Growing old is not so much about chronological age but a consequence of the biochemical processes that happen inside our bodies, the lifestyle choices we make, and how well we can protect our bodies from the toxic elements around us.
Scientists are only now beginning to understand this aging process. Aging is mainly influenced by forces within our bodies including a process called “cellular aging.” Cellular aging is the gradual course over time that leads progressively to the loss of our physiological reserves and functions.
Scientists also developed the free radical theory of aging, which is a theory that the origins of cellular aging are in part the result of the damaging effects of oxidative stress.
Oxidative stress—an imbalance of antioxidant defenses and free radicals—is a product of our environment but also a product of our own metabolism, which brings us to the mitochondrion.
Free Radical Theory of Aging and the Mitochondria
The mitochondrion is a sausage-shaped, double-membrane organelle appropriately nicknamed the cell’s “powerhouse” because of its efficiency in converting food into a form of energy called ATP. The mitochondrion houses the cell’s capacity for “aerobic respiration,” which features the Krebs cycle and the electron transport chain.
The electron transport chain in the mitochondria is the most efficient as it extracts a total of 32 ATP (only 4 ATP are produced from the Kreb’s cycle and glycolysis). The more mitochondria in the cells the more energy produced to meet our cell’s needs. The millions of mitochondria found within our cells in our tissues are what generate the majority of the energy that keeps our organs functioning at their prime: giving our brains the power for thought, and our muscles their power for performance and endurance.
As you’d expect from any efficient power plant, however, there are unwanted side effects. In the case of the mitochondria, the side effects are the generation of electrons, which leave the mitochondria to potentially produce free radicals (reactive oxygen species). Reactive oxygen species such as lipid peroxyl radicals attack all cellular components, especially those that are in close proximity to the mitochondria. These can include intracellular proteins, lipid membranes, mitochondrial DNA and cellular DNA.
The majority of oxidative stress on organelles, cells and bodily organs are bestowed upon them by their own mitochondria. It is part of the process of cellular aging and the mitochondria themselves are particularly susceptible to the damage. They are the body’s primary bioenergetic machinery, and require continuous recycling and regeneration throughout their lifespan.
Further, the effective control of mitochondrial biogenesis and turnover becomes important for maintaining energy levels, preventing endogenous oxidative stress and promoting healthy aging. As mitochondrial and cellular deterioration occur, so does a gradual progressive functional decline. The majority of theories suggest cellular deterioration slowly causes loss of organ function. In addition, the damage of oxidative stress from mitochondria can eventually lead to impaired mitochondrial and cellular DNA, allowing for possible mutations and impaired function of DNA replication.
As changes occur in the cells and the organs over time, old age accumulates, physical function diminishes, and the ability to respond to various stressors diminishes. This can be exacerbated by the onset of a progressive illness associated with aging.
CoQ10 Slows Cellular Aging
Coenzyme Q10 (CoQ10) plays a key role in the mitochondria. As a member of the ubiquinone family, it’s a major fat-soluble antioxidant found in all cell membranes, especially within mitochondrial membranes. It’s one of the cell’s most potent scavengers of free radicals, neutralizing the lipid peroxyl radicals that damage cell membranes, proteins and DNA.
CoQ10 is also an acceptor of electrons for transfer along the electron transport chain; it plays a major role in the generation of ATP energy, and is instrumental in the proton gradient across the mitochondrial membrane that is required to form ATP energy.
Humans and animals synthesize CoQ10 to produce cellular energy and to protect cells from the danger of free radicals. However, humans’ ability to synthesize CoQ10 declines 20 percent every decade of life after the age of 21. The decline leads to deficiency, weakness and fatigue throughout the body. And it is estimated that the average intake of CoQ10 is 3-5 mg per day from normal diet (1) — amounts not nearly enough to return the body to youthful levels.
In addition, pharmaceuticals only worsen age-related low CoQ10 levels and lead to worsened health outcomes. There are 143 known pharmaceuticals that cause decreased serum levels of CoQ10 in patients. These include beta-blockers, antidepressants, antibiotics, chemotherapy, radiation therapy, hormone replacement and, most notably, statin drugs.
Statin therapy, which is used to lower cholesterol for millions in the U.S. and Canada, works by blocking the enzyme HMG-CoA reductase in the liver, which regulates both cholesterol and coenzyme Q10 synthesis (1-3). Although the lower cholesterol levels may reduce risk of atherosclerosis and cardiovascular disease, the added effects are weakened organs such as the heart, muscle weakness, muscle pain, and fatigue from dangerously low CoQ10 levels.
As we age, CoQ10 supplementation is necessary to protect cells from oxidative damage. Lower CoQ10 levels in tissues and cells allows for uncontrolled leakage of electrons from mitochondria, causing damage to nearby lipids, proteins and DNA. Diminished CoQ10 levels also lead to declines in vitamin E, another potent fat-soluble antioxidant, because CoQ10 is the chiefly instrumental (along with selenium) for the regeneration of vitamin E.
As concentrations of CoQ10 and vitamin E diminish, the cell is more susceptible to free radicals (4;5). The concentration of mitochondria is also reduced, affecting cell, tissue and organ function. This is particularly pronounced in organs with normally high levels of CoQ10 such as the heart, brain, liver, and kidneys (4;5). Reduced amounts of CoQ10 also affect muscle energy and performance. The increase in susceptibility to free radicals—from endogenous and exogenous sources—also potentially affects intracellular proteins, lipids and DNA. Supplementation is vital for avoiding damage.
Long-term heart health ultimately requires CoQ10 supplementation. Because of the key role CoQ10 plays in supporting energy levels, maintaining proper levels of CoQ10 in the heart is essential for proper cardiac function. Because CoQ10 is a fat-soluble antioxidant that regenerates vitamin E, healthy levels are also necessary to guard against uncontrolled oxidation of lipoproteins and LDL cholesterol. Supplementation with CoQ10 in a dose-dependent manner supports cellular and mitochondrial integrity as well as an increase in the number of mitochondria in tissues.
The oral intake of CoQ10 can guard against the ill effects produced by age-related reduction of native CoQ10 in the heart, brain and muscle tissues. Supplementation supports health of the heart, kidneys, liver, and brain and helps reduce oxidation on lipids and lipoproteins—including reducing oxidation of LDL cholesterol—and helps keep the body young (6). In addition, CoQ10 supplementation is crucial when using statin drugs for heart health. Clinical dosages of CoQ10 present favorable protection against LDL oxidation and replenish CoQ10 as a vital component for organ function.
CoQ10’s functional support is clearly demonstrated in athletic performance. Studies in animals and humans demonstrate CoQ10’s effects on enhancing performance and guarding against fatigue.
In one randomized, double-blind, crossover study, scientists selected fifteen healthy, sedentary men to take oral CoQ10 or placebo in two 8-week periods and perform repeated bouts of supramaximal exercise. The study found those taking the CoQ10 experienced increased power and reduced fatigue in comparison to those taking placebo (7).
Additionally, a similar study on Finnish cross-country skiers found CoQ10 supplementation improved physical performance and recovery time (8). These studies support the use of the supplement as a valuable aid for performance enhancement.
Enhanced-Absorption Coenzyme Q10
One drawback of CoQ10 is its poor absorption, which has led scientists such as William Judy, Ph.D., to find ways to increase its absorption. He developed a form of CoQ10 for heart health by using a proprietary non-chemical process method that is performed on the coenzyme.
Unlike other CoQ10 products, this form of CoQ10 undergoes an all-natural method with no chemical solvents to enhance absorption, and is lipid stabilized to prevent re-crystallization.
A human clinical study measuring 36-hour peak absorption determined an 8-fold increase in absorption of Dr. Judy’s formula when compared to a dry powder version (most commonly found on the market) in which only 1 percent was absorbed.
The absorption led to a higher amount of CoQ10 in the blood plasma available for use by the body’s cells.
The patent-pending CoQ10 absorption formula is found in Isagenix Ageless Actives™. It’s a product that features 100 mg of CoQ10 and can be expected to restore healthy levels in the body.
Within a few weeks of using Ageless Actives™, people who take it find they notice increased energy levels and the dosage supports cardiovascular health, brain health, kidney health and liver health – apart from muscle and athletic performance.
1. Wang X, Quinn PJ. Vitamin E and its function in membranes. Prog Lipid Res 1999;38:309-36.
2. Galli F, Iuliano L. Do statins cause myopathy by lowering vitamin E levels? Med Hypotheses 2010;74:707-9.
3. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
4. Matthews RT, Yang L, Browne S, Baik M, Beal MF. Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects. Proc Natl Acad Sci U S A 1998;95:8892-7.
5. Dhanasekaran M, Ren J. Curr Neurovasc Res 2005;2:447-59.
6. Schaars CF, Stalenhoef AF. Effects of ubiquinone (coenzyme Q10) on myopathy in statin users. Curr Opin Lipidol 2008;19:553-7.
7. Gokbel H, Gul I, Belviranl M, Okudan N. The effects of coenzyme Q10 supplementation on performance during repeated bouts of supramaximal exercise in sedentary men. J Strength Cond Res 2010;24:97-102.
8. Ylikoski T, Piirainen J, Hanninen O, Penttinen J. The effect of coenzyme Q10 on the exercise performance of cross-country skiers. Mol Aspects Med 1997;18 Suppl:S283-S290.