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Our Aging Mitochondria

If you enter "mitochondria and aging" into the US Library of Medicine website, you'll find over 351 scientific studies published in 2010.
The consensus among researchers is that mitochondrial dysfunction plays a central role in the development of virtually all age-related diseases.
Go back nearly four decades, however, and very little about mitochondria appeared in medical journals. When Life Extension first introduced methods to enhance mitochondrial function, few physicians understood our rationale.
Today's scientific data make it loud and clear that every aging person should take personal responsibility to ensure optimal mitochondrial function and structure. The good news is that nutrients used by Life Extension members to enhance mitochondrial performance have more scientific substantiation than ever.

While compounds like coenzyme Q10, carnitine, and lipoic acid support mitochondrial function, it is critical that new mitochondria are generated if we are to protect against age-related decline.
Mitochondrial biogenesis is the process of creating new mitochondria within cells. Our mitochondria can be regenerated in response to intense aerobic exercise,calorie restriction, and taking certain medications like metformin.

In 2010, researchers at the University of California at Davis released a peer-reviewed publication showing that a natural compound called PQQ (pyrroloquinoline quinone) promotes the formation of new mitochondria within cells.

For the first time, humans are empowered with a natural agent to reverse the deadly decline in functional mitochondria that underlies degenerative disease and premature aging.


About 95% of cellular energy is produced from structures in the cell called mitochondria. Unlike other cell components, mitochondria are able to divide within healthy cells. Mitochondria are required for cellular energy production. Impaired mitochondrial metabolism is now recognized as an underlying factor of many diseases.

The initial interest in taking nutrients like L-carnitine and CoQ10 was to boost mitochondrial function in heart muscle cells. Overlooked was the large amount of energy required by neurons (brain cells) to carry out their specialized functions. Studies published in 2010 (and earlier) corroborate the role of abnormal mitochondria dynamics with neuronal cell death and the onset of Alzheimer's,Parkinson's, Huntington's, and other neurodegenerative disorders.

If you live to 80 years, there is a 30% chance you will develop Alzheimer's dementia. Scientists have identified specific pathologic mechanisms that reveal the role of mitochondrial dysfunction in the initiation and progression of this hideous disease. These findings resulted in the authors of a 2010 report concluding:
"We suggest that mitochondrial protection and subsequent reduction of oxidative stress are important targets for prevention and long-term treatment of early stages of Alzheimer's disease."


Damage to the mitochondria of endothelial cells is an underlying cause of atherosclerosis.
Traditional risk factors for arterial disease such as smoking, obesity,high blood sugar, high cholesterol and high triglycerides, are all linked to mitochondrial injury. When a person suffers persistent coronary artery blockage, a severe weakening of cardiac muscle can occur that results in congestive heart failure.
A study published in 2010 looked at left ventricular heart muscle tissue in patients with endstage heart failure and normal hearts. Compared to normal hearts, mitochondrial DNA was decreased by 40% in failing hearts. This was accompanied by reductions of 25-80% in mitochondrial DNA-encoded proteins of failing hearts. The doctors who conducted this study concluded:

"Mitochondrial biogenesis is severely impaired as evidenced by reduced mitochondrial DNA replication and depletion of mitochondrial DNA in the human failing heart…suggesting novel mechanisms for mitochondrial dysfunction in heart failure."
Nutrients that enhance mitochondrial function (like coenzyme Q10 and L-carnitine) improve clinical and symptomatic indicators of congestive heart failure. The ability of PQQ to promote mitochondrial biogenesis (formation of healthy new mitochondria) could lead to even greater improvements in cardiac output.


In humans, it takes more than 20 years from exposure to a carcinogen before a solid tumor develops. Research published in 2010 explains the many intimate ways that dysfunctional mitochondria contribute to the development of cancer and its metastasis. Cancer is fundamentally connected to mitochondrial dysfunction. A decline in mitochondrial energy production with aging is associated with the generation of increased free radicals, which cause mitochondrial mutations.
These mutations interfere with a normal cell-removal process known as apoptosis.

A critical factor in protecting against cancer is the ability to eliminate damaged cells through apoptosis. Researchers are focusing on the huge energy-dependent processes required to eradicate faulty or abnormally growing cells. It turns out that dysfunctional mitochondria deny cells the ability to go through normal apoptotic removal processes, thus sowing the seeds for cancer initiation and progression. In addition, mitochondria are the source for several apoptotic proteins that activate cell death in the quest to eliminate damaged cells.

Mitochondrial dysfunction that occurs with aging plays a major influence on carcinogenesis. One recent study shows that mitochondrial dysfunction predicts progression of prostate cancer in patients treated with surgery.
Exciting research findings indicate the potential of reversing mitochondrial senescence in nontumor cells using mitochondrial-targeted antioxidants. The benefit is that restored healthy cells are less susceptible to tumor initiation, while cancer cells that have evolved are better controlled by tumor suppressor genes activated by functional mitochondrial cell-signaling.


Type 2 diabetes is often caused by overeating, but some people lose the ability to control glucose because of hereditary factors Glucose Meter or physical inactivity. A study looked at young, lean, sedentary children with insulin resistance whose parents had developed type 2 diabetes. Compared to similar children of non-diabetic parents, muscle biopsies showed that mitochondrial density was reduced by 38% in the offspring of diabetic parents. This study also showed that these insulin-resistant children exhibited increased amounts of fat content in their muscles, which also contributes to insulin resistance. These findings support the concept that hereditary mitochondrial dysfunction contributes to the development of insulin resistance and subsequent type 2 diabetes.

The encouraging aspect to this study is that those genetically predisposed to type 2 diabetes may be able to avert this calamity through either rigorous physical exercise and/or supplementation with PQQ, both of which have been shown to promote mitochondrial biogenesis. (Note that certain anti-diabetic drugs like metformin and thiazolidinediones also induce mitochondrial biogenesis through additional mechanisms.)


Our bodies possess remarkable ability for sustained tissue renewal throughout our lifetimes. This continuous self-renewal process is dependent on reservoirs of somatic stem cells. A report published in 2010 describes how intact mitochondrial function is crucial for maintenance of stem cells. In response to mitochondrial impairment, there is an increase in damaging free radicals accompanied by stem cell compromise. Researchers have discovered that stem cell populations do not necessarily decline with advancing age, but instead lose their restorative potential.

This functional stem cell decline is accompanied by organ malfunction and increased incidence of disease. Mitochondrial dysfunction thus underlies a degenerative cycle that robs aging humans of the renewal benefits of their own stem cells.
The integration of mitochondria into the core "axis of aging" has led researchers to propose that improvements in mitochondrial health (along with other cellular modulations) could yield advanced therapeutic strategies designed to rejuvenate tissues of the aged.


Altered (glycated) proteins can bind to mitochondria and compromise their function. The accumulation of dysfunctional mitochondria results in a vicious cycle whereby increased oxidative and glycation reactions disable more mitochondria, eventually leading to a cell's demise. The mitochondria in cells of elderly people are mostly dysfunctional, whereas young individuals have virtually no mitochondrial damage. A fascinating report published in 2010 describes the lethal cascade that occurs as inactive mitochondria accumulate in cells and how carnosine, acetyl-L-carnitine, and resveratrol can protect against these longevity-shortening molecular interplays.


The aging of the American society is upon us with an accelerated impact on healthcare expenditures. Conventional medicine can affix band-aids to age-related disease, but fails to correct the major underlying cause of mitochondrial dysfunction and the severe shortage of healthy mitochondria within the cell. A search of scientific articles using the terms "mitochondria and aging" going back to the year 1980 reveals the exponential increase in our understanding of the role this cell organelle plays in sustaining healthy life span.

The list below shows how many published papers discuss "mitochondria and aging" in the early 1980s compared to the last two years:
For 1980 there were 54
For 1981 there were 64
For 1982 there were 58
For 1983 there were 64 (This is when coenzyme Q10 was introduced to Americans)
For 2009 there were 438
For 2010 there were 351 (as of September 2010).

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