Certain medical drugs block coenzyme Q10

Q10 is important for cellular energy turnover, and it is also a powerful antioxidant that protects cells and the circulatory system. We synthesize most of our own coenzyme Q10. According to a new in vitro study that is published in Scientific Reports, commonly used medical drugs such as the bisphosphonates, alendronate and zoledronate, for treating osteoporosis block the body’s Q10 synthesis, thereby impairing the energy production in cells, the antioxidant defense, and other metabolic processes. Earlier research has shown that cholesterol-lowering statins lower the endogenous Q10 synthesis, causing side effects such as tiredness, aching muscles, and impotence. It may therefore be a good idea for patients on this type of medication to take a Q10 supplement to prevent or mitigate the adverse effects.

Nitrogen-containing bisphosphonates (NBPs) are medical drugs that are used to treat or prevent osteoporosis. These drugs may also cause dysfunctions of the epithelial cells that line the inside of our blood vessels, cardiac cavity, respiratory tract, and digestive tract. The aim of the new study was to study if six days of treatment with alendronate and zoledronate would affect the energy turnover and function of the endothelial cells. To study this, the scientists used human endothelial cells that had been cultivated in-vitro. The reason for choosing these cells is that endothelial cells line all our blood vessels and are therefore the first cells to come in direct contact with the medicine.
Their study revealed that the two drugs against osteoporosis had the following impact on the endothelial cells:

• Significantly reduced Q10 levels by blocking the cells’ mevalonate pathway that has numerous metabolic functions.
• A reduction of Q10 inhibits the cells’ ability to produce energy in the electron transport chain of their mitochondria
• Lower Q10 levels mean less antioxidant protection and leaves the cells more vulnerable
• Increased anaerobic (without oxygen) energy turnover, which is not very effective
• Oxidative stress where there are too many free radicals and too few protective antioxidants
• Pro-inflammatory conditions
• Downregulation of prenylation-dependent ERK ½ mechanisms, which is a chain of proteins in the cells that send out a signal from a receptor in the cell membrane to the DNA in the cell nucleus.
• Shorter lifespan

The different drugs for treating osteoporosis (NBPs) work by inhibiting farnesyl-diphosphate-synthase, thereby reducing the breakdown of bone tissue and stimulating bone mass formation
Farnesyl-diphosphate-synthase is a key enzyme in the cells’ mevalonate pathway. However, this intracellular and complicated pathway also is involved in the synthesis of Q10 and sex hormones, stress hormones, and vitamin D, all of which are based on cholesterol. Therefore, a number of metabolic disruptions may occur in the cells.
The researchers also mention that the different medical drugs against osteoporosis reduce the endothelial cells’ energy production, metabolism, and antioxidant defense. Furthermore, dysfunctions of the endothelial cells can cause oxidative stress and the development of cardiovascular disease and other problems. These drugs may also affect other cells in the body.

Statins block the endogenous synthesis of Q10 and other compounds

Cholesterol-lowering statins are typically given to older people, diabetics, and to people who have had blood clots or suffered a stroke. Statins affect the mevalonate pathway in cells by blocking HMG CoA, which is an enzyme and a precursor of mevalonate and the subsequent cholesterol synthesis. We also need HMG CoA for making Q10, sex hormones, stress hormones, and vitamin D. By blocking mevalonate, statins therefore interfere with a number of essential compounds in the body.
Studies also suggest that mevalonate is important for the body’s synthesis of selenocysteine, an amino acid that is included in around 25 different selenoproteins. Selenoproteins have numerous tasks in the body such as ensuring optimal utilization of Q10 in its role in the energy turnover and as an antioxidant.
It is commonly known that statins can cause side effects such as fatigue, muscle pain, muscle cramps, joint problems, skin rashes, digestive problems, insomnia, or headache. Impaired memory can also occur, and the same goes for impotence caused by reduced testosterone levels.

• Taking medicine against osteoporosis and/or elevated cholesterol levels can affect the body’s endogenous synthesis of Q10 and other downstream compounds of the mevalonate pathway.
• A high-quality Q10 supplement can compensate for this and prevent the side effects.

References:

Adrianna Budzinska et al. The bisphosphonates alendronate and zoledronate induce adaptations of aerobic metabolism in permanent human endothelial cells. Scientific Reports 2023.

Lain Hargreaves et al. Disorders of Human Coenzyme Q10 Metabolism: An Overview. International Journal of Molecular Sciences. 2020

Manuella Pennisi et al. Vitamin D Serum Levels in Patients with Statin-Induced Musculoskeletal Pain. Disease Markers 2019

Caso Giuseppe et al: Effect of Coenzyme Q10 on Myopathic Symptoms in Patients Treated With Statins. The American Journal of Cardiology. 2007

Moosmann, B & Behl, C. Selenoproteins, cholesterol-lowering drugs, and the consequences: revisiting of the mevalonate pathway. Trends in Cardiovascular medicine. 2004