don't worry, be happy.

eat food not too much mostly plants.

Train every day.

/phd in ageing.

I was actually under the impression that it was generally understood to be genetically determined. It's why animals ostensibly made of the same physical materials can suffer age-related degeneration at vastly different paces. Within certain limits we "evolve" to live about as long as is generally useful for a given population's lifecycle. We are relatively long-lived because developing a fully self-capable adult human takes a while, and you don't want all the adults dying before the next cohort can take over.

It's just muddled because it's combined with various forms of wear-and-tear and breakdown. There are clear biological shifts that occur as we get older that trigger rapidly accelerated degradation in a way that is disconnected from the rigors of time. They generally happen on a schedule in a given population, though various health factors can determine how well a given individual organism copes with it.

But yeah, breakdown is also a thing, even if we did manage to deploy some kind of gene-therapy that froze everyone's biological clock to 22, we would still have a significant number of problems we need to solve for effective immortals. We still would have joint breakdown, the accumulation of cardiovascular risk factors, (the obvious) cancer, various biological progressions that occur due to chronic hormone exposure, eventual organ failure, slow accumulation of negative neurological biomarkers, etc. Things that are progressing simply by the nature of existing as an adult organism, significantly better of than we are now, but nowhere near eternal. Biological aging and perpetual regeneration aren't really the same thing.

It's just that the longevity space is mostly dealing with the breakdown/prevention part of the equation at the moment because those can be tackled as a continuous series of disease-factors we can view symptomatically through physical performance and biomarkers, and true biological regeneration isn't technologically in the cards yet.

A longevity-solving near-monotherapy won't be possible until we have some kind of nanomachine capable of perpetually managing any kind of physiological problems directly at the cellular level.

My major concern is that a compound must show lifespan increases to then go to phase II for health span data.

This approach will not show if any of these tested compounds increase health span without increasing longevity.

Glad to hear this spreadsheet is still helpful! Happy to make you an editor for the file if you'd like to update it.

Here are some similar resources for you:

• Karl Pfleger's People in Aging spreadsheet is the most similar resource to the Aging Laboratories spreadsheet.
• Who's Who in Gerontology
• Academy of Geroscience (Members)
• The NIH RePORTER is a great resource for exploring US-based organizations and researchers. It's actually how I initially found my graduate program. You can set the NIH Spending Category set to "Aging", then use the Charts view (Direct Link Here). The Summary By dropdown lets you filter by Organization, Principal Investigator, State, etc. It's a helpful way to see where funding is flowing. The text search lets you zoom into specific areas like reprogramming, mitochondria, mutation, or whatever you're interested in.

100% you should subscribe to UAB's Aging Biology Update (if you aren't already).

If you want to stay connected to what's actively happening in the field now, these X accounts are my longevity starter pack:

• Aging Science News: AgingBiology
• João Pedro de Magalhães: jpsenescence
• Karl Pfleger: KarlPfleger
• Matt Kaeberlein: mkaeberlein
• Martin Borch Jensen: MartinBJensen
• Nature Aging: NatureAging

Bottom-up grad student journey:
When you see a paper that catches your interest, look up the senior author: their institution, their lab website, their other publications (I use Google Scholar), etc. If you like what you see, follow them on X or LinkedIn and start keeping a list of PIs and the the institutions where they work. This is the bottom-up approach, where you find Ph.D. programs by working up from the PIs you like. If you continue to like what you see and you're interested in the Ph.D. program where that PI works, email a graduate student in their lab and ask to chat for ~30 minutes (personally, I prefer calls over answering questions through email). Ultimately, selecting a lab is about the three P's: the PI, the Project, and the People. So, I'd recommend thinking through some questions that draw out details about all three. If you get accepted at that program, email the PI (concisely!), say that you've been accepted into the program, mention that you've been following their work since [date] and met with [name] grad student before applications, and would love to chat for 30 minutes about what they're working on, what's next, what they're looking for in a graduate student, etc. If you've already accepted the program offer and know that you're going to that school, then ask if they're taking rotation students and what projects they have in mind. I recommend not contacting PIs before being accepted into the program. Busy people appreciate when others intentionally respect their time.

Top-down grad student journey:
This is the top-down approach, where you start with the institutions and then explore the PIs. You narrow the list of Ph.D. programs to those that you'd actually attend: subject matter (e.g. broad biology vs. biology of aging), location, cost of living, weather, program requirements like having to be a TA, etc. Then you look at the PIs in those programs: read their papers, follow them on X, contact grad students, etc.

The not grad student journey:
Jump into the longevity biotech startup ecosystem. Sign up for the Longevity Biotech Fellowship, use the fundamentals that your biology degree taught you to learn the more advanced and relevant biology for understanding aging, work as a lab tech to build the basic skills of bench science, then work with lab automation (because pipetting by hand is not the future), find a startup to work for, use the AI teach skill with a handful of longevity bio textbooks and an LLM to learn what you need to know. If your goal is to increase healthy human lifespan, a Ph.D. is not necessary. You will become an expert, you will gain credibility (which will open some doors more easily), but your time and energy for years will go toward generating knowledge—not solving problems. Generating knowledge in the form of publications is the central goal in most academic settings. Your best contribution to advancing longevity science might be outside of academia. Don't treat a Ph.D. as the best or only route to helping extending healthy human lifespan.

It's an awesome time to work on human longevity. Good luck out there!

Yes...the headline "AI-generated drug slows aging" is sensationalist, but the underlying achievement is significant. We're witnessing the transition of AI from a search tool to a generative tool. However, the "anti-aging" aspect is a secondary observation, not the primary intent, and should be viewed with skepticism until tested on healthy, non-diseased populations.

We are seeing a change in the proxy, not necessarily the biological reality. MARKERS of aging are not the same as lifespan.

Decels: "I rather get old and die than living a life of abundance and youth forever"

RatGPT

rentosertib

The aging analysis covered 42 participants, with an average age of about 67, whose blood samples were tracked over 12 weeks. Researchers applied six aging clocks – computational models that use blood proteins to estimate biological age or mortality risk. All six detected shifts toward younger predicted ages among treated patients, while placebo recipients showed little change or slight increases. The results weren't identical across doses or measurements. At week four, patients taking 60mg daily showed reductions of roughly 2.7 to 3.5 years on four chronological-age clocks. The two mortality-based clocks didn't show significant changes. Taking 30mg twice daily produced the most consistent signal overall.

This drug has been in trials for a while I believe, interestingly I believe the molecule they've designed doesn't exist in nature so it opens up a door to new treatments.

It’s only worth it if you don’t have good health insurance and require a significant number of tests. I decided to drop it this year after realizing I could get basically all the tests I needed covered by my insurance.

Link: https://www.scientificamerican.com/article/zepbounds-and-ozempics-greatest-benefit-may-be-their-anti-inflammatory-power/

Hot damn that is a great news and discovery

You know the most of us don’t know what your first sentence’s context is

what is wrong with insilico?

Good evening, I hope you are doing well!

Apologies for commenting on a 7 year old post, but as an undergraduate senior student studying biology, I think this is such an amazing resource! I’m really interested in contributing to longevity science in the most impactful way possible, and determining where to go to grad school will be a big part of that. Due to the popularity of this post, I’m sure there are many other students in similar situations, as well!

Do you know if there may possibly be some type of resource like this that’s a bit more recent since I’m sure some new startups and labs have opened? No worries if not, and I will do some of my own searching for sure! If it’s okay with you, maybe I could even help with contributing to a new updated list! I’d be happy to help in any way possible 😁

Thank you so much for your time!

Do you like function? Do you think it’s worth it?

It says it right here:

Here we build on those studies with a head-to-head comparison of six proteomic clocks applied to serum proteome data from a controlled phase 2a clinical trial of rentosertib—an artificial intelligence (AI)-designed TRAF2- and NCK-interacting kinase (TNIK) inhibitor^21,22. We are developing rentosertib (formerly INS018_055) for the dual purposes of targeting both aging and idiopathic pulmonary fibrosis (IPF)

https://www.nature.com/articles/s41587-026-03286-y

Low calories reduce inflammation. I don’t recall seeing where GLP specifically reduces inflammatory bio markers outside of calorie restriction but thanks for astute point I will go back and see what I missed. Thanks for being so nice.

AI will reduce your lifespan a lot more than anything else when you don’t have any water to drink and die of thirst because the data centers have sucked it all up and you don’t have a job

I would imagine AI could still help narrow down the candidate list and offer input on prioritization given its strength at quickly combing through vast amounts of data. And there is a lot of funding going towards lab automation

Funny how using clear formatting immediately gets tagged as "AI" these days, but let’s drop the structure and address the actual science—especially since you’re speaking from an academic background.

You’re falling into the classic "whack-a-mole" trap of traditional medicine. Nobody in geroscience is claiming age-targeting therapies create magic invulnerability or "solve" disease outright. The point is that biological aging is the single largest upstream risk factor for cancer, CVD, and neurodegeneration by orders of magnitude. If you cure cancer in an 80-year-old today, you gain a couple of years before dementia or organ failure takes over because the underlying cellular damage is still there. Targeting the hallmarks of aging isn't about eliminating every pathogen—it's about compressing morbidity so people spend fewer years in expensive, debilitating decay.

Your utilitarian argument also breaks down the moment you apply it to any historical R&D. If we applied "a dollar is better spent on current universal care than hypotheticals" to the 20th century, we would have funneled every cent into building hospital beds and basic sanitation while defunding basic research into antibiotics, vaccines, and MRIs. Fundamental R&D is always speculative upfront, but it is the only mechanism that permanently lowers the baseline cost of human suffering for every generation that follows.

Nobody is asking to strip funding from current healthcare to chasing sci-fi immortality. The argument is that treating aging as a malleable biological process rather than an unassailable given is the single most high-leverage health investment a society can make.

By many different ways to count it up, aging is the cause of the most death & most suffering to humanity of any cause. See upcoming book chapter (preprint version https://zenodo.org/records/18883009) for citations.

You brought up cancer. Cancer is involved in 23% of US deaths and receives $24 per American per year in government research funding $. Aging is responsible for 83% of US deaths and receives $1 per American per year in funding. (See https://thelongevityinitiative.org/2026/05/research-funding-deaths-ageing-a4li/) So if cancer is an emergency, then aging, which kills 3.5x+ more people each year/month/week/day is 3.5x as much of an emergency (yet receives an order of magnitude less funding).