What Would You Guess Your Life is Worth?

Longevity News Digest

Funding Aging Research

You are the Healthiest You Will Ever be. But What If¦

Dear Future Centenarian, 

How old are you?

Specific age doesn™t really matter if you™re past maturity. Unless things change, you™ll be worse off physically as years pass.

My friend Dona reminded me of this sad fact.

She beat breast cancer, but treatment side effects made it difficult for her to exercise the way she used to. And she was never one to ignore a good time. Sometimes that meant eating a little too much, choosing what tasted good instead of what was best for her, and even having a drink or three beyond a œsensible limit.

So she weighs a little more than she would like, is not in the condition she used to enjoy¦ and is a bit older than what she remembers as her œbest years.

In other words, she™s normal.

But a few weeks ago, she realized œnormal was not good enough for her. She remembered what it was like to feel great “ and missed it. But more importantly, she realized she only has about 23 more years to live if she™s average, at least according to actuaries.

But if she™s average, the last eight years or so will be dismal. Sadly, she™ll be in a steady state of decline for 15 years¦ and possibly infirmed from then on.

Dona and her husband Tom love vacationing. On and off planes and trains. In and out of water. Up and down hills. But it will be several years before Tom retires, so goodbye to Dona™s best remaining years before they can travel extensively.

After some basic math, she decided to preserve the precious years she has left by adopting positive lifestyle changes.

So in that regard, she™s NOT normal. Too bad for most of the rest. And here™s why:

They may miss a bonus that Dona is setting herself up for. Because she™s almost assuredly going to live better, she™s probably going to live longer too. And because we™re closing in on full body rejuvenating technologies, she may someday be rollerblading again in that hot 22 year old body that used to drive men wild when I first met her.

Emerging technologies could easily add 20 (or WAY) more productive years to your precious life. Extra years and decades to make and realize new dreams. To enjoy your kids™ kids. Continuing growing your business. Traveling. More.

So what are you doing to boost your odds of those rewards?

This morning, I came across this icon™s words of wisdom:

My Twilight Years ~ Clint Eastwood 

œAs I enjoy my twilight years, I am often struck by the inevitability that the party must end. There will be a clear, cold morning when there isn't any "more." No more hugs, no more special moments to celebrate together “ no more phone calls just to chat. 

œIt seems to me that one of the important things to do before that morning comes, is to let everyone of your family and friends know that you care for them by finding simple ways to let them know your heartfelt beliefs and the guiding principles of your life so they can always say, ˜He was my friend, and I know where he stood™." 

Well said Clint, and I have a better idea for you:

More Life,
David Kekich

P.S. October 1st is International Longevity Day. Celebrate with a smoothie and a smooch from your sweetie.
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Latest Headlines from Fight Aging!

Insight into Peter Thiel's Support of Longevity Science - Monday, September 22, 2014
Philanthropist Peter Thiel is one of the patrons of the SENS Research Foundation, perhaps the only organization in the world at this point that is coordinating and funding serious efforts to build rejuvenation treatments.

Thiel recently published a book, and by the alchemy involved in these matters we are thus seeing more press of late on his views and the causes he supports.

Read More https://www.fightaging.org/archives/2014/09/insight-into-peter-thiels-support-of-longevity-science.php

Telomerase has an Off Switch - Monday, September 22, 2014
Telomerase is the enzyme responsible for lengthening telomeres, caps of repeating DNA sequences at the end of chromosomes. Telomere length acts as a clock of sorts, as telomeres shorten with each cell division.

This is one part of a complicated mechanism that limits the replicative life span of ordinary somatic cells that make up the bulk of tissues, producing the well-known Hayflick limit. Telomerase is active in different cell populations to different degrees: in stem cells, for example, it operates to consistently maintain lengthy telomeres, such that the stem cells can renew their own population throughout life, while still periodically creating fresh new batches of somatic cells to replace lost cells in the tissue they support.

Average telomere length is fairly dynamic, depending on the details of tissue maintenance and delivery of fresh cells, and tends to shorten with age and illness. It is most commonly measured in white blood cells, which may have more of a correlation with illness than if measured in other tissues. Telomere length is largely thought of as a marker of age-related damage, not a primary cause of aging, but nonetheless delivery of additional telomerase to mice via genetic engineering has been shown to extend life.

It is still an open question as to how exactly this works: slowing the onset of tissue frailty through cell loss is one possibility, but it has been suggested that telomerase may interact with mitochondria in ways that reduce their impact on aging. Mice have quite different telomere dynamics from humans, and delivery of telomerase comes with an associated concern of raised cancer risk: all cancers incorporate mechanisms to keep telomeres long in their cells despite frequent cell divisions.

Here researchers present an interesting new finding about the mechanisms of telomerase, which will no doubt be incorporated into existing initiatives aiming to use telomerase as a way to intervene in the aging process.

Read More https://www.fightaging.org/archives/2014/09/telomerase-has-an-off-switch.php

A New Approach to Targeting Metastasis in Cancer - Tuesday, September 23, 2014
Most cancers kill through metastasis, the spread of cancerous cells throughout the body to seed numerous secondary tumors. Without this process cancer would be much less threatening and more amenable to treatment. Thus numerous research groups are investigating ways to shut down or otherwise interfere with metastasis, and here is a recent example.

Read More https://www.fightaging.org/archives/2014/09/a-new-approach-to-targeting-metastasis-in-cancer.php

Testing a Bioartificial Liver - Tuesday, September 23, 2014
Artificial organs capable of performing some of the functions of the real thing don't have to look or be structured in the same way as our evolved organs. They just have to work.

Efforts to develop artificial organs have benefited from progress in the ability to control and manage cell populations, giving rise to a first generation of hybrid devices that use both cells and machinery. A number of bulky prototypes to augment various kidney, pancreatic, lung, and liver functions with engineered tissue have been developed in recent years.

In these cases the necessary cells can be grown and maintained outside the body and a patient's blood circulated through them on a regular basis. Miniaturization isn't necessary in order to obtain these benefits, which makes the research and development process much easier. In the future one might imagine that smaller and more efficient versions could be implanted, putting this technology in competition with regenerative medicine and tissue engineering of replacement organs.

Read More https://www.fightaging.org/archives/2014/09/testing-a-bioartificial-liver.php

Proposing Combination Gene Therapy to Slow Aging - Wednesday, September 24, 2014
There are all sorts of longevity-associated genetic manipulations either demonstrated or postulated to produce benefits in mice. Why not try them all at once to see what happens?

If you think that slowing aging through alteration of metabolism to reduce the impact of the cellular and molecular damage that causes aging is a useful strategy, or you believe that aging is programmed and not actually caused by damage, then this is an ambitious (though possibly overoptimistic) plan of exploration that wouldn't require more than a few million dollars to carry out.

This research proposal comes from scientists associated with the Russian language advocacy community and the Science for Life Extension Foundation. They have had some success in the last few years raising funds from the community for smaller projects with mice, and may manage to get this funded the same way.

Read More https://www.fightaging.org/archives/2014/09/proposing-combination-gene-therapy-to-slow-aging.php

Using Songbird Brains to Investigate Regenerative Neurogenesis - Wednesday, September 24, 2014
An unusual characteristic of some songbirds is that parts of their brain vary greatly in size between seasons. Researchers believe that finding the exact mechanisms that trigger this atrophy and regrowth of neurons will lead to ways to spur the latter part of this process in humans, forming the basis for treatments that can increase the slow pace of natural regeneration in the mammalian brain.

Read More https://www.fightaging.org/archives/2014/09/using-songbird-brains-to-investigate-regenerative-neurogenesis.php

The Glenn Research Consortium Continues to Grow - Thursday, September 25, 2014
For some years now the Glenn Foundation for Medical Research has been establishing a network of labs to work on aging and longevity, seeding them with grants of a few million dollars apiece.

The research they carry out is fairly mainstream, such as investigation of calorie restriction mimetics as a way to slightly slow aging, and thus I don't expect to see meaningful results in terms of added years of life in the current form of these laboratory groups. Their primary output will be knowledge and data relating to the fine details of the intersection of metabolism and aging, leading to a better understanding of the causes of natural variations in longevity.

However this is a good example of the growing focus on aging as a treatable condition in the research community, and the Glenn Consortium is exactly the sort of research network we'd like to see pick up work on the rejuvenation biotechnology of SENS in the future. With more results, support, and tools generated by existing SENS research, it will become ever more attractive for scientists working on the go-nowhere path of slowing aging through metabolic manipulation to switch to reversing aging through repair of cellular and molecular damage. That is the only way forward likely to produce meaningful extension of healthy life within our lifetimes. For that switch to happen, it isn't just necessary for SENS to make progress, but there also must be more of a mainstream community whose members are interested in intervention in the aging process in the first place.

Read More https://www.fightaging.org/archives/2014/09/the-glenn-research-consortium-continues-to-grow.php

Nanogel Scaffolding and Cellular Heart Patches - Thursday, September 25, 2014
One approach to scaffolding for tissue engineering is to deliver a dissolving material along with transplanted cells that provides just enough support for those cells to get them past the point of generating their own extracellular matrix scaffold to replace the artificial material. Here researchers test that approach in tissue patches that can restore function to damaged heart tissue.

Read More https://www.fightaging.org/archives/2014/09/nanogel-scaffolding-and-cellular-heart-patches.php

Altered Myeloid Microglia Improve Alzheimer's Symptoms - Friday, September 26, 2014
Growing amounts of amyloid-β (Aβ) between cells forms one part of the pathology of Alzheimer's disease. This is a dynamic process, as much a matter of reduced clearance rates as increased production or simple accumulation: there are systems in the body capable of clearing out this amyloid and which can in theory be altered to increase clearance rates.

One part of the puzzle of what makes Alzheimer's disease an age-related condition is why exactly these clearance mechanisms fail with advancing aging: which of the known forms of cellular and molecular damage associated with aging cause this to happen? These researchers are working with microglia, supporting cells of the innate immune system present in the brain, with an eye to producing therapies to enhance amyloid clearance.

Read More https://www.fightaging.org/archives/2014/09/altered-myeloid-microglia-improve-alzheimers-symptoms.php

How Does Tau Protein Accumulation Harm Brain Cells in Age-Related Neurodegenerative Conditions? - Friday, September 26, 2014
One of the discoveries of past years in Alzheimer's disease research is that the β-amyloid accumulating between cells is less harmful to neurons than other associated proteins involved in the creation of that amyloid. Here is a paper that suggests much the same sort of thing for neurofibillary tangles, the other characteristic form of protein deposit associated with Alzheimer's.

Read More https://www.fightaging.org/archives/2014/09/how-does-tau-protein-accumulation-harm-brain-cells-in-age-related-neurodegenerative-conditions.php
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DISCLAIMER:  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
www.MaxLife.org

"Where Biotech, Infotech and Nanotech
     Meet to Reverse Aging by 2033"

 

 

 



 

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