Lifeboat Foundation

The hypertension drug rilmenidine has been shown to slow down aging in worms, an effect that in humans could hypothetically help us live longer and keep us healthier in our latter years.

Rilmenidine was picked for this latest study because past research has shown it mimics the effects of caloric restriction on a cellular level. Reducing available energy while maintaining nutrition within the body has been shown to extend lifespans in several animal models.

Whether this translates to human biology, or is a potential risk to our health, is a topic of ongoing debate. Finding ways to achieve the same benefits without the costs of extreme calorie cutting could lead to new ways to improve health in old age.

Bryan Johnson releases his rejuvenation protocol:

Blueprint is a public science experiment to determine whether it’s possible to stay the same biological age. This requires slowing down aging processes as much as possible and then reversing the aging that has happened. Currently my speed of aging is .76 (DunedinPACE). That means for every 365 days each year, I age 277 days. My goal is to remain the same age biologically for every 365 days that pass.

Continue reading “My Anti-Aging Protocol Broke a World Record… — YouTube” »

Health tests and reports suggest that Bryan Johnson, 45, has the heart of a 37-year-old and gets erections like a teenager, Bloomberg reported.

We spoke with Dr Morgan Levine 2 years ago concerning the remarkable results that she and a team that included Dr David Sinclair had in restoring vision in mice. In that experiment, published in the journal Nature, older mice had tighter optic nerves crushed causing blindness. Then, using a combination of 3 of the 4 Yamanaka cellular programing factors, they were able to restore the mice’s vision by signally the underlying DNA, rebuilding what had been thought to be permanently damaged cells. This was a remarkable result, as it was restoring a damaged organ, essentially a part of the brain, to its original healthy state. When I spoke to Dr Levine about the next step in her research, she mentioned it may be a more complex organ, such as a mouse liver.

But they went further. In the January issue of Cell, Sinclair published results of their ability to age an entire mouse. That is, to signal the epigenome to cause the underlying mouse DNA to behave as if it were much older. They were also able to do the reverse: to take an older mouse and, by signaling the epigenome, bring its cells and organs to the state of a younger mouse. This is a truly remarkable achievement, and it seems to prove Sinclair’s theory that all of our cells have within them a pristine copy of their DNA, and that aging and the disease associated with aging are the result of miscues from the epigenome. If these miscues can be corrected then the cell can be restored, not to a blank stem cell but to its original condition.

A gene called BPIFB4, discovered in a population of centenarians, could help to reverse the aging of human hearts.

Carriers of healthy mutant genes, including people in so-called “blue zones” of the world, often live to 100 years or more and remain in good health. Cardiovascular complications are also rarer in these individuals. Scientists now believe that a gene may help to keep their hearts young by protecting them against diseases linked to aging.

Recent experiments conducted in Boston labs have shown reverse aging results among mice and could show similar results in people.

The combined experiments — which were conducted during a span of 13 years — published Thursday (January 12) in the scientific journal Cell reported that old, blind mice regained eyesight, developed smarter brains and built healthier muscle and kidney tissue, challenging the theory that DNA was the only cause of aging, as it proved that chemical and structural changes to chromatin played a factor without altering genetic code.

The research showed that a breakdown in epigenetic information caused the mice to age and the restoration of the epigenome reversed aging effects.

Open Longevity Foundation has announced Open Genes, a database of longevity-associated genes and a tool for future anti-aging therapy development. The full press release is included here. Open Longevity Foundation released a novel database of genes involved […].

The year is 2021, and journalism is dead. It does not particularly matter what your personal beliefs or creed are, at this point it has become blindingly apparent that the vast majority of the media are not overly concerned with the truth.

In aging mouse livers, 40% of elongating RNA polymerases are stalled, biasing transcriptional output dependent on gene length. This transcriptional stress appears to be caused by endogenous DNA damage.