Healthy Life Extension

Best Time for Fitness

posted on April 05, 2011

Don’t you just love results?

At what time in your life is fitness most important?

Today.

And it will be even more important tomorrow if health and longevity are your goals.

We get away with a lot when we are young. Our bodies are very forgiving. But as we age, if we want to avoid sickness, disease, immobility and dependence, fitness becomes increasingly important. Paradoxically, most of us exercise more, much more, when we are young. It’s a little easier, we have more time, and lots of it comes with play.

A recent article in USA Today by Janice Lloyd tells us that after 65, we should stay fit to stay healthier. But that applies to the after 45’s and 55’s as well.

 

Ms. Lloyd cautions Baby Boomers to think again if they're longing for a sedentary old age.

She reports that “health experts at the annual meeting of the Gerontological Society of America shed new light on exercise's value as a strong tool in combating diseases often associated with aging.”

"How you live after age 65 is vitally important," says Laura Carstensen, director of the Stanford Center on Longevity. "Up until then, a healthy life is dominated by your genes. After that, it's predominantly about lifestyle. Exercise and nutrition become more important."

Alzheimer's and cardiovascular disease, sarcopenia, osteoporosis, obesity, arthritis, and certain cancers appear more often in later life. To help fight dementia, play memory games if you want, but it might be better to "invest in a good pair of walking shoes," says Peggye Dilworth-Anderson, the gerontology society's president and a board member of the national Alzheimer's Association. That thinking is consistent with a study reported by University of Pittsburgh researchers in October showing older adults who walk 6 to 9 miles a week have a lower risk for cognitive decline later.

One session at the meeting attempted to show how physical activity can restore muscular strength in the elderly. The current genome study by Simon Melov of Buck Institute for Age Research in Novato, Calif., compares the genes of a young person whose leg is immobilized for two weeks in a brace with the genes of an older person who suffers from sarcopenia, a muscle-wasting disease affecting old people. Both age groups responded successfully to exercise and made improvements. But no one has to run a marathon to regain strength. Walking down a hospital wing can jump-start improvement, according to LaDora Thompson of the University of Minnesota's department of physical medicine and rehabilitation.

She studied how physical therapy can reverse the damage of inactivity. Even standing and walking improve muscle strength.

Cancer patients have traditionally been advised to back off exercise and let their bodies rest and recover, but health experts here discussed new research that shows the benefits of exercise for people undergoing treatments.

One reason for all this emphasis on physical activity is the USA's rapidly aging population. Life expectancy has soared to 79.9 years. Boomers currently have a 50% chance of being alive at 85. "Our job is to make use of the added years," says Carstensen. "It would be immoral to receive this gift and squander it."

Report-after-report, study-after-study, confirm these findings. What they don’t mention, and what almost everyone overlooks, is the overriding reason to stay fit. It could be your key to superlongevity and maybe even open-ended, disease-free youthfulness.

The reason most overlook this is they take a linear approach to the future. They assume the future will simply be an extension of the past. So they project incremental gains in lifespan, and they never consider emerging rejuvenation technologies which will translate to age-reversal. They don’t take into account the fact that progress is growing exponentially and is leading to limitless growth.

One way to get moving is to join a boot camp fitness class. If you live in southern california there is a great manhattan beach boot camp, redondo beach boot camp, and hermosa beach boot camp

But you know better, and that’s why you’re going to hit the gym first thing tomorrow morning, isn’t it?

Long Life,
David Kekich
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LATEST HEADLINES FROM FIGHT AGING!

THIOFLAVIN T EXTENDS LIFE IN NEMATODE WORMS Thursday, March 31, 2011 http://www.fightaging.org/archives/2011/03/thioflavin-t-extends-life-in-nematode-worms.php
Another hit in the search for compounds that extend life in lower animals: "Basic Yellow 1, a dye used in neuroscience laboratories around the world to detect damaged protein in Alzheimer's disease - [also] known as Thioflavin T, (ThT) - extended lifespan in healthy nematode worms by more than 50 percent and slowed the disease process in worms bred to mimic aspects of Alzheimer's. The research, conducted at the Buck Institute for Research on Aging, could open new ways to intervene in aging and age-related disease. The study highlights a process called protein homeostasis - the ability of an organism to maintain the proper structure and balance of its proteins, which are the building blocks of life. Genetic studies have long indicated that protein homeostasis is a major contributor to longevity in complex animals. Many degenerative diseases have been linked to a breakdown in the process.

This study points to the use of compounds to support protein homeostasis, something that ThT, did as the worms aged. ThT works as a marker of neurodegenerative diseases because it binds amyloid plaques - the toxic aggregated protein fragments associated with Alzheimer's. In the nematodes ThT's ability to not only bind, but also slow the clumping of toxic protein fragments, may be key to the compound's ability to extend lifespan. We have been looking for compounds that slow aging for more than ten years and ThT is the best we have seen so far. But more exciting is the discovery that ThT so dramatically improves nematode models of disease-related pathology as well. ThT allows us to manipulate the aging process, it has the potential to be active in multiple disease states and it enhances the animal's innate ability to deal with changes in its proteins."

H+ MAGAZINE ON TELOMERES AND TELOMERASE Wednesday, March 30, 2011 http://www.fightaging.org/archives/2011/03/h-magazine-on-telomeres-and-telomerase.php
An introductory article at h+ Magazine looks at the role of telomeres and telomerase in aging: "Several thousand studies have been published on telomeres and telomerase, which are now known to maintain genomic stability, prevent the inappropriate activation of DNA damage pathways, partially determine disease susceptibility/resistance and regulate cellular and organism-wide viability and aging. Telomerase expression [in conjunction with other genetic alterations] also extends the lifespan and reverses senescence-associated pathologies in mice.

In humans telomere length and integrity plays a role in some diseases, disease susceptibility, aging and even in mediating the deleterious effects of long-term psychological stress. Several human genetic diseases are caused by alterations in telomerase function. For example, individuals with dyskeratosis congenita (DC). Many aspects of DC resemble normal aging, although at an accelerated rate. Individuals with DC are born with unusually short telomeres and not surprisingly, the expression of unmutated telomerase in DC cells corrects many of their molecular defects and lengthens their telomeres. Normal cellular telomerase expression is insufficient to prevent telomere shortening with each cell division and hence, telomeres shorten with aging, eventually causing age-related changes. The process is complex, and different cell types and organs show different rates of telomere shortening, although overall telomere shorten most rapidly in growing cell populations. Interestingly, high telomere stability correlates with human longevity while caloric restriction (the only known intervention that increases the [maximum] mammalian lifespan), reduces the rate of telomere shortening, although it does not increase telomerase expression. Last, malignant tumors overexpress telomerase, allowing them to grow indefinitely. One reason why most normal cells of the human body do not express high levels of telomerase might be to prevent cancer."

A BACTERIAL APPROACH TO TARGETED THERAPIES Wednesday, March 30, 2011 http://www.fightaging.org/archives/2011/03/a-bacterial-approach-to-targeted-therapies.php
One approach to developing targeted therapies is to co-opt existing biological structures, such as cells and bacteria: "Scientists have developed bacteria that serve as mobile pharmaceutical factories, both producing disease-fighting substances and delivering the potentially life-saving cargo to diseased areas of the body. [Researchers] chose the term 'bacterial dirigibles' because the modified bacteria actually have the fat-cigar look of blimps and zeppelins, those famous airships of yesteryear. We're building a platform that could allow bacterial dirigibles to be the next-generation disease fighters.  Traditional genetic engineering reprograms bacteria so that they produce antibiotics, insulin, and other medicines and materials. The bacteria grow in nutrient solutions in enormous stainless steel vats in factories. They release antibiotics or insulin into vats, and technicians harvest the medicine for processing and eventual use in people.

The bacterial dirigible approach takes bioengineering a step further. Scientists genetically modify bacteria to produce a medicine or another disease-fighting substance. Then, however, they give the bacteria a biochemical delivery address, which is the locale of the disease. Swallowed or injected into the body, the bacteria travel to the diseased tissue and start producing substances to fight the disease. We have created a genetic circuit that endows E. coli with targeting, sensing and switching capabilities. The 'targeting' molecule is attached to the outer surface of the bacteria. It gives the bacteria an ability to 'hone in' on specific cells and attach to them - in this instance, the intestinal cells where other strains of E. coli cause food poisoning symptoms. Inside the bacteria is a gene segment that acts as 'nanofactory.' It uses the bacteria's natural cellular machinery to make drugs, such as those that can fight bacterial infections, viruses, and cancer. The nanofactory also could produce signaling molecules that enable the dirigible to communicate with natural bacteria at the site of an infection. Some bacteria engage in a biochemical chit-chat, termed 'quorum sensing,' in which they coordinate the activities needed to establish an infection. Bacteria dirigibles could produce their own signaling molecules that disrupt quorum sensing."

THE PROSPECT OF IMPLANTED METABOLIC MONITORS Tuesday, March 29, 2011 http://www.fightaging.org/archives/2011/03/the-prospect-of-implanted-metabolic-monitors.php
Optimizing health, measuring progression of age-related change in metabolism, and detecting disease are far more challenging today than they will be in the future. We can envisage sophisticated implanted devices that cheaply and continuously measure aspects of our biology that are presently expensive to test - and the first steps in the development of such implanted monitors are already underway. "Michael Cima and his team developed an implantable sensor that uses antibodies attached to nanoparticles to detect cancer related biomarkers. In 2009 Cima showed that he could implant these devices into human tumors in mice and then 'read' the cancer growth using MRI. No biopsies needed.

Over the past few years, Cima and his team have adapted their work to create a very similar device that measures biomarkers related to heart damage. This work is very exciting, but still very early in development. As we've said many times before, successes with mice experiments and successes with human experiments can be miles apart. The 5mm cylindrical cancer implant and the 8mm heart monitoring disk both need more time to be perfected. The antibodies used to detect biomarkers have a limited lifetime in the body. Currently an implant probably wouldn't last much longer than two months. If MIT continues to see good results with these early prototypes, there's a good chance we'll see similar devices in clinical trials in the near future. Cima thinks that such experiments could be as little as five years away. The lowest hanging fruit are implants that could monitor for pH levels - acidity is often a hallmark of cancer cells. After that, we may see versions that can accurately detect hormone levels and drug responses."

MORE ON GERM CELLS AND FATTY ACID METABOLISM Tuesday, March 29, 2011 http://www.fightaging.org/archives/2011/03/more-on-germ-cells-and-fatty-acid-metabolism.php
A very readable editorial on recent research into the connection between germ cells and longevity: " For reasons still unknown, a roundworm without its germ cells lives 60% longer than one with those cells intact. And you don't even need to actually remove them - mutations that impair their proliferation also extend life. The authors began their exploration by searching for nuclear receptors that were required for the life-extension effect, reasoning that one or more such receptors were likely to play a key role in controlling longevity pathways. Using RNAi in long-lived worms with a known germline proliferation mutation, they shut down hundreds of receptors, looking for those that would reverse the lifespan extension. They found only one, called nhr-80, which they showed acted specifically within the germline-mediated longevity pathway, and not any of the several other pathways known to extend lifespan. This result provided the first experimental evidence that lifespan extension through ablation of the germline can occur in the absence of insulin signaling, one of the best characterized pathways affecting lifespan.

Mutation of nhr-80 to prevent expression of the gene prevented the longevity effect, while overexpression increased it, in both cases only when germline cells were absent. As a transcription factor, NHR-80 regulates gene expression. Its known targets include a group of enzymes involved in lipid metabolism called desaturases. Desaturases convert saturated fatty acids, such as stearic acid, into unsaturated fatty acids, such as oleic acid, a conversion that significantly alters the physical and biological properties of the fats made from them. The authors show that genes for several desaturases are highly expressed in long-lived germline mutants. While worms are not humans, we share many of the same cellular mechanisms, and it is possible the same life-extending effects of this germline-loss/fatty acid increase pathway will be found in us."

CALORIE RESTRICTION IN PRIMATES Monday, March 28, 2011 http://www.fightaging.org/archives/2011/03/calorie-restriction-in-primates-1.php
Long running studies of calorie restriction in primates remain promising: "In the 75 years since the seminal observation of Clive McCay that restriction of calorie intake extends the lifespan of rats, a great deal has been learned about the effects of calorie restriction (CR; reduced intake of a nutritious diet) on aging in various short-lived animal models. Studies have demonstrated many beneficial effects of CR on health, the rate of aging, and longevity. Two prospective investigations of the effects of CR on long-lived nonhuman primate (NHP) species began nearly 25 years ago and are still under way. This review presents the design, methods, and main findings of these and other important contributing studies, which have generally revealed beneficial effects of CR on physiological function and the retardation of disease consistent with studies in other species.

Specifically, prolonged CR appears to extend the lifespan of rhesus monkeys, which exhibited lower body fat; slower rate of muscle loss with age; lower incidence of neoplasia, cardiovascular disease, type 2 diabetes mellitus, and endometriosis; improved insulin sensitivity and glucose tolerance; and no apparent adverse effect on bone health, as well as a reduction in total energy expenditure. In addition, there are no reports of deleterious effects of CR on reproductive endpoints, and brain morphology is preserved by CR. More research is needed to delineate the mechanisms of the desirable outcomes of CR and to develop interventions that can produce similar beneficial outcomes for humans. This research offers tremendous potential for producing novel insights into aging and risk of disease."

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