Lifeboat Foundation

Of the three great Stoics, Seneca always interested me the least. A playwright and professional philosopher, he seemed unlikely to be acquainted with the more mundane forms of suffering that beset humanity. This made him seem unfit to propound upon a philosophy concerned with right conduct under challenging circumstances.

Marcus Aurelius, ruler of an enormous empire, spent most of his reign embroiled in wars he had no desire to fight. Epictetus, a Greek who endured the hardships of slavery, also embodied the Stoic ideal. Cries of “ad hominem!” aside, it is hard to dispute that our experiences shape our outlooks on living. Biographical criticisms can be flimsy, but the central argument in De Brevitate Vitae — an otherwise inspirational classic — was exceptionally naive for the 1st century.

Although Seneca understood intrigue and exile firsthand, he was not privy to the time-sapping vicissitudes of householding or holding down a job.

How we grow old gracefully—and whether we can do anything to slow down the process—has long been a fascination of humanity. However, despite continued research the answer to how we can successfully combat aging still remains elusive.

Working with non-human primates, scientists have discovered that the protein SIRT2, a member of the sirtuin family, might play an important role in slowing cardiac aging [1].

In this study published in Nature Aging, the researchers used long-tailed macaques to elucidate the molecular aspects of cardiac aging using multi-omics analysis. Unlike short-lived mice and rats, non-human primates like these have hearts that closely resemble those of humans and, due to their relatively long lifespan, suffer from spontaneous heart conditions as well.

When it comes to human longevity, you might envision nanobots helping our bodies operate more efficiently. But our bodies are biological machines in their own right, evolved to handle any situation in the real world from illness to cold to hunger. Our bodies heal themselves, and they can be programmed to do so if we understood that language better.

This video talks about DNA and genes, and the epigenetic mechanisms that read that information. The epigenetic clock is one way to measure the age of cells, and this can be reversed with current technologies. We discuss experiments by David Sinclair, which made blind mice see again, and experiments by Greg Fahy, which regenerated the immune system of humans and reset their cellular age by 2 years.

Continue reading “Unlocking immortality: the science of reversing aging” »

Researchers at the University of Auckland identify platelet factor 4 (PF4) in young blood as a key player in reversing age-related cognitive decline in mice. The study offers a promising avenue for treating dementia-related conditions and enhancing brain function in aging populations.

Researchers developed ‘HistoAge,’ an algorithm that unravels brain aging and neurodegenerative disorders.

As we age, our brains undergo structural and cellular changes influenced by intrinsic and external factors. Accelerated aging in the brain can result in an increased risk of neurodegenerative conditions, bipolar disorder, and mortality. In a bid to deeply understand how an aging brain works, researchers say they have built a powerful AI tool that can identify regions in the brain vulnerable to age-related changes.

The team used AI to develop an algorithm called ‘HistoAge,’ which predicts age at death based on the cellular composition of human brain tissue specimens with an average accuracy… More.

Continue reading “New AI model uncovers how and why the human brain ages” »

This is a bit technical. “nucleocytoplasmic compartmentalization assay”, Yeah buddy.

Life is dependent on the preservation and storage of information. The genome and epigenome are the two central storehouses of information in eukaryotes, and although they work interdependently, they are fundamentally quite different. Genetic information is consistent across all body cells throughout the life of an individual while epigenetic information varies between cells as well as changes over time and as per environment.

Researchers have identified several hallmarks of aging such as epigenetic alterations, genomic instability, cellular senescence, telomere attrition, mitochondrial dysfunction, and others [1]. These are known to play a role in the dysfunction and deterioration of cells with age. David Sinclair and other researchers have previously indicated that loss of epigenetic information can cause changes in gene expression, leading to cellular identity loss. Previous studies in mice have also shown that cell injuries such as cell crushing and DNA double-strand breaks can promote loss of epigenetic information which can accelerate aging along with age-related diseases [2].

Continue reading “Is the reversal of cellular aging possible through chemical means?” »

LEV becoming mainstream medicine.

Centenarians, once considered rare, have become commonplace. Indeed, they are the fastest-growing demographic group of the world’s population, with numbers roughly doubling every ten years since the 1970s.

How long humans can live, and what determines a long and healthy life, have been of interest for as long as we know. Plato and Aristotle discussed and wrote about the ageing process over 2,300 years ago.

The pursuit of understanding the secrets behind exceptional longevity isn’t easy, however. It involves unravelling the complex interplay of genetic predisposition and lifestyle factors and how they interact throughout a person’s life.