You are about to enter the Clinical Studies section of this website. These clinical studies are provided for informational and educational purposes only as scientific publications under Section 5 of the Dietary Supplement Health and Education Act. These scientific publications should not be viewed as suggesting Ubiquinol is intended to have any effect on disease. Ubiquinol is sold as a dietary supplement and is not intended to treat, mitigate, cure, or prevent any disease. No information included on this site should be construed as medical advice. Consult your doctor or qualified health practitioner for medical advice. Never delay or disregard seeking medical advice because of something you have read on this website. You must agree to these terms before proceeding to the Clinical Studies section.
The following are summaries and abstracts of clinical research on ubiquinol and ubiquinol absorption by the body using Kaneka Ubiquinol, along with other scientific studies [or research].
Authors: Langsjoen PH and Langsjoen AM
Presented at the 6th Conference of the International Coenzyme Q10 Association, Brussels, Belgium (2010).
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 percent for Q10 (ubiquinone) and 47.8 percent for Ubiquinol. NYHA Class on Kaneka Ubiquinol was 1.6, while subjects on Kaneka Q10 (ubiquinone) were at 2.5.
Journal: Biofactors. 2008;32(1-4):119-28.
Authors: Langsjoen PH, Langsjoen AM
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 Kaneka Q10 (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 percent (10-35 percent) up to 39 percent (10-60 percent).
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 Kaneka Ubiquinol or Kaneka Q10 (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, Kaneka Ubiquinol supplementation was more effective at increasing total CoQ10 levels in the liver.
Journal: Neuroscience Letters. 2010, 469: 159-163
Authors: Isobe T, Abe T, Terayama Y
Summary/comments: Researchers from Iwate Medical University in Japan examined Kaneka Q10 (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 percent of CoQ10 (which is the percentage of ubiquinone to total CoQ10) was also higher. This shift from the Ubiquinol form to the ubiquinone form may mark the extent of oxidative stress and, conversely, the level of antioxidant protection.
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.
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 (ubiquinone). In one of the animal models, they utilized a neurotoxin called MPTP, which induces effects in the brain designed to be 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.
Journal: Clinical and Experimental Nephrology
Authors: Ishikawa A, Kawarazaki H, Ando K, Fujita M, Fujita T, Homma Y
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.
Journal: Biofactors. 1999;9(2-4):241-6.
Authors: Yamamoto Y, Yamashita S
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 (both ubiquinol and ubiquinone forms) was not reduced. These studies demonstrate that as the level of oxidative stress increases, the ratio of the ubiquinol to ubiquinone declines.
| Control (n=16) |
Hepatitis (n=28) |
Cirrhosis (n=16) |
Hepatoma (n=20) |
|
|---|---|---|---|---|
| Ubiquinol ratio (%) | 93.6 | 87.1 | 89.4 | 81.1 |
| Decline | – | 6.5 | 4.2 | 12.5 |
Journal: Diabetic Medicine. 2006, 23: 1344-1349
Authors: Lim SC, Tan HH, Goh SK, Subramaniam T, Sum CF, Tan IK, Lee BL, Ong CN
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 percent 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 cause 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 |
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
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.
Journal: J Am Geriatr Soc. 2007 Jul;55(7):1141-2.
Authors: Wada H, Goto H, Hagiwara S, Yamamoto Y.
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 both forms of CoQ10 (ubiquinone and ubiquinol) in subjects in different ages was examined. They found that aged subjects not only have reduced CoQ10 biosynthesis, but also their ability to convert ubiquinone to ubiquinol is also diminished.
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
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.