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Methylation clocks are taking the longevity community by storm, but why are they so useful?


Do you know how old you really are? I am not doubting your ability to remember your birthday or questioning the honesty of your parents. Do you, on a fundamental level, know how ‘old’ your body truly is? Now surely that is just the same as the number of years you have been around, which would be your chronological age? Well in reality the answer to how ‘old’ your body is comes down to much more than simply how long you have been around for.

Allow me to explain by falling back to the commonly used automobile analogy. Let’s imagine I bought two identical Ford Escorts in 1982, and then proceeded to place one of them inside a time capsule, where it would be kept at a constant temperature in a non-reactive atmosphere. I then proceeded to drive the second car for the next 40 years. Over that 40 years, this car is going to experience wear and tear, and will most likely break down several times which will require mechanical intervention (analogous to medical intervention). Now, after this 40-year period I am going to take the first car out of storage and compare the two cars side by side. Which car is in the better condition? Well, the car that was preserved, obviously. Which car is likely to last the longest from that point onward? Well, the car which has been preserved, obviously.

“Functional mutations in the growth hormone pathway” meaning it is not active. What’s good for you as a youngster might not be good for you when you’re old.


Dr Nir Barzilai reveals what the longevity genes project found on why Centenarians live longer, not the longevity genes, not healthy lifestyles in this clip.

Dr. Nir Barzilai is the director of the Institute for Aging Research at the Albert Einstein College of Medicine and the Director of the Paul F. Glenn Center for the Biology of Human Aging Research and of the National Institutes of Health’s (NIH) Nathan Shock Centers of Excellence in the Basic Biology of Aging. He is the Ingeborg and Ira Leon Rennert Chair of Aging Research, professor in the Departments of Medicine and Genetics, and member of the Diabetes Research Center and of the Divisions of Endocrinology & Diabetes and Geriatrics.

Dr. Barzilai’s research interests are in the biology and genetics of aging. One focuses on the genetic of exceptional longevity, where we hypothesize and demonstrated that centenarians have protective genes, which allows the delay of aging or for the protection against age-related diseases. In a Program he is leading we take full advantage of phenotypes, DNA, and cells from the Ashkenazi Jewish families with exceptional longevity and the appropriate controls and his group have established at Einstein (over 2,600 samples of which ~670 are centenarians) and discovered underling genomic differences associated with longevity. Longevity Genes Project (LGP) is a cross-sectional, on-going collection of blood and phenotype from families with centenarian proband. LonGenity is a longitudinal study of 1,400 subjects, half offspring of parents with exceptional longevity, validating and following their aging in relationship to their genome.

DISCLAIMER: Please note that none of the information in this video constitutes health advice or should be substituted in lieu of professional guidance. The video content is purely for informational purposes.

After surgery, some cancer patients can safely skip radiation or chemotherapy, according to two studies exploring shorter, gentler cancer care.

Researchers are looking for ways to precisely predict which cancer patients can avoid unneeded treatment to cut down on harmful side effects and unnecessary costs.

One new study used a blood test to determine which colon cancer patients could skip chemotherapy after surgery. Another suggests some low-risk breast cancer patients can omit radiation after lumpectomy.

This is a fantastic podcast exploration of a rapidly maturing, wildley varied fields of science, the military, medicine, the industrialization, exploration, and colonization of our solar system, and the hope for, path to, and purpose of the successful creation of a posthuman, post scarcity future. Its a future destination for humanity that will require a seemless, successful integration of our human biology with artificial intelligence and advanced nonbiological — AND artificially biological — mechanical systems that in one way or another all pass through a very few neccessary technological achievements. In this case it is the seemless communication in both directions of the biological, in this specific case it’s the human sense of touch.


When Brandon Prestwood’s left hand was caught in an industrial conveyor belt six years ago, he lost his arm. Scientists are slowly unraveling the science of touch by trying to tap into the human nervous system and recreate the sensations of pressure for people like Prestwood. After an experimental surgery, Brandon’s prosthetic arm was upgraded with a rudimentary sense of touch—a major development in technology that could bring us all a little closer together.

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A study published today in Cell Reports reveals how populations of a bacterium called Pseudomonas respond to being treated with Colistin, a “last resort” antibiotic for patients who have developed multi-drug resistant infections.

Antibiotics play a key role in by helping to combat , but bacteria can evolve resistance to antibiotics patients rely on. Antibiotic– now cause 1 million deaths worldwide per year.

With a small number of “last-resort” antibiotics available, researchers from the University of Oxford are investigating the processes that drive the rise, and fall, of resistance in common bacterial pathogen populations, which is key to tackling the increase in antimicrobial resistance (AMR).

One theory for is that it is similar to the “death feint” that some animals show. When faced with a predator of overwhelming size or strength, some prey animals will freeze and presumably the predator may not notice them.

One patient in the study vividly described seeing a snake (which also spoke to her). We can’t say from one example that her body was adopting a primitive defence to a predator, but it’s certainly a possibility.

Catatonia remains a mysterious condition, stuck halfway between neurology and psychiatry. At least by understanding what people may be experiencing, we can provide reassurance and empathy.

Our cells perform a marvel of engineering when it comes to packing information into small spaces. Every time a cell divides, it bundles up an amazing 4 metres of DNA into 46 tiny packages, each of which is only several millionths of a metre in length. Researchers from EMBL Heidelberg and the Julius-Maximilians-Universität Würzburg have now discovered how a family of DNA motor proteins succeeds in packaging loosely arranged strands of DNA into compact individual chromosomes during cell division.

The researchers studied condensin, a protein complex critical to the process of chromosome formation. Although this complex was discovered more than three decades ago, its mode of action remained largely unexplored. In 2018, researchers from the Häring group at EMBL Heidelberg and their collaborators showed that condensin molecules create loops of DNA, which may explain how chromosomes are formed. However, the inner workings by which the protein complex achieves this feat remained unknown.

“We have been working on this problem for a long time. But only now, by combining different experimental approaches, we have found an answer to this long-standing question,” said Christian Häring, former Group Leader at EMBL Heidelberg and now Professor at the Julius-Maximilians-Universität Würzburg.