Control Your Own Mortality Risk

Healthy Life Extension

Funding Aging Research

Control Your Own Mortality Risk


posted on December 6th, 2011

Dear Future Centenarian,

Here™s another wellness insight from Reason at www.FightAging.org:

Large-scale studies of health and longevity demonstrate the degree to which we can choose to shift our own risk of disease and death, and along with it the likely level of necessary medical expenditures in our future.

One longevity-related line item that doesn't come up often enough in discussion is the matter of the expected state of your wallet as you move through life.

Given that you have a fair degree of control over your long-term health, do you also have the same degree of control over the funds needed for future medical treatment?

Reliability theory, a consideration of aging as damage, suggests that the only paths to a longer life are those which reduce or repair the accumulated biological damage that leads to aging. Reliability theory also tells us that this will lead to a lower chance of systems failure”which we might interpret as a lower chance of the need for medical intervention at any given time.

So it makes sense to look at the emerging biotechnologies of enhanced longevity as a way to reduce long term expenditures on medicine, on average, for individuals. One might hope that everyone”and not just those who have nursed an aging car through its last years - understands the difference in maintenance costs for a well-repaired machine versus one that's showing all the signs of accumulated wear and tear.

Damaged machines spiral down into ever more expensive breakdowns, and that's just as true of people as it is of the things people build. Yet much of the public debate over medicine seems to focus on the idea that living longer implies greater medical expenditure, possibly another aspect of the Tithonus Error, the naive belief that living longer though biotechnology means being old for longer rather than being young for longer.

One proven way to extend your health span and lifespan is simply moving more.

For light- to moderate intensity activities of daily living, e.g. housework, gardening, stair climbing, walking and bicycling for transportation, an increase of one hour per week compared to no physical activity was associated with a reduction in mortality of four percent.

Even better, Dr. Samitz said that with moderate-intensity leisure activities (e.g. Nordic walking, hiking, social dance) the risk reduction increased to six percent, and with vigorous-intensity aerobic activity or sports (e.g. jogging, bicycling (>10 miles per hour), tennis, ball sport), the reduction in all-cause mortality was even nine percent per one hour increment per week.

Better yet, meeting the WHO´s recommended level of 150 minutes per week of moderate physical activity of daily life or during leisure was associated with a reduction in mortality risk by ten percent. For vigorous exercise and sports the reduction in mortality risk was more than twofold higher (22 %).

I™m not one for New Year Resolutions. There™s no magic in Januarys. But if you did slip a little during the year, maybe a new beginning makes sense for you, especially if you overdo it during the Holidays (or, under-exercise). After all, a 22% reduction in your mortality risk is not something you want to ignore. And that™s just exercise.

Couple it with good nutrition, and 22% is just your starting point.

On second thought, why wait till the new year? Let™s get a 4 week head start!

Long Life,
David Kekich
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LATEST HEADLINES FROM FIGHT AGING!

THE FOSSIL RECORD AND THE HISTORY OF BEING OLD Friday, December  2, 2011 http://www.fightaging.org/archives/2011/12/the-fossil-record-and-the-history-of-being-old.php
From In Search of Enlightenment: "Looking back over our species' history, as told in fossil records, what do we find? Prehistoric human remains have never revealed individuals older than about 50 years of age, and humans had a life expectancy at birth of 30 years or less for more than 99.9% of the time that we have inhabited this planet. So for most of our species' history there was little progress in terms of increasing life expectancy at birth. But things began to change in the 19th century. Advances in technology (e.g. the sanitation revolution), medical knowledge, material resources and changes in behavior helped change the future course of our species.

The fossil records of the 21st century will be unique in our species' history for two reasons. Firstly, there will be more human remains this century than in any other century (because of the size of the human population). Furthermore, the vast majority of these deaths will be caused by chronic disease and will afflict people after the age of 60. Isn't it odd, given how many people are projected to suffer and die from chronic disease and given the rapid progress that is being made in the biomedical sciences, that we don't invest more of our energies into tackling the leading cause of chronic disease? Namely, aging. When future generations look back at the 21st century they will wonder why we didn't act sooner to try to ameliorate the high risks of morbidity and mortality that currently ravage our bodies and minds."

ANOTHER RAPAMYCIN LIFESPAN STUDY Friday, December  2, 2011 http://www.fightaging.org/archives/2011/12/another-rapamycin-lifespan-study.php
Here is another study showing that rapamycin can extend life in mammals: "The nutrient-sensing TOR (target of rapamycin) pathway is involved in cellular and organismal aging. Rapamycin, an inhibitor of TOR, extends lifespan in yeast, fruit flies and genetically heterogeneous mice. Here, we demonstrate that lifelong administration of rapamycin extends lifespan in female 129/Sv mice characterized by normal mean lifespan of [two years]. Importantly, rapamycin was administrated intermittently (2 weeks per month) starting from the age of [two months].

Rapamycin inhibited age-related weight gain, decreased aging rate, increased lifespan (especially in the last survivors) and delayed spontaneous cancer. 22.9% of rapamycin-treated mice survived the age of death of the last mouse in control group. Thus we demonstrated for the first time in normal inbred mice that lifespan can be extended by rapamycin. This opens an avenue to develop optimal doses and schedules of rapamycin as an anti-aging modality."

THE STATE OF DNA SEQUENCING Thursday, December  1, 2011 http://www.fightaging.org/archives/2011/12/the-state-of-dna-sequencing.php
As a follow up to an earlier post on why DNA sequencing is of interest to those of us who follow longevity science, here is a look at the present state of the sequencing industry: "BGI, based in China, is the world's largest genomics research institute, with 167 DNA sequencers producing the equivalent of 2,000 human genomes a day. BGI churns out so much data that it often cannot transmit its results to clients or collaborators over the Internet or other communications lines because that would take weeks. Instead, it sends computer disks containing the data, via FedEx. ... the ability to determine DNA sequences is starting to outrun the ability of researchers to store, transmit and especially to analyze the data.

Data handling is now the bottleneck. It costs more to analyze a genome than to sequence a genome. That could delay the day when DNA sequencing is routinely used in medicine. In only a year or two, the cost of determining a person's complete DNA blueprint is expected to fall below $1,000. But that long-awaited threshold excludes the cost of making sense of that data, which is becoming a bigger part of the total cost as sequencing costs themselves decline. We believe the field of bioinformatics for genetic analysis will be one of the biggest areas of disruptive innovation in life science tools over the next few years."

PRINTING BONE SCAFFOLDS Wednesday, November 30, 2011 http://www.fightaging.org/archives/2011/11/printing-bone-scaffolds.php
The use of 3D printers is spreading in medical research and development: "researchers have used a 3D printer to create a bone-like material and structure that can be used in orthopedic procedures, dental work, and to deliver medicine for treating osteoporosis. Paired with actual bone, it acts as a scaffold for new bone to grow on and ultimately dissolves with no apparent ill effects. The authors [say] they're already seeing promising results with in vivo tests on rats and rabbits. It's possible that doctors will be able to custom order replacement bone tissue in a few years.

If a doctor has a CT scan of a defect, we can convert it to a CAD file and make the scaffold according to the defect. The material grows out of a four-year interdisciplinary effort involving chemistry, materials science, biology and manufacturing. A main finding of the paper is that the addition of silicon and zinc more than doubled the strength of the main material, calcium phosphate. The researchers also spent a year optimizing a commercially available ProMetal 3D printer designed to make metal objects. The printer works by having an inkjet spray a plastic binder over a bed of powder in layers of 20 microns, about half the width of a human hair. Following a computer's directions, it creates a channeled cylinder the size of a pencil eraser. After just a week in a medium with immature human bone cells, the scaffold was supporting a network of new bone cells."

SENS FOUNDATION ON PLURIPOTENT STEM CELLS AND PARKINSON'S DISEASE Tuesday, November 29, 2011 http://www.fightaging.org/archives/2011/11/sens-foundation-on-pluripotent-stem-cells-and-parkinsons-disease.php
A commentary from the SENS Foundation: "Rejuvenation biotechnology encompasses a suite of advanced medical therapies, each of which removes, repairs, replaces, or renders harmless one of the forms of cellular or molecular damage that accumulates in an aging tissue over time and impairs its function. Through the comprehensive abatement of all such aging damage to levels approximating those of younger adults, tissue structure and function can be made more youthful, restoring the health and vigor of aging persons to that of persons years or decades younger. This approach is most prominently under pursuit in the development of cell therapy and tissue engineering, of which the most striking success to date has been the use of fetal and embryonic mesencephalic tissue grafts to replace dopaminergic (DA) neurons lost to the age-related neurodegenerative processes driving Parkinson's disease (PD).

The promise of this approach has been foreshadowed in murine models of PD, in which DA neurons derived from mouse [embryonic stem cells] have been found highly effective in reversing motor symptoms. But the performance of ostensibly DA neurons derived from human pluripotent stem cells in the same systems has so far been poor, due to uncertain and unstable differentiation of the cells. In a new study, a team of researchers [have] used their novel DA neuron differentiation strategy to resolve these difficulties, leading to robust and stable engraftment of human pluripotent stem cell-derived DA neurons into the striatum and substantial evidence of efficacy in two rodent models of the disease, and provided preliminary data on the viability of their approach in nonhuman primates."

A VIEW OF THE BREADTH OF RESEARCH AIMED AT SLOWING AGING Monday, November 28, 2011 http://www.fightaging.org/archives/2011/11/a-view-of-the-breadth-of-research-aimed-as-slowing-aging.php
The mainstream of aging research is only interested in slowing aging through manipulation of metabolic processes, rather than trying to reverse aging through repair biotechnologies. Here is a look at the breadth of that potential research: "Aging is the major biomedical challenge of this century. The percentage of elderly people, and consequently the incidence of age-related diseases such as heart disease, cancer, and neurodegenerative diseases, is projected to increase considerably in the coming decades. Findings from model organisms have revealed that aging is a surprisingly plastic process that can be manipulated by both genetic and environmental factors.
Here we review a broad range of findings in model organisms, from environmental to genetic manipulations of aging, with a focus on those with underlying gene-environment interactions with potential for drug discovery and development. One well-studied dietary manipulation of aging is caloric restriction, which consists of restricting the food intake of organisms without triggering malnutrition and has been shown to retard aging in model organisms. Caloric restriction is already being used as a paradigm for developing compounds that mimic its life-extension effects and might therefore have therapeutic value.

The potential for further advances in this field is immense; hundreds of genes in several pathways have recently emerged as regulators of aging and caloric restriction in model organisms. Some of these genes, such as IGF1R and FOXO3, have also been associated with human longevity in genetic association studies. The parallel emergence of network approaches offers prospects to develop multitarget drugs and combinatorial therapies. Understanding how the environment modulates aging-related genes may lead to human applications and disease therapies through diet, lifestyle, or pharmacological interventions. Unlocking the capacity to manipulate human aging would result in unprecedented health benefits."

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