CoQ10 Bioavailability, Formulation (Co-operation, Competition in the CoQ10 Market)

However, the pharmaceutical treatment of high cholesterol may adversely affect the body’s CoQ10 levels. The enzyme hydroxymethylglutaryl (HMG)-CoA reductase plays an important role in regulating cholesterol synthesis; inhibiting this activity is the goal of the statin class of cholesterol-reducing pharmaceuticals. Unfortunately, the same HMG-CoA reductase pathway also regulates CoQ10 synthesis. Italian researchers noted statin treatment generally results in lower plasma levels of CoQ10, possibly related to the fact that the drugs lower levels of LDL, the primary transport molecule for CoQ10; however, there is also a decrease of CoQ10 seen in the platelets and lymphocytes, suggesting CoQ10 synthesis itself may be inhibited.⁶

Intervention studies with statins have examined the impact of the drugs on CoQ10 levels. A new Japanese open study examined the impact of pitavastatin or atorvastatin on plasma levels of CoQ10 in patients with hypercholesterolemia, and found the drugs did significantly reduce total and LDL cholesterol and increase HDL cholesterol.⁷ However, treatment with atorvastatin also significantly reduced (-26.1 percent) plasma levels of CoQ10, more so than pitavastatin (-7.7 percent). Similarly, Italian researchers reported three months of statin therapy dose dependently reduced total cholesterol, as well as levels of ubiquinol and ubiquinone in plasma.⁸ The researchers concluded: “The concomitant administration of ubiquinone with statins, leading to its increase in plasma, lymphocytes and liver may cooperate in counteracting the adverse effects of statins.”

Interestingly, there is a growing interest in the use of statins as an adjunct treatment for heart failure (HF); however, reviewers out of Norway noted low concentrations of cholesterol are generally associated with a worse prognosis in HF patients, possibly because of reduced CoQ10 levels.⁹

CoQ10 may also be an important neuroprotective agent. Because CoQ10 levels decline with age,10 accelerating precursors of beta-amyloid deposition, CoQ10 supplementation may be preventive against Alzheimer’s disease (AD), Parkinson’s disease (PD) and other neurodegenerative disorders.¹¹ In one study, CoQ10 therapy attenuated amyloid beta-peptide toxicity in brain mitochondria isolated from elderly rats.¹² Hong Kong researchers similarly found in a group of 48 mice (four genotypes), those treated with CoQ10 (1,200 mg/d) after ischemic injury for 28 days had amyloid precursor protein mutations and smaller infarct volumes, while the volumes of hemisphere and hippocampus on the infarcted side were larger than those treated with placebo, suggesting CoQ10 could protect the brain from ischemic-related atrophy in aged and susceptible transgenic mice.¹³

A recent study out of Weill Medical College of Cornell University, New York, found administration of CoQ10 via the diet could protect against the loss of dopamine, exerting neuroprotective effects in a model of PD.¹⁴ Japanese researchers also found a link between oxidized CoQ10 levels in cerebrospinal fluid of patients with amyotrophic lateral sclerosis (ALS), suggesting mitochondrial oxidative damage may play a role in pathogenesis of ALS.¹⁵

Researchers are also examining CoQ10’s effects on energy production and athletic performance. Japanese researchers recently reported providing oral CoQ10 (100 or 300 mg/d) to healthy adults for one week prior to a workload trial found CoQ10 could improve subjective fatigue and physical performance.¹⁶ Another study out of Japan found CoQ10 supplementation (300 mg/d) reduced exercise-induced muscular injury, possibly due to its antioxidant effects.¹⁷ And a trial in 22 aerobically trained and 19 untrained male and female adults who received a placebo or fast-melt CoQ10 supplement for 14 days reported supplementation increased muscle CoQ10 concentration and lowered serum superoxide dismutase (SOD) oxidative stress, while also increasing plasma CoQ10 concentrations and time to exercise exhaustion.¹⁸

There are many evolving areas of research as well. There is currently an ongoing FDA- and NIH-funded clinical trial using Tishcon’s liquid ubiquinol (LiQNOL®) in mito-patients. In fact, Tishcon holds orphan drug designation for CoQ10 in the treatment of mitochondrial cytopathies, conditions characterized by defects in the mitochondria often related to DNA mutations.