An essential nutrient?
CoQ10 (Ubiquinone) is a coenzyme, which is a vital substance in the body that has many important functions. It plays a key role in the generation of energy in the mitochondria, which are the “powerhouses” of the cells. It also acts as one of the few fat-soluble antioxidants for mopping up Reactive Oxygen Species (ROS) that are released during energy production. If they are not removed, they cause damage to the cells. This applies especially to the muscles, which includes the heart. Because of its importance in the body, some workers in the field recommend that it should be regarded as a vitamin.
It has been shown that with certain genetic conditions there is a deficiency in the amount of CoQ10 that can be produced, which includes:
- Severe infantile multisystemic disease;
- Cerebellar ataxia;
- Isolated myopathy;
- Nephrotic syndrome (1).
It has also been established that the ability to produce adequate supplies falls off as people grow old. Patients with various types of heart disease often have a deficiency of CoQ10 and can be treated successfully by taking a supplement. CoQ10 is fat soluble and is naturally present in small amounts in a wide variety of foods but is particularly high in organ meats such as heart, liver and kidney, as well as beef, soy oil, sardines, mackerel, and peanuts.
Deficiencies of CoQ10
A detailed explanation of the background and role of CoQ10 has been prepared by Professor Peter Langsjoen (2).
He notes that the normal blood and tissue levels of CoQ10 have been well established by numerous investigators around the world. In particular it has been established in both animal and human studies that there are significantly decreased levels of CoQ10 in a wide variety of diseases. This deficiency can be caused by insufficient dietary CoQ10, impairment in CoQ10 biosynthesis, excessive utilization of CoQ10 by the body, or any combination of the three. Because there is an increased demand for CoQ10 in those who take exercise, these individuals have an increased risk of experiencing a deficiency.
The heart muscle cells have a particularly high energy requirement and consequently have a very high demand for CoQ10. So it is not in the least surprising that congestive heart failure has been strongly correlated with significantly low blood and tissue levels of CoQ10. Furthermore the severity of heart failure correlates with the severity of CoQ10 deficiency. This raises the possibility that some of these heart conditions could be treated by the administration of CoQ10. The results of investigations designed to study this approach have been very positive. In some there have been dramatic improvements, especially in patients who started CoQ10 soon after the onset of congestive heart failure, with recovery of normal heart size and function. In others, there has been improvement in heart function accompanied by the relief of symptoms including fatigue, chest pain and palpations.
There have now been numerous clinical studies in many different using CoQ10 to treat these diseases of the heart. The results have been remarkably consistent in that invariably there have been significant improvements in heart muscle function without any adverse effects or drug interactions.
Statins lower blood cholesterol (TC) by blocking a pathway involved in its synthesis. However this action also suppresses the synthesis of CoQ10. Therefore it is inevitable that treatment with statins will reduce the amount of CoQ10 in the body. There is ample research to confirm this. In one of the studies (3), 34 subjects had the CoQ10 concentration in blood measured before and after the introduction of treatment with atorvastatin. Their average age was 70 years. It was found that a reduction in the blood plasma concentrations of CoQ10 was evident 14 days after the statin treatment started and was even more marked after 30 days.
Although there have been relatively few studies, which specifically focus on the impact of statins on the CoQ10 levels in the body, the vast majority show essentially similar results. This is not in the least surprising since our knowledge of the mechanism of action by statins predicts that that this is exactly as expected. Now that we understand the functions of CoQ10, this helps to explain some of the problems that are often reported by those who are taking statins. In particular, the muscle damage that is associated with aches and pains especially among those taking exercise. Obviously these muscles include those in the heart so it follows that any reduction in CoQ10 will result in impairment of these muscles as described above. This is rather ironic because it means that although the justification for statin use is to improve the operation of the heart, the drug also has an effect that is likely to be damaging. In order alleviate this undesirable side effect, it is sometimes recommended that statin treatment should be accompanied by CoQ10, this is certainly not the standard procedure. Hence it follows that if statins are used without supplementary CoQ10, there will almost certainly be INCREASED risk of congestive heart failure.
I have encountered numerous individuals who have suffered muscle pains that are associated with the use of statins. Invariably they experience relief when the statins are stopped. This, of course, is entirely predictable and is consistent with a deficiency of CoQ10. Therefore it would be advisable for those on statins to take CoQ10 as well.
But does this make any kind of sense? The reality is that the case for using statins in the first place is extremely weak. The benefits are minimal. Even Dr Mark Baker of NICE accepts that 77 people have to be on statins for three years so that ONE person benefit, which may be just a few more months of life (4). On the other hand, the risks of adverse side effects remain substantial.
The latest information indicates that as people get older, there may be inadequate levels of CoQ10 in the body and so it may be beneficial to take supplements, even if statins are not being used. It is advised that if this is being done the reduced form, ubiquinol, should be taken (5).
- C M Quinzii & M Hirano (2010). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097389/pdf/nihms292488.pdf
- P Langsjoen (1994). https://www.grc.com/sr6dev/misc/coq10/Coenzyme%20Q10.pdf
- T Rundek et al (2004). http://jamanetwork.com/pdfaccess.ashx?url=/data/journals/neur/13750/