Studies Prove Exercisers Live Longer

Healthy Life Extension

Funding Aging Research

Studies Prove Exercisers Live Longer

posted on September 27, 2011

Dear Future Centenarian,

A large study at the National Health Research Institutes in Zhunan, Taiwan published in The Lancet found that as little as 15 minutes of physical activity a day can reduce the risk of dying by 14% and increase lifespan by three years.

More exercise led to greater life gains. Every additional 15 minutes of daily exercise further reduced all-cause death rates by 4%. This trend continued until a person was exercising for 100 minutes a day.

High intensity exercise though, is the gold standard for fitness¦ and longevity. It was recently endorsed by the European Society of Cardiology. A study conducted among cyclists in Copenhagen, Denmark showed it™s the relative intensity, and not the duration of cycling, which is most important in relation to all-cause mortality. It™s even more pronounced for coronary heart disease mortality. The study concluded that men with fast intensity cycling survived 5.3 years longer, and men with average intensity 2.9 years longer than men with slow cycling intensity. For women, the figures were 3.9 and 2.2 years longer, respectively.

Exercise reduces disease and death dramatically for all major progressive diseases. According to a study involving over 13,000 participants cited by Ray Kurzweil in The Future of Aging, the overall death rate for moderate exercisers was 60% less than the sedentary group”and the high fitness group scored much better. Yet some 70% of Americans do not participate in any type of physical activity.

As Dona Folk, my close friend and breast cancer survivor will tell you, exercise can also treat serious diseases such as cancer. A new report issued by Macmillan Cancer Support argues that exercise should be part of standard cancer care. It recommends all patients getting cancer treatment should engage in moderate-intensity exercise for two and a half hours every week.

A previous Harvard Medical School study found that breast cancer patients who exercise moderately for three to five hours a week cut their odds of dying from cancer by about half. In fact, any amount of weekly exercise increased a patient's odds of surviving breast cancer. This benefit also remained constant regardless of whether women were diagnosed early on or after their cancer had spread. Finally, research has found that exercise reduces the risk of breast cancer recurrence by about 40 percent.

Research has also shown that exercise can reduce your risk of dying from prostate cancer by up to 30 percent.

If you have cancer or any other chronic disease, tailor your exercise routine to your individual scenario, taking into account your stamina and current health. Always listen to your body, and if you feel you need a break, take time to rest. But even exercising for just a few minutes a day is better than not exercising at all.

Exercise is critical to help dodge or reduce diabetes as well as most other diseases. According to the American Diabetes Association, exercising moderately for only thirty minutes a day coupled with a 5“10% reduction in body weight resulted in an astonishing 58% reduction in diabetes. They also report that 90% of all people with diabetes are overweight.

Any exercise that gets the heart pumping may even reduce the risk of dementia and slow the condition's progression once it starts, reported a Mayo Clinic study published in the September 2011 issue of Mayo Clinic Proceedings.

Long Life,
David Kekich


Via ScienceDaily: researchers "have identified more than 70 genes that play a role in regenerating nerves after injury, providing biomedical researchers with a valuable set of genetic leads for use in developing therapies to repair spinal cord injuries and other common kinds of nerve damage such as stroke. The scientists detail their discoveries after an exhaustive two-year investigation of 654 genes suspected to be involved in regulating the growth of axons - the thread-like extensions of nerve cells that transmit electrical impulses to other nerve cells.

We don't know much about how axons re-grow after they're damaged. When you have an injury to your spinal cord or you have a stroke you cause a lot of damage to your axons. And in your brain or spinal cord, regeneration is very inefficient. That's why spinal cord injuries are basically untreatable. While scientists in recent decades have gained a good understanding of how nerve cells, or neurons, develop their connections in the developing embryo, much less is known about how adult animals and humans repair - or fail to repair - those connections when axons are damaged. Of particular interest [are] the six genes that appear to repress the growth of axons. The discovery of these inhibitors is probably the most exciting finding [because] identifying and eliminating the inhibiting factors to the re-growth of axons could be just as essential as the biochemical pathways that promote axon re-growth in repairing spinal cord injuries and other kinds of nerve damage."

From In the Pipeline: "I'd say that the whole sirtuin story has split into two huge arguments: (1) arguments about the sirtuin genes and enzymes themselves, and (2) arguments about the compounds used to investigate them, starting with resveratrol and going through the various sirtuin activators reported by Sirtris, both before and after their (costly) acquisition by GlaxoSmithKline. That division gets a bit blurry, since it's often those compounds that have been used to try to unravel the roles of the sirtuin enzymes, but there are ways to separate the controversies. I've followed the twists and turns of argument #2, and it has had plenty of those. It's not safe to summarize, but if I had to, I'd say that the closest thing to a current consensus is that (1) resveratrol is a completely unsuitable molecule as an example of a clean sirtuin activator, (2) the earlier literature on sirtuin activation assays is now superseded, because of some fundamental problems with the assay techniques, and (3) agreement has not been reached on what compounds are suitable sirtuin activators, and what their effects are in vivo.

It's a mess, in other words. But what about argument #1, the more fundamental one about what sirtuins are in the first place? That's what these latest results address, and boy, do they ever not clear things up. There has been persistent talk in the field that the original model-organism life extension effects were difficult to reproduce, and now two groups (those of David Gems and Linda Partridge) at University College, London (whose labs I most likely walked past last week) have re-examined these. They find, on close inspection, that they cannot reproduce them. It's important to keep in mind that these aren't the first results of this kind. Others had reported problems with sirtuin effects on lifespan (or sirtuin ties to caloric restriction effects) in yeast, and as mentioned, this had been the stuff of talk in the field for some time. But now it's all out on the table, a direct challenge."

One possible form of future immune therapy involves growing vast numbers of tailored immune cells, far more than would ever naturally be present in the body, and then infusing them to sweep away the target problem - cancer being an early target for this sort of approach. Here is some groundwork for these future therapies: "Adult stem cells from mice converted to antigen-specific T cells - the immune cells that fight cancer tumor cells - show promise in cancer immunotherapy and may lead to a simpler, more efficient way to use the body's immune system to fight cancer.

Tumors grow because patients lack the kind of antigen-specific T cells needed to kill the cancer. An approach called adoptive T cell immunotherapy generates the T cells outside the body, which are then used inside the body to target cancer cells. It is complex and expensive to expand T cell lines in the lab, so researchers have been searching for ways to simplify the process. [They] found a way to use induced pluripotent stem (iPS) cells, which are adult cells that are genetically changed to be stem cells. Any cell can become a stem cell. It's a very good approach to generating the antigen-specific T cells and creates an unlimited source of cells for adoptive immunotherapy. By inserting DNA, researchers change the mouse iPS cells into immune cells and inject them into mice with tumors. After 50 days, 100 percent of the mice in the study were still alive, compared to 55 percent of control mice, which received tumor-reactive immune cells isolated from donors."

A possible road to rejuvenating some portions of the declining mechanisms of tissue regeneration in the old: "The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases. We demonstrated that we were able to reverse the process of aging for human adult stem cells by intervening with the activity of non-protein coding RNAs originated from genomic regions once dismissed as non-functional 'genomic junk'.

Adult stem cells undergo age-related damage. And when this happens, the body can't replace damaged tissue as well as it once could, leading to a host of diseases and conditions. The team began by hypothesizing that DNA damage in the genome of adult stem cells would look very different from age-related damage occurring in regular body cells. They compared freshly isolated human adult stem cells from young individuals, which can self-renew, to cells from the same individuals that were subjected to prolonged passaging in culture. This accelerated model of adult stem cell aging exhausts the regenerative capacity of the adult stem cells. Researchers looked at the changes in genomic sites that accumulate DNA damage in both groups. ... We found the majority of DNA damage and associated chromatin changes that occurred with adult stem cell aging were due to parts of the genome known as retrotransposons. By suppressing the accumulation of toxic transcripts from retrotransposons, we were able to reverse the process of human adult stem cell aging in culture." The next step would be to look at this process in old animals, and see what happens when it is reversed.

Yet another benefit of regular exercise: "Researchers have long known that regular exercise increases the number of organelles called mitochondria in muscle cells. Since mitochondria are responsible for generating energy, this numerical boost is thought to underlie many of the positive physical effects of exercise, such as increased strength or endurance. Exercise also has a number of positive mental effects, such as relieving depression and improving memory. However, the mechanism behind these mental effects has been unclear. In a new study in mice, [researchers] have discovered that regular exercise also increases mitochondrial numbers in brain cells, a potential cause for exercise's beneficial mental effects.

The researchers assigned mice to either an exercise group, which ran on an inclined treadmill six days a week for an hour, or to a sedentary group, which was exposed to the same sounds and handling as the exercise group but remained in their cages during the exercise period. Confirming previous studies, the results showed that mice in the exercise group had increased mitochondria in their muscle tissue compared to mice in the sedentary group. However, the researchers also found that the exercising mice also showed several positive markers of mitochondria increase in the brain. The study authors note that this increase in brain mitochondria may play a role in boosting exercise endurance by making the brain more resistant to fatigue, which can affect physical performance. They also suggest that this boost in brain mitochondria could have clinical implications for mental disorders, making exercise a potential treatment for psychiatric disorders, genetic disorders, and neurodegenerative diseases."

NEURONS FROM BONE MARROW Tuesday, September 20, 2011
Via EurekAlert!: "The ability to produce neuroprotectors, proteins that protect the human brain against neurodegenerative disorders such as Parkinson's and ALS, is the holy grail of brain research. A technology developed at Tel Aviv University does just that, and it's now out of the lab and in hospitals to begin clinical trials with patients suffering from amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease. The technology is now a patent-pending process that takes stem cells from a patient's own bone marrow and causes them to differentiate into astrocyte-like cells, which are responsible for the well-being of the brain's neurons.

The cells release neurotrophic factors, or neuroprotectants, which have been shown to play a key role in reducing the progress of ALS, a debilitating disease characterized by the progressive degeneration of motor neurons, resulting in paralysis of a patient's limbs and organ function. In the mouse model, we were able to show that the bone marrow derived stem cells prevent degeneration in the brain following injection of selective neurotoxins. Researchers also demonstrated that transplantation of these cells increased the survival rate in the mouse model of ALS and significantly delayed the progress of motor dysfunction. The technology was licensed to BrainStorm Cell Therapeutics that has developed it into a clinical grade product called NurOwn, which is now being used in a clinical trial at Jerusalem's Hadassah Medical Center. BrainStorm Cell Therapeutics has recently struck an agreement to expand clinical trials to Massachusetts General Hospital in collaboration with the University of Massachusetts Medical School."

Another study that points to the value of regular exercise: "Low aerobic exercise capacity is a powerful predictor of premature morbidity and mortality for healthy adults as well as those with cardiovascular disease. For aged populations, poor performance on treadmill or extended walking tests indicates closer proximity to future health declines. Together, these findings suggest a fundamental connection between aerobic capacity and longevity. Through artificial selective breeding, we developed an animal model system to prospectively test the association between aerobic exercise capacity and survivability (aerobic hypothesis).

Laboratory rats of widely diverse genetic backgrounds [were] selectively bred for low or high intrinsic (inborn) treadmill running capacity. Cohorts of male and female rats from generations 14, 15, and 17 of selection were followed for survivability and assessed for age-related declines in cardiovascular fitness including maximal oxygen uptake (VO(2max)), myocardial function, endurance performance, and change in body mass. Median lifespan for low exercise capacity rats was 28% to 45% shorter than high capacity rats. VO(2max), measured across adulthood was a reliable predictor of lifespan. During progression from adult to old age, left ventricular myocardial and cardiomyocyte morphology, contractility, and intracellular Ca(2+) handling in both systole and diastole, as well as mean blood pressure, were more compromised in rats bred for low aerobic capacity. Physical activity levels, energy expenditure (Vo(2)), and lean body mass were all better sustained with age in rats bred for high aerobic capacity."


Researchers establish a link between calorie restriction, aging, and telomere length in yeast, but one which poses more questions than it answers: "Dietary restriction promotes longevity in many species, ranging from yeast to primates, and delays aging-related pathologies including cancer in rodent models. There is considerable interest in understanding how nutrient limitation mediates these beneficial effects. Much of what we have learned about the genetics of aging comes from studying isogenic model organisms, where the effects of single gene changes can be examined independently of other genetic alterations. In order to explore a broader spectrum of genetic variation and to gain insight into aging-related phenotypes as polygenic traits, we analyzed the chronological lifespan of 122 S. cerevisiae strains derived from a cross between laboratory and vineyard yeast strains. The major genetic locus controlling chronological lifespan was found to be identical to a previously mapped locus that controls telomere length. Identification of the responsible polymorphism in BUL2, a gene involved in controlling amino acid permeases, allowed us to establish a previously unrecognized link among cellular amino acid intake, chronological aging, and telomere maintenance. While human epidemiological studies have linked shortened telomeres with increased mortality, it is unclear how these processes are connected. Our results suggest that, in yeast, reduced amino acid uptake and consequent reduced nutrient signaling extend chronological lifespan but reduce telomere length."

Back to Top