Longevity News Digest
One Simple Change = 17 More Quality Years
Dear Future Centenarian,Â
Calorie restriction (CR) still proves to be the ONLY way to extend maximum life span in mammals. Much more so in shorter lived smaller mammals (up to 30% or more).
If it could do the same for humans, the food industry landscape would change dramatically. But it doesn™t. We might be able to squeeze out a few extra years at best.
But again, that™s maximum life span. CR does sooo much more. It™s the most sure fire way to totally AVOID, and at least delay virtually every single aging-related disease on the planet.
So it won™t extend human™s maximum life spans from 120 to 150, but it will significantly extend average life spans. In fact, a reasonable estimate is 10-15 years.
And it gets even better. Not only will you probably live a lot longer, but you will live BETTER. Without CR, we may expect to live to around late 70™s on average. The bad part about that is, most can expect to suffer for over seven years, lingering, waiting for death to relieve the agony.
But those who practice CR can expect about 90 active independent years, and then die relatively quickly and comfortably. Adding it up, look for over 17 more QUALITY years.
You still die though¦ unless¦ we see likely breakthrough radical life-extending technologies during the extra years you bought.
Then the lid is off, and you may be on the path to full body rejuvenation.
CR is a tough lifestyle for almost everyone though, in spite of the life or death benefits.
So what do we do? Eat comfort foods? And a lot of them? We could, and most do, in spite of the long term consequences.
Fortunately. There™s a middle ground that could give you most, if not all the benefits of CR that is much easier to adopt. It does take committing to a consistent habit, but is there anything worth having that doesn™t? Don™t think about that. I™ll answer it for you.
Plan B is regular intermittent fasting (IF) such as alternate day fasting, doing one or two 24 hour fasts a week¦ or eating every day, but spacing your last meal of the day and your first meal of the next about 17 hours apart.
All three variations may work as well as CR, assuming your food is nutritious and you consume less calories overall. (This may also be the most effective weight loss strategy on the planet)
The latest research looks at the relationship between fasting and immune function, which turns out to interest the cancer research community, among others.
Ways to better recover from treatments like chemotherapy that greatly weaken the immune system are high on the priority list. There is already a fair amount of work underway on generating better outcomes for cancer patients by combining CR with chemotherapy. So it shouldn't be surprising to find that there is funding for work on IF as well.
Prolonged fasting cycles (no food for two to four days at a time over the course of six months) kill older and damaged immune cells and generate new ones. The research also has implications for chemotherapy tolerance and for those with a wide range of immune system deficiencies, including autoimmunity disorders.
This may be effective because fasting triggers stem cell regeneration of damaged aging immune systems.
Some research info is at:
Latest Headlines from Fight Aging!
Towards Intestinal Tissue Engineering - Monday, October 20, 2014
Researchers are making progress towards a methodology for growing intestinal tissues from a patient's cells.
As is usually the case in this sort of work, the first results are not intended for use in therapies, but will instead provide raw materials that can help to speed further research.
Calico Undertaking Neural Plasticity Drug Research - Monday, October 20, 2014
Probably indicative of the Calico Labs strategy for the foreseeable future, here is a piece of news from last month that I missed at the time.
The initiative will be taking over funding of an established drug development program aimed at increasing neural plasticity, trying to find ways to spur the brain to generate more new neurons to compensate for damage. Like much of what goes on in modern medical research for age-related conditions, this is a compensatory approach, addressing proximate rather than root causes of degeneration.
For many conditions, this may be useful and possibly even sufficient - Parkinson's disease, for example, affects a mechanical part of the brain that has little to do with the structure of the mind, and the cells there could in theory be replaced wholesale over and again as needed.
Generally, however, we want a research community that works to repair and prevent the root causes of aging, rather than one focused on trying to patch up late stage age-related damage after the fact, or worse, trying to alter the operation of metabolism to make it run slightly better when damaged.
If the Calico Labs leadership intend to build an establishment rapidly over the next few years by adopting promising research programs, then the less optimal paths are largely what they'll be funding, however.
NT3 and Regeneration from Noise-Induced Deafness - Tuesday, October 21, 2014
Deafness due to noise exposure is apparently due in part to destruction of specific forms of synapses linking hair cells and nerve cells. Researchers are here manipulating cells in search of ways to boost the regrowth of these synapses.
Using Olfactory Bulb Cells to Treat Spinal Injury - Tuesday, October 21, 2014
Here is recent news of an approach to spinal injury that has produced benefits in one patient. It is worth tempering optimism until larger trials are attempted, however, as nerve regeneration has proven to be highly variable between individuals. The published paper on the results is open access, but very slow to load at the moment.
Physical Exercise is Protective of Brain Function, but Some of the Effects Decline in Old Age - Wednesday, October 22, 2014
There is plenty of evidence to link regular exercise with specific aspects of better health, such as measures of functionality in the brain and cardiovascular system.
Here, however, researchers produce data to suggest that some of the protective effects of exercise decline in later old age. This may well be the case, but it is worth noting that this is a small study, and that other past studies have indicated that exercise at any age is beneficial.
Aging and Brain Rejuvenation as Systemic Events - Wednesday, October 22, 2014
It is always good to see more researchers talking openly about the prospects for treating aging, reversing dysfunction, and extending life. This review is open access, but the full paper is only available in PDF format at the moment.
Mitochondrial Mutations Contribute to Autoimmune Disease? - Thursday, October 23, 2014
Mitochondria, the cell's power plants, contain their own DNA. This is a legacy of their origin as symbiotic bacteria, but it makes them vulnerable to damage.
Mitochondrial DNA is not as well protected and maintained in comparison to nuclear DNA, and it sits right next to an energetic biochemical process that generates plenty of potentially harmful reactive oxygen species.
More serious mutational damage such as deletions are thought to contribute to aging by creating mitochondria that lack the proteins needed for proper function. Here, however, researchers speculate that other types of mutation that alter the produced proteins rather than block their production can contribute to the development of autoimmune disease.
The Other Activities of Telomerase - Thursday, October 23, 2014
Telomerase extends telomeres, the protective ends of chromosomes. A portion is lost with each cell division, and this mechanism forms part of a clock regulating the replicative life span of ordinary cells.
Stem cells maintain long telomeres. and when active, work to introduce into tissues a continual supply of new daughter cells with long telomeres. Average telomere length declines with illness or age most likely largely because of disturbances to this process of tissue maintenance: as the creation rate of new cells with long telomeres falls, the average telomere length in tissue will also fall.
Telomerase is vital to most cancers, in which individual cells maintain long lives and act more like unlimited stem cells than the ordinary cells they are descended from. A fair amount of modern research into telomeres and telomerase is conducted by the cancer research community. Ways to selectively block the activity of telomerase would be a potent cancer therapy.
One of the possible reasons why artificially increased levels of telomerase extends life in mice is that it improves stem cell function in this way. Extending telomeres is not the only function of telomerase, however. Evolution tends to produce systems in which components are promiscuously reused in many processes. For example, telomerase has been shown to improve mitochondrial function, and mitochondria are important in the aging process.
Towards the Production of New Photoreceptor Cells In Situ - Friday, October 24, 2014
The evolution of cell therapies will most likely be towards treatments that alter cell type and behavior in place, drawing from the existing pool of cells and changing them to suit the needs of the patient.
Given sufficient control over cell activities and cell state old cells might be repaired and entire organs could be regenerated through this approach. Present efforts in tissue engineering and transplants are a stepping stone to this more sophisticated future of regenerative medicine. Here is an early example of this trend underway.
Screening for Stress Resistance Mutations in Mice - Friday, October 24, 2014
The open access paper quoted below provides some insight into increasing sophistication of the work involved in identifying longevity-related genes and proteins in mammals.
Many of these have been discovered over the past twenty years, leading to numerous ways to alter the operation of metabolism in order to slow aging and thus extend healthy life. This should probably be considered a part of the bigger picture of progress towards a better understanding of the fine details of biochemistry, however, and not a stepping stone to longer lives for you and I.
Slowing aging by building a better metabolism is not a great strategy at this point in time in comparison to working on repair of damage. Researchers know much more about the damage that causes aging than they do about metabolism, so the choice is between easier and more promising lines of research versus much harder work that will produce far less useful results.
Unfortunately for us, since scientists are in the business of gaining knowledge rather than changing the world, most research is in fact directed towards the harder work that will do little to produce meaningful treatments for aging. That is why we need advocacy and grassroots fundraising programs and organizations aimed at changing the strategic direction of aging research.
Read More https://www.fightaging.org/archives/2014/10/screening-for-stress-resistance-mutations-in-mice.php
DISCLAIMER:Â News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.fightaging.org/
David A. Kekich
Maximum Life Foundation
"Where Biotech, Infotech and Nanotech
Â Â Â Â Meet to Reverse Aging by 2033"