Rejuvenate Your Cells Now

Healthy Life Extension

Funding Aging Research

Rejuvenate Your Cells Now

posted on February 14th, 2012

Dear Future Centenarian,

During the course of normal aging, a host of debilitating disorders followed by death are set up by the diminishing number of functional mitochondria. As you may recall, mitochondria are the power plants of every one of your tens of trillions of cells.

Mitochondrial dysfunction is a primary cause of age-related decline. In a revealing study, a team of researchers showed that muscle tissue of a 90-year-old man contained 95% damaged mitochondria compared to almost no damage in that of a 5-year-old.

When you look at the dynamic energy of a child compared to an elderly person, the devastating impact of mitochondrial degradation becomes instantly apparent. Stacks of recent scientific reports link defective and deficient mitochondria to virtually all degenerative diseases including Alzheimer™s, type 2 diabetes, heart failure, and cancer.

Human cells may house anywhere from 2 to 2,500 mitochondria, depending on tissue type, antioxidant status, and other factors. A growing number of biologists theorize that mitochondrial number and function determine human longevityand greater overall health and durability. The problem is that as we age, our mitochondria degrade and become dysfunctional.

Sounds grim, huh?

But in an unprecedented breakthrough, a compound has been discovered that promotes the growth of new mitochondria structures within aging cells by activating genes that stimulate the generation of new mitochondria!

This compound is called PQQ.

Essentially, PQQ helps reverse cellular aging.

As an ultra potent antioxidant, it provides extraordinary defense against mitochondrial decay: PQQ™s chemical structure enables it to withstand exposure to oxidation up to 5,000 times greater than vitamin C. When combined with CoQ10, research shows just 20 mg per day of PQQ can significantly preserve and enhance memory, attention, and cognition in aging humans.

PQQ™s critical biological roles stem from its ability to activate genes directly involved in cellular energy metabolism, development, and function. And  when PQQ is introduced back into the diet, it reverses effects of aging, restoring systemic function while simultaneously increasing mitochondrial number and energy efficiency.

PQQ has been shown to optimize function of the entire central nervous system while reversing cognitive impairment caused by chronic oxidative stress in pre-clinical models.

In humans, supplementation with 20 mg per day of PQQ resulted in improvements on tests of higher cognitive function in a group of middle-aged and elderly people. These effects were significantly amplified when the subjects also took 300 mg per day of CoQ10.

Supplementation with PQQ reduces the size of ischemia-reperfusion damaged areas in animal models of acute heart attack too. This occurs whether the supplement is given before or after the heart attack itself.

How to get your PQQ:

If you are a Life Extension Foundation member, you are probably already taking it. If not, why not?

If you are not a member, how would you like a FREE $75 membership with the privilege of getting a 25% discount on PQQ¦ as well as a 25% discount on every other product? It™s easy to do. Simply click on, make a $100 donation, and get $300 worth of goodies. Larger donations earn you even more.

Or, If you don™t want to donate and want to get your own membership, go to and click on Membership.

When you go to this link, you don™t even need to buy a membership. You can get a FREE one year subscription to Life Extension Magazine. the ultimate source for new health and medical findings from around the world. Each month, Life Extension fills over 100 pages with fully referenced articles on the very latest topics and nutritional supplements that affect our health and wellness, as well as the many steps you can take to help gain better control of your health.

Life Extension Magazine is routinely the first to report new discoveries involving nutrition, hormones and anti-aging supplements. In addition, Life Extension reports innovative findings concerning the diseases that threaten many of us.

I have been a member and subscriber since 1983, and I swear by it.

Long Life,
David Kekich


Research is fundamentally broken by regulation in much of the world. One facet of this problem is that the cost of obtaining approval for new drugs and technologies is so astronomical that large swathes of the research community are directed towards finding marginal new uses for drugs that are already approved by regulators. This activity is, despite occasional successes like the one linked here, always going to be far less productive and useful than tailoring new technologies to the problem at hand. This is one of many ways in which regulation slows progress to a grinding crawl. Because people only pay attention to the occasional successes, they don't see or much care about the many other potential successes that never happened and were never worked on because of the perverse financial incentives put upon the research community by the regulators:

FASTING VERSUS CANCER Thursday, February  9, 2012
As researchers continue to explore calorie restriction, intermittent fasting, and other forms of lowering food intake, then make discoveries like this: "Man may not live by bread alone, but cancer in animals appears less resilient, judging by a study that found chemotherapy drugs work better when combined with cycles of short, severe fasting. Even fasting on its own effectively treated a majority of cancers tested in animals, including cancers from human cells.

For example, multiple cycles of fasting combined with chemotherapy cured 20 percent of mice with a highly aggressive type of children's cancer that had spread throughout the organism and 40 percent of mice with a more limited spread of the same cancer. No mice survived in either case if treated only with chemotherapy. Only a clinical trial lasting several years can demonstrate whether humans would benefit from the same treatment. As with any potential cancer treatment, fasting has its limits. The growth of large tumor masses was reduced by multiple fasting and chemotherapy cycles, but cancer-free survival could not be achieved. [Researchers] speculated that cells inside a large tumor may be protected in some way or that the variety of mutations in a large mass may make it more adaptable. The cell is, in fact, committing cellular suicide. What we're seeing is that the cancer cell tries to compensate for the lack of all these things missing in the blood after fasting. It may be trying to replace them, but it can't. A way to beat cancer cells may not be to try to find drugs that kill them specifically but to confuse them by generating extreme environments, such as fasting that only normal cells can quickly respond to."

SPEEDING UP THE REPAIR OF BROKEN BONE Wednesday, February  8, 2012
News of "fracture putty," an evolution in the use of scaffold material for bone regeneration: recent studies "show promise to significantly shorten the healing time and revolutionize the course of fracture treatment. ... Healing of critical-size defects is a major challenge to the orthopedic research community. Large-bone defects must be stabilized and necessitate technologies that induce rapid bone formation in order to replace the missing tissue and allow the individual to return to rapid function. To date, no single material can suffice. In our experiences with large animal models, following the guidelines established by our animal care and use committee, we have been successful in formulating a product that contains mesenchymal stem cells and allows them to survive in the environment of the fracture long enough to elicit the rapid formation of new bone.  

To start the bone regeneration process, the [researchers] used adult stem cells that produce a protein involved in bone healing and generation. They then incorporated them into a gel, combining the healing properties [into] 'fracture putty.' [The] team used a stabilizing device and inserted putty into fractures in rats. Video of the healed animals at two weeks shows the rats running around and standing on their hind legs with no evidence of injury. [The] researchers are testing the material in pigs and sheep, too. Our approach is biological with the putty. Other groups are looking at polymers and engineering approaches like implants and replacements which may eventually be combined with our approach. We are looking at other applications, too, using this gel, or putty, to improve spinal fusion outcomes."

If you think that telomere length is a secondary marker of aging and health, then it makes perfect sense that exercise would lengthen telomeres. There is ample evidence to show that average telomere length, while declining with age, is somewhat dynamic in response to circumstances, at least in the white blood cells examined by most present day research: "Leukocyte telomere length (LTL) is a potential indicator of cellular aging; however, its relation to physical activity and sedentary behavior is unclear. The authors examined cross-sectionally associations among activity, sedentary behavior, and LTL among 7,813 women aged 43-70 years in the Nurses' Health Study.

Participants self-reported activity by questionnaire in 1988 and 1992 and sedentary behavior in 1992. Telomere length in peripheral blood leukocytes, collected in 1989-1990, was measured by quantitative polymerase chain reaction. For total activity, moderately or highly active women had a 0.07-standard deviation (SD) increase in LTL compared with those least active. Greater moderate- or vigorous-intensity activity was also associated with increased LTL. Associations remained after adjustment for body mass index. Although associations were modest, these findings suggest that even moderate amounts of activity may be associated with longer telomeres, warranting further investigation in large prospective studies."

As you might imagine, exercise affects the behavior of muscle stem cells: "researchers determined that an adult stem cell present in muscle is responsive to exercise, a discovery that may provide a link between exercise and muscle health. The findings could lead to new therapeutic techniques using these cells to rehabilitate injured muscle and prevent or restore muscle loss with age. Mesenchymal stem cells (MSCs) in skeletal muscle have been known to be important for muscle repair. Since exercise can induce some injury as part of the remodeling process following mechanical strain, we wondered if MSC accumulation was a natural response to exercise and whether these cells contributed to the beneficial regeneration and growth process that occurs post-exercise.

The researchers found that MSCs in muscle are very responsive to mechanical strain. They witnessed MSC accumulation in muscle of mice after vigorous exercise. Then, they determined that although MSCs don't directly contribute to building new muscle fibers, they release growth factors that spur other cells in muscle to fuse and generate new muscle, providing the cellular basis for enhanced muscle health following exercise. Next, the group hopes to determine whether these cells contribute to the decline in muscle mass over a person's lifetime. Preliminary data suggest MSCs become deficient in muscle with age. The team hopes to develop a combinatorial therapy that utilizes molecular and stem-cell-based strategies to prevent age-related muscle loss."

Osteoporosis is a pervasive issue in the old, and potential methods for reversing its effects are welcome: scientists have "developed a novel technique to enhance bone growth by using a molecule which, when injected into the bloodstream, directs the body's stem cells to travel to the surface of bones. Once these cells are guided to the bone surface by this molecule, the stem cells differentiate into bone-forming cells and synthesize proteins to enhance bone growth. There are many stem cells, even in elderly people, but they do not readily migrate to bone. Finding a molecule that attaches to stem cells and guides them to the targets we need is a real breakthrough.

The researchers made use of a unique hybrid molecule, LLP2A-alendronate. The researchers' hybrid molecule consists of two parts: the LLP2A part that attaches to mesenchymal stem cells in the bone marrow, and a second part that consists of the bone-homing drug alendronate. After the hybrid molecule was injected into the bloodstream, it picked up mesenchymal stem cells in the bone marrow and directed those cells to the surfaces of bone, where the stem cells carried out their natural bone-formation and repair functions. Twelve weeks after the hybrid molecule was injected into mice, bone mass in the femur (thigh bone) and vertebrae (in the spine) increased and bone strength improved compared to control mice who did not receive the hybrid molecule. Treated mice that were normally of an age when bone loss would occur also had improved bone formation, as did those that were models for menopause." This is an example of the future of stem cell medicine - more about directing and altering stem cells in the body to create in-situ effects than providing new cells or growing tissue for transplant.

Back to Top