Lifeboat Foundation: Safeguarding Humanity
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Category: life extension

Aging is by far the dominant risk factor for the development of cardiovascular diseases, whose prevalence dramatically increases with increasing age reaching epidemic proportions. In the elderly, pathologic cellular and molecular changes in cardiac tissue homeostasis and response to injury result in progressive deteriorations in the structure and function of the heart. Although the phenotypes of cardiac aging have been the subject of intense study, the recent discovery that cardiac homeostasis during mammalian lifespan is maintained and regulated by regenerative events associated with endogenous cardiac stem cell (CSC) activation has produced a crucial reconsideration of the biology of the adult and aged mammalian myocardium. The classical notion of the adult heart as a static organ, in terms of cell turnover and renewal, has now been replaced by a dynamic model in which cardiac cells continuously die and are then replaced by CSC progeny differentiation. However, CSCs are not immortal. They undergo cellular senescence characterized by increased ROS production and oxidative stress and loss of telomere/telomerase integrity in response to a variety of physiological and pathological demands with aging. Nevertheless, the old myocardium preserves an endogenous functionally competent CSC cohort which appears to be resistant to the senescent phenotype occurring with aging. The latter envisions the phenomenon of CSC ageing as a result of a stochastic and therefore reversible cell autonomous process. However, CSC aging could be a programmed cell cycle-dependent process, which affects all or most of the endogenous CSC population. The latter would infer that the loss of CSC regenerative capacity with aging is an inevitable phenomenon that cannot be rescued by stimulating their growth, which would only speed their progressive exhaustion. The resolution of these two biological views will be crucial to design and develop effective CSC-based interventions to counteract cardiac aging not only improving health span of the elderly but also extending lifespan by delaying cardiovascular disease-related deaths.

Over the last decades, average life expectancy has significantly increased worldwide although several chronic diseases continue to grow, with aging as their main risk factor [1]. Aging is a natural and inevitable degenerative process of biological functions characterized by the progressive decline in tissue and organ homeostasis and function. Despite the significant improvements in diagnosis and treatment, the majority of individuals older than 65 years of age suffer from an elevated risk to develop cardiovascular diseases (CVDs), with a decline in the quality of life and in the ability to perform the normal activities of daily living [1]. Aging produces numerous changes in the human heart at structural, molecular, and functional levels [2].

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Dr. Sandra Kaufmann

The Author of the book, The Kaufmann Protocol: Why we age and how to stop it.

The Kaufmann Protocol is the first comprehensive approach to aging that tackles why we age and then recommends a strategic, scientific formulation to decelerate the process.

The book brings practical information to everyday people and takes the science of aging out of the laboratory and into the real world.

The first half of The Kaufmann Protocol discusses aging on a cellular level, which separates it from all other anti-aging fads. We age because our cells age and it is this understanding that allows the protocol to combat aging for people from all walks of life.

This is presented in terms of the seven tenets, or categories, of aging which comprise topics such as DNA alterations, mitochondrial energy, and aging pathways. These are explained in both scientific and laymen terms, such that anyone can understand the process. A series of analogies paralleling the cell to a factory assist the reader in following the logic.

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The colorful Clownfish lives longer than 20 years in the aquarium. Researchers of the Scuola Normale Superiore in Pisa, Italy, in collaboration with the Leibniz Institute on Aging (FLI) in Jena, Germany, have investigated the genetics behind the longevity of clownfish. By sequencing the genome and comparing the sequences with other species, they were able to show, that the secret of this longevity lies in the mitochondria and lysosomes of the clownfish. Because it is uncomplicated to keep and breed clownfish, they represent an interesting new animal model for research on longevity. The results are now published in the journal BMC Evolutionary Biology.

Clownfish, famous because of the Disney movie “Finding Nemo,” are a bright orange-white-black colored fish with three vertical stripes, which occur in the western Pacific and Indian Oceans. Clownfish live in symbiotic relationship with sea anemone. They are reliant on sea anemone for shelter in their natural habitat, which offer protection for the fish with its tentacles. The Clownfish’s mucus protection prevents it from being stung by the tentacles of the sea anemone. Thanks to this survival strategy, have a lower mortality rate than other fishes and can grow quite old. Until now there was not much known about the lifespan of this interesting sea dweller.

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Sirtuins have long been implicated in playing a role in the longevity of various species, including our own, and researchers at the University of Rochester have now discovered more supporting evidence that they do.

What are sirtuins?

Sirtuins are a family of proteins that facilitate cellular function and have long been known to play a role in aging. In particular, they are responsible for functions such as gene expression and are involved in DNA repair. It has long been understood that sirtuins played a role in aging, but the key factor in how well they function is the presence of nicotinamide adenine dinucleotide (NAD+), a coenzyme found in all living cells. NAD+ biology is central to deregulated nutrient sensing and a reason why we age, and sirtuins play a key role in this biology.

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Keith Comito, interviewed by Adam Ford at the Undoing Aging 2019 conference in Berlin, discusses why solving the diseases of old age is a powerful cause.

How can solving aging reduce suffering? What are some common objections to the ideas of solving aging? How does Anti-Aging stack up against other cause…

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AI Overlords

Musk has repeatedly warned of evil AI overlords in the past, saying that AI could become “an immortal dictator from which we could never escape” in a 2018 documentary called “Do You Trust This Computer?”

Most of what Neuralink is working on, including any plans for a brain computer interface, are still tightly under wraps. In one tantalizing clue, Bloomberg recently reported on a still unpublished academic paper by five authors who have been employed by or associated with Neuralink — though it’s unclear whether Musk’s tweet referred to their work.

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Mesenchymal stem cells (MSCs) have been a topic of great interest in the last decade or so due to their ability to improve tissue regeneration merely by their presence and the secreted signals they give out.

Adult MSCs have traditionally been used for regenerative medicine with hit-and-miss results, depending on the quality and age of the harvested MSCs. It has been discovered in recent years that the efficacy of these cells greatly depends on how damaged by aging they are, which explains why MSC therapy sometimes works very well in one person but not so much in another.

However, what about aged cells that are reprogrammed back to pluripotency then guided into becoming mesenchymal stem cells through cellular reprogramming?

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