Your question illustrates the confusion out there about statins.
On the one hand...studies show anti-inflammatory effects of statins that are independent of their cholesterol lowering actions. It is this anti-inflammatory effect that is supposed to be the "heart" of their success in studies.
Many many studies are on PubMed about this subject. But I don't know how accurate they are. I recall a similar blitz of positive studies with hormone replacement therapy that were all erroneous, as well as antidepressants use in children that were positive and then withdrawn. (drug companies forced to reveal the negative studies).
So it is really hard to know who to believe these days.
If you Google this subject you will find doctors who claim that there is an "epidemic" of heart failure now and they believe it is from statin use-- like this example:
Quote:
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According to Dr. Langsjoen, "In my practice of 17 years in Tyler, Texas, I have seen a frightening increase in heart failure secondary to statin usage: statin cardiomyopathy. Over the past five years, statins have become more potent, have been prescribed in higher dosages, and have been used with reckless abandon in the elderly and in patients with normal cholesterol levels. We are in the midst of a congestive heart failure epidemic in the U.S., with a dramatic increase over the past decade. Are we causing this epidemic through our zealous use of statins? In large part, I think the answer is yes. We are now in a position to witness the unfolding of the greatest medical tragedy of all time. Never before in history has the medical establishment knowingly created a life-threatening nutrient deficiency in millions of otherwise healthy people."
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from
http://www.townsendletter.com/FebMar2006/coq100206.htm
We do know that statins DAMAGE mitochondria. And since the heart is the most active muscle in the body, it is only logical that damage here would be signficant and deadly.
Quote:
Toxicol Appl Pharmacol. 2007 Jun 21; : 17658574 PubMed
Mitochondrial impairment by PPAR agonists and statins identified via immunocaptured OXPHOS complex activities and respiration.
MitoSciences, Inc., 1850 Millrace Drive, Eugene, OR 97403, USA
Sashi Nadanaciva , James A Dykens , Autumn Bernal , Roderick A Capaldi , Yvonne Will
Mitochondrial impairment is increasingly implicated in the etiology of toxicity caused by some thiazolidinediones, fibrates, and statins. We examined the effects of members of these drug classes on respiration of isolated rat liver mitochondria using a phosphorescent oxygen sensitive probe and on the activity of individual oxidative phosphorylation (OXPHOS) complexes using a recently developed immunocapture technique. Of the six thiazolidinediones examined, ciglitazone, troglitazone, and darglitazone potently disrupted mitochondrial respiration. In accord with these data, ciglitazone and troglitazone were also potent inhibitors of Complexes II+III, IV, and V, while darglitazone predominantly inhibited Complex IV. Of the six statins evaluated, lovastatin, simvastatin, and cerivastatin impaired mitochondrial respiration the most, with simvastatin and lovastatin impairing multiple OXPHOS Complexes. Within the class of fibrates, gemfibrozil more potently impaired respiration than fenofibrate, clofibrate, or ciprofibrate. Gemfibrozil only modestly inhibited Complex I, fenofibrate inhibited Complexes I, II+III, and V, and clofibrate inhibited Complex V. Our findings with the two complementary methods indicate that (1) some members of each class impair mitochondrial respiration, whereas others have little or no effect, and (2) the rank order of mitochondrial impairment accords with clinical adverse events observed with these drugs. Since the statins are frequently co-prescribed with the fibrates or thiazolidinediones, various combinations of these three drug classes were also analyzed for their mitochondrial effects. In several cases, the combination additively uncoupled or inhibited respiration, suggesting that some combinations are more likely to yield clinically relevant drug-induced mitochondrial side effects than others.
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Using CoQ-10 may be protective, but we don't know what doses to use compared to the doses of statin. For example I have never seen a recommendation for say 100mg of CoQ-10 for 10mg Lipitor, etc. It is rather hit and miss.
In Dr. Jay Cohen's book, he has many many reports from older patients who saw lowered cholesterol without damage in doses quite low. 2.5mg of Lipitor, 10mg Pravachol, 5 mg of Zocor. He believes that statins may help without harming people if used in much lower doses. That the high doses we are suggested to use are not accurate or necessary.
Personally I think it is possible. I have seen patients coming to me in their 40's with CHF...and before statins, that was pretty rare.
When the patents run out on statins soon, that is when the NEGATIVE studies will appear. That is the way other drugs' problems are eventually revealed and the truth then comes out.
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All truths are easy to understand once they are discovered; the point is to discover them.-- Galileo Galilei
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Weezie looking at petunias 8.25.2017
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