Study: Supplementation with the reduced form of Coenzyme Q10 decelerates phenotypic characteristics of senescence and induces a peroxisome proliferatoractivated receptor-alpha gene expression signature in SAMP1 mice.
Journal: Mol Nutr Food Res. 2010 Jun;54(6):805-15.
Authors: Schmelzer C, Kubo H, Mori M, Sawashita J, Kitano M, Hosoe K, Boomgaarden I, Doring F, Higuchi K.
Department: Institute of Human Nutrition and Food Science, Molecular Prevention, Christian-Albrechts-University of Kiel, Heinrich-Hecht-Platz 10, Kiel, Germany.
Summary/comments: In this study, the researchers conducted broad genome expression profiling in various tissues (liver, kidney, heart and brain) of SAMP1 mice supplemented with Ubiquinol or Ubiquinone. The scientists detected the presence of redox-sensitive genes, specifically Ubiquinol-dependent gene networks that are involved in inflammation and lipid metabolism. These Ubiquinol sensitive genes involved in cholesterol and lipid metabolism were not effected by Ubiquinone. The research also indicated that, in comparison to Ubiquinone, Ubiquinol supplementation was more effective at increasing total CoQ10 levels in the liver.
Study: Supplemental Ubiquinol in the Treatment of Heart Failure; Five Year Experience
Authors: Langsjoen PH and Langsjoen AM
Presented at the 6th Conference of the International Coenzyme Q10 Association, Brussels, Belgium.
Summary/comments: Based on the initial study published in 2008, Dr Langsjoen expanded the number of patients on Ubiquinol. For a variety of markers associated with cardiovascular function ranging from plasma CoQ10 levels to Ejection Fraction, the Ubiquinol form showed better benefit with less amounts required. For instance, ejection fractions were at 40.9% for Ubiquinone and 47.8% for Ubiquinol; NYHA Class on Ubiquinol was 1.6, while subjects on Ubiquinone were at 2.5.
Study: Supplemental Ubiquinol in patients with advanced congestive heart failure.
Journal: Biofactors. 2008;32(1-4):119-28.
Authors: Langsjoen PH, Langsjoen AM
Department: East Texas Medical Center and Trinity Mother Francis Hospital, TX, USA.
Summary/comments: An initial group of subjects with end stage congestive heart failure (NYHA Class IV) were being given an average of 450 mg per day of Ubiquinone. Despite the supplemental Ubiquinone, blood values were a mean of 1.6 mcg/mL plasma. Dr Langsjoen changed subjects to the Ubiquinol form (average of 580 mg/day) and found blood values rose from 1.6 microg/ml up to 6.5 microg/ml. The researchers noted remarkable clinical improvement with NYHA class improving from a mean of IV to a mean of II, and mean Ejection Fraction improved from 22% (10-35%) up to 39% (10-60%).
Brain & Neurological Health
Study: Levels of reduced and oxidized coenzymeQ-10 and 8-hydroxy-2′-deoxyguanosine in the cerebrospinal fluid of patients with living Parkinson's disease demonstrate that mitochondrial oxidative damage and/or oxidative DNA damage contributes to the neurod
Journal: Neuroscience Letters. 2010, 469: 159-163
Authors: Isobe T, Abe T, Terayama Y
Department: Department of Neurology, Iwate Medical University, 19-1 Uchimaru, Morioka, Iwate 020-0805, Japan.
Summary/comments: Researchers from Iwate Medical University in Japan examined Ubiquinone and Ubiquinol levels in the cerebrospinal fluid from a small number of untreated Parkinsonʼs Disease patients, in order to ascertain the oxidative balance. There was no correlation between the content of Ubiquinone (oxidized CoQ10) and age of the patients. However, the Parkinsonʼs Disease patients did have higher concentrations of Ubiquinone relative to the control group, and the %CoQ10 (which is the percentage of Ubiquinone to Total CoQ10) was also higher. This shift from the Ubiquinol to the Ubiquinone form may mark the extent of oxidative stress and, conversely, the level of antioxidant protection.
Study: Therapeutic effects of coenzyme Q10 (CoQ10) and reduced CoQ10 in the MPTP model of Parkinsonism.
Journal: J Neurochem. 2008 Mar;104(6):1613-21. Epub 2007 Oct 31.
Authors: Cleren C, Yang L, Lorenzo B, Calingasan NY, Schomer A, Sireci A, Wille EJ, Beal MF.
Department: Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York-Presbyterian Hospital, New York, New York 10021, USA.
Summary/comments: Beal offered his groupʼs most recent findings on mitochondrial dysfunction and neurodegenerative diseases, specifically involving animal models of Parkinsonʼs and Huntingtonʼs disease to compare Ubiquinol and conventional CoQ10. In one of the animal models, they utilized a neurotoxin called MPTP, which induces effects in the brain that are analogous to clinical and biochemical changes seen in patients with Parkinsonʼs disease. The rodents treated with CoQ10 (both Ubiquinone and Ubiquinol forms) had significantly less formation of alpha synuclein aggregates, which is a major pathological hallmark found in Parkinsonʼs disease patients. Additionally, the scientists noted that the Ubiquinol form resulted in higher plasma levels and exerted a greater neuroprotective effect against the damaging effect of MPTP.
Antioxidants & Aging
Study: Renal preservation effect of Ubiquinol, the reduced form of coenzyme Q10.
Journal: Clinical and Experimental Nephrology
Authors: Ishikawa A, Kawarazaki H, Ando K, Fujita M, Fujita T, Homma Y
Department: Department of Urology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Summary/comments: Researchers from the University of Tokyo have been examining the role of antioxidants in Chronic Kidney Disease. As a preliminary study, an animal model of chronic kidney disease was developed. Three experimental groups were created: a control group, a high salt diet group, and a high salt diet plus Ubiquinol group. In comparison to the control group, the high salt diet increased oxidative stress (measured by the generation of superoxide anion in kidney tissue), increased hypertension, and induced albuminuria. However, the high salt diet plus Ubiquinol group exhibited results indicating significant renoprotection by Ubiquinol, including decreased generation of superoxide anion (antioxidant effect), decreased urinary albumin, and amelioration of hypertension. This study marks the first experimental research with the antioxidant Ubiquinol in an animal model of chronic kidney disease.
Study: Plasma Ubiquinone to Ubiquinol ratio in patients with hepatitis, cirrhosis, and hepatoma, and in patients treated with percutaneous transluminal coronary reperfusion.
Journal: Biofactors. 1999;9(2-4):241-6.
Authors: Yamamoto Y, Yamashita S
Department: Research Center for Advanced Science and Technology, University of Tokyo, Japan.
Summary/comments: Scientists found a loss of Ubiquinol with subjects that have certain types of liver disease. Certain liver conditions are also known to have elevated oxidative stress, as witnessed by the increase in biomarkers such as TBARS (serum thiobarbituric acid reactive substances). Researchers at the University of Tokyo showed that patients with hepatitis, cirrhosis, and hepatoma all exhibited a decrease in the Ubiquinol ratio percent (chart below), while the total levels of amounts of CoQ10 (Ubiquinol + Ubiquinone) was not reduced. These studies demonstrate that as the level of oxidative stress increases, the ratio of the Ubiquinol:Ubiquinone declines. This is both an indication that these type of physical states particularly require Ubiquinol and provides support for the use of the ratio as a biomarker of oxidative stress.
|Ubiquinol ratio (%)||93.6||87.1||89.4||81.1|
Study: Oxidative burden in prediabetic and diabetic individuals: evidence from plasma coenzyme Q10
Journal: Diabetic Medicine. 2006, 23: 1344-1349
Authors: Lim SC, Tan HH, Goh SK, Subramaniam T, Sum CF, Tan IK, Lee BL, Ong CN
Department: Department of Medicine, Alexandra Hospital, Singapore 159964, Republic of Singapore.
Summary/comments: Singaporean researchers demonstrated that Ubiquinol ratios are low in diabetics, however the extent of Ubiquinol loss is very severe: diabetics exhibited approximately 75% less Ubiquinol as opposed to control (nondiabetic) subjects (chart below). These diabetics were defined by a fasting plasma glucose of ≥ 6.9 mmol/L (blood glucose of ≥ 124 mg/dL). This research demonstrates that the diabeticʼs oxidative stress may causes the conversion of Ubiquinol to Ubiquinone.
|Blood Glucose||≤ 99 mg/dL||101 – 124 mg/dL||≥ 124 mg/dL|
|Ubiquinol ratio (%) Male||93 ± 6||43 ± 25||24 ± 11|
|Ubiquinol ratio (%) Female||95 ± 6||41 ± 15||29 ± 16|
Study: Coenzyme Q10 (Ubiquinol-10) Supplementation Improves Oxidative Imbalance in Children With Trisomy 21
Journal: Pediatr Neurol. 2007 Dec;37(6):398-403
Authors: Miles MV, Patterson BJ, Chalfonte-Evans ML, Horn PS, Hicke FJ, Schapiro MB, Steele PE, Tang PH, Hotze SL
Department: Division of Pathology and Laboratory Medicine, Cincinnati Children's Hospital Medical Center and University of Cincinnati Medical Center, Cincinnati, OH 45229-3039, USA.
Summary/comments: This is the first study to indicate a pro-oxidant state in plasma of children with trisomy 21, as assessed by Ubiquinol-10: total coenzyme Q10 ratio. The scientists found the redox status of coenzyme Q10 in children with trisomy 21 is significantly altered compared with that of healthy children. In addition, after 3 months of supplementation with Ubiquinol, the antioxidant:oxidant imbalance was positively affected in most of these children. Though this did not prove a clinical effect, the results provide a foundation for further research.
Study: Redox status of coenzyme Q10 is associated with chronological age.
Journal: J Am Geriatr Soc. 2007 Jul;55(7):1141-2.
Authors: Wada H, Goto H, Hagiwara S, Yamamoto Y.
Department: Department of Respiratory Medicine, Kyorin University, School of Medicine, Tokyo, Japan.
Summary/comments: Research has continued to uncover the association between oxidative stress and aging, and recent work done at Kyorin University in Japan demonstrates that Ubiquinol is involved. The blood levels of the both forms of CoQ10 in subjects in different ages was examined. They found that aged subjects not only have reduced CoQ10 biosynthesis, but their ability to convert Ubiquinone to Ubiquinol is also diminished.
Study: Reduced coenzyme Q10 supplementation decelerates senescence in SAMP1 mice.
Journal: Experimental Gerontology 41 (2006) 130–140
Authors: Yan J, Fujii K, Yao J, Kishida H, Hosoe K, Sawashita J, Takeda T, Mori M, Higuchi K
Department: Department of Aging Biology, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, 3-1-1, Asahi, Matsumoto 390-8621, Japan.
Summary/comments: Scientists from Shinshu University (Department of Aging Biology) investigated the effects of Ubiquinol on a senescence-accelerated mouse strain called SAMP1. Ubiquinol improved the behavior and appearance of the SAMP1 mice, and delayed senescence during middle-age.