Study on Coenzyme Q10 and CMT and Muscular Diseases

[Guest guest]

Here is an excerpt from the article. A Dr. friend sent me this

information. The study gives results of the effects of Coenzyme Q10

and CMT patients along with those who have other Muscular Diseases.

I have the whole study if anyone would like a copy of it please

email me.

Excerpt - These results indicate that the impaired myocardial

function of such patients with muscular disease may have some

association with impaired function of skeletal disease, both of

which may be improved by CoQ10 therapy.

Here is some information on the publisher of the study:Dr. Folkers

(author of this article) is well known for his research regarding

CoQ10. In fact, his research is commonly cited in research books

and nutritional product brochures. Muscular dystrophy is a

devastating condition that yet has a proven medical cure. A common

problem associated with muscular dystrophy is degradation of heart

tissue leading towards poor cardiac function. Dr. Folkers indicates

the positive benefits of CoQ10 supplementation to help prevent

cardiac disease in muscular dystrophy patients.

muscle disease to therapy with coenzyme Q10

(cardiac disease/dystrophy/myopathy/chemotherapy)

KARL FOLKERS*, JANUSZ WOLANIUK*, RODNEY SIMONSENt, MASAYUKI

MORISHITA*,

AND SURASI VADHANAVIKIT*

*Institute for Biomedical Research, The University of Texas at

Austin, Austin, TX 78712; and tPhysical Medicine-Rehabilitation,

Austin, TX 78701

Contributed by Karl Folkers, March 4, 1985

ABSTRACT Cardiac disease is commonly associated with

virtually every form of muscular dystrophy and myopathy. A

double-blind and open crossover trial on the oral administration

of coenzyme Qio (CoQ1o) to 12 patients with progressive

muscular dystrophies and neurogenic atrophies was conducted.

These diseases included the Duchenne, Becker, and

limb-girdle dystrophies, myotonic dystrophy, Charcot-Marie-

Tooth disease, and Welander disease. The impaired cardiac

function was noninvasively and extensively monitored by

impedance cardiography. Solely by significant change or no

change in stroke volume and cardiac output, all 8 patients on

blind CoQ1o and all 4 on blind placebo were correctly assigned

(P < 0.003). After the limited 3-month trial, improved physical

well-being was observed for 4/8 treated patients and for 0/4

placebo patients; of the latter, 3/4 improved on CoQ10; 2/8

patients resigned before crossover; 5/6 on CoQ1o in crossover

maintained improved cardiac function; 1/6 crossed over from

CoQ1o to placebo relapsed. The rationale of this trial was based

on known mitochondrial myopathies, which involve respiratory

enzymes, the known presence of CoQ1o in respiration, and

prior clinical data on CoQ1j and dystrophy. These results

indicate that the impaired myocardial function of such patients

with muscular disease may have some association with impaired

function of skeletal muscle, both of which may be

improved by CoQ1o therapy. The cardiac improvement was

defmitely positive. The improvement in well-being was subjective,

but probably real. Likely, CoQ1o does not alter genetic

defects but can benefit the sequelae of mitochondrial impairment

from such defects. CoQ10 is the only known substance that

offers a safe and improved quality of life for such patients

having muscle disease, and it is based on intrinsic bioenergetics.

Best Regards,

Jay