Longevity News Digest
A Different Car Analogy for Increased Human Longevity
Dear Future Centenarian,Â
Following is a reprint of one of Reason™s recent essays. It™s an important message for most of you, since we tend to be in the upper end of age groups.
I agree with Reason on almost everything, but I lean more toward biotech and other interventions in the aging process to achieve extreme lifespans in the next 20 years or so.
However, I™m fully in Reason™s œrepair camp during the interim. Many of us over 60 (and probably younger) will almost assuredly depend on repair. So I urge you to support SENS Research Foundation any way you can.
Following is Reason™s essay with my comments at the end:
The car analogy that shows up most often in my circles relates to repair and the biological damage of aging. We, like cars, are machines. We differ only in complexity, and the same methods arising from reliability theory can be used to model progressive dysfunction and systems failure over time in both vehicles and people.
Given sufficient tools and resources a car can be maintained in good working condition indefinitely, a Ship of Theseus pattern progressing forward into the indefinite future. This is something we could achieve now for any model of car in the world, but for the most part choose not to. The only reason we cannot presently achieve the same result for people is that we lack the tools, the rejuvenation toolkit outlined in the SENS research proposals, ways to repair the known forms of damage that distinguish old tissue from young tissue.
In principle we could all become Ships of Theseus once rejuvenation therapies exist, with the unit of replacement being individual cells where the precise details of structure and molecular arrangements matter (largely in the brain) and anything up to whole organs elsewhere in the body. This is entirely possible and plausible, and given sufficient funding could arrive soon enough to matter for most of us.
This is the car analogy for rejuvenation research supporters, used as a way to help convince uninformed audiences skeptical about the prospects for prevention and reversal of aging. We can maintain cars, therefore it is reasonable to work on ways to maintain people.
Insofar as thinking about maintenance goes, people and cars are basically the same class of entity. The rejuvenation research crowd are not the only set of folk thinking about extending life, however, and they are (unfortunately) far from the most numerous at this time. The majority of people inside and outside the scientific community with an interest in enhanced longevity think in terms of slowing aging and altering the operation of metabolism: incremental, small advances towards better operation of the human machine.
In comparison to rejuvenation research vast sums are directed towards that goal, though it is still a very small field in comparison to medicine as a whole. As long-time readers will know by now, I think little of slowing aging as a goal: it is the expensive road to a near-useless end result. What good is slowing aging for those who are already old? Metabolism is fantastically complex and the prospects for significant progress in altering it to extend life are remote, judging by the time and money expended and lack of results obtained to date, and this is generally acknowledged as true by scientists in the field.
Outside the scientific community, people are more enthusiastic about the prospects to extend life by incremental advances in drugs, supplements, and other things I'd consider a pointless waste of time in comparison to the more serious modern applications of biotechnology in SENS research. These folk have their own car analogy, which is sketched in the post quoted below. It is a helpful read if you're looking to understand the mindset that has people chasing the mythical ever-better combination of supplements and prospective new ways to manipulate metabolism to slow aspects of aging:
What do we need to do to live longer, healthier lives? An editorial tale of cars and people
Can we expect to live longer and longer as the first part of this century rolls by? I think so, probably by a large amount. Will this extension of human lives be because of basic new scientific breakthroughs? Yes, but only in part. Collectively, such breakthroughs are likely to be important. Curiously though, I don't think that any single such breakthrough will make an immense difference.
What will matter is a process issue, and whether and how such breakthroughs are applied is only one consideration.
So, how then will it happen? I argue here that extended longevity is likely to happen via a number of incremental steps, probably small ones at that. Most will involve improvements in lifestyle and diet. Others will involve selective application of stresses and consumption of health-producing phytosubstances and selected dietary supplements.
I think you can move along the increasing longevity curve by pursuing a long string of incremental lifestyle and dietary modifications over time, each of which may seem to produce only modest results. Some steps may seem to be very tiny and insignificant, such as getting up from the computer and walking around a bit every hour.
Let's start by talking about, my grandmother's 1950 Chevy Bel Air, purchased new. If you were middle class and lived in Detroit you were expected to turn your car in every year for a new car, or at least every 2-3 years. Most cars did not survive the junk heap for more than 4-5 years. A three-year-old car was a seriously old car and you could expect to put less than 50,000 miles on it before it died.[In contrast, consider] our 2005 Subaru Impreza which we purchased in 2004. Expected lifespan: 15-20 years, perhaps 200,000 miles. This 10 year old car is still healthy, vigorous and a reliable family workhorse with no known problems at 100,000 miles. No sign of rust.
What was the big scientific or technical breakthrough that made the difference in lifespan and performance between the earlier cars and our Subarus? Lifespan extension of a factor of at least four and MPG improvement by a factor of two? None! In fact, it wasn't any single big scientific or engineering breakthrough. The difference is because of thousands of incremental improvements made year after year in just about every component and system. Virtually everything has been improved to make cars more reliable, last longer and operate more economically.
To be clear, I think it is arrant nonsense to state, as the author does above, that we could incrementally move to doubling our life spans without the application of modern biotechnology, interventions that meaningfully and directly repair cellular damage.
Not diet, not drugs, not random compounds dredged from the natural world because they turn out to do more good than harm, but designed applications of molecular machinery that achieve specific goals in our biochemistry, reverting most or all forms of low-level damage in and between our cells. This is a night and day difference in goals, ambition, and methodology. If you had a perfect diet and lifestyle, you'd still mostly likely die before age 90 in the environment of today's medical technology - because it is medical technology that overwhelmingly determines your life span, not your lifestyle.
Putting that aside, the rest of the article actually has little to do with specific implementation details and is more concerned with a vision of organized incremental improvement in life span. It is long and worth reading as a matter of interest.
My Comments: It is exactly major technology breakthroughs that will make radical life extension possible, not incremental gains for diet, exercise, supplement and other lifestyle modifications. However, lifestyle factors are what pave the way to being HERE when the technology breakthroughs emerge.
Depending on your age and condition, buying yourself a few more years could be the difference between being part of the first generation to NEVER die from aging¦ or being left behind.
So keep up you healthy habits, and enjoy¦
Latest Headlines from Fight Aging!
A Press Article on the Cryonics Institute - Monday, August 4, 2014
This press article on the history of cryonics and the work of the Cryonics Institute skips over a lot of the important technical details, such as the fact that patients are vitrified these days rather than frozen, a technique that minimizes ice crystal formation in tissues, but is still worth reading.
An Example of Continuing Legal Opposition to Cryonics - Monday, August 4, 2014
The small four decades old cryonics industry provides low-temperature storage at the end of life, an attempt to preserve the fine structure of the brain until future technologies can restore a preserved individual to life.
This is not beyond the realm of the possible: it will require at the very least mature molecular nanotechnology and near complete control over cells, but both of these are expected to come to pass over the next century.
Cryonics has long faced legal opposition, and it remains illegal in many regions for reasons that have less to do with actual directed opposition and more to do with a state of bureaucracy surrounding death and funerary arrangements in which everything not explicitly permitted is forbidden.
The tiny size of the cryonics community makes effective lobbying a challenge at this level; its membership can oppose local government and win, as happened in the US some years back, but that is about it at this time. This post outlines another similar situation in Canada, but here the legislative opposition to cryonics is more deliberate.
A Mainstream Press Article on Longevity Science - Tuesday, August 5, 2014
These days the mainstream press is giving a larger sliver of attention to various ongoing efforts to treat aging as a medical condition and thereby extend healthy life. We should expect to see an increasing number of articles similar to this one as funding for proactive aging research grows and more large institutions with publicity teams become involved.
Towards Cell Therapy to Treat Neurodegeneration - Tuesday, August 5, 2014
A range of neurodegenerative conditions that primarily involve cell loss, such as Parkinson's disease, might be treated with transplants of neural stem cells or more specialized differentiated cells.
Replacing the cells doesn't address the underlying causes that led to their loss, the rising toll of molecular damage that accompanies aging, but it may be a far more effective patch treatment than those presently available. Perhaps more importantly, it is expected that any more general rejuvenation toolkit that does address underlying causes will still need some way of making up the numbers in various small populations of long-lived nerve cells of the brain and central nervous system that have diminished over time. Progress towards this goal is to be welcomed.
Read More https://www.fightaging.org/archives/2014/08/towards-cell-therapy-to-treat-neurodegeneration.php
Most Gains in Life Expectancy are Now Realized Late in Life - Wednesday, August 6, 2014
Much of the gain in life expectancy at birth over the past two centuries was realized through reductions in early mortality. This was achieved through sanitation, increased wealth, and control of infectious disease.
As this paper notes, that trend is largely done with now, and the gains in life expectancy overwhelmingly arrive in later life due to advances in medical technologies aimed at treating the diseases of aging. The authors, economists rather than biogerontologists, see this as a potential problem because of increased length of retirement. In reality retirement is just a tradition, however, already unjust where it is enforced by law, and removed from the reality that individuals who remain healthy for longer thanks to modern medicine can just carry on being productive and working for a living. Do people serve laws or do laws serve people?
As life spans lengthen, retirement as an institution will change, as the reason for its existence - the ill health and incapacity that accompanies aging - will ultimately vanish.
Similarly the culture of government-enforced entitlement in which resources are transferred from comparatively poor and disempowered young people to comparatively wealthy and empowered old people must also be dismantled in the years ahead: it is unsustainable and morally bankrupt besides. All of the financial problems that the political chattering classes fret about with respect to increasing longevity are created by the present system of governance and its entitlements and rules, which together threaten to make a grand and damaging economic ruin out of what would otherwise be a great benefit.
Testing PTB as an AGE-Breaker in Bone - Wednesday, August 6, 2014
Advanced glycation endproducts, AGES, are a class of undesirable sugary metabolic waste that accumulate in tissues over time. They gum together important protein structures and cause cells to react to their presence in ways that are damaging and raise levels of chronic inflammation.
There are many different types of AGE, but most are not all that relevant to the aging process in healthy people, being short-lived and well controlled by our biochemistry. More hardy types of AGE that cannot be effectively cleared are a fundamental difference between old and young tissues, and a contribution to degenerative aging. Of these glucosepane is the most important in human tissues.
Much of the limited work of past decades that aimed to produce AGE-breaker drugs capable of clearing out AGEs went nowhere, as drug candidates established in animal studies performed very poorly in people. It turned out that the types of AGE important in mice and rats are quite different from those that are important in humans.
So researchers now realize that they have to work with human tissues to draw any reasonable conclusions, such as in this study. Note that the drug candidate PTB has been known as a potential AGE-breaker on the basis of animal studies for some years now, but it remains unclear as to its utility as a treatment for people.
Claiming a Cure for Rheumatoid Arthritis in Mice - Thursday, August 7, 2014
Autoimmunity is one of the remaining dark frontiers of human disease, and the collection of medical conditions in which the immune system starts to attack a patient's own tissues are largely poorly understood.
In the case of rheumatoid arthritis, for example, there is no real consensus on root cause or how the disease mechanisms work in detail, and it even may be a collection of several distinct issues lumped under one heading because the outcome looks the same. The effectiveness of treatments has been improving, but some patients just don't respond to the standard approach of trying to suppress the unwanted immune responses via TNF inhibitors.
Here researchers are making the bold claim of an effective cure for rheumatoid arthritis in mice, with a method that sounds like a more targeted way of suppressing unwanted immune activity rather an advance towards addressing root causes, and are heading for clinical trials.
AGEs Contribute to the Development of Osteoporosis - Thursday, August 7, 2014
Osteoporosis is the characteristic loss of bone mass and strength that occurs with aging, with proximate causes that include an imbalance in the distinct populations of cells responsible for bone creation and destruction, as well as the general decline in stem cell maintenance activities that occurs for every tissue in the body.
For root causes you have to look to cellular and molecular damage of the sort listed in the SENS research programs, which include an accumulation of sugar-based metabolic waste molecules called advanced glycation endproducts (AGEs).
These gum together important proteins in the extracellular matrix between cells and degrade tissue elasticity, but they also trigger increased levels of chronic inflammation through reacting with RAGE, the receptor for AGEs. Chronic inflammation is an unpleasant thing, a source of damage and dysfunction in and of itself, and it contributes meaningfully to many age-related conditions - such as osteoporosis.
Considering Cerebrospinal Fluid Flow Disruption as a Contributing Cause of Alzheimer's Disease - Friday, August 8, 2014
Alzheimer's disease is associated with buildup of amyloid-Î² in the brain, aggregates formed of misfolded proteins.
The amount of amyloid present at any given time is dynamic, however, which has long suggested that Alzheimer's is in part caused by a slow decline in the mechanisms responsible for clearing amyloid from the cerebrospinal fluid. You might look at investigations of the choroid plexus, for example, which acts as a filtration mechanism for cerebrospinal fluid. Here a researcher theorizes on the possible role of disruptions in the flow of cerebrospinal fluid in Alzheimer's disease, another way in which clearance of amyloid might be impacted with the progression of aging
Compensating for Cognitive Decline in Alzheimer's Disease - Friday, August 8, 2014
In this open access paper researchers report on a way to somewhat compensate for the measurable cognitive dsyfunction resulting from Alzheimer's disease by boosting synaptic activity.
This is characteristic of much of what emerges from the medical research community in that it makes no attempt to engage with the causes of the condition, but rather adjusts biological processes so as to better force continued operation despite the underlying disease pathology.
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"