Lifeboat Foundation: Safeguarding Humanity
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Category: life extension

The current market is expected to balloon to $1.0-$1.5 trillion in the next 20 years. Not even the anti-aging industry is worth that much!

The next decade is going to be an important one, with declining costs & advanced technology propelling the space economy to new highs. We have never been closer to the final frontier.

Reprinted with permission from the author.

Faisal Khan is a prolific Canada-based tech blogger and influencer. He is the founder and editor of the Technicity publication which focuses on technical, scientific and financial knowledge sharing. Follow him on Twitter @fklivestolearn.

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Scientists at USC Dornsife College of Letters, Arts and Sciences may have found the beginnings of a path toward increasing human lifespan.

The research, published July 10 by the Journal of Gerontology: Biological Sciences, shows the drug can extend the lives of two very different species used in , suggesting the findings may apply to other species, including human beings.

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Reprogramming of differentiated cells into induced pluripotent stem cells has been recently achieved in vivo in mice. Telomeres are essential for chromosomal stability and determine organismal life span as well as cancer growth. Here, we study whether tissue dedifferentiation induced by in vivo reprogramming involves changes at telomeres. We find telomerase-dependent telomere elongation in the reprogrammed areas. Notably, we found highly upregulated expression of the TRF1 telomere protein in the reprogrammed areas, which was independent of telomere length. Moreover, TRF1 inhibition reduced in vivo reprogramming efficiency. Importantly, we extend the finding of TRF1 upregulation to pathological tissue dedifferentiation associated with neoplasias, in particular during pancreatic acinar-to-ductal metaplasia, a process that involves transdifferentiation of adult acinar cells into ductal-like cells due to K–Ras oncogene expression. These findings place telomeres as important players in cellular plasticity both during in vivo reprogramming and in pathological conditions associated with increased plasticity, such as cancer.

Keywords: in vivo reprogramming, telomeres, stem cells, TRF1, tumorigenesis, cellular plasticity, cancer, transdifferentiation, ADM, regeneration.

Reprogramming into full pluripotency has been achieved in vivo in the context of mouse tissues (Abad et al., 2013). Thus, induction of the reprogramming factors in transgenic mice (so-called reprogrammable mice) results in reprogramming events marked by the expression of the pluripotency factor NANOG in multiple organs, tissue dedifferentiation, and teratoma formation. Therefore, these mice could be useful for a deeper understanding of the molecular mechanisms that govern tissue dedifferentiation in vivo. Interestingly, mammalian cell reprogramming can also occur spontaneously during regeneration after injury or damage conditions (Yanger et al., 2013). Differentiated cells can be converted in vivo into another cell type and also into functional multipotent stem-like cells (Tata et al., 2013). This capacity of somatic cells to dedifferentiate into stem-like cells in vivo may have a pivotal role in physiological tissue regeneration or during tumorigenesis.

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A little-studied liver protein may be responsible for the well-known benefits of exercise on the aging brain, according to a new study in mice by scientists in the UC San Francisco Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research. The findings could lead to new therapies to confer the neuroprotective effects of physical activity on people who are unable to exercise due to physical limitations.

Exercise is one of the best-studied and most powerful ways of protecting the from and has been shown to improve cognition in individuals at risk of neurodegenerative disease such as Alzheimer’s disease and frontotemporal dementia —even those with rare gene variants that inevitably lead to dementia.

But many are not able to exercise regularly due to or disabilities, and researchers have long searched for therapies that could confer some of the same neurological benefits in people with low physical activity levels.

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Aging/longevity/heathspan fans!!

Higher levels of humanin, a peptide encoded in the small genome of the mitochondria, in the body is linked to longer lifespans and better health.

Aging Journal – The mitochondrial derived peptide humanin is a regulator of lifespan and healthspan

The scientists observed that species which are already predisposed to long life, including the naked mole rat had high levels of humanin, while mice, in contrast, experience a 40% decrease in humanin over the first 18 months of their life and primates experienced a similar notable decrease between the ages of 19 and 25.

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Study after study has shown that statins can prevent heart attacks, strokes and death in middle-aged adults. But in 28 major clinical trials of statins, only 2 percent of participants have been 75 years or older. This means that even though older adults are at greater risk of heart disease and death, there is scant data on whether statins should be prescribed for them.

A new study led by investigators from Brigham and Women’s Hospital and VA Boston Healthcare System leverages national data from the U.S. Veterans Health Administration Services and Centers for Medicare & Medicaid Services to shed new light on the role statins may play for older adults who have not yet experienced a , stroke or other cardiovascular event. In their retrospective analysis, the researchers found that the risk of dying from any cause was lower by 25 percent among veterans who were using statins compared to those who were not treated with statins. The risk of dying from a cardiovascular event, such as a heart attack or stroke, was lower by 20 percent. The team’s results are published in JAMA.

“Based on these data, age is not a reason to not prescribe statins,” said lead and corresponding author Ariela Orkaby, MD, MPH, a physician scientist at VA Boston Health Care System and in the Division of Aging at the Brigham. “Statins are commonly studied and prescribed for middle-aged adults but understudied in people over age 75. One of the most remarkable things about our results is that we found the benefit of statins held true regardless of whether a person was older or younger or had a condition such as dementia.”

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Very interesting.

New UCLA research conducted in mice could explain why some people suffer more extensive scarring than others after a heart attack. The study, published in the journal Cell, reveals that a protein known as type 5 collagen plays a critical role in regulating the size of scar tissue in the heart.

Once formed, remains for life, reducing the heart’s ability to pump blood and adding strain to the remaining heart muscle. People who develop larger scars have a higher risk of heart rhythm problems, heart failure and sudden cardiac death.

“Two individuals with the same degree of can end up with different amounts of scar tissue,” said Dr. Arjun Deb, the study’s senior author and a member of Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. “Given the clear correlation between scar size and survival rates, we set out to understand why some hearts scar more than others. If we can reduce this scarring, we can greatly improve survival.”

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Infertility is one of the most striking effects of aging. The impact of aging on females’ fertility is more severe and much better understood, but it also affects males. Male reproductive aging is less researched, but of those studies that do address it, most focus on sperm. However, ejaculate contains more than just sperm. Proteins in the seminal fluid are important for fertility, and in many animals, they have a dramatic effect on female physiology and behavior. Little is currently known about the impact of male aging on these proteins, and whether any changes contribute to poorer ejaculates in older males.

To resolve these questions, researchers at the University of Oxford’s Department of Zoology conducted experiments in a model organism, the fruit fly, Drosophila melanogaster. This species typically lives for less than five weeks, which means that researchers can very rapidly measure the impact of age on male fertility, and their and seminal fluid proteins. This species is also highly amenable to genetic studies, which allowed the researchers to genetically manipulate , to see how this impacted the decline in fertility with age.

Published this week in PNAS are their results which show that both sperm and quality and quantity decline with male age, making distinct contributions to declining reproductive performance in older males. However, the relative impacts on sperm and seminal fluid often differ, leading to mismatches between ejaculate components. Despite these differences, experimental extension of male lifespan improved overall ejaculate performance in later life, suggesting that such interventions can delay both male reproductive aging and death.

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A better deal than any supernaturalist religion can offer; that seems to me what Julian Huxley intended. Some relief from fear of death. Morality self judged and perhaps situational – but not ethical codes forced on you by an imaginary invisible bullying tyrant(s) or a human calling upon His name…

A lot – possibly most- individuals on trans/ singul/ posthuman lists are drawn to radical futurism for specific reasons of extending life and attaining immortality (continuation of awareness) after physical death by technology. Different groups are working on different projects, but posthuman.org is concentrating on MVT analog circuits with Zenet interface. This is much less ambitious than approaches involving whole brain/ personality/ memory preservation, since there is only need to retain signals relating to game decision making. But who wants to be particularly aware of being dead?

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New research from the University of Colorado Boulder has offered some of the clearest evidence to date showing how the gut microbiome produces a metabolite that, over time, contributes to age-related declines in cardiovascular health.

High blood levels of trimethylamine-N-Oxide (TMAO), a metabolic byproduct of digestion, have been strongly linked to negative cardiovascular health. When one eats red meat, eggs or other animal proteins, certain types of gut bacteria feed on chemicals in those foods and produce TMA, or trimethylamine, which is then turned into TMAO in the liver.

A number of studies have linked TMAO to heart disease, however, until now it hasn’t been clear exactly how this metabolite causes cardiovascular damage. A robust new study, published in the journal Hypertension, is offering one of the first thorough mechanistic investigations illustrating how TMAO damages the cardiovascular system.

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