Lifeboat Foundation

From the beginning of time, humankind has searched for the secret to a long life. Now science may have found an answer, in the form of molecular augury. The pattern of chemical chains that attach to the DNA in your cells—on-off switches known as epigenetic markers—can reveal how swiftly you are aging, and perhaps even how much longer you will live. While genetic testing might tell you where you came from, epigenetics promises a glimpse into the future. Now, a handful of companies are offering commercial blood or saliva tests based on the science of epigenetics—a chance to find out how old you truly are.

Companies claim they can now easily calculate your biological age. Should you take them up on it?

Objective Failing to properly repair damaged DNA drives the ageing process. Furthermore, age-related inflammation contributes to the manifestation of ageing. Recently, we demonstrated that the efficiency of repair of diethylnitrosamine (DEN)-induced double-strand breaks (DSBs) rapidly declines with age. We therefore hypothesised that with age, the decline in DNA damage repair stems from age-related inflammation.

Design We used DEN-induced DNA damage in mouse livers and compared the efficiency of their resolution in different ages and following various permutations aimed at manipulating the liver age-related inflammation.

Results We found that age-related deregulation of innate immunity was linked to altered gut microbiota. Consequently, antibiotic treatment, MyD88 ablation or germ-free mice had reduced cytokine expression and improved DSBs rejoining in 6-month-old mice. In contrast, feeding young mice with a high-fat diet enhanced inflammation and facilitated the decline in DSBs repair. This latter effect was reversed by antibiotic treatment. Kupffer cell replenishment or their inactivation with gadolinium chloride reduced proinflammatory cytokine expression and reversed the decline in DSBs repair. The addition of proinflammatory cytokines ablated DSBs rejoining mediated by macrophage-derived heparin-binding epidermal growth factor-like growth factor.

Rejuvenation Roundup November 2019

Quite a number of readily understandable reviews were published this month, along with an X10 episode on epigenetic alterations; if you’re new to the biology of aging or want to introduce someone else to the topic with new material, this is a great time to start.

LEAF News

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This study involved 4,717 participants from two different community-based cohorts. A meta-analysis of both cohorts showed that elevated sCD14 was associated with a 12 percent increased risk of dementia as people got older. Higher levels of sCD14 were also associated with accelerated brain aging in both cohorts, a faster progression of age-related brain atrophy, and a more rapid decline of executive functions.

The authors sum up their findings: “sCD14 is an inflammatory marker related to brain atrophy, cognitive decline, and incident dementia.”

“Higher levels of sCD14 were associated with markers of brain aging and injury, such as total brain atrophy and a decline in executive functioning—the decision-making needed for many activities of daily life,” first author Matthew Pase, of the Florey Institute for Neuroscience and Mental Health in Melbourne, Australia, said in a news release.

You are invited to Perpetual Life for The Remembrance of the Resurrectables and Age Reversal & Cryonics by Bill Faloon.

Before and After the service, we will celebrate the Remembrance of the Resurrectables in the Sanctuary, A ceremony of remembering all of the patients that are in Cryonic Suspension.

Continue reading “Remembrance of the Resurrectables and Age Reversal & Cryonics” »

Changes to gene activity in mice show the ageing process can be slowed or even reverse, leading to hopes it could be replicated in humans.

Cognitive Behavioural Therapy (CBT) for patients with social anxiety not only helps to reduce anxiety levels but also seems to protect against accelerated cellular ageing, a study involving researchers at Karolinska Institutet published in the journal Translational Psychiatry reports.

“This is the first step towards better understanding the link between cellular ageing and the treatment of psychiatric issues,” says lead author Kristoffer Månsson, researcher at the Department of Clinical Neuroscience at Karolinska Institutet in Sweden.

Individuals affected by mental illness are at greater risk of developing somatic conditions, such as high blood pressure and diabetes, earlier in life than unaffected individuals. While the reasons for this are unclear, one possible contributory factor is that mental health disorders are associated with shorter telomeres and accelerated cellular ageing.

Article courtesy of Dr. Nicholas DiNubile, Vice President of the A4M, an orthopedic surgeon specializing in sports medicine, best selling author, keynote speaker, and one of our medical editors who is dedicated to keeping you healthy in body, mind and spirit.

We’ve extended the warranty on the human heart, and people are living longer. We’ve improved care for skin, and people look better. But it’s your frame that gets you where you need to go whenever you need to get there. Without the proper care, your bones and joints can all too easily become the limiting factor in your enjoyment of life. Have you outlived the warranty on your frame? Would you like an extended warranty?

I have come to believe that the achievement of longevity will bring the challenge of durability to the forefront of modern healthcare.