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Interpreting Coenzyme Q10 Blood levels


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#1 nameless

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Posted 20 March 2009 - 07:40 PM


I just got back some blood tests I had done on CoQ10 levels, and am hoping one of the more scientific-minded individuals out there would help me interpret them.

What I have is:

CoQ10 Total 2402 ug/L (range 433-1532)
CoQ10 Reduced 2279.4 ug/L (range 415-1480)
CoQ10 % Reduced 95% (92-98)

I interpret this as (using the more traditional mg/ml ranges):

CoQ10 2.402 and Reduced 2.279 mg/ml

Previous to getting these results, I was taking Healthy origins CoQ10, 100mg, twice daily.

About a year ago I had a similar test done, using dry capsules taken at the same time as fish oil -
I used a different lab (Labcorp) for this one, and received results of CoQ10, Total 3.62 (range .37-2.20). Previous to this test I used dry capsules, Jarrow 100mg/twice daily. Although I may have skewed this, as I looked up my old Iherb orders and noticed I had taken JarrowQH Ultra about a month previously before changing to the dry capsules. I'm not sure if serum levels would have normalized within several weeks, or if the higher CoQ10 levels could be due to the Jarrow Ultra.

So... it appears my reduced CoQ10 is just fine, at 95%, so ubiquinol supplementation would probably be unnecessary. I'd like my total CoQ10 in the 3.5-4.0 range, at least, so it looks like I'll need to take a bit more CoQ10.

What would be the most cost effective way to get my CoQ10 a bit higher? 300mg-400mg CoQ10 appears necessary for this, unless that dry capsule test from a year ago actually was accurate and the Ultra didn't skew it high.

I'm not sure if a regular gel form has any advantages over a dry capsule taken with fats, but a specialized formula (like Jarrow QH, limonene, or Tishchon) probably would. I'll have to figure out if it'd be more cost effective to simply take more dry CoQ10 or a more soluble form.

And does dosing schedule matter for CoQ10? Would 300mg all at once absorb less than 100mg split into three doses? I expect the smaller doses split up would be better, but I don't recall seeing any direct studies comparing dosing like that.

#2 VespeneGas

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Posted 21 March 2009 - 12:04 AM

it's fat soluble and has a 30-50 hour half-life, so taking it all at once is fine.

Why do you want your CoQ10 levels so high above the reference range? Just curious :)

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#3 nameless

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Posted 21 March 2009 - 12:27 AM

I have a somewhat weird heart, as I was diagnosed with idiopathic cardiomyopathy about 4 years ago. And that's just a fancy way for doctors to say my heart muscle isn't beating as strong as it should be, but they really have no idea why. They suspect it could be viral or genetic in cause, but there is no easy way to prove it (without a biopsy -- taking a piece of my heart out). And I'm not too fond of that idea.

Although with all the Lyme posts lately (and noticing a lot of similar symptoms), I'm going to investigate that a bit further.

My cardiologist recommended I take CoQ10, although she doesn't know what the optimal blood levels should be. I am guessing 3.5-4.0 would be a pretty safe and hopefully somewhat helpful blood level to shoot for.

And thanks for info. I forgot CoQ10 does have a long half-life. It could save me a little money taking a larger dose 1-2x daily vs a smaller dose 3x daily.

#4 VespeneGas

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Posted 21 March 2009 - 02:51 AM

Interesting. I've read that forskolin increases the contractile strength of the heart, you might want to look into that. Good luck!

#5 krillin

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Posted 21 March 2009 - 11:09 PM

CoQ10 does have a long half-life, but absorption seems to diminish with dosage so divided doses would be more effective.

Forskolin is an inotrope, which are bad for damaged hearts over the long run.

Biofactors. 2005;25(1-4):219-24.
Effect on absorption and oxidative stress of different oral Coenzyme Q10 dosages and intake strategy in healthy men.
Singh RB, Niaz MA, Kumar A, Sindberg CD, Moesgaard S, Littarru GP.

Halberg Hospital and Research Institute, Moradabad, India. icn2005@mickyonline.com

INTRODUCTION: The effect of various dosages and dose strategies of oral coenzyme Q(10) (Q(100) administration on serum Q(10) concentration and bioequivalence of various formulations are not fully known. SUBJECTS AND METHODS: In a randomized, double blind, placebo controlled trial 60 healthy men, aged 18-55 years, were supplemented with various dosages and dose strategies of coenzyme Q(10) soft oil capsules (Myoqinon 100 mg, Pharma Nord, Denmark) or crystalline 100 mg Q(10) powder capsules or placebo. After 20 days blood levels were compared and oxidative load parameters, malondialdehyde (MDA) and thiobarbituric acid reactive substances (TBARS) were monitored to evaluate bioequivalence. All the subjects were advised to take the capsules with meals. Blood samples were collected after 12 hours of overnight fasting at baseline and after 20 days of Q(10) administration. Compliance was evaluated by counting the number of capsules returned by the subjects after the trial. RESULTS: Compliance by capsule counting was >90%. Side effects were negligible. Serum concentrations of Q(10) (average for groups) increased significantly 3-10 fold in the intervention groups compared with the placebo group. Serum response was improved with a divided dose strategy. TBARS and MDA were in the normal ranges at baseline. After 20 days intervention in the 200 mg group TBARS and MDA decreased, but the decrease was only significant for MDA (Fig. 2). Conclusions: All supplementations increased serum levels of Q(10). Q(10) dissolved in an oil matrix was more effective than the same amount of crystalline Q(10) in raising Q(10) serum levels. 200 mg of oil/soft gel formulation of Q(10) caused a larger increase in Q(10) serum levels than did 100 mg. Divided dosages (2 x 100 mg) of Q(10) caused a larger increase in serum levels of Q(10) than a single dose of 200 mg. Supplementation was associated with decreased oxidative stress as measured by MDA-levels. Indians appear to have low baseline serum coenzyme Q(10) levels which may be due to vegetarian diets. Further studies in larger number of subjects would be necessary to confirm our findings.

PMID: 16873950

Crit Care Med. 2008 Jan;36(1 Suppl):S106-11.
Inotropes in the management of acute heart failure.
Petersen JW, Felker GM.
Division of Cardiovascular Medicine, Duke University Medical Center, Durham, NC, USA.

Impaired cardiac contractility is a fundamental component of the heart failure syndrome, initiating the cycle of vasoconstriction, neurohormonal and inflammatory activation, and adverse ventricular remodeling that leads to heart failure progression. Based on this core paradigm, drugs that increase cardiac contractility (positive inotropes) are theoretically appealing as a heart failure therapy, and such agents have been extensively investigated in both acute and chronic heart failure. Although these agents clearly improve cardiac output, their use in heart failure has consistently been associated with increased myocardial oxygen demand, cardiac arrhythmias, and mortality in a variety of clinical settings. Based on these data, the routine use of inotropes as heart failure therapy is not indicated in either the acute or chronic setting. Inotropes may be a necessary evil in a subset of acute heart failure patients, such as those with acute heart failure decompensation in the setting of clinically evident hypoperfusion or shock, or as a bridge to more definitive treatment, such as revascularization or cardiac transplantation. Currently available inotropes, such as dobutamine and milrinone, act (directly or indirectly) by increasing cyclic adenylate monophosphate and therefore intracellular calcium flux. Whether newer inotropes with differing mechanisms of action will realize the potential clinical benefits of inotropic therapy without the risk remains a subject of ongoing investigation.

PMID: 18158469

#6 nameless

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Posted 22 March 2009 - 12:37 AM

Thanks for the reply. I recall the inotropic info you posted for pcynogenol in another post, so figured forskolin wouldn't be the best idea. The 'heart' supplements I currently take are CoQ10, D/K2, grapeseed, fish oil and mag orotate. I'm too much of a scaredy cat to try other things. As for CoQ10, I was thinking of trying 200mg, dry caps taken with fish oil, split into two doses, and see how that works. Although based on the study above, I may be better off going with 100mg doses. 100mg 3x daily may result in higher levels than 200mg 2x daily, or be equivalent. I guess I'll look into which is the cheaper option.

I did try ubiquinol a while back, but didn't notice any benefits over regular CoQ10. I'm not entirely sold on ubiquinol being better than CoQ10 for most people anyway.

I'm not sure if my heart would exactly be considered damaged in the traditional sense... it's just not working at full power, I guess. It was caught pretty early, so there is no structural damage. Even though diagnosed as 'idiopathic dilated cardiomyopathy', my heart was never really dilated either. No scar tissue, arteries all clean, microvessels all normal. I had a bunch of tests, and they couldn't find anything besides the fact my ejection fraction was lower than it should be.

And although I tried pycnogenol a while ago, I switched to grapeseed due to cost. I contacted one of the pycnogenol scientist/doctors from Horphag a while back regarding the inotropic issue. I'll paste his response below, in case anyone else has heart issues and are interested.

------

The in vitro test with embryonic chicken cardiomyocytes suggests that
Pycnogenol might act as a beta agonist, that means it has the opposite
activity as a beta-blocker. In any case such studies with cells grown in a
petri dish are more of academic interest and it would be far-fetched to
conclude any effects for humans.

There are several clinical trials ongoing which investigate Pycnogenol in
heart failure patients. One of them has recently revealed very positive
preliminary findings suggesting significant better heart ejection volume.
These patients were able to consequently walk longer distances (tested on a
treadmill) because their hearts were able to pump blood more efficiently.

Best regards,


Frank Schonlau, PhD

#7 tlm884

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Posted 22 March 2009 - 03:08 AM

I just got back some blood tests I had done on CoQ10 levels, and am hoping one of the more scientific-minded individuals out there would help me interpret them.

What I have is:

CoQ10 Total 2402 ug/L (range 433-1532)
CoQ10 Reduced 2279.4 ug/L (range 415-1480)
CoQ10 % Reduced 95% (92-98)

I interpret this as (using the more traditional mg/ml ranges):

CoQ10 2.402 and Reduced 2.279 mg/ml

Previous to getting these results, I was taking Healthy origins CoQ10, 100mg, twice daily.

About a year ago I had a similar test done, using dry capsules taken at the same time as fish oil -
I used a different lab (Labcorp) for this one, and received results of CoQ10, Total 3.62 (range .37-2.20). Previous to this test I used dry capsules, Jarrow 100mg/twice daily. Although I may have skewed this, as I looked up my old Iherb orders and noticed I had taken JarrowQH Ultra about a month previously before changing to the dry capsules. I'm not sure if serum levels would have normalized within several weeks, or if the higher CoQ10 levels could be due to the Jarrow Ultra.

So... it appears my reduced CoQ10 is just fine, at 95%, so ubiquinol supplementation would probably be unnecessary. I'd like my total CoQ10 in the 3.5-4.0 range, at least, so it looks like I'll need to take a bit more CoQ10.

What would be the most cost effective way to get my CoQ10 a bit higher? 300mg-400mg CoQ10 appears necessary for this, unless that dry capsule test from a year ago actually was accurate and the Ultra didn't skew it high.

I'm not sure if a regular gel form has any advantages over a dry capsule taken with fats, but a specialized formula (like Jarrow QH, limonene, or Tishchon) probably would. I'll have to figure out if it'd be more cost effective to simply take more dry CoQ10 or a more soluble form.

And does dosing schedule matter for CoQ10? Would 300mg all at once absorb less than 100mg split into three doses? I expect the smaller doses split up would be better, but I don't recall seeing any direct studies comparing dosing like that.


Hawthorn Berry is effective in increasing the contractions of the heart.

#8 nameless

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Posted 22 March 2009 - 08:59 PM

I recall reading mixed results on Hawthorn berry in some studies. I'm also concerned about possible drug interactions.

The only other supplement I've been considering is D-Ribose. But I'll need to research it a little more, regarding safety, drug interactions, etc.

#9 shaggy

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Posted 22 March 2009 - 10:06 PM

@ OP....Wouldn't creatine monohydrate or similar be helpful to someone with your symptoms?

#10 nameless

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Posted 23 March 2009 - 12:15 AM

I read somewhere that creatine may not be so healthy for mitochondria, which could be problematic for me. I think the studies using creatine for cardiomyopathy weren't that promising either, but I could be wrong there.

Carnitine might be worth looking into. I probably should ask to get my levels checked.

Edited by nameless, 23 March 2009 - 12:17 AM.


#11 ortcloud

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Posted 27 March 2009 - 01:36 AM

I have a somewhat weird heart, as I was diagnosed with idiopathic cardiomyopathy about 4 years ago. And that's just a fancy way for doctors to say my heart muscle isn't beating as strong as it should be, but they really have no idea why.


Have you checked for mercury ?

mercury concentration was 22,000 times higher (178,400 ng/g vs. 8 ng/g) in the idiopathic cardiomyopathy group compared with secondary cardiac dysfunction.

http://www.ncbi.nlm....pubmed/10334427
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#12 FunkOdyssey

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Posted 27 March 2009 - 01:58 AM

I read somewhere that creatine may not be so healthy for mitochondria, which could be problematic for me. I think the studies using creatine for cardiomyopathy weren't that promising either, but I could be wrong there.


Can you provide a supporting reference for the creatine/mitochondria claim?

#13 nameless

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Posted 27 March 2009 - 02:01 AM

I have a somewhat weird heart, as I was diagnosed with idiopathic cardiomyopathy about 4 years ago. And that's just a fancy way for doctors to say my heart muscle isn't beating as strong as it should be, but they really have no idea why.


Have you checked for mercury ?

mercury concentration was 22,000 times higher (178,400 ng/g vs. 8 ng/g) in the idiopathic cardiomyopathy group compared with secondary cardiac dysfunction.

http://www.ncbi.nlm....pubmed/10334427


Yeah, first thing I did after diagnosis was a mercury hair test. Later on my cardiologist checked mercury levels via blood (arsenic too). All came back very low. I'm going with some sort of Lyme or tick theory right now, due to recent blood test positive for ehrlichiosis.

#14 nameless

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Posted 27 March 2009 - 02:15 AM

I read somewhere that creatine may not be so healthy for mitochondria, which could be problematic for me. I think the studies using creatine for cardiomyopathy weren't that promising either, but I could be wrong there.


Can you provide a supporting reference for the creatine/mitochondria claim?

I think it was this article that mentioned creatine/mitochondria, although it is mostly about aspartame and mitochondria. I don't know how accurate it is, (I would guess it probably isn't) and it isn't like pubmed study or anything, but I tend to be conservative with these sorts of things --

http://www.wnho.net/...omaspartame.htm

I thought I read it somewhere else too, in a more scientific-oriented article, but can't recall right now where. If I find it again, I'll post it here.
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#15 krillin

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Posted 11 April 2009 - 07:41 AM

So... it appears my reduced CoQ10 is just fine, at 95%, so ubiquinol supplementation would probably be unnecessary. I'd like my total CoQ10 in the 3.5-4.0 range, at least, so it looks like I'll need to take a bit more CoQ10.

Here's an article on CoQ10 by an ND. This guy's website floors me. I haven't read through it all yet, but most of what I've read is Imminst-caliber stuff. He warns that the Quest blood test maxes out at 4.0.

As for an ideal level, if you can't titrate via symptoms, I think we should target LDL oxidation. If we prevent that, then Aubrey's proposed mitochondrial free radical aging mechanism should be neutralized. (For those who aren't familiar with it, the mitochondrial free radicals delete the DNA needed for the electron transport chain, so the cell produces its energy by doing LOTS of glycolysis. The pyruvate gets turned into CO2 and NADH in the Kreb's cycle, and the NADH gets oxidized back to NAD+ at the plasma membrane. The electrons get taken up by oxygen in the blood to form superoxide, which oxidizes LDL, which spreads damage throughout the body. Aubrey says we can't stop LDL oxidation because vitamin E can't do it. But CoQ10 is what protects LDL, not E. All E does is lower (Q + QH2), lower QH2/Q, and increase oxidation. Make sure to differentiate between high- and low-radical flux experiments. The low-flux experiments mimic physiological conditions, while the high-flux experiments are what conned us into thinking megadose alpha tocopherol would be good for us.)

I think it's impossible to affordably saturate LDL with CoQ10 (300 mg/day puts only 2.8 molecules in each LDL particle.), so I think the best plan is to take enough to minimize oxidized LDL cholesterol. I've not had the test, so I have no clue how low we want to take it.

Saturation might be a bad idea, anyway. PMID: 15059645 gave mice a human equivalent of ~600 mg/day.

One notable finding was that 16 mice in the Q10-supplemented group showed deposition of a crystalline-appearing, insoluble material in areas of the heart, liver, and kidney.


http://www.haidumed....ripleMarker.pdf
http://www.shiel.com/oxldl.htm

Free Radic Res. 2000 Sep;33(3):329-40.
Antioxidative efficacy of parallel and combined supplementation with coenzyme Q10 and d-alpha-tocopherol in mildly hypercholesterolemic subjects: a randomized placebo-controlled clinical study.
Kaikkonen J, Nyyssönen K, Tomasi A, Iannone A, Tuomainen TP, Porkkala-Sarataho E, Salonen JT.
Research Institute of Public Health, University of Kuopio, Finland.

It has been claimed that coenzyme Q10 (Q10) would be an effective plasma antioxidant since it can regenerate plasma vitamin E. To test separate effects and interaction between Q10 and vitamin E in the change of plasma concentrations and in the antioxidative efficiency, we carried out a double-masked, double-blind clinical trial in 40 subjects with mild hypercholesterolemia undergoing statin treatment. Subjects were randomly allocated to parallel groups to receive either Q10 (200 mg daily), d-alpha-tocopherol (700 mg daily), both antioxidants or placebo for 3 months. In addition we investigated the pharmacokinetics of Q10 in a separate one-week substudy. In the group that received both antioxidants, the increase in plasma Q10 concentration was attenuated. Only vitamin E supplementation increased significantly the oxidation resistance of isolated LDL. Simultaneous Q10 supplementation did not increase this antioxidative effect of vitamin E. Q10 supplementation increased and vitamin E decreased significantly the proportion of ubiquinol of total Q10, an indication of plasma redox status in vivo. The supplementations used did not affect the redox status of plasma ascorbic acid. In conclusion, only vitamin E has antioxidative efficiency at high radical flux ex vivo. Attenuation of the proportion of plasma ubiquinol of total Q10 in the vitamin E group may represent in vivo evidence of the Q10-based regeneration of the tocopheryl radicals. In addition, Q10 might attenuate plasma lipid peroxidation in vivo, since there was an increased proportion of plasma ubiquinol of total Q10.

PMID: 10993487

Arterioscler Thromb Vasc Biol. 1996 May;16(5):687-96.
Cosupplementation with coenzyme Q prevents the prooxidant effect of alpha-tocopherol and increases the resistance of LDL to transition metal-dependent oxidation initiation.
Thomas SR, Neuzil J, Stocker R.
Biochemistry Group, Heart Research Institute, Camperdown, Sydney, NSW, Australia.

There is considerable interest in the ability of antioxidant supplementation, in particular with vitamin E, to attenuate LDL oxidation, a process implicated in atherogenesis. Since vitamin E can also promote LDL lipid peroxidation, we investigated the effects of supplementation with vitamin E alone or in combination with coenzyme Q on the early stages of the oxidation of isolated LDL. Isolated LDL was obtained from healthy subjects before and after in vitro enrichment with vitamin E (D-alpha-tocopherol, alpha-TOH) or dietary supplementation with D-alpha-TOH (1 g/d) and/or coenzyme Q (100 mg/d). LDL oxidation initiation was assessed by measurement of the consumption of alpha-TOH and cholesteryl esters containing polyunsaturated fatty acids and the accumulation of cholesteryl ester hydroperoxides during incubation of LDL in the transition metal-containing Ham's F-10 medium in the absence and presence of human monocyte-derived macrophages (MDMs). Native LDL contained 8.5 +/- 2 molecules of alpha-TOH and 0.5 to 0.8 molecules of ubiquinol-10 (CoQ10H2, the reduced form of coenzyme Q) per lipoprotein particle. Incubation of this LDL in Ham's F-10 medium resulted in a time-dependent loss of alpha-TOH with concomitant stoichiometric conversion of the major cholesteryl esters to their respective hydroperoxides. MDMs enhanced this process. LDL lipid peroxidation occurred via a radical chain reaction in the presence of alpha-TOH, and the rate of this oxidation decreased on alpha-TOH depletion. In vitro enrichment of LDL with alpha-TOH resulted in an LDL particle containing sixfold to sevenfold more alpha-TOH, and such enriched LDL was more readily oxidized in the absence and presence of MDMs compared with native LDL. In vivo alpha-TOH-deficient LDL, isolated from a patient with familial isolated vitamin E deficiency, was highly resistant to Ham's F-10-initiated oxidation, whereas dietary supplementation with vitamin E restored the oxidizability of the patient's LDL. Oral supplementation of healthy individuals for 5 days with either alpha-TOH or coenzyme Q increased the LDL levels of alpha-TOH and CoQ10H2 by two to three or three to four times, respectively. alpha-TOH-supplemented LDL was significantly more prone to oxidation, whereas CoQ10H2-enriched LDL was more resistant to oxidation initiation by Ham's F-10 medium than native LDL. Cosupplementation with both alpha-TOH and coenzyme Q resulted in LDL with increased levels of alpha-TOH and CoQ10H2, and such LDL was markedly more resistant to initiation of oxidation than native or alpha-TOH-enriched LDL. These results demonstrate that oral supplementation with alpha-TOH alone results in LDL that is more prone to oxidation initiation, whereas cosupplementation with coenzyme Q not only prevents this prooxidant activity of vitamin E but also provides the lipoprotein with increased resistance to oxidation.

PMID: 8963727

Biochim Biophys Acta. 1992 Jun 26;1126(3):247-54.
Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation.
Mohr D, Bowry VW, Stocker R.
Biochemistry Group, Heart Research Institute, Sydney, Australia.

Ubiquinol-10 (CoQH2, the reduced form of coenzyme Q10) is a potent antioxidant present in human low-density lipoprotein (LDL). Supplementation of humans with ubiquinone-10 (CoQ, the oxidized coenzyme) increased the concentrations of CoQH2 in plasma and in all of its lipoproteins. Intake of a single oral dose of 100 or 200 mg CoQ increased the total plasma coenzyme content by 80 or 150%, respectively, within 6 h. Long-term supplementation (three times 100 mg CoQ/day) resulted in 4-fold enrichment of CoQH2 in plasma and LDL with the latter containing 2.8 CoQH2 molecules per LDL particle (on day 11). Approx. 80% of the coenzyme was present as CoQH2 and the CoQH2/CoQ ratio was unaffected by supplementation, indicating that the redox state of coenzyme Q10 is tightly controlled in the blood. Oxidation of LDL containing various [CoQH2] by a mild, steady flux of aqueous peroxyl radicals resulted immediately in very slow formation of lipid hydroperoxides. However, in each case the rate of lipid oxidation increased markedly with the disappearance of 80-90% CoQH2. Moreover, the cumulative radical dose required to reach this 'break point' in lipid oxidation was proportional to the amount of CoQH2 incorporated in vivo into the LDL. Thus, oral supplementation with CoQ increases CoQH2 in the plasma and all lipoproteins thereby increasing the resistance of LDL to radical oxidation.

PMID: 1637852

#16 RoadToAwe

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Posted 11 April 2009 - 06:29 PM

So... it appears my reduced CoQ10 is just fine, at 95%, so ubiquinol supplementation would probably be unnecessary. I'd like my total CoQ10 in the 3.5-4.0 range, at least, so it looks like I'll need to take a bit more CoQ10.

Here's an article on CoQ10 by an ND. This guy's website floors me.

Thanks Krillin for the great link. Most sites on Naturopathy are a bit suspect but this one is good. Some great articles there.

#17 nameless

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Posted 11 April 2009 - 06:55 PM

That is an interesting site. Thanks for posting it and the studies too. Do any commercial labs currently test oxidized LDL, besides Shiel Labs? I'll have to see if my insurance will pay for that one.

As for dosing and type of CoQ10, I've tried Ubiquinol in the past, first at a pre-load of 400mg/daily for 4 weeks, then 300mg/daily for around 2-3 months. I didn't notice any difference in symptoms or how I felt, Actually, the only difference I noticed was increased muscle twitching. But I get that sometimes even when I don't take Ubiquinol.

To be scientific, I should have had CoQ10 levels tested before and after supplementing with ubiquinol, and had echos right before and after. But I wasn't due for my echo then, and my doctor doesn't usually give a script for one more than 1-2 times yearly anyway. I'm not sure if my heart issue is even related to CoQ10, so for all I know CoQ10 supplementation isn't doing much.

Some CoQ10 questions (for anyone who knows the answers):

Why would a crystalline-appearing substance appear in rat hearts taking high dose CoQ10?
Is it because they use CoQ9? Or if too much is consumed, there are health problems (like crystal hearts)?
Ubiquinol may result in higher CoQ10 serum levels, but is that actually a good thing?
Not a ton of studies to back up Ubiquinol yet...
And are the higher ubiquinol levels due to ubiquinol itself or the carrier in the gels? I recall reading one ubiquinone/ubiquinol article stating that once digested, ubiquinol becomes oxidized in the stomach anyway.

And that site has a ton of interesting articles not about CoQ10 too. I just noticed articles regarding Aromatase Inhibitors and Arthritis ... and Grape Seed Extract: aromatase Inhibition... hmm...
*wonders if his neck pain problems can be related to grape seed extract now*

#18 krillin

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Posted 12 April 2009 - 02:44 AM

My theory is that the crystals appear because the CoQ10 transport system gets overwhelmed and CoQ10 can diffuse wherever it wants. Since it's insoluble, most of the unchaperoned CoQ10 will precipitate as crystals.

As uptake does not appear to be passive, we speculate that in yeast there is a process for trafficking exogenous ubiquinones from the plasma membrane to mitochondria and that it is selective for ubiquinones with isoprenoid tails. Such a process is suggested by some earlier work on yeast where accumulation of exogenous CoQ6 in mitochondria was deficient in some strains (85). It is unclear whether a similar pathway would exist in mammalian cells; however, in a clinical case where CoQ10 supplementation ameliorated the symptoms of CoQ deficiency, subsequent switching to idebenone caused clinical and metabolic worsening, which disappeared on return to CoQ10 supplementation (86). As the final steps of CoQ synthesis are in mitochondria, it is not clear why a putative CoQ uptake system should exist. However, it is possible there is a pathway that allows the export mitochondrial CoQ to the plasma membrane, and in the presence of exogenous CoQ it can operate in reverse to insert CoQ into mitochondria. This may explain why dietary supplementation with CoQ10 leads to only small increases in mitochondrial CoQ10 concentration except when there is an underlying CoQ10 deficiency (20–24, 87). Our results suggest that short chain ubiquinone analogs containing isoprenoid side chains may accumulate more effectively within mitochondria than saturated exogenous ubiquinones and are worth exploring as potential therapies for human diseases with CoQ deficiencies.


The ubiquinol advantage can't be due to the vehicle. 300 mg/day ubiquinol yields 8.28, while 300 mg/day Q Absorb yields only 3.64. Both are liposome products.

Edited by krillin, 12 April 2009 - 02:54 AM.


#19 nameless

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Posted 12 April 2009 - 03:59 AM

My theory is that the crystals appear because the CoQ10 transport system gets overwhelmed and CoQ10 can diffuse wherever it wants. Since it's insoluble, most of the unchaperoned CoQ10 will precipitate as crystals.

The ubiquinol advantage can't be due to the vehicle. 300 mg/day ubiquinol yields 8.28, while 300 mg/day Q Absorb yields only 3.64. Both are liposome products.


At what dosage would you estimate the transport system becoming overwhelmed? Or, better yet, at what serum levels would it become overwhelmed?

And regarding ubiquinol, I remember reading this article:
http://ubiquinolubiq...e.blogspot.com/

Which basically stated that ubiquinol becomes oxidized anyway, so it may not be that different than simply taking ubiquinone. I don't know if this is true or not though.

Here is the recent Jarrow study on ubiquinol ---

http://www.npicenter...w...99&zoneid=8

Total increase at 300mg/daily was: 0.70 mcg/mL to 6.14

There was also a reduction in the mean oxidized Co-Q10 levels in the plasma from 12% to 7%. But was this reduction in oxidized levels due to ubiquinol supplementation, or due to higher total plasma CoQ10? By this I mean, if a person just gulped down a lot of ubiquinone and achieved levels of 6.14, could their bodies have simply converted more of it to the reduced form on its own?

And I think (if I remember their little bottle chart correctly), Q-absorb ubiquinone 300mg/day + exercise showed an increase to 4.0.

And their Ultra version with limonene was at least in the 5s, or maybe higher -- I think. I tried it once, but I cannot remember the exact values on the label. But it is in the same ballpark as their ubiquinol product, unless my memory is failing.

So... although ubiquinol does show higher serum levels, how do we know if it's not the carrier, or a better liposome process? The studies so far have been done on very small groups of people, usually by the companies selling ubiquinol. I don't mean to say ubiquinol is worse in any way (besides being more expensive), as I expect it probably is more absorbable regardless of carrier, but I'd like to see better (and larger) studies head-to-head.

Edited by nameless, 12 April 2009 - 04:01 AM.


#20 krillin

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Posted 12 April 2009 - 05:58 PM

At what dosage would you estimate the transport system becoming overwhelmed? Or, better yet, at what serum levels would it become overwhelmed?

Based on that mouse study, 600 could be enough to do it. But the safety review below paints a rosy picture.

There was also a reduction in the mean oxidized Co-Q10 levels in the plasma from 12% to 7%. But was this reduction in oxidized levels due to ubiquinol supplementation, or due to higher total plasma CoQ10? By this I mean, if a person just gulped down a lot of ubiquinone and achieved levels of 6.14, could their bodies have simply converted more of it to the reduced form on its own?

One of my references said "Q10 supplementation increased and vitamin E decreased significantly the proportion of ubiquinol of total Q10, an indication of plasma redox status in vivo." A crude way of thinking about it is that there is going to be a relatively constant number (not fraction) of oxidized Q molecules and plasma antioxidants will keep the rest reduced. By increasing total Q, you thus increase percentage reduced. The only reason I see to take ubiquinol is if it is a cheaper way to achieve a desired concentration. I only take 100, so I'm switching to a limonene product. At that intake, the blood level will be the same, for a lower price, and with the added benefits of limonene.


And I think (if I remember their little bottle chart correctly), Q-absorb ubiquinone 300mg/day + exercise showed an increase to 4.0.

PMID: 16882678 said 3.64, so I guess they rounded up.

And their Ultra version with limonene was at least in the 5s, or maybe higher -- I think. I tried it once, but I cannot remember the exact values on the label. But it is in the same ballpark as their ubiquinol product, unless my memory is failing.

Could you dig up the limonene data? All I have is 60 mg/day of CoQSol-CF providing 2.75 mcg/ml.


So... although ubiquinol does show higher serum levels, how do we know if it's not the carrier, or a better liposome process?

That's possible, but with Jarrow's QH Absorb being so much better than Jarrow's Q Absorb, I say it's the better water solubility of QH2. The transport paper I cited said that shorter chain Q's were better absorbed because of their better solubility. But that also makes them fumble more electrons from the ETC because they stick out of the membrane further and can bump into more oxygen molecules.


Biofactors. 2008;32(1-4):199-208.
Safety assessment of coenzyme Q10 (CoQ10).
Hidaka T, Fujii K, Funahashi I, Fukutomi N, Hosoe K.
Functional Food Ingredients Division, Healthcare Products Business Unit, Kaneka Corporation, Osaka, Japan.

Coenzyme Q10 (CoQ10) is a naturally occurring component present in living cells. Its physiological function is to act as an essential cofactor for ATP production, and to perform important antioxidant activities in the body. In most countries, CoQ10 has been widely used as a dietary supplement for more than 20 years. Recently, the use of CoQ10 as a dietary supplement has grown with a corresponding increase in daily dosage. The present review describes the safety profile of CoQ10 on the basis of animal and human data. The published reports concerning safety studies indicate that CoQ10 has low toxicity and does not induce serious adverse effects in humans. The acceptable daily intake (ADI) is 12mg/kg/day, calculated from the no-observed-adverse-effect level (NOAEL) of 1200 mg/kg/day derived from a 52-week chronic toxicity study in rats, i.e., 720 mg/day for a person weighing 60 kg. Risk assessment for CoQ10 based on various clinical trial data indicates that the observed safety level (OSL) for CoQ10 is 1200 mg/day/person. Evidence from pharmacokinetic studies suggest that exogenous CoQ10 does not influence the biosynthesis of endogenous CoQ9/CoQ10 nor does it accumulate into plasma or tissues after cessation of supplementation. Overall, these data from preclinical and clinical studies indicate that CoQ10 is highly safe for use as a dietary supplement. Additionally, analysis of CoQ10 bioavailability or its pharmacokinetics provides the pertinent safety evaluation for CoQ10.

PMID: 19096117

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#21 nameless

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Posted 13 April 2009 - 12:55 AM

Based on that mouse study, 600 could be enough to do it. But the safety review below paints a rosy picture.

The only reason I see to take ubiquinol is if it is a cheaper way to achieve a desired concentration. I only take 100, so I'm switching to a limonene product. At that intake, the blood level will be the same, for a lower price, and with the added benefits of limonene.

Could you dig up the limonene data? All I have is 60 mg/day of CoQSol-CF providing


Have there been long term (like 15-20 year) studies on people checking for crystallization in organs or odd side effects? Only concern I have is high dose (300mg + over a long period of time). Although in my own case, the rewards outweigh any potential risk anyway. But for those taking high dose ubiquinol or megadosing CoQ10, it may be an issue.

I'm afraid I didn't get the Jarrow limonene CoQ10 serum data from a published study. It was printed on the bottle of Jarrow Ultra, 100mg, from a study I presume they did but never made public. I tried the product last summer, and recall seeing the little chart printed on it, but don't remember the exact data. I can try emailing Jarrow for the info, but they don't always write me back.

And I agree that it probably isn't the carrier, since both Jarrow products should use similar carriers. But they do use different ingredients in their Jarrow Q-absorb vs QH, and they don't list the exact lecithin amounts in each.... so there could be some differences.

I sometimes wonder if most of the advances in CoQ10 bioavailablity even matter for most people -- Dry CoQ10 - gel - liposome - limonene - ubiquinol. And what I mean by that is, it may be more cost effective to take dry capsules with fats (like fish oil) vs the more expensive formulations. Once you get into limonene or ubiquinol products, you are talking about approx. 2-4x the price of dry capsules. Even if absorption is better, why not just take 2-4x as much as dry capsules? I realize if a person is shooting for big serum increases or have mitochondrial issues, that a more bioavailable form may be needed, but I don't think most people taking CoQ10 really need super high serum levels.




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