Lifeboat Foundation

As transhumanists, we aim at the so-called continuity of subjectivity by the means of advanced technologies. Death in a common sense of the word becomes optional and cybernetic immortality is within our reach during our lifetimes. By definition, posthumanism (I choose to call it ‘cyberhumanism’) is to replace transhumanism at the center stage circa 2035. By then, mind uploading could become a reality with gradual neuronal replacement, rapid advancements in Strong AI, massively parallel computing, and nanotechnology allowing us to directly connect our brains to the Cloud-based infrastructure of the Global Brain. Via interaction with our AI assistants, the GB will know us better than we know ourselves in all respects, so mind-transfer, or rather “mind migration,” for billions of enhanced humans would be seamless, sometime by mid-century.

By 2040, mind-uploading may become a norm and a fact of life with a “critical mass” of uploads and cybernetic immortality. Any container with a sufficiently integrated network of information patterns, with a certain optimal complexity, especially complex dynamical systems with biological or artificial brains (say, the coming AGIs) could be filled with consciousness at large in order to host an individual “reality cell,” “unit,” or a “node” of consciousness. This kind of individuated unit of consciousness is always endowed with free will within the constraints of the applicable set of rules (“physical laws”), influenced by the larger consciousness system dynamics. Isn’t too naïve to presume that Universal Consciousness would instantiate phenomenality only in the form of “bio”-logical avatars?

Keith Comito, president of Life Extension Advocacy Foundation, joins me for a discussion to preview the 2020 Eding Age Related Diseases conference, to be held online, August 20–21, 2020. Go HERE to register for the conference, and use discount code SeekingDelphiEARD

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The answer is in their genes—especially those that encode for basic life functions, such as metabolism. Thanks to the lowly C. elegans worm, we’ve uncovered genes and molecular pathways, such as insulin-like growth factor 1 (IGF-1) signaling that extends healthy longevity in yeast, flies, and mice (and maybe us). Too nerdy? Those pathways also inspired massive scientific and popular interest in metformin, hormones, intermittent fasting, and even the ketogenic diet. To restate: worms have inspired the search for our own fountain of youth.

Still, that’s just one success story. How relevant, exactly, are those genes for humans? We’re rather a freak of nature. Our aging process extends for years, during which we experience a slew of age-related disorders. Diabetes. Heart disease. Dementia. Surprisingly, many of these don’t ever occur in worms and other animals. Something is obviously amiss.

In this month’s Nature Metabolism, a global team of scientists argued that it’s high time we turn from worm to human. The key to human longevity, they say, lies in the genes of centenarians. These individuals not only live over 100 years, they also rarely suffer from common age-related diseases. That is, they’re healthy up to their last minute. If evolution was a scientist, then centenarians, and the rest of us, are two experimental groups in action.

We take a trip down Lifespan.io’s Rejuvenation Roadmap – and it’s a journey towards Longevity progress.

Could there really be a magic pill for immortality?

NSD2 is the fourth protective factor of cellular senescence that our team has identified,” said Professor Mitsuyoshi Nakao. “With the discovery that NSD2 protects against cellular senescence, this study clarifies a basic mechanism of aging.

Researchers from Kumamoto University in Japan have used comprehensive genetic analysis to find that the enzyme NSD2, which is known to regulate the actions of many genes, also works to block cell aging. Their experiments revealed 1) inhibition of NSD2 function in normal cells leads to rapid senescence and 2) that there is a marked decrease in the amount of NSD2 in senescent cells. The researchers believe their findings will help clarify the mechanisms of aging, the development of control methods for maintaining NSD2 functionality, and age-related pathophysiology.

As the cells of the body continue to divide (cell reproduction), their function eventually declines and they stop growing. This cellular senescence is an important factor in health and longevity. Cell aging can also be stimulated when genomic DNA is damaged by physical stress, such as radiation or ultraviolet rays, or by chemical stress that occurs with certain drugs. However, the detailed mechanisms of aging are still unknown. Cell aging can be beneficial when a cell becomes cancerous; it prevents malignant changes by causing cellular senescence. On the other hand, it makes many diseases more likely with age. It is therefore important that cell aging is properly controlled.

Continue reading “NSD2 shapes the program of cell senescence [image] Science News” »

https://www.youtube.com/watch?v=gwylNmYrjoo&feature=share

And older vid but it addresses various anti-life extension topics.

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Continue reading “Immortalism vs Deathism: Should we Live Forever?” »

Well, they don’t.

Thousands are currently engaged in solving the problem of death. Maybe they’ll succeed, and out of sheer boredom I’ll reread this sentence when I’m 900 years old, reflecting fondly on the first wasted century of my life. In the meantime, billions are going to die—some from disease, some in freak accidents, and a substantial number from what we generally call “old age.” That last sounds like a pleasant way to go, comparatively—a peaceful winding-down. But what exactly does it look like? What does it really mean to die from old age? For this week’s Giz Asks, we reached out to a number of experts to find out.

A study from researchers at KAIST (Korea Advanced Institute of Science and Technology) is providing new insights into a cellular energy pathway that has been linked to longer lifespan. The research, conducted in human cells and roundworms, raises the prospect of anti-aging therapeutics that can extend lifespan by activating this pathway.

AMPK (adenosine monophosphate-activated protein kinase) is an enzyme that acts as a metabolic master switch. It has been described as a “magic bullet” protein, conferring broad beneficial health effects, from improving cardiovascular health to extending lifespan. It is activated in response to low cellular energy levels, as is often seen during exercise or periods of caloric restriction.

An increasing volume of study has found activating AMPK in animal models leads to notable increases in lifespan, prompting a surge in research investigating this enzyme.