Today, we’re officially launching @HalePrevention with a film called “Grow Old With Them”. You won’t see us founders in it. We wanted you to meet one of our customers, and hear his story in his own words. It captures why we built Hale better than any founder introduction could.

Glycine will likely be the "next creatine" Although glycine imho is way more effective And all my favorite peptides have glycine residues "Either glycine or DT-109-treatment provides an athero-protective effect evidenced by reduced atherosclerosis in the whole aorta and aortic sinus concomitant with reduced superoxide formation. DT-109 activity was superior compared to that of glycine."

Can we please remove all the neuroticism from the performance and longevity field Why is everyone attracted to this field so damn neurotic We need to focus on resiliency and defense, not fragility Anti Fragile Longevity Thrive DESPITE suboptimal inputs

Human brain organoids record the passage of time over multiple years nature.com/articles/s41586-0…

I put eight years of Fitbit data into Claude. It spent a couple of hours analyzing everything, looking for correlations, etc. What it found: When I stay up late, I don't get as much sleep

Growth and movement of cells in a human hair follicle. From this paper: Mapping cell dynamics in human ex vivo hair follicles suggests pulling mechanism of hair growth nature.com/articles/s41467-0…

it used to be really hard to consume enough protein to make working out worthwhile. your choices were to eat enough chicken breast until you’re nauseous or drink some whey isolate chalky disgusting proteinslop for about 15g of protein.

Most exercise and aging studies can't answer a basic question: is muscle deterioration from aging itself, or just from decades of moving less? A new Nature Aging study solved this by recruiting older adults who moved as much as people in their twenties. The researchers from Amsterdam UMC and Maastricht University recruited four distinct groups: young adults in their twenties, older adults whose daily step counts and high-intensity activity matched the young group, older adults who had trained consistently for years (three structured hour-long sessions per week for over a year), and older adults with early physical impairment. They took muscle biopsies before and after a one-hour cycling session, then measured over 24,000 gene transcripts, 135 metabolites, and 1,383 lipid species. By matching activity levels between young and older groups, any molecular differences couldn't be blamed on the older adults simply moving less. This isolated aging from inactivity for the first time at this molecular depth. Key findings: • The defining molecular signature of muscle aging is an energy crisis. Comparing young adults to activity-matched older adults, 1,106 genes were downregulated with age. These genes build the mitochondrial machinery that produces cellular energy: ATP synthase, cytochrome c oxidase, and NADH dehydrogenase subunits. Mitochondria are the power plants of cells, converting nutrients into ATP, the energy currency cells use to function. When these genes decline, cells lose their ability to generate energy efficiently. • NAD+ levels declined and triglycerides accumulated inside aging muscle. NAD+ is a molecule required for energy production and cellular repair. Lower NAD+ means less capacity to convert fuel into usable energy. Triglycerides are stored fats, their accumulation inside muscle indicates unburned fuel piling up as the tissue loses its ability to process it. • More than half the molecular signature of muscle aging was absent in trained older adults. Specifically, 57.1% of age-related gene downregulation and 55.9% of upregulation were missing in the trained group. Their muscle resembled young adults far more than their chronological age would predict. • The changes training preserved were specifically the energy metabolism ones. Genes like NDUFS1 and COX5A, which were depleted in normally active and impaired older adults, sat at youthful levels in the trained group across all five mitochondrial respiratory complexes. The single most prominent feature of muscle aging turned out to be the single most preventable. • Being generally active was not enough. Structured training was the difference. The normally active older adults walked as much as young adults, and their energy metabolism genes declined anyway. What preserved the youthful molecular profile was structured, sustained training. Filling a step counter and being genuinely trained are not equivalent at the molecular level. • Roughly half of muscle aging persisted regardless of training. Changes in genes controlling synaptic transmission (how nerves communicate with muscle) and WNT signaling (a pathway regulating tissue maintenance and stem cell function) appeared in all older adults, trained or not. This unavoidable half is where drugs will have to work. • The fittest muscle mounted the largest inflammatory response to exercise. All groups activated stress and immune genes after exercise, including IL6, IL1B, and TNF. But the magnitude scaled with fitness. Trained older adults most closely resembled young adults in their response, followed by normally active, with impaired older adults showing the most blunted response. The stress response to exercise appears to be the mechanism of adaptation, not damage to be minimized. This raises a concern about anti-inflammatory longevity strategies. If the inflammatory stress response is how exercise produces its benefits, chronically suppressing inflammation may blunt the adaptation that exercise depends on. It doesn't mean inflammation is beneficial in general, but the timing and context matter. A separate discovery: the proteasome appears to regulate NAD+. The proteasome is the cellular machinery that breaks down damaged proteins. When researchers inhibited it, NAD+ levels rose in both muscle and liver cells to a degree comparable to NAD+ precursor supplements. This opens a new route to understanding NAD+ decline that operates through protein turnover rather than just supplying more raw material. The study draws a clear line between what lifestyle can address and what will require therapeutics. The energy metabolism decline, mitochondrial deterioration, and NAD+ depletion that define muscle aging are largely preventable through structured training. The synaptic and signaling changes that persist in all older adults represent the unavoidable half where drugs will need to work. The decisions made about structured training in midlife determine which molecular trajectory muscle follows in later decades. Half of muscle aging is optional. The other half isn't. Knowing which changes belong to each category is knowing where behavior ends and biology takes over.

Andrew Huberman shares a simple, science-backed trick to fall asleep faster when your mind races or you can't stop noticing your body position: Close your eyes and do slow, deliberate eye movements to shut down proprioception (body awareness) and signal your brain it's time to transition into sleep. Try this tonight (takes ~1–2 minutes): - Slowly move eyes left → right (a few times) - Then counterclockwise circle → clockwise circle Look up → down - Gently attempt to look toward the bridge of your nose (faux cross-eyed) - Finish with a long exhale to slow heart rate Why it works: Eye movements coordinate with your vestibular system & cerebellum to mimic the natural forgetting of body position that happens at sleep onset (similar to slow rocking or boat motion calming the brain). It gives your racing mind something active to focus on instead of "just relax." Huberman: "Many people find it helps them fall asleep quickly—it's not kooky; it's physiology." No apps, no gadgets—just your eyes. Game-changer for insomniacs or restless nights. Try it & report back.

HUGE breakthrough out today, in arguably the single most neglected aspect of aging, extracellular matrix damage. Top researchers have tried & failed for decades to do this. Massive kudos to Aaron and his team! (Proud to note that Revel is a SENS spinout.) revelpharmaceuticals.com/new…

Most people have no idea how long it actually takes to build muscle after a workout. The biology runs on a much slower clock than many realize. A single resistance session raises muscle protein synthesis fast, and synthesis is the process that lays down new contractile protein. MacDougall measured it directly: it climbed about 50 percent by 4 hours after exercise and peaked near 109 percent above baseline at 24 hours. Phillips found the same arc, still elevated at 48 hours before returning to rest. The response is large, it is brief, and within 36 to 48 hours the muscle is back to baseline. That is one full cycle from a single workout. Damas and colleagues tracked untrained men through ten weeks and measured synthesis and muscle damage at the same time points. In week one the synthesis response was highest, but so was muscle damage, the structural disruption that unaccustomed training causes. Early synthesis was being spent repairing that damage rather than adding new tissue, and the magnitude of the early response did not predict who gained the most muscle later. By around week three the damage response had attenuated, and by week ten, with damage minimal, synthesis finally correlated with actual hypertrophy. The same group showed that the apparent size increase in the first few sessions is largely swelling and edema, not growth. Durable muscle is built over months, not hours. What you measure should follow that timeline. The acute spike is necessary but not sufficient, so a supplement or technique that raises synthesis acutely has not demonstrated it builds muscle. Judge a program or a product by the trend across two to three months, not by how the session felt or what the scale did the next morning. The first weeks of scale weight overstate real tissue because some of it is water, so do not over-read it when it moves. The synthesis response is the fast part. Adding muscle is the slow part, and it only shows up with consistency. References: MacDougall et al., Canadian Journal of Applied Physiology, 1995 Phillips et al., American Journal of Physiology, 1997 Damas et al., Journal of Physiology, 2016 Damas et al., European Journal of Applied Physiology, 2018

Whole body scans in asymptomatic people won't save lives overall. They will mostly find benign incidentalomas that cause anxiety for otherwise healthy people. Many of us have benign growths that mimic cancer but are harmless. These will be discovered leading to unnecessary panic and additional testing that causes harm. If you want to live a long healthy life, skip the scan and instead go the gym and eat a salad.