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Category: life extension – Page 347

Sauna Exercise Mimetic — The Science Of The Amazing Health & Longevity Benefits

It is true. From its effect on biomarkers such as heat shock proteins and Fox 03, through to real world impacts on cardiovascular health, to improving mood, helping you live longer healthier and reducing your chance of dying before your time. I think we all know saunas are really great for you, but this will give you all the scientific reasons why… Taking it easy and relaxing for half an hour… Is not just wasting your time… Changes today will make tomorrow better. #saunas

I am going to give you the best reasons in the world to sit back and take it easy in a nice warm environment, and to just forget the troubles of the world.
Maybe play some music, or a podcast, or listen to a book, or just meditate, just relax and take it easy.
It is for your own health after all!!

How about clicking here and watching the video I did on good and bad stress.

The science in the video.

Modulation of body temperature and LH secretion by hypothalamic KNDy (kisspeptin, neurokinin B and dynorphin) neurons.

Continue reading “Sauna Exercise Mimetic — The Science Of The Amazing Health & Longevity Benefits” | >

Healthy skin with OneSkin — Interview//Presentation with Carolina Reis Oliveira

Oneskin — the first skin cream that destroys senescent cells:

Longevity, Health, Long Lifespans, and Halthspans, Psychology, Spirituality — I and Carolina Reis Oliveira talk about all these things in relation to the skin. Find out how you can have very healthy skin with OneSkin!

Visit OneSkin’s website — https://www.oneskin.co/

0:00 — Logo & Title.
0:17 — H! & Intro.
1:40 — Presentation.
2:20 — Presentation | Skin Health — Longevity.
3:57 — Presentation | The Root Cause of Aging.
4:46 — Presentation | Senescent Cells.
5:49 — Presentation | Current solutions.
6:32 — Presentation | OneSkin Approach.
7:47 — Presentation | Let’s Dive Deeper into the Science.
9:51 — Presentation | Replicating Skin Aging.
11:42 — Presentation | Developing an Algorithm to Measure Skin Aging.
12:58 — Presentation | A Drug Discovery Process.
14:23 — Presentation | Senotherapeutic Compounds.
15:00 — Presentation | OS1
15:42 — Presentation | OS1 & UVB Radiation.
17:13 — Presentation | OS1 — Validate effects in 3D models.
19:33 — Presentation | OS1 — Treatment in Skin Biopsies.
20:55 — Presentation | OS1 — Safety.
21:43 — Presentation | OS1 — Clinical Study Results.
23:18 — Presentation | OS1 — Applications Beyond Skin.
26:14 — Presentation | Team.
28:07 — Q&A + the Conversation.
28:25 — Futuristic Psychology & Spirituality.
31:34 — Myths Regarding Immortality.
34:20 — The Collective Rejuvenation.
37:10 — Biologic Hygiene.
41:56 — Cellular Senescence.
46:00 — The Molecular Clock.
48:04 — Morphogenesis of a Scar.
51:15 — Differences Between Skin Types on a Body.
52:35 — Skin Types Regarding Different Races.
54:44 — Skin Conditions.
56:03 — Closing & Ending

Presentación de “La Mort de la Mort” (inglés)

NOT curing aging is immoral.

El libro de José Luis Cordeiro y David Wood, “La Muerte de la Muerte”, cuya publicación en español cubrimos en su día, se ha presentado ahora en francés. Los autores han hecho esta presentación en inglés para promocionarlo.

Todos los beneficios son donados a organizaciones que trabajan para acabar con el envejecimiento.

“La mort de la mort — les avancées scientifiques vers l’immortalité” was published on 21st January 2021 and is available in bookshops throughout France, Belgium, Luxembourg, and Switzerland, as well as online — see e.g. https://www.amazon.fr/mort-avancées-scientifiques-vers-limmortalité/dp/2875422200/

To mark the occasion of the publication, Sergey Young, Founder of the Longevity Vision Fund, asked a number of questions to the book’s co-authors, José Cordeiro and David Wood.

Continue reading “Presentación de “La Mort de la Mort” (inglés)” | >

Quantifying Biological Age With Aging.ai: 24 Blood Tests Since 2009

The maximal reduction for biological age when using the biological age calculator, Phenotypic Age, is ~20 years. In other words, if I’m 80 years old and my biomarkers are all reflective of youth, the lowest possible biological age will be ~60 years old. One reason for that is the inclusion of chronological age in the prediction of biological age, which adds strength to the correlation while simultaneously limiting the maximal biological age reduction.

To account for the possibility that youthful biomarkers at an older chronological age can yield a biological age that is more than 20 years younger, it’s important to quantify biological age using a tool that doesn’t include chronological age in its calculation. Aging.ai fits that criterion, and in the video I present biological age data with use of aging.ai for 24 blood tests since 2009.

‘Exercise protein’ doubles running capacity, restores function and extends healthy lifespans in older mice

A new study shows that humans express a powerful hormone during exercise and that treating mice with the hormone improves physical performance, capacity and fitness. Researchers say the findings present new possibilities for addressing age-related physical decline.

The research, published on Wednesday in Nature Communications, reveals a detailed look at how the encodes instructions for regulating physical capacity, performance and metabolism during aging and may be able to increase healthy lifespan.

“Mitochondria are known as the cell’s energy source, but they are also hubs that coordinate and fine-tune metabolism by actively communicating to the rest of the body,” said Changhan David Lee, assistant professor at the USC Leonard Davis School of Gerontology and corresponding author of the study. “As we age, that seems to break down, but our study suggests you can restore that network or rejuvenate an older mouse so it is as fit as a younger one.”

Chinese scientists may have key to delaying ageing

Scientists in Beijing may be one step closer to having the answer to living longer and reversing the effects of ageing. A group of biologists at the Chinese Academy of Sciences say they have developed a world-first new gene therapy and have been running tests on mice. It involved screening around 10000 genes in search of particularly strong drivers of cellular ageing. They identified 100 genes in that pool, but the one that really stood out was the kat7. They then inactivated that kat7 gene in the livers of mice, Professor Qu Jing explained some of their findings: “These mice show after six to eight months, they show overall improved appearance and grip strength and most importantly they have extended lifespan for about 25%.” Kat7 is one of tens of thousands of genes found in the cells of mammals. The scientists also tested the function of the gene in human stem cells, human liver cells and more. So far there have been no side effects of cellular toxicity. Despite this, the method still has a long way to go from being ready for human trials and will require a lot of funding and much more research. “In the end we do hope that we can find a way to delay ageing even by a very minor percentage we want to delay the human ageing in the future.” For now, there’s no final answer to cheating death, but the scientists plan on testing the function of kat7 in other cell types of humans and other organs of mice.

A genome-wide CRISPR-based screen identifies KAT7 as a driver of cellular senescence

Whereas cellular senescence is known to promote aging, many of the mechanisms controlling this process remain poorly understood. Using human mesenchymal precursor cells (hMPCs) carrying pathogenic mutations of the premature aging diseases Werner syndrome and Hutchinson-Gilford progeria syndrome, the authors conducted a genome-wide CRISPR-Cas9–based screen to identify genes that could affect cellular senescence. They identified KAT7, a histone acetyltransferase gene, as a driver of senescence. Inactivation of Kat7 in mice aging normally and in prematurely aging progeroid mice extended their life span. Although KAT7 requires further study in other cell types, these experiments highlight the utility of genome-wide CRISPR-Cas9 screens and shed further light on mechanisms controlling senescence.

Understanding the genetic and epigenetic bases of cellular senescence is instrumental in developing interventions to slow aging. We performed genome-wide CRISPR-Cas9–based screens using two types of human mesenchymal precursor cells (hMPCs) exhibiting accelerated senescence. The hMPCs were derived from human embryonic stem cells carrying the pathogenic mutations that cause the accelerated aging diseases Werner syndrome and Hutchinson-Gilford progeria syndrome. Genes whose deficiency alleviated cellular senescence were identified, including KAT7, a histone acetyltransferase, which ranked as a top hit in both progeroid hMPC models. Inactivation of KAT7 decreased histone H3 lysine 14 acetylation, repressed p15INK4b transcription, and alleviated hMPC senescence.

Study reveals immune driver of brain aging

A brain aging link ~~~.

Suppose Smokey the Bear were to go on a tear and start setting forest fires instead of putting them out. That roughly describes the behavior of certain cells of our immune system that become increasingly irascible as we grow older. Instead of stamping out embers, they stoke the flames of chronic inflammation.

Biologists have long theorized that reducing this inflammation could slow the and delay the onset of age-associated conditions, such as , Alzheimer’s disease, cancer and frailty, and perhaps even forestall the gradual loss of mental acuity that happens to nearly everyone.

Yet the question of what, exactly, causes particular of the immune system to kick into inflammatory overdrive has lacked a definitive answer.

NAD+ can restore age-related muscle deterioration

The older we grow, the weaker our muscles get, riddling old age with frailty and physical disability. But this doesn’t only affect the individual, it also creates a significant burden on public healthcare. And yet, research efforts into the biological processes and biomarkers that define muscle aging have not yet defined the underlying causes.

Now, a team of scientists from lab of Johan Auwerx at EPFL’s School of Life Sciences looked at the issue through a different angle: the similarities between muscle aging and degenerative muscle diseases. They have discovered aggregates that deposit in skeletal muscles during natural aging, and that blocking this can prevent the detrimental features of muscle aging. The study is published in Cell Reports.

“During age-associated muscle diseases, such as (IBM), our cells struggle to maintain correct protein folding, leading these misfolded proteins to precipitate and forming toxic protein aggregates within the muscles,” explains Auwerx. “The most prominent component of these protein aggregates is , just like in the in the brains of patients with Alzheimer’s disease.”

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