DTPP), which consists of TPP and the alkyl chain, but not by TPP alone. Surprisingly, MitoQ-induced mitochondrial swelling occurred in the absence of a decrease in oxygen consumption rate. We also found that DTPP directly increased the permeability of artificial liposomes with a cardiolipin content similar to that of the IMM. In summary, MitoQ causes mitochondrial swelling and depolarization in PT cells by a mechanism unrelated to anti-oxidant activity, most likely because of increased IMM permeability due to insertion of the alkyl chain.

PMID: 29611340

 

 

 

 

[gregmacpherson]

This is a snippet of some recent research - see attached image. 

 

The image on the far left is a cross section of an young mouse aorta,  the next image is a cross section of an old mouse aorta.  The image on the far right is a cross section of an old mouse aorta after 4 weeks of MitoQ. 

 

Taken from this paper;  https://www.ncbi.nlm...pubmed/29074712

 

This paper is from the same lab that completed our recent clinical study.  We hope to be able to share the paper with you soon. 

 

Thanks all.

 

Greg

Attached Files

•  image001.png   282.76KB   2 downloads

[ta5]

The study you refer to is very flawed/poor quality it just shows that high concentrations of hydrophobic TPP cations in vitro are accumulated and can cause swelling. 

 

Are you saying that you agree that MitoQ caused the swelling, but that it's not a problem?

[zorba990]

I've tried idebenone several times from different vendors. It always gave me horrible burning diahhrea. No problem with ubiquinol or pqq. So just wondering if mitoQ is going to cause the same problem.

[gregmacpherson]

Are you saying that you agree that MitoQ caused the swelling, but that it's not a problem?

 

What I am saying is that anything in high doses, including sucrose, would cause swelling and that ultimately it is not an issue because the dose of MitoQ being used in this study is way beyond what you would normally see in standard doses. 

[gregmacpherson]

I've tried idebenone several times from different vendors. It always gave me horrible burning diahhrea. No problem with ubiquinol or pqq. So just wondering if mitoQ is going to cause the same problem.

 

 

Hi Zorba990, 

 

It is unlikely but also hard for me to confirm that you wouldnt. The best way would be to just try it.  If you do get that reaction contact customer services and they will refund.  Just tell them to check with Greg and I will make sure we take care of it for you. 

[ta5]

What I am saying is that anything in high doses, including sucrose, would cause swelling and that ultimately it is not an issue because the dose of MitoQ being used in this study is way beyond what you would normally see in standard doses. 

 

I appreciate your replies to my questions, Greg.

 

Do you know what the kidney blood levels would be from normal doses of MitoQ? The authors admit they didn't know, but they seemed to think 500 nmol/L was a low dose:

 

"We are not aware of any previous kidney studies that have reported blood concentrations of MitoQ to directly relate our data to, but we found clear evidence of deleterious effects in vitro at a concentration of only 500 nmol/L. Moreover, evidence suggests that MitoQ does not undergo significant modification or metabolism in vivo (Smith and Murphy 2010)."

 

And, they compared it to a much higher dose of SS-31:

 

"In contrast, SS-31 at a 1000 fold higher dose (500 umol/L) had no discernible impact on mitochondrial structure/function (Fig. 1B), showing that the response to MitoQ is unique to this compound, rather than a common feature of all mitochondrial targeted anti-oxidants."

[gregmacpherson]

Its great to be back talking with the LongeCity community Ta5 - happy to answer your questions. 

 

I have checked with our lead scientist, just to confirm my thinking, and whilst I don't want to be critical of this paper the dose of MitoQ is excessive and too much of anything will have a deleterious impact on cells and mitochondria. 

 

When all said and done, I am not concerned with this paper as we have established safety with MitoQ over the past 15 years.  

 

There are ongoing clinical trials with MitoQ specifically for Kidney health (https://clinicaltria...rm=mitoq&rank=6 ) and the feedback I get from researchers to date indicate they have no concern with MitoQ. I look forward to seeing the unblinded data!

 

We are just about to have the results published from a clinical trial looking at vascular aging that I will be able to share with you sometime in the next few weeks. I can share that the trial showed that in a group of adults aged 60-79 we were able to improve their arterial function as measured by Flow Mediated Dilation by 42% after 6 weeks.  We were also able to normalise artery flexibility and reduce oxidative stress markers in the blood stream.  Trial participants took 20mg a day and some took up to 160mg as a one off dose (with some mild gastric side effects I might add) and that should give you some confidence that at the recommended dose of MitoQ of 10mg there is no risk of mitochondrial swelling issues.

 

I hope that helps allay any concerns you have. 

 

Kind regards

 

Greg

 

 

[TRUGAN]

Its great to be back talking with the LongeCity community Ta5 - happy to answer your questions. 

 

I have checked with our lead scientist, just to confirm my thinking, and whilst I don't want to be critical of this paper the dose of MitoQ is excessive and too much of anything will have a deleterious impact on cells and mitochondria. 

 

When all said and done, I am not concerned with this paper as we have established safety with MitoQ over the past 15 years.  

 

There are ongoing clinical trials with MitoQ specifically for Kidney health (https://clinicaltria...rm=mitoq&rank=6 ) and the feedback I get from researchers to date indicate they have no concern with MitoQ. I look forward to seeing the unblinded data!

 

We are just about to have the results published from a clinical trial looking at vascular aging that I will be able to share with you sometime in the next few weeks. I can share that the trial showed that in a group of adults aged 60-79 we were able to improve their arterial function as measured by Flow Mediated Dilation by 42% after 6 weeks.  We were also able to normalise artery flexibility and reduce oxidative stress markers in the blood stream.  Trial participants took 20mg a day and some took up to 160mg as a one off dose (with some mild gastric side effects I might add) and that should give you some confidence that at the recommended dose of MitoQ of 10mg there is no risk of mitochondrial swelling issues.

 

I hope that helps allay any concerns you have. 

 

Kind regards

 

Greg

 

Why didnt they test 10mg as well?  It would have been nice to know if years of taking 10mg had a positive effect. Any plans to sell a higher 20mg dose?

[gregmacpherson]

In a short clinical study we looked to get the best result in the shortest timeframe - hence the 20mg.   You will see the same benefit over time with the 10mg - it just wont happen quite as quickly.

 

Yes, 20mg dose coming later this year.

[TRUGAN]

In a short clinical study we looked to get the best result in the shortest timeframe - hence the 20mg.   You will see the same benefit over time with the 10mg - it just wont happen quite as quickly.

 

Yes, 20mg dose coming later this year.

 

 

thanks! I may have to try 20mg for a while when its ready.....if I can afford it. I've been on the 10 mg for a few years.

[gregmacpherson]

You are welcome!! I am coming up 6 years on MitoQ.  I just wish I had started it before I lost a good portion of my hair

[TRUGAN]

hmmm...I dont think its slowed my hair loss. Maybe I do need a higher dose!

[aribadabar]

hmmm...I dont think its slowed my hair loss. Maybe I do need a higher dose!

 Or, more than likely, it has no effect on the rate of hair loss.

[gregmacpherson]

Greetings from New Zealand. 

 

We are very excited to be able to share the first of a number of clinical trials that are currently underway evaluating MitoQ in a range of health settings. 

 

This study comes from the Vascular Aging Lab at Colorado University and was published in Hypertension; A journal of the American Heart Association.  

 

Abstract—Excess reactive oxygen species production by mitochondria is a key mechanism of age-related vascular dysfunction. Our laboratory has shown that supplementation with the mitochondrial-targeted antioxidant MitoQ improves vascular endothelial function by reducing mitochondrial reactive oxygen species and ameliorates arterial stiffening in old mice, but the effects in humans are unknown. Here, we sought to translate our preclinical findings to humans and determine the safety and eficacy of MitoQ. Twenty healthy older adults (60–79 years) with impaired endothelial function (brachial artery ow–mediated dilation <6%) underwent 6 weeks of oral supplementation with MitoQ (20 mg/d) or placebo in a randomized, placebo-controlled, double-blind, crossover design study. MitoQ was well tolerated, and plasma MitoQ was higher after the treatment versus placebo period (P<0.05). Brachial artery flow–mediated dilation was 42% higher after MitoQ versus placebo (P<0.05); the improvement was associated with amelioration of mitochondrial reactive oxygen species–related suppression of endothelial function (assessed as the increase in flow-mediated dilation with acute, supratherapeutic MitoQ [160 mg] administration; n=9; P<0.05). Aortic stiffness (carotid–femoral pulse wave velocity) was lower after MitoQ versus placebo (P<0.05) in participants with elevated baseline levels (carotid–femoral pulse wave velocity >7.60 m/s; n=11). Plasma oxidized LDL (low-density lipoprotein), a marker of oxidative stress, also was lower after MitoQ versus placebo (P<0.05). Participant characteristics, endothelium-independent dilation (sublingual nitroglycerin), and circulating markers of inflammation were not different (all P>0.1). These findings in humans extend earlier preclinical observations and suggest that MitoQ and other therapeutic strategies targeting mitochondrial reactive oxygen species may hold promise for treating age-related vascular dysfunction.

 

What Is New?

• This is the first trial in humans to show that 6 weeks of daily oral supplementation with the mitochondrial-targeted antioxidant MitoQ improves vascular endothelial function.

• We provide the first in vivo evidence in humans that MitoQ improves endothelial function by suppressing mitochondrial-derived oxidative stress.

• We provide the initial evidence in humans that MitoQ supplementation reduces aortic stiffness in adults with elevated baseline levels.

What Is Relevant?

• Older individuals have a greater risk for cardiovascular diseases largely because of vascular dysfunction, including reduced endothelial function and aortic stiffening. Thus, it is important to establish evidence-based therapeutic options to improve vascular function in this group.

• This study demonstrates that mitochondrial-targeted antioxidant MitoQ improves endothelial function and aortic stiffness in healthy late middle- aged and older adults with impaired baseline vascular function, thus establishing initial evidence for eficacy.

Summary

 

MitoQ supplementation improved vascular endothelial function in healthy late middle-aged and older adults by reducing the tonic suppressive effects of excessive mitochondrial-specific reactive oxygen species. MitoQ also reduced aortic stiffness in individuals with age-related arterial stiffening.

 

[mitomutant]

 

Greetings from New Zealand. 

 

We are very excited to be able to share the first of a number of clinical trials that are currently underway evaluating MitoQ in a range of health settings. 

 

This study comes from the Vascular Aging Lab at Colorado University and was published in Hypertension; A journal of the American Heart Association.  

 

Abstract—Excess reactive oxygen species production by mitochondria is a key mechanism of age-related vascular dysfunction. Our laboratory has shown that supplementation with the mitochondrial-targeted antioxidant MitoQ improves vascular endothelial function by reducing mitochondrial reactive oxygen species and ameliorates arterial stiffening in old mice, but the effects in humans are unknown. Here, we sought to translate our preclinical findings to humans and determine the safety and eficacy of MitoQ. Twenty healthy older adults (60–79 years) with impaired endothelial function (brachial artery ow–mediated dilation <6%) underwent 6 weeks of oral supplementation with MitoQ (20 mg/d) or placebo in a randomized, placebo-controlled, double-blind, crossover design study. MitoQ was well tolerated, and plasma MitoQ was higher after the treatment versus placebo period (P<0.05). Brachial artery flow–mediated dilation was 42% higher after MitoQ versus placebo (P<0.05); the improvement was associated with amelioration of mitochondrial reactive oxygen species–related suppression of endothelial function (assessed as the increase in flow-mediated dilation with acute, supratherapeutic MitoQ [160 mg] administration; n=9; P<0.05). Aortic stiffness (carotid–femoral pulse wave velocity) was lower after MitoQ versus placebo (P<0.05) in participants with elevated baseline levels (carotid–femoral pulse wave velocity >7.60 m/s; n=11). Plasma oxidized LDL (low-density lipoprotein), a marker of oxidative stress, also was lower after MitoQ versus placebo (P<0.05). Participant characteristics, endothelium-independent dilation (sublingual nitroglycerin), and circulating markers of inflammation were not different (all P>0.1). These findings in humans extend earlier preclinical observations and suggest that MitoQ and other therapeutic strategies targeting mitochondrial reactive oxygen species may hold promise for treating age-related vascular dysfunction.

 

What Is New?

• This is the first trial in humans to show that 6 weeks of daily oral supplementation with the mitochondrial-targeted antioxidant MitoQ improves vascular endothelial function.

• We provide the first in vivo evidence in humans that MitoQ improves endothelial function by suppressing mitochondrial-derived oxidative stress.

• We provide the initial evidence in humans that MitoQ supplementation reduces aortic stiffness in adults with elevated baseline levels.

What Is Relevant?

• Older individuals have a greater risk for cardiovascular diseases largely because of vascular dysfunction, including reduced endothelial function and aortic stiffening. Thus, it is important to establish evidence-based therapeutic options to improve vascular function in this group.

• This study demonstrates that mitochondrial-targeted antioxidant MitoQ improves endothelial function and aortic stiffness in healthy late middle- aged and older adults with impaired baseline vascular function, thus establishing initial evidence for eficacy.

Summary

 

MitoQ supplementation improved vascular endothelial function in healthy late middle-aged and older adults by reducing the tonic suppressive effects of excessive mitochondrial-specific reactive oxygen species. MitoQ also reduced aortic stiffness in individuals with age-related arterial stiffening.

 

 

Good to know that mitoQ improves endothelial function, but so does old-plain CoQ10[1] at a fraction of the cost. Why placebo ? Compare it with CoQ10 to really see whether targeting the mitochondria has some clinical advantage or not.

 

[1] https://www.ncbi.nlm...pubmed/22088605

[Harkijn]

https://www.scienced...80419141523.htm

[ceridwen]

MitoQ has brought a slight amount of memory back and has helped me to dream at night again

[gregmacpherson]

Good to know that mitoQ improves endothelial function, but so does old-plain CoQ10[1] at a fraction of the cost. Why placebo ? Compare it with CoQ10 to really see whether targeting the mitochondria has some clinical advantage or not.

 

[1] https://www.ncbi.nlm...pubmed/22088605

 

Hi Mitomutant, 

 

I will have to do a little digging to see the actual quant of benefit from CoQ10 from that paper.  Will do so. 

 

We have a MitoQ vs CoQ10 study that will be underway in May.  I hope to have data for you early next year. 

[gregmacpherson]

Mitomutant, 

 

We found the paper you refer to. 

 

The meta-analysis covered 5 papers with doses of CoQ10 ranged between 150mg and 300mg per day and were studied over 4 to 12 weeks.  The results showed an change in FMD by between 1.16 and 4.35%.  So, whilst you are correct that CoQ10 improves endothelial function it is between 5-10% of that seen with MitoQ over 6 weeks.  

 

I am happy to send you the paper by direct message but cant upload it for all.  Someone else may be able to though. 

 

Thanks.