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This may be good news for those who have damaged joints due to sports or old age.

😃


Human knees are notoriously vulnerable to injury or wearing out with age, often culminating in the need for surgery. Now researchers have created new hybrid bioinks that can be used to 3D print structures to replace damaged cartilage in the knee.

The meniscus is the rubbery cartilage that forms a C-shaped cushion in your knee, preventing the bones of your upper and lower leg from rubbing against each other. This stuff is susceptible to damage from sports injuries, but can also wear out with age – and if it gets particularly bad, sometimes the only thing left to do is surgically remove some of the damaged meniscus.

A new synthetic probe offers a safe and straightforward approach for visualizing chromosome tips in living cells. The probe was designed by scientists at the Institute for Integrated Cell-Material Science (iCeMS) and colleagues at Kyoto University, and could advance research into aging and a wide range of diseases, including cancers. The details were published in the Journal of the American Chemical Society.

“Chromosome ends are constantly at risk of degradation and fusion, so they are protected by structures called telomeres, which are made of long repeating DNA sequences and bound proteins,” says iCeMS chemical biologist Hiroshi Sugiyama, who led the study. “If telomeres malfunction, they are unable to maintain chromosome stability, which can lead to diseases such as cancer. Also, telomeres normally shorten with each cell division until they reach their limit, causing cell death.”

Visualizing telomeres, especially their physical arrangements in , is important for understanding their relevance to disease and aging. Several visualization approaches already exist, but they have disadvantages. For example, some can only observe telomeres in preserved, or fixed, cells. Others are time-consuming or involve harsh treatments that denature DNA.

TEL AVIV — November 18, 2020: In a scientifically verified approach, signalling an important breakthrough in the study of aging, Tel Aviv University and The Sagol Center for Hyperbaric Medicine and Research at Shamir Medical Center announced today that, for the first time in humans, two key biological hallmarks of aging, telomere length shortening, and accumulation of senescent cells, can be reversed. The prospective clinical trial, published in peer-reviewed Journal Aging, utilizes Hyperbaric Oxygen Therapy protocols to demonstrate cellular level improvement in healthy aging adults.


For the first-time a human study shows the reversal in the biology of aging including telomere shortening with Hyperbaric Oxygen Therapy.

Fantastic news for a change!


The ageing process has been biologically reversed for the first time by giving humans oxygen therapy in a pressurised chamber.

Scientists in Israel showed they could turn back the clock in two key areas of the body believed to be responsible for the frailty and ill-health that comes with growing older.

As people age, the protective caps at the ends of chromosomes – called telomeres – shorten, causing DNA to become damaged and cells to stop replicating. At the same time, “zombie” senescent cells build up in the body, preventing regeneration.

NAD+ (nicotinamide adenine dinucleotide), a key metabolite central to an efficient and healthy metabolism, declines with age. This previously unexplained phenomena is associated with numerous age-related diseases and has spawned the development of many nutritional supplements aimed at restoring NAD+ to more youthful levels. Publishing in Nature Metabolism, researchers at the Buck Institute have identified chronic inflammation as a driver of NAD+ decline. They show that an increasing burden of senescent cells, which is also implicated in the aging process, causes the degradation of NAD via the activation of CD38 (cyclic ADP ribose hydrolase) a protein that is found on the cell membranes both inside and on the surface of many immune cells.

“We are very excited to link two phenomena which have been separately associated with aging and age-related disease,” said Eric Verdin, MD, Buck Institute President and CEO and senior author of the paper. “The fact that NAD+ decline and are intertwined provides a more holistic, systemic approach to aging and the discovery of CD38 macrophages as the mediator of the link between the two gives us a new target for therapeutic interventions.”


AgelessRx claims that PEARL is the first nationwide telemedicine trial and one of the first large-scale intervention trials on Longevity. The human trial is a stepping stone to the way to bringing rapamycin to the Longevity market. PEARL (Participatory Evaluation of Aging with Rapamycin for Longevity) is a $600,000 trial with the University of California. They will evaluate the safety and effectiveness of rapamycin in 200 healthy adults for Longevity in double-blind, randomized, placebo-controlled trial.

Interested patients will be screened for eligibility using telemedicine. Eligible patients include those aged 50–85 of any sex, any ethnicity, in relatively good health, with only well-managed, clinically stable chronic diseases.

TAME is a separate $75 million trial to clinically evaluate Metformin drugs for Longevity properties. TAME has a composite primary endpoint – of stroke, heart failure, dementia, myocardial infarction, cancer and death. Rather than attempting to cure one endpoint, it will look to delay the onset of any endpoint, extending the years in which subjects remain in good health – their healthspan. A $40 million donation has been combined with a $35 million NIH grant to fund the TAME trial.

Where do you typically go to get the most up-to-date news on anti-aging research studies?

I’ve been digging around and found some longevity journals and other resources but curious to know what else is out there.


One of the most-frequent questions prominent longevity experts get asked is, “How can I contribute?”

Dr. Aubrey de Grey typically responds that, “The main way to get involved other than donating, unless you’re a biologist and can help with the actual research, is in raising awareness.”

– and Why We Don’t Have To — A conversation with David Sinclair.

David Andrew Sinclair AO is an Australian biologist who is a professor of genetics and co-Director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School.

The Italian version is “Longevità”, here: https://www.verduci.it/prodotto/longevita/

https://media.blubrry.com/drjohnday/p/drjohnday.com/podcasts/Podcast217.mp3 Podcast: Play in new window | DownloadSubscribe: Apple Podcasts | Android | RSS6 Foods to Reverse Aging with Lithium Could a microscopic dose of the psychoactive drug lithium, which occurs naturally in mineral water and certain foods, actually be the secret to less heart disease, better moods, and a longer life? In this article, I share how eating six foods may reverse aging with lithium.

“In our current study we were able to uncover important limitations for the use of metformin as longevity medicine,” says Dr. Ermolaeva. In contrast to the positive longevity effects in young organisms that received metformin, lifespan is shortened through metformin intake at an older age. “Previous studies that provided evidence of an extended longevity by metformin usually examined animals treated with metformin from young adult or middle age until the end of life. In contrast, we have looked at treatment windows covering the entire life span, or restricted to early life or to late life”. The study also utilized a human cell culture model of replicative aging to assess human responses to metformin at a cellular level and compare them to organismal responses of the worms.

**Metformin longevity benefits are reversed with age**

The research team led by Dr. Ermolaeva found that the very same metformin treatment that prolonged life when C. elegans worms were treated at young age, was highly toxic when animals of old age were treated. Up to 80% of the population treated at old age were killed by metformin within the first 24 hours of treatment. Consistently, human primary cells demonstrated a progressive decrease in metformin tolerance as they approached replicative senescence. The researchers were able to link this detrimental phenotype to the reduced ability of old cells and old nematodes to adapt to metabolic stressors like metformin. Under these circumstances, the exact same dose of the drug that increased longevity of young-treated organisms by triggering adaptive stress responses was harmful in animals treated at old age, which were unable to activate such protective signals.


Metformin is a common type 2 diabetes drug. Recently, it was found to extend life span of young non-diabetic animals but the responses of older organisms to metformin remain unexplored. Researchers at the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena, Germany, and the Friedrich Schiller University Jena found that mitochondrial dysfunction abrogates metformin benefits in aged C. elegans and late passage human cells. Moreover, the same metformin regime that prolongs the lifespan of young nematodes was toxic in old animals by inducing deleterious metabolic changes. These findings suggest that aging sets a limit for the health span benefits of metformin outside of diabetes.