Founder of nonprofit AgingBiotech.info Investor in rejuvenation startups: portfolio on LinkedIn Organizer of VitaminDforAll.org AI/ML Stanford PhD & ex-Google
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My longer intro to the aging/longevity field Zoom talk for the Collaborative Drug Discovery virtual seminar is now live on YouTube:
FDA Approvals of Aging Therapies Have Started: The Motivation for, Status of, & Path to Eliminating Aging
Jul 2026
My longest, most thorough talk
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FYI, my latest podcast interview just dropped. It was a great conversation with @NikoTHems & Miguel Medina Stanivukovic on their Return on Health podcast:
piped.video/P7dHrpQsJTk?list=PL…
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Immunis is my portfolio company that I currently expect to achieve phase 2 success & eventual FDA approval first amongst all the 35+ companies I've invested in. Congrats to them on their first-place grand-prize win in a significant competition.
🏆 Congratulations to the winners of our 2026 Healthy Longevity Global Grand Prize Competition!
🔗 Read the full announcement and explore all 2026 awardees: nam.edu/news-and-insights/na…
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Many interesting new databases recently added to AgingBiotech.info/databases
4 added past 3 days:
-BioLens: mouse lifespan research
-DLPFC Lifespan Atlas: cortex transcriptome across lifespan
-Oliver's mTOR Atlas: all things mTOR
-TranslAGE: human epigenetics
10 added in 2026.
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I can't help but think there is a wealth of interesting & useful aging-related data in here, much of it machine readable. I continue to think there are probably interesting pairs (or triples) of these DBs that could unlock interesting things if combined in the right ways.
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Great work by Dr. Neri & all the compilers of these DBs who decided to make them widely available!
Especially @jpsenescence, whose lab has made available over a half dozen, far more than any other group.
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Warning: this post may seem heretical to some in the aging field.
It is nonetheless important, maybe my most important message for the field.
The aging field suffers from an inappropriate fixation on its main outcome metric.
New substack tries to explain why this is bad:
Made with AI
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Here is the monolithic way to think about aging and the geroscience hypothesis, whether thinking about therapeutics (targeting to interfere in aging) or biomarkers (measuring aging as a whole).
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Lastly, here is the divide-and-conquer ("multifactorial") way to think about aging, as a collection of separable subproblems (subpathologies), to be treated separately & measured separately, each of which embodies a kind of separated geroscience hypothesis in the sense of causing multiple age-related diseases. Many biotechs embody this thinking in the way their interventions target only 1 aging subpathology, but few in the field think about ignoring lifespan/healthspan/surrogates as metrics of interest and focusing entirely on measures of subpathology mitigation and/or effectiveness vs. multiple diverse age-related indications. Also, only a small minority of what goes on in the biomarkers corner of the field is measurement of or estimation of individual subpathologies rather than of aging as a whole.
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Vitamin D is fat-soluble. Overweight & obese people usually need higher vitamin D intake to maintain sufficient levels so deficiency is more common in these contexts to begin with & those with high BMIs should be more careful about monitoring levels & getting sufficient intake. I never thought about how this interacts with GLP-1 drugs but it seems complicated.
The relevant biology evolved before supplementation & food fortification when a large fraction of humanity lived in places where vitamin D could be synthesized from sun only for a fraction of the year but not during winter. During those centuries of evolution food was also easier to get during non-winter months. People put on adipose tissue partly to get them through the leaner winter. So sequestering vitamin D in that adipose tissue made a lot of sense. As the fat was consumed during winter, the sequestered vitamin D was released maintaining levels.
Thinking about fat sequestering vitamin D we can conclude several things: When gaining weight, one needs a higher aggregate intake of vitamin D, regardless of exact source distribution (sun, fortified food, or supplements) because some goes into the fat. During fat loss the fat loss acts as another source possibly decreasing needs from other sources.
During rapid weight loss this should decrease intake requirements, but only if the fat being lost got a good supply of vitamin D when it was accumulated.
GLP-1 drugs thus could decrease vitamin D needs. But might not. And the decreased appetite could decrease intake from fortified food, so if one gets their D primarily from such food (eg fortified milk), GLP-1 drugs could create a need to increase intake from other sources.
So the take-home message is, more testing of levels is probably warranted, under all 3 conditions: weight increase, weight (or food intake) decrease, or steady-state overweight.
All this applies to adults as well as children. Sad that so many in both groups need GLP-1 drugs.
About 1 in 8 children and adolescents were diagnosed with vitamin D deficiency within a year of starting a GLP-1 drug.
Nearly 17% received at least one new diagnosis of a nutritional deficiency or related complication. Vitamin D deficiency alone affected 12.4%. Yet fewer than one in four received nutrition counseling within six months.
This doesn't prove the medications caused the deficiencies (obesity itself increases the risk of low vitamin D). But GLP-1 drugs suppress appetite by design, and when the body is undergoing rapid growth and development, nutritional sufficiency matters enormously.
Vitamin D supports calcium absorption and skeletal development, along with muscle function, immune regulation, and neurodevelopment.
The takeaway here is not that children should avoid GLP-1 drugs when appropriate. It’s that treatment should include nutrition counseling and monitoring of vitamin D and iron status, protein intake, and growth, not just weight loss.
PS: Adults using GLP-1 drugs should pay attention to micronutrient status, too!
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My last day at Boston Longevity Week is today at the Biomarkers of Aging meeting. 5 days in a row of events for me here starting with 2 days of ARDD has felt like old 5-day 8am-8pm ARDD. Tiring but exciting with a lot going on in the field. I hope everyone else had a great time at whichever of the many early Oct (& late Sep) meetings they ended up at.
In 2 weeks, I'll be at the Longevity Partnering Forum in South San Francisco Oct 19-20 presenting an overview of the 2026 status of the aggregate pipeline of all the biotechs in the field. Register at longevitypartnering.com/ (free for pharma & investors). Sandwiched right between 2 other conferences in the SF bay area that are focused more on current clinical longevity practice (making the best of what we have now), this event will be squarely focused on the next-gen stuff that is on the way.
Something amazing is about to happen.
The greatest day in the history of aging/longevity conferences is coming up!
And greatest month.
It seemed like unfortunate scheduling conflicts at first,
but the result is something worth celebrating as a sign of significant field growth.
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Nonetheless, those issues seem easier to deal with than using anencephaly or hydranencephaly as mechanistic models to engineer functional young bodies with zero ethical issues.
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Upon cursory further reading it seems like "2 separate organs" language is a bit inappropriate. Many organs develop from diff sets of progenitor cells but are considered 1 organ. What's shocking here is most people thought all neural tissue came from a homogeneous set of progenitors, but this work showed it's really 2 very different groups.
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The phase 3 clinical trials table of AgingBiotech.info (top trials DB of AgingBiotech.info/trials) now updated thanks to work by @tliu44.
- New approvals (eg Scholar Rock).
- Failed ph3s marked as such.
- Prev Ph2 programs now in ph3 added.
The pipeline progresses (slowly).
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This should have generated more reaction 2 weeks ago as it's a big deal. Soluble PD-L1 (sPD-L1) helps tumors avoid immune clearance. This published study by Mayo shows that depleting sPD-L1 helps against a tough cancer type.
After 15 years of our discovery of soluble PD-L1(B7-H1), we finally have a proof of it as a therapeutic target and have a way to specifically remove it in vivo to restore antitumor immunity. businesswire.com/news/home/2…
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NaNots (nanoparticles w/ shielded capture agents) uniquely can deplete soluble targets w/o touching membrane bound versions. Conventional approaches to PD-L1 inhibition could bind mPD-L1 causing autoimmunity to healthy mPD-L1 expressing non-cancer cells (as I understand things).
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Great work by my portfolio company NaNotics, a company w/ a platform that is at the moment still underappreciated but I think is destined for great things. The platform has potential in many therapeutic areas.
New paper published w/ Mayo direct link:
pmc.ncbi.nlm.nih.gov/article…
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