CoQ10-H2™

Throughout the years, researchers have extensively studied the antioxidant coenzyme Q10 for its ability to support heart and cognitive functions plus enhance mitochondrial production of ATP, the cellular energy molecule. However, just like with any nutritional supplement, the ability of the body to absorb coenzyme Q10 is critical to its effectiveness. Recently, a new breakthrough has revealed that the first generation of supplemental coenzyme Q10, called ubidecarone or CoQ10-Ox, while still absorbed by the human body to produce some benefits, isn’t nearly as effective at increasing blood levels as its newer, more biochemically active, second generation form, CoQ10-H2™. This is important because increased blood levels help ensure that CoQ10 reaches important cellular sites.

Prior to the introduction of this new, reduced form, known as ubiquinol, individuals were often required to consume significant dosage levels of Co-Q10-Ox in order to achieve clinical benefits. With CoQ10–H2, however, higher blood levels can be achieved with smaller doses, indicating that less is required to produce optimal results. Fifty to one hundred milligrams (50-100 mg) of CoQ10–H2 yields higher blood levels, which produce prolonged bioenergetic and improved antioxidant benefits. As an example, individuals who are consuming 100 to 150 mg per day of the first generation form of coenzyme Q10 to replenish the depletion of this antioxidant caused by statin drugs, can now consume considerably less of the new CoQ10–H2 and achieve the same therapeutic benefits with fewer side effects.

In next month’s issue of Vitamin Research News, a leading expert on CoQ10–H2 will delve deeper into the research conducted on this fascinating new form of one of nature’s most important bio-energetic catalysts and powerful, fat-soluble antioxidants. In this article, I will review some of the research that I mentioned in last month’s article and address more of the reasons why I believe CoQ10–H2 will become the preferred choice for physicians, nutritionists and patients who want to improve cardiac function, and increase vitality and longevity.

Better Absorption Equals Better Efficacy
The human body is continually recycling its cellular stores of coenzyme Q10. Before the introduction of CoQ10-H2, this cycle was “primed” with the oxidized form of coenzyme Q10, known as CoQ10–Ox or ubidecarone because, obviously, this was the only form of CoQ10 available in supplement form. During biochemical transformations in the mitochondria, the body transforms CoQ10-Ox into the reduced form, CoQ10–H2. It is, in fact, actually CoQ10–H2 that the body uses to catalyze the synthesis of ATP in the mitochondria. In addition, in order for coenzyme Q10 to trap and inactivate free radicals, particularly the highly reactive hydroxyl radical (OH.) and the superoxide radical (O2-) to protect the integrity of the lipid membranes of cells and their mitochondria, it must first be changed into the reduced form, CoQ10–H2. In both coenzyme Q10’s primary mechanism of actions (the ability to catalyze the production of ATP in the mitochondria and to act as a fat soluble antioxidant), CoQ10–H2 is more effective than the more extensively studied, oxidized form of coenzyme Q10, the only form available to clinicians, patients and health conscious consumers previously.

The emerging research documents the superior bioavailability of CoQ10–H2 in animals and humans. A published single-blind, placebo controlled, four week study of healthy Japanese subjects has shown that CoQ10–H2 was absorbed rapidly and efficiently from the gastrointestinal tract after oral administration. The Japanese researchers reported that the benefits of reduced Coenzyme Q10, CoQ10–H2, were attributable to the over 210 percent increase in blood levels of ubiquinol. This is a dramatic and therapeutically efficacious elevation when compared to the oxidized form of coenzyme Q10. Importantly, this study also revealed no abnormal laboratory values seen in blood chemistry panels or any other indications of clinically relevant safety concerns, as evidenced by the clinicians’ assessments of adverse events related to higher dosages of CoQ10–H2 up to 300 mg. per day.1

Less is More?
One of the advantages to consuming this new, reduced form of coenzyme Q10, as CoQ10–H2, may be that lower doses are required to achieve the same or improved responses. This is important because many of the clinical studies that have shown positive neurological effects actually used rather large doses of the first generation, oxidized form of CoQ10. For example, a 16-month randomized, placebo-controlled pilot trial in 80 subjects with mild Parkinson’s disease found significant benefits for oral CoQ10-Ox at 1,200 mg per day. At this dose, oxidized coenzyme Q10 appeared to slow functional deterioration.2 However, 1,200 mg per day is a substantial and expensive dose of this antioxidant; achieving similar benefits with a much lower amount of CoQ10-H2 would obviously be ideal. It’s likely that, although first generation coenzyme Q10 has demonstrated efficacy in supporting the health of patients with heart disease in many studies, the reason why some of the earlier coenzyme Q10 trials have not produced as dramatic a result as would be expected may be because the subjects were not absorbing enough of the 150 mg to 200 mg of oxidized CoQ10 used in these trials, to produce the blood levels of coenzyme Q10 required to produce a positive, clinical outcome.

One group of researchers, who reviewed the use of CoQ10 in congestive heart failure, ischemic heart disease, hypertensive heart disease, diastolic dysfunction of the left ventricle, and reperfusion injury after coronary artery bypass graft surgery, concluded, “The attainment of higher blood levels of CoQ10 with the use of higher doses of CoQ10 appears to enhance both the magnitude and rate of clinical improvement.”3 CoQ10-H2 can be expected to produce the higher blood levels required to produce these desired clinical improvements.

Conclusion
Coenzyme Q10 plays well documented roles in cardiovascular and mitochondrial health. Researchers have stated that, “Supplemental coenzyme Q10 alters the natural history of cardiovascular illnesses and has the potential for prevention of cardiovascular disease through the inhibition of LDL cholesterol oxidation and by the maintenance of optimal cellular and mitochondrial function.”3 Coenzyme Q10 deficiency also has been observed in patients with congestive heart failure, angina pectoris, coronary artery disease, cardiomyopathy, hypertension, and mitral valve prolapse.4

Furthermore, coenzyme Q10 is a powerful, fat soluble antioxidant that mitigates the potential adverse consequences of free radicals produced in the inner mitochondrial membrane. The biochemical pathologies produced by oxidative stress result in depletion of glutathione and oxidant “nicks” in both nuclear and mitochondrial DNA, plus damage to proteins. This free radical mediated pathology has been implicated in many neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease and Huntington’s disease.2

Although it is too early to state with absolute certainty, I feel confident that all previously published study outcomes and personal experience benefits provided by the first generation of supplemental coenzyme Q10, in its oxidized form, will be significantly superceded by the appropriate dosages of the new, stabilized CoQ10–H2.

References
1. Hosoe K, Kitano M, Kishida H, Kubo H, Fujii K, Kitahara M. Study on Safety and Bioavailability of Ubiquinol (QH™) after Single and 4-week Multiple Oral Administration to Healthy Volunteers. Regulatory Toxicology Pharmacology. 2007 February; 47(1):19-28.
2. Young AJ, Johnson S, Steffens DC, Doraiswamy PM. Coenzyme Q10: a review of its promise as a neuroprotectant. CNS Spectr. 2007 Jan;12(1):62-8.
3. Langsjoen PH, Langsjoen AM. Overview of the use of CoQ10 in cardiovascular disease. Biofactors. 1999;9(2-4):273-84.
4. [Anonymous]. Physiological aspects of ubiquinone supplementation under cardiovascular pathology. [Article in Ukrainian]. Fiziol Zh. 2006;52(5):80-91.