10. Statins and Heart Failure

A paper titled simply "Lovastatin decreases coenzyme Q levels in humans" [16] states unequivocally in the abstract: "It is established that Coenzyme Q10 is indispensable for cardiac function." The heart is a muscle, and hence it is subject to all the same laws of physics as the skeletal muscles. It faces the same problem of fuel deficiency due to the various effects statins have on metabolism discussed above. Heart muscle cells would also have to cannibalize themselves to get enough fuel, and would also suffer damage to their cell membranes due to exposure to Ferryl myoglobin.

An article published in 2004 [42] provides a plausible theory for the process by which muscle cells in the heart become dysfunctional with old age, leading ultimately to heart failure. The argument blends perfectly with the logical deductions associated with the mechanism by which statins damage cells, and leads to the unavoidable conclusion that statins make you age at an accelerated pace. The process involves a downward spiral caused by deficiencies in both the mitochondria and the lysosomes. Recall that the mitochondria are responsible for providing fuel to the cell, and the lysosomes are responsible for digesting and decomposing residues of waste products. The article claims that the downward spiral is caused by "continuous physiological oxidative stress." Oxidative stress is greatly enhanced by statins, because they deplete the supply of both antioxidants like coenzyme Q10 and fresh phospholipids and cholesterol to rebuild damaged cell walls. Debris from damaged phospholipids in the cell wall, the mitochondrial walls, and the lysosome walls must be taken up by the lysosomes, digested, and disposed of. Under normal circumstances the lysosomes would easily break them down in their highly acidic environment, using their powerful digestive enzymes.

When the lysosomes are unable to digest the debris that accumulates from damaged cell walls, the residue that remains is called "lipofuscin." Lipofuscin is considered to be a signature of old age, accumulating in the liver, kidney, heart muscle, and nerve cells as we get older. Lipofuscin is believed to be the product of oxidation of unsaturated fatty acids, and is indicative of membrane damage, whether to the cell's outer wall or to the walls of the lysosomes and mitochondria [17].

For long-term statin users, lipofuscin almost certainly accumulates, because their lysosomes are dysfunctional. This condition would arise not just in the heart, but in all the cells of the body. As I mentioned earlier, statins cripple the production of the dolichols, antioxidants that play a crucial role in protecting the lysosomes from hydrogen ion leakage. Lysosomes also depend upon cholesterol in their membranes to provide additional insulation against charge dissipation. With a constant leakage outward of H⁺ ions, lysosomes can not maintain their pH at a sufficiently acidic level to allow their enzymes to work. As a consequence, undegradable debris, i.e., lipofuscin, accumulates within the lysosomes, and the cell has no backup repair system to salvage the disaster. The last sentence in the abstract of [42] says: "This interrelated mitochondrial and lysosomal damage eventually results in functional failure and death of cardiac myocytes {heart muscle cells]."

Doctor Peter Langsjoehn believes that statins are inducing an epidemic rise in the incidence of heart failure. He wrote: "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, are being prescribed in higher doses, and are being used with reckless abandon in the elderly and in patients with 'normal' cholesterol levels. We are in the midst of a CHF epidemic in the US 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. " (Statins and Heart Failure) .

Dr. Duane Graveline, a long-time advocate of the dangers of statin therapy, has provided a very clear description ( Duane Graveline on Statins and Heart Failure) of the role of coenzyme Q10 in the heart and the reason why its inhibition by statins would lead to heart failure. You can find several references to relevant articles by Dr. Langsjoehn on that page.

A very recent study (November, 2009) [8] found that patients with diastolic heart failure who were taking statins had a significantly poorer outcome than patients who were not on statin therapy. Diastolic heart failure is distinguished from systolic heart failure in that it is associated with dysfunction of the heart during the resting phase rather than the contracting phase. However, it is the cause of nearly half of the cases of heart failure, and it is equally as fatal as the systolic form. In the study, it was confirmed that people with diastolic heart failure who were on statin therapy were more likely to have problems with their lungs and were less able to exert themselves (weaker muscles, poorer exercise tolerance) than those not on statins.