A study about Mitochondrial alpha lipoic acid, creatine monohydrate and coenzyme Q10.
February 22, 2007 The study indicated that mitochondrial disorders have several things in common, including reduced production of ATP (the energy molecule in our bodies), increased reliance on non-oxygen energy sources and increased production of oxygen free radicals. In this study, patients with mitochondrial disorders were treated in a randomized, double-blinded, placebo-controlled manner with crossover using the three above noted nutrients. The combination therapy appeared to lower plasma lactate levels and decreased decline in ankle muscle strength.
This study suggest that combination of nutritional stratagies targeting common pathways of mitochondrial dysfunction (mitochondrial cytopathy) showed favorable benefits in the markers of cellular energy.
Abstract
Mitochondrial disorders share common cellular consequences: (1) decreased ATP production; (2) increased reliance on alternative anaerobic energy sources; and (3) increased production of reactive oxygen species. The purpose of the present study was to determine the effect of a combination therapy (creatine monohydrate, coenzyme Q10, and lipoic acid to target the above-mentioned cellular consequences) on several outcome variables using a randomized, double-blind, placebo-controlled, crossover study design in patients with mitochondrial cytopathies.
Three patients had mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), four had mitochondrial DNA deletions (three patients with chronic progressive external ophthalmoplegia and one with Kearns-Sayre syndrome), and nine had a variety of other mitochondrial diseases not falling into the two former groups. The combination therapy resulted in lower resting plasma lactate and urinary 8-isoprostanes, as well as attenuation of the decline in peak ankle dorsiflexion strength in all patient groups, whereas higher fat-free mass was observed only in the MELAS group. Together, these results suggest that combination therapies targeting multiple final common pathways of mitochondrial dysfunction favorably influence surrogate markers of cellular energy dysfunction. Future studies with larger sample sizes in relatively homogeneous groups will be required to determine whether such combination therapies influence function and quality of life.
Muscle & Nerve: Feb 2007 Volume 35, Issue 2, Pages 235 - 242
Source: Muscle & Nerve
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