Lifeboat Foundation

This product came out months ago with some shocking numbers as to effect. But those effects were in mice tests. 10–20% increase in lifespan and 55% increase in healthspan. It is AKG, Rejuvant, it’s a product you can buy now. There will be a part 2 of this interview so I hope to hear about human data.

Here we present an interview with Tom Weldon the founder and CEO of Ponce de Leon Health, which makes Rejuvant a Calcium AKG based supplement. In this video Tom talks through the process and reasons for selecting CaAKG. He also talks about some of the other results that they found in their tests, especially with respect to mixing different supplements and their combined effects.

Continue reading “CaAKG — The Science Behind Rejuvant | Tom Weldon Interview Series Part I” »

There are Sirt6 activators on the market, but since we are not seeing any major news about results I would question their value.

SPONSOR: Longevity. Technology — https://www.longevity.technology/?utm_source=SSS&utm_medium=…aign=Sirt6

Continue reading “The longevity sirtuin – what you need to know about SIRT6” »

The population on Earth is increasingly growing and people are expected to live longer in the future. Thus, better and more reliable therapies to treat human diseases such as Alzheimer’s and cardiovascular diseases are crucial. To cope with the challenge of ensuring healthy aging, a group of international scientists investigated the potential of biosynthesising several polyamines and polyamines analogs with already known functionalities in treating and preventing age-related diseases.

One of the most interesting molecules to study was spermidine, which is a natural product already present in people’s blood and an inducer of autophagy that is an essential cellular process for clearing damaged proteins, e.g., misfolded proteins in brain cells that can cause Alzheimer’s. When people get older the level of spermidine in the blood decrease and dietary supplements, or certain food products are needed to maintain a stable and high level of spermidine in the blood. However, those products are difficult to produce with traditional chemistry due to their structural complexity and extraction of natural resources is neither a commercially viable nor a sustainable approach.

Therefore, the researchers instead decided to open their biochemical toolbox and use classical metabolic engineering strategies to engineer the yeast metabolism to produce polyamines and polyamines analogs.

Research conducted by Qiang et al has discovered a link between a protein in red blood cells and age-related decline in cognitive performance. Published in the open access journal PLOS Biology on 17th June 2021, the study shows that depleting mouse blood of the protein ADORA2B leads to faster declines in memory, delays in auditory processing, and increased inflammation in the brain.

As life expectancies around the world increase, so are the number of people who will experience age-related cognitive decline. Because the amount of oxygen in the blood also declines with age, the team hypothesized that aging in the brain might be naturally held at bay by adenosine receptor A2B (ADORA2B), a protein on the membrane of red blood cells which is known to help release oxygen from the blood cells so it can be used by the body. To test this idea, they created mice that lacked ADORA2B in their blood and compared behavioral and physiological measures with control mice.

The team found that as the mice got older, the hallmarks of cognitive decline—poor memory, hearing deficits, and inflammatory responses in the brain—were all greater in the mice lacking ADORA2B than in the control mice. Additionally, after experiencing a period of oxygen deprivation, the behavioral and physiological effects on young mice without ADORA2B were much greater than those on normal young mice.

BES/BZR転写因子ファミリー間の競合関係は維管束幹細胞の増殖と分化のバランスを安定化させ幹細胞の永続的な維持に貢献する。

A new study led by University of Maryland and UCLA researchers found that DNA from tissue samples can be used to accurately predict the age of bats in the wild. The study also showed age-related changes to the DNA of long-lived species are different from those in short-lived species, especially in regions of the genome near genes associated with cancer and immunity. This work provides new insight into causes of age-related declines.

This is the first research paper to show that animals in the wild can be accurately aged using an epigenetic clock, which predicts age based on specific changes to DNA. This work provides a new tool for biologists studying animals in the wild. In addition, the results provide insight into possible mechanisms behind the exceptional longevity of many bat species. The study appears in the March 12, 2021, issue of the journal Nature Communications.

“We hoped that these epigenetic changes would be predictive of age,” said Gerald Wilkinson, a professor of biology at UMD and co-lead author of the paper. “But now we have the data to show that instead of having to follow animals over their lifetime to be sure of their age, you can just go out and take a tiny sample of an individual in the wild and be able to know its age, which allows us to ask all kinds of questions we couldn’t before.”

The inside of a mitochondria is made up of a folded membrane, which has evolved to produce the greatest surface area possible between two parts of the mitochondria known as the intermembrane space (the outer part) and the mitochondrial matrix (the inner part). To drastically oversimplify this entire process, the mitochondria uses glucose (and ethanol if it’s available) to pump hydrogen ions (with the occasional deuterium and tritium ion) across the membrane which separates these two compartments of the mitochondria (known as the cristae) into the intermembrane space. These hydrogen ions then flow back into the mitochondrial matrix through a very special protein called ATP synthase, which uses the electrostatic potential energy of the hydrogen ion to manufacture ATP.

Unfortunately, as we get older this inner membrane starts to decay and become smaller. As the cristae starts to shrink, there is less space for ATP synthase, which means there is less ATP produced, which ultimately means that our cells do not have enough energy to maintain all of our cellular functions. As you can imagine, this lack of energy is catastrophic for the health of the cell, and will eventually lead to either cell senescent (where the cell essentially becomes dormant), or complete cell death.

Numerous different suggestions have been put forward as to explain why exactly why mitochondria decay in this way, including mutations within the DNA of the mitochondria (they have their own chromosomes), as well as the build up of oxidative agents within the cell itself which cause direct damage to the mitochondria. However, a group of scientists lead by Dr Hazel Szeto have discovered that the decay of the mitochondrial cristae is linked to declining levels of a phospholipid (fat) called cardiolipin. It turns out that as we age, oxidative agents within our body destroy this phospholipid, which is essential for maintaining the folded inner membrane of the mitochondria.

Several different causes of aging have been discovered, but the question remains whether there are common underlying mechanisms that determine aging and lifespan. Researchers from the Max Planck Institute for Biology of Ageing and the CECAD Cluster of Excellence in Ageing research at the University Cologne have now come across folate metabolism in their search for such basic mechanisms. Its regulation underlies many known aging signaling pathways and leads to longevity. This may provide a new possibility to broadly improve human health during aging.

In recent decades, several cellular signaling pathways have been discovered that regulate the lifespan of an organism and are thus of enormous importance for aging research. When researchers altered these signaling pathways, this extended the lifespan of diverse organisms. However, the question arises whether these different signaling pathways converge on common metabolic pathways that are causal for longevity.

We probably cannot slow the rate at which we get older because of biological constraints, an unprecedented study of lifespan statistics in human and non-human primates has confirmed.

The study set out to test the ‘invariant rate of aging’ hypothesis, which says that a species has a relatively fixed rate of aging from adulthood. An international collaboration of scientists from 14 countries, including José Manuel Aburto from Oxford’s Leverhulme Centre for Demographic Science, analyzed age-specific birth and death data spanning centuries and continents. Led by Fernando Colchero, University of Southern Denmark and Susan Alberts, Duke University, North Carolina, the study was a huge endeavor requiring monitoring wild populations of primates over several decades.

Jose Manuel Aburto says, Our findings support the theory that, rather than slowing down death, more people are living much longer due to a reduction in mortality at younger ages. We compared birth and death data from humans and non-human primates and found this general pattern of mortality was the same in all of them. This suggests that biological, rather than environmental factors, ultimately control longevity.