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Topic : Congestive Heart Failure And CoQ10 by: Greg Post Since the 1960’s there have been numerous controlled clinical trials concerning the relationship between congestive heart failure and Coenzyme Q10 (CoQ10). As its - mncguru.com Mobile app version of mncguru.com
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: Congestive Heart Failure And CoQ10 by: Greg Post Since the 1960’s there have been numerous controlled clinical trials concerning the relationship between congestive heart failure and Coenzyme Q10 (CoQ10). As its

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Posted in: #Health #Heart #Coq10 #Patients #Improvement #Failure #Treatment #Heart-Failure #Trials #Studies

Congestive Heart Failure And CoQ10

by: Greg Post


Since the 1960’s there have been numerous controlled clinical trials concerning the relationship between congestive heart failure and Coenzyme Q10 (CoQ10). As its name implies CoQ10 is a coenzyme that is necessary for the proper functioning of other substances, one of the most important of which is ATP (adenosine triphosphate). ATP is necessary for the production of cellular energy. By proxy CoQ10 is likewise essential for this process.
Clinical trials have attempted to study the relationship between CoQ10 and many chronic diseases including, but not limited to, heart disease, cancer and AIDS. But heart disease has gained the most attention; congestive heart failure being one of the primary subjects. Because heart muscle cells require so much energy to function and CoQ10 is at the core of the cellular energy process it makes sense to suspect that congestive heart failure might be linked to CoQ10 deficiency. With that theory in mind many studies like the ones that follow have been conducted. These trials have been presented in this essay in thumbnail format.
One early Japanese trial (1972) involved 197 patients with varying levels of severity of cardiac failure. The study reported significant improvement of cardiac function supplementing with 30 mg per day of CoQ10. Another Japanese study demonstrated similar results with 38 patients also supplementing with 30 mg. In 1985 a U.S. clinical study prescribed daily supplementation with 100 mg of the coenzyme for treatment periods of three months for patients with low ejection fraction measurements. The ejection fraction is the measure of the heart’s ability to pump blood. A low ejection fraction is a classic symptom of congestive heart failure. Again, significant improvements in heart function were reported. Other clinical trials followed prescribing the same level of supplementation with similar results.
Studies in the early 1990s showed improvement for patients suffering from ischemic cardiomyopathy (a low oxygen state usually due to obstruction) with supplemental levels of 200 mg per day. Supplementing with 100 mg per day demonstrated improvement for patients suffering from idiopathic dilated cardiomyopathy, an enlarged heart syndrome of unknown cause.
One of the largest trials of the 1990s involves 641 patients randomly divided into two groups. The first group received a placebo. The other group received CoQ10 supplements. During the one-year follow-up period 118 patients in the placebo group were hospitalized for heart failure compared to 73 in the group that received the supplements.
All of the preceding trials were relatively short-term studies. The level of improvement among patients varied depending on how long they had been suffering from some aspect of congestive heart failure. Through the years it has become increasing clear that the greatest improvements were shown in patients that had suffered from their condition the least amount of time. In other words, the longer a person had been suffering from the disease before he or she received CoQ10 treatments the less improvement was demonstrated. People who had received treatments early in the development of the disease showed the most dramatic improvement often returning to normal heart function. Long-term sufferers received less relief and were less likely to return to full heart function. Whatever the reasons for this disparity in health improvement, it demonstrates the importance of receiving treatment as early as possible.
But what about long-term studies? Do they show the same marked improvement with similar treatment? In the short-term trials it was apparent that even high level supplementing with CoQ10 seemed to produce no ill effects. In order to determine if this is only true for short durations a number of long-term studies were conducted.
In 1990 observations were published concerning 126 patients with dilated cardiomyopathy. Unlike previously noted studies this one followed the patients’ progress for six years. Long-term benefits from CoQ10 supplementing were noticed with no harmful side effects. Similar observations were made in a trial involving 2,664 patients treated with CoQ10 at levels up to 150 mg per day.
A 1994 study involving 424 patients with a variety of myocardial (refers to the heart's muscle mass) diseases. Among these conditions were the following: Valvular heart disease (pertaining to dysfunction of heart valves), hypertension, diastolic dysfunction (failure of the heart to properly refill itself with blood), dilated cardiomyopathy (group of disorders where the heart muscle is weakened and enlarged and cannot pump effectively) and ischemic cardiomyopathy (low oxygen state usually due to obstruction of the arterial blood supply). Patients were treated with an average of 240 mg of CoQ10 daily during their treatment period. They were then followed-up for up to eight years with an average follow-up period of 18 months. Overall results demonstrated measurable cardiac improvements in one month with maximum improvements at about six months. With continued CoQ10 treatment the improvement in most patients was sustained. However, discontinuing the treatment usually resulted in a decline of cardiac function with eventual return to pre-treatment conditions.
As always in the medical community many more studies will need to be conducted to determine the future of CoQ10 treatment. However, the research to date seems to support CoQ10 as a viable treatment for many diseases that are caused or exacerbated by inadequate production of cellular energy.


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