Dear Future Centenarian,
In the 1990s, I forged my life’s mission which is to 1) Keep you (and me ?) alive until we perfect the ability to completely rejuvenate us and 2) Help make #1 a reality.
It seemed like an unrealizable dream last century with a tiny underfunded but devoted life extensionists leading what conventional wisdom considered a hopeless charge.
But besides being wildly optimistic dreamers, we were armed with insights into several emerging technologies that when integrated gave us a logical scientific roadmap to “curing” aging.
And we were united in our dedication to reversing aging in our lifetimes.
Since then, the concept of age reversal has finally been accepted by mainstream media, by gerontologists and researchers who avoided involvement to keep from being shunned by their peers, by Silicon Valley billionaires, and by the investment community who are making our mission a reality.
This is all very encouraging, but we still have a ways to go.
During this process, I wrote a how to book 13 years ago on why we can cure aging in our lifetime… and especially what you and I can do now through lifestyle habits and by incorporating newest technologies, products, and medical interventions.
Over the years, I rewrote and updated the book and republished it under a new title.
One thing that did not change was my emphasis on PART II: Seven Steps You Can Take Now to Put Extreme Longevity Odds on Your Side.
I consider that part the most critical since it shows you how to stay alive and well long enough be with us when emerging technologies will be able to rejuvenate you.
In other words, your life could very well depend on incorporating these lifestyle changes that could add over ten vibrant years to your life.
However, due to time constraints, I have not had a chance to update it since 2016.
But because the 7 steps are a matter of life or death, especially for the aging population, I decided to update each step, featuring them in easy to digest seven individual e-books.
The first one, Volume 1 — NUTRITION: Eat Your Way to a Maximum Healthy Lifespan, is complete, with the rest soon to follow. It’s available now as a Kindle publication on Amazon.
However, as a subscriber, you can download it at no cost. All I ask in return are two simple requests. 1) Please give it a good review at Amazon.com, and 2) Share this letter with your network.
CLICK HERE for your free e-book.
I will send you the other six volumes soon. They are almost complete and ready to publish.
Further Evidence for Cellular Senescence to Contribute Meaningfully to the Progression of Diabetic Retinopathy
Ever more of the research community is drawn to work on cellular senescence by the clear, robust, and expanding evidence for senescent cell accumulation to be a major contributing cause of aging.
Clearance of senescent cells by senolytic treatments produces extension of healthy life span and rejuvenation in mice, the reversal of many different age-related conditions. Senolytics are presently in the early stages of human clinical trials, with promising results for some of the approaches taken, such as use of the dasatinib and quercetin combination.
The Aging Microvasculature and Alzheimer’s Disease
The microvasculature of the body diminishes with age, and this is thought to be a major contributing factor in the progression of age-related loss of organ function, particularly in energy-hungry tissues such as muscles and the brain.
Every tissue is densely packed with tiny blood vessels, hundreds of capillaries passing through every square millimeter in cross-section. This small-scale microvasculature is needed in order to efficiently deliver sufficient nutrients to all cells in a tissue.
Bcl-xL in Cellular Senescence and Human Longevity
An accumulation of lingering senescent cells takes place with advancing age. Senescent cells are created throughout life, entering the senescent state in response to reaching the Hayflick limit on replication, or DNA damage, or signaling from other senescent cells, or to a toxic environment.
Senescent cells cease replication and instead generate a potent mix of inflammatory and pro-growth signals, the senescence-associated secretory phenotype (SASP). In youth near all senescent cells are rapidly destroyed, either by programmed cell death, or by the immune system. With advancing age, however, the processes of clearance slows down and the pace of creation picks up.
The Longevity FAQ at Nintil
Given the increased interest in the treatment of aging as a medical conditions, and the establishment of a longevity industry focused on building therapies that target the mechanisms of aging, it is now the case that more people are writing on the topic.
Most Children Born this Century Will Live to be Centenarians if Present Trends in Longevity Continue
Present trends in human life expectancy were established in an era in which little to nothing was being done to target the mechanisms of aging. As of fairly recently, this is changing.
There is now a growing contingent of researchers, entrepreneurs, and clinicians attempting to treat aging as a medical condition. This introduces a shift from (a) trying – and largely failing – to address the symptoms of aging, to (b) trying to control the causes of aging.
Immunosenescence and COVID-19
It is very clear from the data, as is the case for influenza, the mortality of the COVID-19 pandemic is suffered near entirely by the old.
This is because the aged immune system is less capable of fighting off pathogens, but also because the state of chronic inflammation and other dysfunctions resulting from immune system aging makes the cytokine storm of a severe SARS-Cov-2 viral infection that much more likely and that much more severe.
Patients with inflammatory age-related conditions, or conditions associated with obesity, a prominent cause of chronic inflammation, are much more likely to die from SARS-Cov-2 infection.
Ischemic Conditioning Reduces Inflammatory Signaling
Ischemic conditioning involves reducing the blood flow to part of the body for a period of time, such as to limbs via use of a tourniquet. When carried out correctly, the right degree of restriction for the right length of time, this provokes a beneficial stress response in cells that is similar in some ways to that produced by exercise.
Here, researchers show that ischemic conditioning reduces the inflammatory signaling and state of chronic inflammation that contributes to many age-related conditions, including the age-related hypertension that the is the focus on these studies.
The Damage of a Heart Attack Causes the Immune System to Overreact
Researchers here note a mechanism that causes T cells of the adaptive immune system to spur chronic inflammation and tissue damage following a heart attack.
As the researchers note, not all inflammation is the same. Some is maladaptive, and this is particularly the case in older individuals. The aged immune system is more prone to a sustained inflammatory response, provoked by pro-inflammatory signaling of senescent cells and the signs of cell damage that circulate in the body.
Suppressing all inflammation is too blunt of a tool, however, as short-term inflammation is still necessary for regeneration and response to pathogens even in later life.
Most Core Longevity Industry Venture Investment Vehicles are Companies, Not Funds
The prevailing model for the investment vehicles at the core of the longevity industry is the business development company, not venture funds.
The canonical example is Juvenescence, while the Longevity Vision Fund and Life Biosciences look very similar, and, as noted here, Cambrian Biopharma – that started out as a venture fund, as I recall – is now following the same playbook.
The objective of a venture fund is to exist for a set period of time, invest in startups, and return gains to investors at the end of that time. The objective of a business development company is to go public.
Incidence of Stroke is Declining in People Aged 70 and Older
The decline of cardiovascular disease in older people is the result of improved health practices, primarily less smoking, and a focus on lowering blood cholesterol via lifestyle change and drugs such as statins.
The formation of fatty plaque in blood vessel walls occurs in later life, the condition known as atherosclerosis. The plaque narrows and weakens blood vessels throughout the body. The rupture of a vessel or disintegration of a plaque followed by a a downstream blockage is the mechanism that causes both stroke and heart attack.
Beta-hydroxybutyrate as a Mediator of the Benefits of Exercise
Exercise is broadly beneficial to health, an effect in part mediated by the mild stress it inflicts on cells, causing increased cell maintenance activities in response, and in part by a vast and complex array of cell signaling that produces sweeping changes in cellular behavior.
Some of that signaling is the result of the aforementioned mild stress, some of it not. Researchers here look one of these signals, the secretion of beta-hydroxybutyrate, and its beneficial effects on tissue function.
Further Evidence for a Diversity of Cellular Senescence and Variable Efficacy of Senolytic Drugs
Cellular senescence is important in aging, as these cells disrupt tissue function and provoke chronic inflammation where they linger in old tissues.
The phenomenon is found in cell types throughout the body, but researchers have shown that meaningful differences between cell types exist in the biochemistry of cellular senescence, and possibly between senescent states for the same cell type.
A senolytic drug that can efficiently destroy one type of senescent cell may perform poorly for another type. This indicates that a diversity of development of senolytic therapies, and combinations of multiple therapies, will likely prove beneficial. Alternatively, approaches such as the suicide gene therapy developed by Oisin Biotechnologies may win out as p16 expression proves to be a more general characteristic of senescence than others.
Heart Attacks are More Severe in Sedentary Individuals
Researchers here provide epidemiological evidence to suggest that exercise, an active lifestyle, reduces the impact of heart attacks, making them less severe.
Modeling Age-Related Disease Risk as Accumulation of Senescent Cells
Researchers here find that a simple model of senescent cell accumulation, with thresholds at which disease occurs, can be made to match the observed variations in risk of most age-related diseases.
Operation of the Circadian Clock is Altered in Senescent Cells
The circadian clock operates at various levels, in cells, in tissues, and in the whole organism. In animals, aging disrupts the biochemistry of the circadian clock.
Researchers here show that in individual cells, entering the state of senescence alters the circadian clock.