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.pdfhttp://www.shiel.com/oxldl.htmFree 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
