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 can’t help but ask myself: is it that they don’t know better, or that they do know better and choose to keep presenting bad information?
My wife once said, “This is a draft idea. No one will ever listen to you.” And here we are now. She’s since said, “Yeah, I was wrong.”
We were still left with about a $150,000 shortfall for the study, and that’s where my wife let us remortgage our house.
How we understood the surface of the Earth in 500 BC—I feel like that’s how we understand the biology of aging today. There’s a lot we don’t 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 aren’t 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 we’ve met in person. I’ve been on your podcast a couple of times and we’ve done some other things together, which I’m sure we’ll talk about. Great to connect in person. We’ll 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. I’ll say “longevity,” but you can choose a different word if you like. Maybe talk about your background, what you’re doing now, and how you got into your YouTube channel and day job.
Brad’s 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 aging—are 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 wasn’t for me. I took a year out and worked in the emergency department. During that time I kept thinking: I’m really interested in the aging process, but I want to bring science into this field—especially because there’s so much misinformation online.
People were extrapolating single-cell research straight to human supplements: “Look what happened in a single cell, therefore you should take this.” 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, “This is a daft idea, no one will ever listen to you, you shouldn’t do this.” But here we are now. She admits she was wrong—and that’s the only time I’ve heard her say that. She’s been very supportive.
I started the channel at the end of 2019, while working in the emergency department. My early videos—now deleted—were 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. There’s so much misinformation and people genuinely want to be healthy, not misled.
People seem to appreciate that I’m guideline-driven. Primary care guidelines are fantastic, but most of the public don’t know about them. I try to democratize that information in a way that isn’t too dreary. I think that approach resonated.
Host:
When I first saw your videos, I had to get past the “YouTube style” to get to the content. But your work is very data-driven and stays scientific. In my view, you’re more conservative in presenting science than I am. I really like how rigorous you are.
Brad:
I appreciate that. Honestly, I’m scared when I publish a video in case I’ve got something wrong. With the channel size I have, if I make mistakes and people follow that advice, that’s a real problem—especially as a practicing physician. The advice I give on YouTube needs to match what I give to patients in clinic.
If I’m wrong on YouTube, I’m potentially wrong with patients too. So I double-check guidelines, make sure I haven’t missed key clinical trials, and focus on randomized controlled trials. A lot of people quote observational data—vitamin D, magnesium—huge 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 imperfect—even clinical trials. You have to synthesize everything and form a probabilistic understanding of what’s most likely to be true, recognizing it can change.
I also care deeply about accuracy, but we’re going to make mistakes. The key is being willing to say, “I got this wrong, here’s what the evidence actually says.” That separates people trying to do their best from those chasing clicks.
Brad:
Exactly. I’ve 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 “elders” in the field instead of applying my usual standards.
I think people appreciate that I say, “I got it wrong, here’s why, and here’s what I’m changing.”
Host:
Many people got fooled by the resveratrol story. It’s frustrating that some big, well-credentialed names still misrepresent aging biology and sirtuin data, especially when they should know better by now.
There’s a very high-profile medical doctor who consistently misstates basic aging biology and sirtuin/resveratrol literature. It’s unfortunate.
Brad:
I don’t really watch that person’s content.
Rapamycin Trial: Motivation, Design & Funding
Host:
Let’s 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 resources—which is uncommon. Talk about that trial: what it tested, how it worked, and where it’s 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 there’s 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 test—sensitive 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.
That’s when my wife agreed we could remortgage our house to get the trial done.
We’ve completed the study, written it up, and submitted it for peer review. Once that’s done, we can share the results. I think they’re exciting and informative for how to dose rapamycin in healthy individuals to affect muscle performance.
Host:
Your wife sounds extremely supportive.
Brad:
I’m very lucky. Still paying off that mortgage though.
Host:
Why 6 mg once a week?
Brad:
We lack definitive human data—that’s 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 “on/off” 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. It’s a major gap we wanted to help fill. Big pharma has little incentive to fund these trials, so it required unconventional funding.
We’ve submitted the paper; it hasn’t been rejected and has been under review for a while, which is a good sign.
PhD Plans & Doing High-Quality Trials
Host:
You’re also starting a PhD. Why, given you’re an MD with a successful channel and a supplement brand?
Brad:
Presenting other people’s data is one thing. I want to generate high-quality data myself—especially because many studies in this space aren’t 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 I’ll connect them with the correct people at the university.
Prevention Culture: New Zealand vs US
Host:
We’ve talked offline about prevention. My view is that US primary care is reactive, not focused on keeping people healthy. You’ve said New Zealand is different.
Brad:
New Zealand has a predominantly public system. A key goal is to prevent hospitalizations because they’re expensive. Preventing heart attacks and strokes in primary care is more cost-effective than treating them.
The government incentivizes prevention, and training reflects that. There’s a strong prevention culture. It’s jarring to hear how different it is in the US, where incentives favor procedures and hospital care.
Host:
Insurers in the US don’t reliably value prevention, and many patients won’t do something if insurance doesn’t 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 “more data is better,” 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 don’t know how to interpret vitamin D levels in a way that meaningfully changes outcomes for most people.
Trials using ~800 IU daily seem to “lock in” 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 haven’t strongly supported routine testing as a driver of better outcomes.
Given cost constraints and limited benefit, broadly testing everyone isn’t 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:
I’m skeptical of guideline committees because of past failures like hormone replacement therapy (HRT) after the Women’s Health Initiative. I worry they overweight small safety signals and underweight quality-of-life and broader benefits.
Brad:
I see guidelines as our “least bad” option. They’re produced by domain experts reviewing the evidence. Not perfect, but better than individual “cowboy” 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:
Let’s talk about one of your big concerns: biological age scores.
Brad:
Right. I see two main problems:
-
Lack of clinical validation. We don’t 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. That’s premature.
I see biological age tests as interesting research tools, but they shouldn’t guide routine clinical decisions on preventing heart disease, stroke, or cancer.
Host:
I agree. No doctor should recommend a test they don’t understand, can’t quantify in terms of accuracy/precision, or that doesn’t 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 won’t 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. It’s not my job to dictate; it’s my job to present benefits, risks, and options, and support informed decisions.
If patients ask what I’d recommend, I’ll say, “Based on this evidence and these guidelines, I suggest X,” but it’s their decision.
Host:
Many US doctors are still more paternalistic. I like your approach, though it can be hard when the “true” information is uncertain and evolving.
How to Judge Clinical Trials (CONSORT)
Brad:
To judge trial quality:
If a trial doesn’t meet these standards, I’m cautious about its conclusions. Many non-replicating early results come from underpowered or poorly designed studies.
GLP-1s, SGLT2s & Risk–Benefit
Host:
On risk–benefit, you often say benefits should “vastly” outweigh risks. Why “vastly”?
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:
They’re 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.
- There’s 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.
That’s outside strict guideline indications but is a fully informed, patient-centered decision—where in this case I’m the patient.
If a patient similarly informed wanted SGLT2s as second-line with an ARB, I’d consider it, making clear it’s not yet guideline standard.
Are We Close to “Solving” Aging?
Host:
You wanted to discuss whether treating the “hallmarks of aging” 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 map—useful but crude, with huge unknowns. I’d say we’re closer to 10% than 90% understanding.
Two implications if that’s true:
-
Our current framework is useful. We know enough to improve healthspan and probably lifespan in humans and companion animals.
-
We underfund discovery. The hallmarks framework has narrowed focus. It’s now hard to fund work that doesn’t 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 “curing aging,” we’d expect to beat that routinely in mice. We haven’t.
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:
Agreed—there’s a lot to be done. This has been great; let’s continue the discussion another time.
Host:
Absolutely. Thanks for sitting down.
If you’d 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.
