Fatigue and mitochondrial function – Ubiquinol’s therapeutic benefits

The importance of the mitochondria

There are many reasons that people may experience low levels of energy, with diet, lifestyle and illness all key influencers, but if you have been putting your low energy levels down to too little sleep, ongoing stress or just feeling ‘under the weather’, you might want to think a little deeper.

We generally consider food as the fuel that gives us energy, but if the body is simply inefficient at converting food into energy then it may be worth looking at measures that can be taken to improve the process that, ultimately, fuels our everyday functions at both the cell and molecular levels.  The first port of call is to the humble mitochondria – tiny structures within cells, often referred to as the cell ‘powerhouse’ due to their generation of adenosine tri-phosphate (ATP) – the energy molecule upon which all cellular functions in the body depend. There are three main pathways used to generate energy: cellular respiration, including glycolysis and the citric acid cycle; oxidative phosphorylation; beta-oxidation. All of these are involved in the breakdown of carbohydrate, fat and protein from food. Normal mitochondrial function is therefore imperative for optimal energy production; mitochondrial dysfunction may lead to decreased ATP production and, thus, to low energy and fatigue.  For the mitochondria to function normally, it relies on the successful input of several ‘team players’, which participate in a series of reactions transferring molecules (called electrons) from a donor molecule to an acceptor molecule and, collectively, as the ‘electron transport chain’, this culminates in the release of energy. One of the major team players is a vitamin-like nutrient called coenzyme Q10 (CoQ10), which acts as a catalyst for mitochondria to produce ATP.


ATP is essentially an adenosine molecule joined to three phosphate groups.  Mitochondria produce energy by taking a molecule of ATP and chopping off one of its three phosphate groups, releasing energy in the production of adenosine diphosphate (ADP).  When the reaction is over, CoQ10 donates electrons required for the reattachment of the phosphate group to ADP to produce ATP.  Once CoQ10 has delivered its electrons and ATP is reformed, the cycle then repeats.  As long as the body is fuelled (in the form of food), and CoQ10 is present, it’s a perpetual energy process.  If, however, CoQ10 levels become depleted, the recycling of ATP from ADP is significantly affected.  For many people, low energy may simply be a symptom of CoQ10 deficiency.


As part of the cycling of ATP to ADP, CoQ10 itself is cycled between two states.  As CoQ10 accepts electrons, it becomes ‘reduced’ (to ubiquinol) and as it gives up electrons, it becomes ‘oxidised’ (to ubiquinone), and both forms are necessary to shuttle electrons between the ADP to ATP energy-producing reactions.  One of the major benefits of ubiquinol is that it acts as a powerful antioxidant ’mopping up’ potentially harmful free radicals – unstable free-floating electrons – that, when not attached to other molecules, are capable of causing damage to cell membranes.  Approximately 96% of total CoQ10 is found as ubiquinol, reflecting the importance of the reduced, antioxidant form over the oxidised form [1].


Small amounts of CoQ10 (as ubiquinone) can be found in foods – primarily meat and fish, with the highest amounts found in organ meat such as heart, liver and kidneys.  The body can also make ubiquinone, and levels within the body peak around the age of 20, after which they begin to decline, with the body’s ability to convert ubiquinone into ubiquinol also diminishing with age.   In addition, individuals taking cholesterol-lowering drugs (commonly known as statins) are very likely to have low CoQ10 levels as a direct side effect of the treatment.  This is because these drugs act by blocking the activity of the enzyme HMG-CoA reductase involved in cholesterol synthesis.  As the cholesterol and CoQ10 biosynthesis share the same pathway, inhibiting cholesterol synthesis will also block the body’s ability to make CoQ10, leading to a condition known as statin-induced myopathy.


Symptoms include fatigue, muscle pain, muscle tenderness, muscle weakness, nocturnal cramping and tendon pain. [2] Taking CoQ10 supplements can correct the deficiency caused by such medications without affecting the medication’s positive effects on cholesterol levels, and can improve statin-induced myopathy. [3]

Supplementing offers a direct method to restore CoQ10 levels, but, as with many other supplements, there are a number of versions commonly available, offering different (and confusing information about) levels of bioavailability; ensuring you source the most efficient form and delivery method will impact significantly on treatment outcomes.

Ubiquinone was originally discovered in the 1950s, [4] but because (reduced form) ubiquinol is easily oxidised outside the body, the stabilised form of ubiquinol(Kaneka QH™) has only been available for use in supplements since 2006.  It is generally accepted that this antioxidant version of CoQ10 is superior to ubiquinone supplements at both the cellular and molecular levels.  As both ubiquinone and ubiquinol are lipid-soluble nutrients, their absorption and bioavailability are generally poor.  Most commonly available formulations of CoQ10 are ubiquinone, in powder form or dispersed in oil suspensions, and with relatively poor bioavailability.  A product containing ubiquinol will achieve superior results over one that contains ubiquinone, but because the clinical outcomes of treatment with ubiquinol are dependent on increasing its bioavailability, rendering ubiquinol water-soluble allows superior uptake over a non-solubilised version.   Combining solubilised ubiquinol with a unique delivery system (known as VESIsorb™) that works to mimic the naturally occurring transport system of the intestine leads to unprecedented absorption, tissue distribution and superior health benefits over any other form of openly available CoQ10 product.


Supplementing with colloidal-solubilised ubiquinol leads to significantly higher blood serum levels of CoQ10 than with comparable doses of other available products. Increasing ubiquinol levels increases energy levels and improves the activity of the body’s high-energy tissues, such as the heart, skeletal muscles, liver and brain.   Ubiquinol supplementation is particularly useful for conditions where mitochondrial dysfunction and coenzyme Q10 (CoQ10) deficiency are implicated, such as chronic fatigue syndrome [5] and fibromyalgia. [6]  In addition to fighting fatigue, ubiquinol’s potent antioxidant activity may also be of additional benefit in cardiovascular disease, neurological diseases such as Parkinson’s disease, cancer and diabetes [7-11].

Given that there is age-related decline in total CoQ10 levels and in the body’s ability to convert ubiquinone to ubiquinol, supplementing with highly bioavailable ubiquinol could benefit a range of individuals, as well as offer a therapeutic benefits for conditions in which mitochondrial dysfunction and CoQ10 deficiency are key players.


1. Tang PH, Miles MV, DeGrauw A, Hershey A, Pesce A: HPLC analysis of reduced and oxidized coenzyme Q(10) in human plasma. Clinical chemistry 2001, 47:256-265.

2. Fernandez G, Spatz ES, Jablecki C, Phillips PS: Statin myopathy: a common dilemma not reflected in clinical trials. Cleveland Clinic journal of medicine 2011, 78:393-403.

3. Fedacko J, Pella D, Fedackova P, Hanninen O, Tuomainen P, Jarcuska P, Lopuchovsky T, Jedlickova L, Merkovska L, Littarru GP: Coenzyme Q10 and selenium in statin-associated myopathy treatment. Canadian journal of physiology and pharmacology 2013, 91:165-170.

4. Crane FL, Hatefi Y, Lester RL, Widmer C: Isolation of a quinone from beef heart mitochondria. Biochimica et biophysica acta 1957, 25:220-221.

5. Maes M, Mihaylova I, Kubera M, Uytterhoeven M, Vrydags N, Bosmans E: Coenzyme Q10 deficiency in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardiovascular disorder. Neuro endocrinology letters 2009, 30:470-476.

6. Cordero MD, Alcocer-Gomez E, de Miguel M, Culic O, Carrion AM, Alvarez-Suarez JM, Bullon P, Battino M, Fernandez-Rodriguez A, Sanchez-Alcazar JA: Can Coenzyme Q10 improve clinical and molecular parameters in Fibromyalgia? Antioxidants & redox signaling 2013.

7. Lance J, McCabe S, Clancy RL, Pierce J: Coenzyme Q10–a therapeutic agent. Medsurg nursing : official journal of the Academy of Medical-Surgical Nurses 2012, 21:367-371.

8. Lee BJ, Lin YC, Huang YC, Ko YW, Hsia S, Lin PT: The relationship between coenzyme Q10, oxidative stress, and antioxidant enzymes activities and coronary artery disease. TheScientificWorldJournal 2012, 2012:792756.

9. Mancuso M, Orsucci D, Volpi L, Calsolaro V, Siciliano G: Coenzyme Q10 in neuromuscular and neurodegenerative disorders. Current drug targets 2010, 11:111-121.

10. Chai W, Cooney RV, Franke AA, Shvetsov YB, Caberto CP, Wilkens LR, Le Marchand L, Henderson BE, Kolonel LN, Goodman MT: Plasma coenzyme Q10 levels and postmenopausal breast cancer risk: the multiethnic cohort study. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2010, 19:2351-2356.

11. Chai W, Cooney RV, Franke AA, Caberto CP, Wilkens LR, Le Marchand L, Goodman MT, Henderson BE, Kolonel LN: Plasma coenzyme Q10 levels and prostate cancer risk: the multiethnic cohort study. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2011, 20:708-710.

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