Interview with Markus Look, MD, internist from Bonn, Germany, and author of the report of the Drug Commission of the German Medical Association (AKDÄ) on statins and Q10. In a statement for the AKDÄ, Dr. Look compiled the existing knowledge about the connection between the intake of cholesterol-lowering drugs from the current family of statins and the reduction of the vital endogenous substance Q10: Statins simultaneously inhibit the production of Q10 along with cholesterol synthesis.
Avoiding Q10 deficiency with statins?
Based on these biochemical reaction processes in the body, it is plausible that Q10, taken together with statins, may avoid an undesirable Q10 deficiency for the patient. But the evidence for this in the form of large clinical studies according to the current state of science is lacking. The substance Q10 is available over the counter as a food supplement and cannot be patented. Should every statin patient now buy and swallow Q10 himself? Dr. Look advises an individual decision after consultation with a physician or pharmacist.
What does our body need the energy enzyme Q10 for?
Dr. Look: Coenzyme Q10 (“ubiquinol”) fulfills an important function in energy production in the power plants of every body cell, the mitochondria. Here, food energy is converted into metabolic energy. However, Q10 is also one of the most important antioxidants in the organism, i.e. it protects the cell walls from aggressive molecules.
Why does the heart in particular consume so much Q10?
Dr. Look: It stands to reason that all organs with high energy requirements rely on optimal Q10 supply – the ever-beating heart is one such organ.
Where does Q10 come from, which is essential for us to live?
Dr. Look: Q10 is both ingested with food and synthesized by the organism itself. For example, to get 100 milligrams of Q10 from food, you would have to eat about 1.6 kilograms of sardines.
Among the four million Germans who take statins to lower elevated cholesterol, there may be an undersupply of Q10. Why?
Dr. Look: You are quite right to say “may.” Studies in the sense of the highest level of evidence I, that is, the highest level of evidence, as we must have for official population-wide recommendations, are unfortunately not available. Statins are, from the current point of view, intended as long-term therapy, even lifelong therapy. In the elderly, lower Q10 levels are already found without statin therapy than in the young. Accordingly, it is plausible to expect Q10 deficiency in the elderly under long-term statin therapy and especially at high doses. Regarding the possible mechanism, the substance provided by the key enzyme of cholesterol synthesis is needed for the formation of Q10 in addition to cholesterol synthesis. Statins inhibit this enzyme, the body forms less cholesterol. It is a logical hypothesis that throttling this enzyme by statins may consequently decrease Q10 production.
What may be the consequences of Q10 deficiency in patients with elevated cholesterol and heart failure?
Dr. Look: Heart failure may be due to myocardial infarction or may have developed without relevant narrowing of the coronary arteries due to other factors (viruses, genetic, other reasons). But, not every patient with high cholesterol suffers from heart failure, and not everyone needs to be treated with a statin. However, one can well imagine that an impairment of energy production in the “power plants” of the cell (mitochondria, see question 1) leads to stress in the muscles or death of muscle cells. The individual perceives this as muscle pain and weakness, and elevated levels of a muscle enzyme (the creatine kinase), may be found in the laboratory. It is conceivable that Q10 deficiency may exacerbate existing heart failure and contribute to pump failure.
What do you recommend for statin patients to prevent Q10 deficiency?
Dr. Look: Given the lack of large-scale studies on the subject, this is an individual decision between physician and patient in light of the described inhibition of Q10 synthesis by statins. However, the number of those studies investigating joint administration of Q10 and statin or Q10 administration as an attempt to remedy statin-mediated side effects is too small. Therefore, it is not possible to make a universally valid recommendation, even at the expense of health insurers.
Are physicians aware of the problem of potential Q10 deficiency in statin patients? How can education be contributed?
Dr. Look: I assume that this is specialist knowledge, but I do not have representative data on possible questioning of colleagues on this topic. Only large, so-called head-to-head studies comparing statins alone with statins plus Q10 can provide clarity. These studies must be carried out on several thousand patients and last for several years. Presenting the Q10 hypothesis to colleagues at this time may be correct on the one hand, but also carries the risk of raising unfounded fears among patients as well. Conservative institutions therefore view this somewhat critically. For as long as the proving studies I have outlined do not take place, colleagues in practice are always in the dilemma of having to interpret the data situation according to their own feelings. In my opinion, it is a minor scandal that the scientific community has not yet managed to conduct these head-to-head studies. In the last 20 years, tens of thousands of patients have been treated with statins in studies. The fact that a statin/Q10 comparison group has never been compared with the exclusive statin group is highly criticizable. One could have easily looked ten years ago to see if the combination therapy, Q10 plus statin, had fewer side effects or even a better overall result in reducing heart attacks and mortality, especially in high-risk patients, than statin monotherapy. Dr. Look, thank you for the interview.
