Abstract

Coenzyme Q10 (also known as Ubiquinone) and its active form, Ubiquinol, are essential for the body’s energy production processes, including those which take place in the heart. Thus, a deficiency of heart and blood CoQ10 could be a risk factor for the development of cardiovascular diseases.
The latest advance in supplemental Coenzyme Q10 is the reduced, active form Ubiquinol. While traditional, oxidized CoQ10 has to be converted into Ubiquinol before it works in the body, Ubiquinol can work quickly and directly without such conversion. It is effective at lower dosages. Ubiquinol daily doses range from 100 to 600 mg and can increase blood plasma levels of CoQ10 to more than 3.5 mg/l, which is the level required by patients with severe heart problems for improving heart function. Clinical studies support the safety of Ubiquinol in CHF patients and demonstrate that Ubiquinol is more effective than oxidized Coenzyme Q10.

INTRODUCTION

In today’s industrialised countries, cardiovascular diseases are the most common cause of death, with congestive heart failure (CHF) being the third most common cause in this category. In 2009, one in nine death certificates (274,601 deaths) in the United States mentioned heart failure, and heart failure was the underlying cause in 56,410 of those deaths. The number of deaths attributable to heart failure was approximately as high in 1995 (287,000) as it was in 2009 (275,000) (1).
As a constantly active organ, the heart muscle has to be supplied on a permanent basis with enough energy for optimal function. CoQ10 and its reduced form, Ubiquinol, play important roles in the body’s energy production processes, including those which take place in the heart. In fact, Coenzyme Q10 occurs in every cell of the body and is an essential cofactor in the mitochondrial electron transport system. It interacts with at least three mitochondrial enzyme complexes involved in oxidative phosphorylation during ATP production (2). A deficiency of Coenzyme Q10 causes reduced energy delivery in the cardiac myocyte, despite an optimal mitochondrial subst ...