Lifeboat Foundation

Now fast forward 10 more years. That same man and his peers will have counted 70 circles round the sun. But John will remain biologically 60. At the same time, someone who is 30 years old in the year 2033 could theoretically begin the therapy at age 30, and stick at a biological age of 30 for the next 30 years, when their calendar would call them 60. That’s what gene therapies for longevity could do.

Longevity startups are riding high as a wave of gene therapies advance through clinical trials. Can they actually turn back the clock?

So far, gene therapy has been approved by the U.S. Food and Drug Administration (FDA) for only a couple of applications like rare inherited diseases and blood cancer. That said, more than 2,000 clinical trials are taking place in 2023, with 200 of them having already reached phase 3 clinical trials. A slew of upcoming gene therapies could be approved—possibly in the months to come—in the United States and Europe, targeting everything from sickle cell disease and hemophilia to metastatic skin cancer. In this future, gene therapy will be approved for everything we can imagine—and many things we can’t.

I’m going to start bringing you Smart Brevity™ versions of books I find worthy of your time.

Zoom in: “Outlive: The Science & Art of Longevity,” by Peter Attia, M.D., is getting tons of buzz, and has spent 18 weeks on the N.Y. Times bestseller list (no. 2 for hardcover nonfiction in the list for Aug. 13).

Rotifers are excellent research organisms for studying the biology of aging, DNA repair mechanisms, and other fundamental questions. Now, using an innovative application of CRISPrCas9, scientists at the Marine Biological Laboratory, Woods Hole, have devised a method for making precise, heritable changes to the rotifer genome, enabling the larger community of scientists to deploy the rotifer as a genetically tractable lab organism.

Local and federal authorities spent months investigating a warehouse in Fresno County, California, that they suspect was home to an illegal, unlicensed laboratory full of lab mice, medical waste and hazardous materials.

The Fresno County Public Health Department has been “evaluating and assessing the activities of an unlicensed laboratory” in Reedley, the health department’s assistant director, Joe Prado, said in a statement Thursday. All of the biological agents were destroyed by July 7 following a legal abatement process by the agency.

“The evaluation required coordination and collaboration with multiple federal and state agencies to determine and classify biological and chemical contents onsite, in addition to assessing jurisdictional authority under this unique situation,” Prado said.

The skin is the largest organ of the body, comprising several compartments and about 20 different cell types that are involved in various skin functions – complexity that is more than skin deep! [1] Skin aging is a multifactorial process that is impacted by several intrinsic and extrinsic factors. Constant exposure of the human skin to such stimuli impacts its function and accelerates aging resulting in dry skin, wrinkling, thinning of the epidermis, and reduced barrier integrity. While we notice most of those changes by looking in a mirror – something the cosmetics industry has leveraged to multi-billion dollar effect – older skin is more at risk of injury, less able to sense touch, heat and cold, slower to heal and more prone to cellulitis and other skin infections.

Aging is a complex and gradual process characterized by a reduction in function and reproducibility along with an increase in the incidence of degenerative diseases. Skin aging has been reported to be associated with the presence and accumulation of senescent cells. “A number of diseases that increase in older people may have a unifying underlying mechanism having to do with senescence,” says Ruth Montgomery, PhD, professor of medicine and epidemiology (microbial diseases) at Yale School of Medicine [2].

Senescent cells are those that have lost their proliferative capacity, are resistant to apoptosis, and secrete factors that can cause tissue deterioration and inflammation [3]. These factors are termed senescence-associated secretory phenotype (SASP) and can lead to extracellular matrix (ECM) deposition, impact epidermal stem cell renewal and worsen melanin synthesis.

Heterochronic parabiosis ameliorates age-related diseases in mice, but how it affects epigenetic aging and long-term health was not known. Here, the authors show that in mice exposure to young circulation leads to reduced epigenetic aging, an effect that persists for several months after removing the youthful circulation.

Yang and co-workers state that “using inducible changes to the epigenome, we find that the act of faithful DNA repair advances aging at physiological, cognitive, and molecular levels, including erosion of the epigenetic landscape, cellular exdifferentiation, senescence, and advancement of the DNA methylation clock, which can be reversed by OSK-mediated rejuvenation. These data are consistent with the information theory of aging, which states that a loss of epigenetic information is a reversible cause of aging.” There is extensive evidence that the key reagent, restriction endonuclease I-PpoI, is cytotoxic. Moreover, the corresponding author published two papers—neither cited—showing that I-PpoI targeted to specific cell types causes a p53 response and cell elimination within a month. Despite globally inducing I-PpoI activation for seven times as long as required to induce a progeric effect, no analysis of mice during this critical window was presented. No significant conclusion of Yang was demonstrated.

In Switzerland, there’s a new cryonics company: and they invited me to have a look around. I had questions: legal, practical, and ethical, and I want to be clear: this is not an endorsement. I just wasn’t going to turn down that invitation. ■ Tomorrow Bio: https://www.tomorrow.bio/

Camera: Martin Bäbler.

Continue reading “Storing dead people at —196°C” »

As we age, our bodies undergo various changes that can impact our overall health and make us more susceptible to diseases. One common factor in the aging process is low-grade inflammation, which contributes to age-related decline and impairment. However, the precise pathways responsible for this inflammation and their impact on natural aging have remained elusive until now.

A new study led by Andrea Ablasser at EPFL now shows that a molecular signaling pathway called cGAS/STING plays a critical role in driving chronic inflammation and functional decline during aging. By blocking the STING protein, the researchers were able to suppress inflammatory responses in senescent cells and tissues, leading to improvements in tissue function.

The findings are published in the journal Nature.