Multilingualism emerged as a protective factor in cross-sectional and longitudinal analyses, whereas monolingualism increased risk of accelerated aging
A review on how SGLT2 inhibitors target ectopic fat (specifically epicardial fat). Ectopic fat is the excess fat that gets stored in organ tissue. The paper outlines the different mechanisms of how it does so. For anyone not familiar with SGLT2 inhibitors, they cause you to urinate 60-80g of glucose, so it can cause a mild caloric deficit. It would be interesting to see a side by side comparison of how SGLT2i's compare to GLP1 reduction in ectopic fat.
People talk about a single morning HRV, either celebrating a high one or panicking about a low one. One night barely tells you anything on its own. Alcohol, a late meal, travel, sleeping in a different bed, a minor cold you don't even feel yet, any one of those can swing a single reading more than most real physiological changes do.
What actually makes an HRV number worth trusting is consistency over time, not any single measurement. A rolling average across two to three weeks smooths out the noise from any one bad night and starts showing you your actual baseline and how it moves. The individual number is mostly noise. The trend is the signal.
The other thing worth knowing: your baseline is personal and not comparable to anyone else's. Genetics, age, and fitness level all set a different starting point, so comparing your raw HRV to a friend's or to some number you saw online is close to useless. What matters is whether your own trend is moving up, down, or holding steady relative to your own history, nothing else. If you're new to tracking, give it three or four weeks before you trust any single day's reading over what the trend is telling you.
ARPA-H was established in 2022 and approved two programs in 2024 led by researchers in this field: PROSPR aims to establish biomarkers and clinical indications of aging, i.e. "intrinsic capacity" and run FDA-approved clinical trials to build the rail lines for future preventative trials against aging, offering an alternative to the stepping-stone approach of targeting an age-related pathology and then expanding from there. FRONT is led by Jean Hebert, who argues for sidestepping most of the complexities of aging biology by replacing failing tissues and organs. His program focuses on piecemeal replacement of damaged neocortical tissue. Various other programs also focus on aspects of aging biology.
XPrize Healthspan launched in 2023 and has a prize purse up to $101 million to a team that restores 10+ years of healthy function across muscular, cognitive, and immune systems. Forty teams have advanced to semi-finals, and the competition intends to end in 2030.
A roadmap on research and innovation integrating replacement and next-generation damage-removal therapeutics to modulate the ageing process in the whole body, restore biological function, and extend healthy lifespan.
Influencers and ultra-rich people looking to extend their lifespan are trading tips and tricks on how to eke out extra years.
One thing I found interesting is how many different paths people think could lead to healthier aging, senolytics, stem cells, epigenetic reprogramming, AI-driven drug discovery, regenerative medicine, and more.
If you had to bet on one area that will have the biggest real-world impact over the next 10–15 years, which would it be and why?
Personally, I'm especially interested in regenerative medicine. The idea of helping aging tissues repair themselves feels like one of the most exciting directions in the field.
For anybody interested in the metabolic hypothesis of Alzheimer's, this is an interesting overview of research on the overabundance of glycan protein modifications and the failure to clear them as contributors to Alzheimer's pathology.
One of the more interesting callouts was glucosamine usage was associated with a 25% higher mortality risk in patients with established Alzheimer's disease-related dementia, and a 25 percent higher rate of progression from mild cognitive impairment to full dementia.
Major caveats are needed to process that finding because it seems like this finding does really translate to healthy people taking glucosamine. The biological mechanism through which it could worsen outcomes in an already hyperglycosylating brain is coherent though.
As people age, their muscles don't just get weaker, they may also stop doing something that's been quietly protecting them from cancer. A study published in Nature Communications by researchers at Duke-NUS Medical School found that healthy muscle releases tiny molecular packages into the bloodstream carrying a specific microRNA that actively suppresses tumor growth in other tissues. Aging muscle releases far fewer of these packages, and what it does release carries much less of the protective cargo. When researchers exposed colorectal, lung, and bile duct cancer cells to vesicles from young, healthy mouse muscle, the vesicles sharply reduced cancer cell growth. Vesicles from old muscle couldn't do the same. The pathway controlling this entire system, the researchers found, can be reactivated through exercise.
A couple of providers, coaches and I whipped up this lab service since we were getting a lot of complaints about expensive labs: https://dirtcheaplabs.com
As the name suggests, these are meant to be dirt cheap (quest) labs.
We're using it for our clients, but if you guys want to join in, more volume helps lower our platform fee (selfishly) and you guys get (dirt) cheap labs.
There is a slight mark up on each marker just to cover the platform fee that gives us the bulk pricing, but this is by no means a business meant to make money.
If we can pay off this month's fee with relative ease, we can start offering labcorp as well.
Feel free to DM me if you want to help with the project at all!
In this presentation, Michael Levin proposes a new perspective on aging, framing it as a cognitive and cybernetic disorder rather than just a result of physical damage or biological programming. He suggests that our bodies function as a "Ship of Theseus," where maintaining the overall structure relies on information stored in bioelectric patterns that guide cells toward a specific anatomical goal (0:00 - 2:45).
Key takeaways from his research include:
• Anatomical Homeostasis: Biological systems use electrical networks to store a "set point" or plan for the body's structure, allowing cells to collaborate toward complex goals like limb regeneration, even when individual cells lack the full picture (3:45 - 8:30).
• Bioelectric Manipulation: Levin's team has developed techniques—using ion channel drugs and optogenetics—to read and rewrite these patterns. They have successfully induced organ formation (like eyes) and triggered appendage regeneration in frogs by resetting their bioelectric state, essentially providing a "prompt" for the tissue to build toward a new goal (8:40 - 12:20).
• Aging as Degradation: The central hypothesis is that aging involves the blurring or degradation of these instructive bioelectric patterns, causing cells to lose their precise guidance. This leads to "atavistic dissociation," where cells no longer align their transcriptomes to the body's collective evolutionary age (12:35 - 14:15; 20:30 - 21:45).
• Cybernetic Model of Aging: Levin suggests that once a goal-directed system achieves its primary objective (development), the lack of new challenges can lead to a breakdown in order, similar to a psychological crisis. He posits that interventions could potentially reverse aging by "sharpening" these fuzzy patterns and re-engaging the system with new, organized goals (17:35 - 19:45).
https://www.nature.com/articles/s43587-026-01138-7
Abstract:
Different species age in similar ways but their lifespans differ by orders of magnitude. It is not clear how these similarities and differences arise from the accumulation of damage that underlies aging. Does long lifespan arise from reduced damage production, increased removal or enhanced robustness to damage? Here we apply the saturating removal model—a stochastic model of damage accumulation and removal—and fit it to survival data from well-studied species. Several parameters have near-universal values including ratios of removal rate, noise amplitude and death threshold. The model parameter that best predicts lifespan is the damage production rate, which spans seven orders of magnitude. We identify two distinct aging regimes: ballistic aging where damage production outpaces removal, characterizing yeast, nematodes, flies and mice, and quasi-steady-state aging, where damage tracks a moving set point of balanced production and removal, characterizing humans, dogs, guinea pigs and cats. These results provide a mechanistic model-based basis of comparative aging that awaits experimental validation.
theoretically? how does one go about finding metformin? My mother takes it but I do not wish to steal her medication.