Lifeboat Foundation

The maximum lifespan varies more than 100-fold in mammals. This experiment of nature may uncover of the evolutionary forces and molecular features that define longevity. To understand the relationship between gene expression variation and maximum lifespan, we carried out a comparative transcriptomics analysis of liver, kidney, and brain tissues of 106 mammalian species. We found that expression is largely conserved and very limited genes exhibit common expression patterns with longevity in all the three organs analyzed. However, many pathways, e.g., “Insulin signaling pathway”, and “FoxO signaling pathway”, show accumulated correlations with maximum lifespan across mammals. Analyses of selection features further reveal that methionine restriction related genes whose expressions associated with longevity, are under strong selection in long-lived mammals, suggesting that a common approach could be utilized by natural selection and artificial intervention to control lifespan. These results suggest that natural lifespan regulation via gene expression is likely to be driven through polygenic model and indirect selection.

The authors have declared no competing interest.

Uncover the truth behind the human lifespan. From Ancient Rome to modern America, discover the progress we’ve made in extending life expectancy and the flaws in measuring it. Join us as we explore the science of aging, the pursuit of immortality, and the ongoing debate on the limits of human longevity.

Why do cells, and by extension humans, age? The answer may have a lot to do with mitochondria, the organelles that supply cells with energy. Though that idea is not new, direct evidence in human cells had been lacking. Until now.

In a study published Jan. 12 in Communications Biology, a team led by Columbia University researchers has discovered that human cells with impaired mitochondria respond by kicking into higher gear and expending more energy. While this adaptation—called hypermetabolism—enhances the cells’ short-term survival, it comes at a high cost: a dramatic increase in the rate at which the cells age.

“The findings were made in cells from patients with rare mitochondrial diseases, yet they may also have relevance for other conditions that affect mitochondria, including neurodegenerative diseases, inflammatory conditions, and infections,” says principal investigator Martin Picard, PhD, associate professor of behavioral medicine (in psychiatry and neurology) at Columbia University Vagelos College of Physicians and Surgeons.

This process can occur endlessly and allows the jellyfish to escape death.

Achieving immortality has driven human beings throughout much of their history. Many peculiar legends and fables have been told about the search for the elixirs of life. Medieval alchemists worked tirelessly to find the formula for the philosopher’s stone, which granted rejuvenating powers. Another well-known story is the travels of Juan Ponce de León, who searched for the mysterious fountain of youth while conquering the New World.

But to this day, no one has discovered the keys to eternal life. However, there is one exception — a creature no more than four millimeters in size, Turritopsis dohrnii.

Continue reading “Immortal jellyfish: Scientists are deciphering genes to learn secrets” »

Loss of epigenetic information can drive aging, restoration can reverse it.

Sources:

Continue reading “How to Reverse Aging? David Sinclair — Epigenetic Information” »

We take a look at and why some researchers think it could be useful in combating aging.

Rapamycin is a macrolide, a class of antibiotic that includes erythromycin, roxithromycin, azithromycin, and clarithromycin. exhibits potent antitumor and immunosuppressive activity.

Where is found?

Aging is characterized by changes in cellular identity and function over time. This process is driven by changes in chromatin factor localization during DNA break repair, which alters the epigenome and advances the epigenetic clock. Expression of a subset of Yamanka factors, OSK, can reverse these changes and modulate aging.

The rebooting came in the form of a gene therapy involving three genes that instruct cells to reprogram themselves—in the case of the mice, the instructions guided the cells to restart the epigenetic changes that defined their identity as, for example, kidney and skin cells, two cell types that are prone to the effects of aging. These genes came from the suite of so-called Yamanaka stem cells factors—a set of four genes that Nobel scientist Shinya Yamanaka in 2006 discovered can turn back the clock on adult cells to their embryonic, stem cell state so they can start their development, or differentiation process, all over again. Sinclair didn’t want to completely erase the cells’ epigenetic history, just reboot it enough to reset the epigenetic instructions. Using three of the four factors turned back the clock about 57%, enough to make the mice youthful again.

“We’re not making stem cells, but turning back the clock so they can regain their identity,” says Sinclair. “I’ve been really surprised by how universally it works. We haven’t found a cell type yet that we can’t age forward and backward.”

Rejuvenating cells in mice is one thing, but will the process work in humans? That’s Sinclair’s next step, and his team is already testing the system in non-human primates. The researchers are attaching a biological switch that would allow them to turn the clock on and off by tying the activation of the reprogramming genes to an antibiotic, doxycycline. Giving the animals doxycycline would start reversing the clock, and stopping the drug would halt the process. Sinclair is currently lab-testing the system with human neurons, skin, and fibroblast cells, which contribute to connective tissue.

This might be important. It might not be over for metformin just yet though as a mice study showed that rapamycin combined with metformin removed each other’s side effects.

If you are a non-diabetic who takes metformin for longevity, I highly recommend you stop immediately. Hear me out, and at the end of the video I’ll share what to do instead.

Continue reading “Metformin For Anti-Aging: Disproved & Dangerous!” »