What do “epigenetic clocks” actually measure? These lab tests have become popular tools for studying biological aging, or how the body’s cellular function changes at a faster or slower rate than expected. However, the underlying biology behind each of these measurements has remained largely unknown until now.
Last summer I sat down with Adam Becker and asked him to name the most confident story in tech.
He picked the one nobody in Silicon Valley is allowed to question: that godlike #AI, digital immortality, and space empires are simply where history is headed. Not a hope. A destination.
Becker has a PhD in astrophysics and fifteen years as a science journalist. In his book More Everything Forever, he takes that story apart and shows where it actually came from: misread science fiction, fringe mailing lists, and a very old colonial logic about who deserves the future. From there it walked straight into university labs, congressional hearings, and your feed.
His line from our conversation stayed with me: Silicon Valley has confused science fiction with science, and science with branding.
The stakes are not academic. While we debate the welfare of trillions of hypothetical posthuman minds, the actual world runs on war, climate collapse, widening inequality, and a shared reality coming apart. Becker calls the grand visions a distraction. I asked him whether a civilization can function without a myth of the future at all.
I do not agree with everything Adam argues, and that is exactly why this one is worth your time. Watch it and tell me who you think is right about the #Singularity.
Bosch and colleagues described that one-time AAV-FGF21 gene therapy in aged mice induced whole-body tissue-specific adaptations, including improved metabolic and mitochondrial function, restored proteostasis, and reduced adiposity, inflammation, fibrosis, and amyloidosis, thereby maintaining systemic cell fitness, preventing multi-organ age-related pathology, and prolonging health span.
Researchers have found that an upstream promoter of two extracellular matrix proteins increases healing and strength capabilities in the tendons of rats.
Tendon injuries in older people
Previous research has found that, like with many other injuries, tendon injuries have an age-related component. The tendons of the biceps and rotator cuffs are more commonly injured in older people than in younger people [1], and older people heal slower after forearm injuries and have less range of motion in the fingers for a longer time [2].
Dr. Michael Lustgarten earned his Ph.D. in Physiology from the University of Texas Health Science Center at San Antonio in 2009. Since then, he has contributed to 38 peer-reviewed publications that have been cited more than 5,000 times.
What if medicine stopped treating diseases one at a time and started repairing the human body as a system? This conversation explores why longevity research is accelerating faster than ever.
In a study recently published in Nature Communications, researchers from Berlin, Potsdam, and Jena present a new method for analyzing the epigenome. The machine-learning method identifies differentially methylated DNA regions without sample labels—a prerequisite for many existing algorithms. This makes it possible to identify previously hidden biological patterns as well as new subgroups of cells or diseases.
The activity of our genes is not determined by DNA sequence alone. The attachment of small chemical compounds—known as methyl groups—influences which genes are active and which remain silenced. DNA methylation is thus a central component of the epigenome.
Changes to the epigenome play a crucial role in the development of our bodies, influence the aging process and are relevant to numerous diseases, such as cancer. To understand such changes, researchers specifically search for differentially methylated DNA regions (DMRs). However, existing methods usually require samples under investigation to be assigned to known groups—such as healthy or diseased tissue. With complex clinical datasets, however, this information is often unknown.
However, the trajectory of wearables is evident. Oura is contributing to the widespread use of continuous health and recovery monitoring. Apple is showcasing how wearable technology can integrate safety, communication, and wellness. Hume is a part of the growing trend for health span and longevity. Garmin specializes in navigation and performance tracking. Fitbit provides data analytics with its interaction with Google’s ecosystem. And by trying to quantify the neurological system and cognitive function itself, Pison is pushing the boundaries.
When taken as a whole, these companies and their products suggest a time when wearables will be more than just clothing. It turns into a conduit between the digital world and our biology. The ultimate promise of this technology is not that doctors, coaches, or human judgment will be replaced by machines. It’s that we’ll know more about ourselves, and that knowledge will be accessible when it counts most.
Therefore, the new world of wearables may be less about watches, rings, and bands and more about a much larger transformation: providing people with previously unheard-of visibility into their skills, performance, and health.
Researchers have identified a cellular “aging switch” driving age-related skin decline and chronic inflammation, centered on the interaction between two proteins, BMAL1 and YAP. While these proteins independently maintain cellular structure in youth, age-related tissue stiffening and the immune signaling protein Interleukin-17 (IL-17) cause them to alter their behavior, binding to new DNA regions to aggressively activate inflammatory genes and impair wound healing. In a study published in Nature Aging, experiments on mice demonstrated that temporarily blocking IL-17 suppressed this BMAL1-YAP inflammatory pathway and significantly reversed visible signs of skin aging, highlighting a promising new therapeutic target for treating age-related epidermal deterioration in humans.
Chronic inflammation is a hallmark of aging, yet the underlying molecular mechanisms are incompletely understood. Here the authors show that, in the skin, BMAL1 and YAP cooperate at enhancers to maintain epidermal homeostasis. During aging, this cooperation is increased at inflammatory enhancers, driven by age-associated changes in the microenvironment, promoting epidermal inflammation.