Claude failed to do the transcript, but I have the transcript from chatGPT
Introduction
Host:
The very high-profile medical doctor continues to get the fundamental biology of aging literature wrong and presents it incorrectly. I canât help but ask myself: is it that they donât know better, or that they do know better and choose to keep presenting bad information?
My wife once said, âThis is a draft idea. No one will ever listen to you.â And here we are now. Sheâs since said, âYeah, I was wrong.â
We were still left with about a $150,000 shortfall for the study, and thatâs where my wife let us remortgage our house.
How we understood the surface of the Earth in 500 BCâI feel like thatâs how we understand the biology of aging today. Thereâs a lot we donât understand. If we were really getting closer to solving aging, we ought to be able to increase the lifespan of a mouse by more than what Rick and Roy did 50 years ago. We arenât doing it.
One of my biggest concerns is that no doctor should be recommending these tests.
Meeting at the Longevity Investors Conference
Host:
Hey guys, look who I ran into at the Longevity Investors Conference in Gstaad, Switzerland: Brad Stanfield. This is the first time weâve met in person. Iâve been on your podcast a couple of times and weâve done some other things together, which Iâm sure weâll talk about. Great to connect in person. Weâll just talk about whatever comes to mind and see where it goes.
Brad:
Absolutely. A lot of people watching will know of you or have seen your podcast, but may not know much about you or how you got interested in this space. Iâll say âlongevity,â but you can choose a different word if you like. Maybe talk about your background, what youâre doing now, and how you got into your YouTube channel and day job.
Bradâs Background & Starting the YouTube Channel
Brad:
My day job is as a primary care physician in Auckland, New Zealand. Getting there was a bit of a journey.
As a junior doctor working in hospitals, I noticed some wrinkles around my eyes. That kicked off my interest in agingâare we closer to slowing the aging process, what can we do about wrinkles, are there breakthroughs underway? That led me into things like metformin and IGF-1, and that really started my journey.
Originally, I had the idea of becoming an orthopedic surgeon. I spent about a year fixing broken bones and hips but realized that lifestyle wasnât for me. I took a year out and worked in the emergency department. During that time I kept thinking: Iâm really interested in the aging process, but I want to bring science into this fieldâespecially because thereâs so much misinformation online.
People were extrapolating single-cell research straight to human supplements: âLook what happened in a single cell, therefore you should take this.â You still see that all the time. That motivated me to start my YouTube channel.
I had no idea it would grow or that people would listen. My wife told me, âThis is a daft idea, no one will ever listen to you, you shouldnât do this.â But here we are now. She admits she was wrongâand thatâs the only time Iâve heard her say that. Sheâs been very supportive.
I started the channel at the end of 2019, while working in the emergency department. My early videosânow deletedâwere filmed on a couch in a hospital residence after night shifts. One thing led to another.
Host:
Your channel has done great. What do you think led to its success?
Brad:
I think people were craving clear communication of human, clinical trial data. Thereâs so much misinformation and people genuinely want to be healthy, not misled.
People seem to appreciate that Iâm guideline-driven. Primary care guidelines are fantastic, but most of the public donât know about them. I try to democratize that information in a way that isnât too dreary. I think that approach resonated.
Host:
When I first saw your videos, I had to get past the âYouTube styleâ to get to the content. But your work is very data-driven and stays scientific. In my view, youâre more conservative in presenting science than I am. I really like how rigorous you are.
Brad:
I appreciate that. Honestly, Iâm scared when I publish a video in case Iâve got something wrong. With the channel size I have, if I make mistakes and people follow that advice, thatâs a real problemâespecially as a practicing physician. The advice I give on YouTube needs to match what I give to patients in clinic.
If Iâm wrong on YouTube, Iâm potentially wrong with patients too. So I double-check guidelines, make sure I havenât missed key clinical trials, and focus on randomized controlled trials. A lot of people quote observational dataâvitamin D, magnesiumâhuge associative datasets suggesting benefits, but randomized human trials often show mixed or null results. Vitamin D and cancer is a classic; the VITAL trial is one I often cite.
How to Treat Evidence & Admitting Mistakes
Host:
All evidence is imperfectâeven clinical trials. You have to synthesize everything and form a probabilistic understanding of whatâs most likely to be true, recognizing it can change.
I also care deeply about accuracy, but weâre going to make mistakes. The key is being willing to say, âI got this wrong, hereâs what the evidence actually says.â That separates people trying to do their best from those chasing clicks.
Brad:
Exactly. Iâve publicly corrected myself on resveratrol, sulforaphane supplements, metformin, and more. I went wrong when I deviated from my clinical training and got pulled along by charismatic individuals in the aging space. I trusted âeldersâ in the field instead of applying my usual standards.
I think people appreciate that I say, âI got it wrong, hereâs why, and hereâs what Iâm changing.â
Host:
Many people got fooled by the resveratrol story. Itâs frustrating that some big, well-credentialed names still misrepresent aging biology and sirtuin data, especially when they should know better by now.
Thereâs a very high-profile medical doctor who consistently misstates basic aging biology and sirtuin/resveratrol literature. Itâs unfortunate.
Brad:
I donât really watch that personâs content.
Rapamycin Trial: Motivation, Design & Funding
Host:
Letâs switch topics to rapamycin. You became very interested in testing rapamycin in the context of exercise response in healthy older adults. You raised funds with philanthropic support, viewer donations, and your own resourcesâwhich is uncommon. Talk about that trial: what it tested, how it worked, and where itâs at.
Brad:
My interest in rapamycin came from the Interventions Testing Program, where rapamycin repeatedly extended lifespan in male and female mice.
Clinically, rapamycin has a bad reputation as an immunosuppressant for transplant patients, so thereâs concern that if we get the dose wrong in healthy people, we might increase infections or cancer. Fortunately, some human trials show that if mTOR inhibitors are dosed correctly, those risks can be managed. But we still lack robust data in healthy individuals.
A lifespan study in humans would take decades, so we needed a functional outcome. I focused on muscle performance, which declines with age and is linked to overactive mTOR in older muscle. Overactive mTOR may limit autophagy. The idea: dose rapamycin intermittently to turn mTOR down, allow autophagy and cellular cleanup, then use exercise to reactivate mTOR to rebuild healthier tissue.
With your input, we designed a trial: exercise three days a week (Mon/Wed/Fri) plus 6 mg rapamycin once weekly on Saturday. The primary endpoint was the 30-second chair stand testâsensitive to lower-body power in older adults.
It was only a 40-person study, but took about two years to fund. Viewers donated; Vadell contributed; the total cost was about USD $500,000. After two years we were only a quarter funded. To close the remaining gap we created a supplement line, with the idea that profits could fund clinical trials like this. Another funder came on board, but we still had a ~$150,000 shortfall.
Thatâs when my wife agreed we could remortgage our house to get the trial done.
Weâve completed the study, written it up, and submitted it for peer review. Once thatâs done, we can share the results. I think theyâre exciting and informative for how to dose rapamycin in healthy individuals to affect muscle performance.
Host:
Your wife sounds extremely supportive.
Brad:
Iâm very lucky. Still paying off that mortgage though.
Host:
Why 6 mg once a week?
Brad:
We lack definitive human dataâthatâs exactly why we did the study. We chose intermittent dosing to create windows of mTOR inhibition (to boost autophagy) followed by drug washout so that exercise could reactivate mTOR for muscle building. The hope is that this âon/offâ pattern optimizes the balance.
Host:
You need mTOR to build muscle, so chronic suppression is a concern. Animals on rapamycin show better muscle function with age, but human data are sparse.
Brad:
Exactly. Itâs a major gap we wanted to help fill. Big pharma has little incentive to fund these trials, so it required unconventional funding.
Weâve submitted the paper; it hasnât been rejected and has been under review for a while, which is a good sign.
PhD Plans & Doing High-Quality Trials
Host:
Youâre also starting a PhD. Why, given youâre an MD with a successful channel and a supplement brand?
Brad:
Presenting other peopleâs data is one thing. I want to generate high-quality data myselfâespecially because many studies in this space arenât robust.
I want our trials to be rock-solid and CONSORT-compliant: proper randomization, blinding, powering, reporting, minimizing bias. A PhD at the University of Auckland gives me supervision, structure, and better access to funding pathways. Our rapamycin work is fully non-profit, and the university is happy to sponsor it; 100% of donations go to the studies.
If people want to donate, they can contact me via my website, drstanfield.com, or through my YouTube channel, and Iâll connect them with the correct people at the university.
Prevention Culture: New Zealand vs US
Host:
Weâve talked offline about prevention. My view is that US primary care is reactive, not focused on keeping people healthy. Youâve said New Zealand is different.
Brad:
New Zealand has a predominantly public system. A key goal is to prevent hospitalizations because theyâre expensive. Preventing heart attacks and strokes in primary care is more cost-effective than treating them.
The government incentivizes prevention, and training reflects that. Thereâs a strong prevention culture. Itâs jarring to hear how different it is in the US, where incentives favor procedures and hospital care.
Host:
Insurers in the US donât reliably value prevention, and many patients wonât do something if insurance doesnât pay. That culture plus misaligned incentives makes change hard.
Brad:
Because funding is constrained in New Zealand, there are clear guard rails on what tests I can order. I spend a lot of time on my channel discussing which tests are worthwhile and which are not. People often think âmore data is better,â but unnecessary testing can be wasteful or harmful.
Vitamin D: Testing vs Population-Level Strategy
Brad:
Vitamin D is a good example. There was (and is) a big push to test vitamin D levels. Recent Endocrine Society guidelines essentially say we donât know how to interpret vitamin D levels in a way that meaningfully changes outcomes for most people.
Trials using ~800 IU daily seem to âlock inâ bone and immune benefits for the general population. Higher doses have shown potential harm. Vitamin D blood levels often track frailty or indoor living rather than cause outcomes. Retrospective data havenât strongly supported routine testing as a driver of better outcomes.
Given cost constraints and limited benefit, broadly testing everyone isnât a great use of resources in my setting. People can still self-pay if they wish, but at the population level we prioritize interventions with clearer impact.
Host:
Iâm skeptical of guideline committees because of past failures like hormone replacement therapy (HRT) after the Womenâs Health Initiative. I worry they overweight small safety signals and underweight quality-of-life and broader benefits.
Brad:
I see guidelines as our âleast badâ option. Theyâre produced by domain experts reviewing the evidence. Not perfect, but better than individual âcowboyâ interpretations. Medicine should move cautiously; reversing widespread recommendations is difficult.
Host:
But that caution can cause harm too, as many women lost access to HRT benefits for decades.
Brad:
We can debate that specific history, but my broader point is: following well-constructed guidelines usually reduces errors at the population level, while allowing for justified individual deviations.
Biological Age Tests: Why Brad is Concerned
Host:
Letâs talk about one of your big concerns: biological age scores.
Brad:
Right. I see two main problems:
-
Lack of clinical validation. We donât have solid evidence that a given biological age score should drive interventions.
-
Misuse in decision-making. Some clinicians recommend supplements or treatments based on these scores. Thatâs premature.
I see biological age tests as interesting research tools, but they shouldnât guide routine clinical decisions on preventing heart disease, stroke, or cancer.
Host:
I agree. No doctor should recommend a test they donât understand, canât quantify in terms of accuracy/precision, or that doesnât clearly inform care. That describes most biological age tests today.
Brad:
If patients want to pay for them and they find them motivating, fine. But I explain that our management plan for real risks wonât change based on that number.
Patient-Centered Care vs Paternalism
Brad:
In my training there was a strong shift away from paternalism and toward patient-centered care. Itâs not my job to dictate; itâs my job to present benefits, risks, and options, and support informed decisions.
If patients ask what Iâd recommend, Iâll say, âBased on this evidence and these guidelines, I suggest X,â but itâs their decision.
Host:
Many US doctors are still more paternalistic. I like your approach, though it can be hard when the âtrueâ information is uncertain and evolving.
How to Judge Clinical Trials (CONSORT)
Brad:
To judge trial quality:
If a trial doesnât meet these standards, Iâm cautious about its conclusions. Many non-replicating early results come from underpowered or poorly designed studies.
GLP-1s, SGLT2s & RiskâBenefit
Host:
On riskâbenefit, you often say benefits should âvastlyâ outweigh risks. Why âvastlyâ?
Brad:
Because harms can be large for a minority of patients. With GLP-1 agonists, most people benefit, but some experience severe GI issues or very rare serious complications. Medications always carry risks; I want to be confident that for almost everyone, net benefit is clearly positive.
I explain risks and benefits and let patients decide. Fear is a real driver, so they need honest numbers.
Host:
How do you see GLP-1s and SGLT2 inhibitors?
Brad:
Theyâre effective preventative tools in the right context:
- In type 2 diabetes, GLP-1s and SGLT2s reduce cardiovascular events and slow kidney decline.
- In obesity, GLP-1s reduce diabetes risk.
- Thereâs growing discussion about using them earlier (e.g., prediabetes), potentially instead of metformin, given stronger weight and metabolic effects.
Personally, I take:
- An ARB for genetically driven hypertension.
- An SGLT2 inhibitor as an add-on for blood pressure and diuretic effect, after consulting a nephrologist.
Thatâs outside strict guideline indications but is a fully informed, patient-centered decisionâwhere in this case Iâm the patient.
If a patient similarly informed wanted SGLT2s as second-line with an ARB, Iâd consider it, making clear itâs not yet guideline standard.
Are We Close to âSolvingâ Aging?
Host:
You wanted to discuss whether treating the âhallmarks of agingâ is enough and how close we are to understanding aging biology.
I often use the Hecataeus map analogy: our current view of aging is like a 500 BC world mapâuseful but crude, with huge unknowns. Iâd say weâre closer to 10% than 90% understanding.
Two implications if thatâs true:
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Our current framework is useful. We know enough to improve healthspan and probably lifespan in humans and companion animals.
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We underfund discovery. The hallmarks framework has narrowed focus. Itâs now hard to fund work that doesnât fit those boxes, so we get deep dives into known pathways but too little true discovery.
A telling point: the largest lifespan extension in a mammal (discounting extreme developmental manipulations) is still classic caloric restriction work by Walford and others ~50 years ago. If we were close to âcuring aging,â weâd expect to beat that routinely in mice. We havenât.
So: lots of good progress, but we need more resources for exploring the unknown alongside targeted, mechanistic work. We should walk and chew gum at the same time.
Brad:
Agreedâthereâs a lot to be done. This has been great; letâs continue the discussion another time.
Host:
Absolutely. Thanks for sitting down.
If youâd like, next step I can: (a) turn this into a clean article-style piece, or (b) strip it down to a bullet-point summary + key themes for rapid reference.
