Did The Most Promising Longevity Drug Fail? | Brad Stanfield

0:00 The dream of longevity medicine is surprisingly elegant.

0:03 You think we'll be potentially taking a pill in 10

0:07 years time every couple of weeks that will make us younger.

0:10 Can you explain to me that prediction?

0:12 One day a single pill could radically

0:14 extend a person's active and healthy years.

0:17 The promise of such a medical breakthrough

0:19 has been with humanity since the very beginning,

0:21 mentioned both in the very first cuneiform manuscript 4,500 years

0:25 ago in the Epic of Gilgamesh and in a 2,000-year-old

0:29 manuscript by the Chinese emperor Qin Shi Huang

0:32 which revealed a nationwide search for an immortality elixir.

0:36 The dream survived on Greek papyrus through medieval

0:38 alchemists and even radioactive cocktails during the atomic age.

0:42 But it wasn't until 2011 that modern

0:45 scientists came across a chemically proven longevity agent

0:49 that extended the lives of worms and flies

0:51 and mice and showed promise in humans, too.

0:55 So, what is rapamycin?

0:56 So, rapamycin is a drug Rapamycin, also known as sirolimus and Rapamune,

1:02 is an immunosuppressant drug first isolated from bacteria

1:06 harvested on the island of Rapa Nui,

1:08 also known as Easter Island where those moai sculptures are,

1:11 in the 1960s whose properties really did seem miraculous.

1:16 It is one of the most potent antifungal agents known to science and also has

1:19 the remarkable property to suppress the immune system

1:23 enough to stop it from rejecting organ transplants.

1:26 It has saved hundreds of thousands of lives, but its story was far from over.

1:31 In 2011, researchers discovered that it acts on a cellular pathway

1:36 eponymously named the mTOR pathway and that's for target of rapamycin.

1:41 It suppresses certain chemical signals that relate to aging.

1:44 The mechanisms, they looked really promising.

1:48 That's when the biohacking community took notice.

1:50 Longevity influencers like Peter Attia began taking

1:53 it and encouraged his followers to follow suit, but there was a problem.

1:57 No one had actually studied how rapamycin actually

2:00 did anything for human longevity in human studies.

2:05 That's where Brad Stanfield came in.

2:07 He teamed up with Matt Kaeberlein, who's a friend of this channel,

2:10 and crowdfunded almost $750,000 to run

2:14 an actual clinical trial on the longevity prospect.

2:18 His results, they came out this month.

2:21 And rather than going into it all myself,

2:23 I invited Stanfield onto the channel today to talk about what they found.

2:27 Thanks so much for being on the show today, Brad.

2:29 Yeah, thanks, Scott.

2:30 I'm excited to have this conversation with you.

2:32 I've, you know, followed your channel for a while now,

2:34 so it's cool to actually meet you face-to-face.

2:40 Well,

2:41 yeah, and I have absolutely cited your channel when we were doing, you know,

2:45 you were one of the first people to call out David Sinclair,

2:49 and I just basically stole stuff from your videos and put it in mine.

2:54 So, you know, thanks for being doing the work that you do.

2:57 Yeah, no worries.

2:58 And I think, you know, one of the reasons why I started my channel

3:00 in the first place was to actually get, you know,

3:02 some of these stories out there because, you know,

3:04 while there are some snake oil,

3:06 there are some genuine things that do help people.

3:09 And, you know, that's what kind of led me onto rapamycin in the first place cuz,

3:12 as you mentioned in the intro,

3:14 this is one of the things that really took the longevity field by storm.

3:17 And it was hoped, and still hoped, that it may play a role in human aging.

3:23 So, yeah, that's why I wanted to set up

3:24 this study to see if we could make some progress.

3:26 Yeah, you actually did a You crowdfunded your own study,

3:29 which is amazing for a number of reasons, and we're going to get to that.

3:33 But, let's, you know, Brad, we got to get the painful part out of the way first.

3:38 The study didn't exactly go to plan.

3:41 Tell me what happened.

3:42 Yeah, so I think it starts at the design of the study.

3:45 So, you know, the in the intro you mentioned how in worms,

3:49 flies, and mice it extends lifespan.

3:51 Now, if you try and design a human study looking at lifespan,

3:53 you're going to be waiting decades and you're going to need

3:55 hundreds and hundreds of patients

3:57 to actually reach a statistically significant result.

4:00 So, instead what we tried to do was go back to the groundwork and say,

4:04 "What endpoints could we measure that may

4:06 improve with rapamycin compared to placebo?" And one

4:09 of the things that we noted was that in human muscle um uh so,

4:14 everyone kind of knows that as we get a bit older,

4:16 our muscles start to weaken and deteriorate.

4:18 And it almost seems like the muscles recognize

4:20 that and they try to compensate for that weakening.

4:23 So, what they do is they over-activate mTOR complex 1

4:26 cuz they're trying to rebuild proteins and rebuild their strength.

4:29 The trouble is if you over-activate mTOR complex 1,

4:32 you don't allow for another process to happen, which is called autophagy.

4:35 So, that's the cell clearance process.

4:37 So, you can imagine that your muscles are holding all of these old,

4:40 damaged components um and never having a chance to flush them away.

4:44 So, they're holding onto these.

4:45 So, the hope was that if we could use rapamycin intermittently,

4:49 we could dial down mTOR complex 1 and allow autophagy to happen.

4:53 And then we could have separate periods of time

4:55 where we ramp mTOR complex 1 back up with exercise.

4:58 So, that kind of led to the design

4:59 of the study where if we had both groups exercising,

5:02 so we gave them exercise bikes at home.

5:04 So, they exercised on Monday, Wednesday, and Friday.

5:07 And then if we dosed either the rapamycin or placebo on the Saturday.

5:11 Um so, the hope again that we would

5:13 have these separate periods of time of dialing mTOR

5:15 complex 1 down via rapamycin and other periods

5:18 of time where we're ramping back up again with exercise.

5:21 And it was hoped that that cycling hypothesis

5:23 would allow improved muscle performance for older adults.

5:26 So, that's what we um that that's how we designed the the the study

5:31 and and why we chose our primary endpoint as the 30-second chair stand test.

5:35 So, how many times could you stand up and then sit back down in 30 seconds?

5:39 And the reason why we chose that is that it's a very sensitive

5:42 uh measurement for older adults in terms of their muscle strength and power.

5:46 So, that's the overall uh hypothesis that uh that we were testing in the study.

5:52 So, it was a 13-week trial involving 40 participants,

5:56 so 20 participants in each.

5:57 And again, both groups were exercising here.

6:00 So, we thought that at worst,

6:02 we wouldn't see any difference between the 30-second

6:05 chair stand test in the two groups.

6:07 But at best, we were hoping that the rapamycin group would

6:10 improve their 30-second chair stand test more compared to the placebo group.

6:15 We didn't anticipate that it would actually cause the 30-second

6:19 chair stand test to perform worse than the placebo group.

6:22 So, it it opens up a lot of interesting questions and you know,

6:27 also validates the warnings that I suppose I've been giving people

6:31 that we don't yet know enough about rapamycin in otherwise healthy individuals,

6:35 and we need these clinical trials to actually see whether rapamycin actually

6:39 does have a role to play in healthy aging or you know,

6:42 whether our hopes have been misguided.

6:44 Yeah, I want to just underline what you said because

6:48 you use the words placebo and all sound very scientific.

6:50 But basically, you found that people who took rapamycin got weaker

6:54 compared to people who got in a very minor way, right?

6:58 But but got weaker compared to people who were taking,

7:00 I guess, dextrose or whatever your your placebo was.

7:04 So, it it it wasn't quite that they were getting weaker.

7:06 It was that they improved less.

7:08 So, both groups improved their muscle performance

7:10 in terms of the 30-second chair stand test,

7:12 but it seems that the rapamycin group

7:15 again improved less compared to the placebo group.

7:18 So, based on these results,

7:20 I I think it it it does suggest that yeah, rapamycin,

7:24 at least at the doses that we used,

7:26 blunted some of the positive effects of exercise.

7:29 And one of the reasons why you chose, you know, exercise, right?

7:33 Is because, you know, we I think you mentioned this, right?

7:36 If we're going to study humans over our lifespan.

7:39 So, the average human's what?

7:40 I mean, New Zealand, you probably live a little longer,

7:42 but I think in America we live probably like 74 or so so.

7:46 And uh when we the reason you studied uh muscle is because you you don't

7:52 have time to to wait for humans to age and die on this very specific protocol.

7:58 And then also you can't isolate um

8:00 a a particular data point for that long anyway.

8:04 So, when you looked at muscle and and and and and why

8:07 was the muscle such an important uh target for you?

8:11 Yeah, so you know, gym goers when they when they

8:15 go to when they go to the gym they are

8:16 activating mTOR complex one to to build up their their muscles

8:20 and and build up their um well activate protein synthesis.

8:23 So, there was the concern at the time that if you did get

8:26 the dose wrong uh that you could

8:28 impede some of those performance enhancements from exercise.

8:31 So, there there was a safety concern um with taking rapamycin off-label.

8:36 But again, we were hoping that if we got the dose correct,

8:39 we would actually improve muscle performance.

8:40 And the reason for that when you have a look at the mice research,

8:44 when uh you get the dose of rapamycin correct,

8:47 you do see markers of improved muscle performance um you know,

8:51 compared to the placebo group.

8:53 So, there was the preclinical work um to actually suggest that yes,

8:57 this may have merit in humans.

8:59 Um and again, we we we chose muscle because um we thought that that was

9:04 going to be probably the best uh marker of improvement with um with rapamycin.

9:11 So, you know, we we could choose heart disease, we could choose cancer,

9:14 but all of those are going to require a lot of time and quite large studies.

9:18 So, we thought what is the what is the study that we

9:20 could feasibly do um that would give us uh that would

9:24 hopefully take the safety concern off the table um and and allow

9:29 uh us to springboard uh for future studies as well.

9:32 So, that's why we overall chose muscle.

9:33 We thought that it was going to be the yeah,

9:35 that the best bang for buck if you like.

9:37 Do you think that that that your results,

9:39 I mean, your your you're studying just 40 people,

9:42 but again, it's the only study of its kind that's out there.

9:45 So, this is the data that we have as a community.

9:49 You know, and and when we're talking about statistical significance, right?

9:52 You have a statistically significant result in several cases,

9:56 but that's very different from the we use the word significance,

10:00 um and I think that in English, it just sounds like that's a big result.

10:03 And and and in statistics, it just means,

10:05 no, we measured something and it's real versus substantial.

10:10 And the and that's the word that we actually

10:11 that in that that that is the the linguistic mistake that so many people make.

10:15 It's Did you see a substantial change um because of this?

10:19 And just, you know, do you think you have any substantial

10:22 results to report at all from from the study that you did?

10:25 Yeah, I think we do.

10:26 So, with a 40-person um study,

10:29 you're only going to get statistically significant results

10:31 if you have quite a large effect size.

10:33 So, at a large clinically relevant effect size.

10:36 Um so, I I I do want to um just take a step back.

10:40 There there's When we set up the study,

10:43 what we did is that we registered the study um on a clinical uh registry.

10:48 And that just means that you there's nowhere to hide.

10:50 You know exactly what you're going to measure,

10:52 how you're going to measure, and you have to report those results.

10:54 Um so, all of these measurements uh yeah, again, there was nowhere to hide.

10:59 And as part of that, uh the the main uh

11:03 primary endpoint is called the uh um intention to treat analysis.

11:07 Now, that one, it didn't reach statistical significance,

11:10 but when we looked at the sensitivity analysis,

11:13 so for example, the per protocol analysis,

11:15 and I know that I'm getting in the weeds here, but I think it is important just

11:17 to make sure that we report the study correctly.

11:20 In the per protocol analysis,

11:21 so this is people who performed 75% or more of the exercise

11:25 protocol and took 75% or more of the study drug,

11:29 that's when we saw the statistically significant results.

11:33 So, it seems that the more people stuck to this protocol,

11:36 um the more blunting effect there was uh from rapamycin in terms of exercise.

11:40 Now, it it wasn't just the 30-second chair stand test that we measured.

11:44 We also saw that the same trend um

11:46 for the 6-minute walk test as well as grip strength.

11:49 So, to me, we've got three different muscle performance measures all trending

11:53 in the same direction that the 6-mg dose that we used once a week,

11:57 I I think we we do have solid evidence now that that at least

12:01 over a 13-week time horizon blunts the positive effects of exercise.

12:05 So, when you're talking about the adherence um uh to rapamycin,

12:09 this is something that I've written about not about rapamycin,

12:12 but I've written about adherence in terms of the placebo effect quite

12:15 frequently and and I didn't get into the weeds enough in your article,

12:19 but uh in the the the journal article,

12:22 but did the Did you have a similar number of people who had

12:25 adhered to the exercise protocols in both the active and the control group?

12:29 Yes, we did.

12:30 Yes, we did.

12:31 Oh, did.

12:31 Oh, that's fascinating.

12:33 So, you're So, what you're not seeing is that So,

12:35 one of the things with adherence is even if you

12:37 just give two sugar pills to two two different people,

12:40 but the person who adheres to the protocol more almost always shows a more

12:44 substantial benefit uh to that protocol regardless

12:48 of the actual effectiveness of the drug,

12:50 which is one of the weird things about the placebo effect as well.

12:53 It's like how much you put into it yourself versus not.

12:56 But you But what you're just told me is that that luckily

12:59 those two groups had the same number of people who were just like,

13:02 "Yeah, I'm not so into it." Which is great.

13:05 Yeah.

13:05 Yeah.

13:05 So, that that was one of the things that we

13:07 looked into cuz when we when we first saw the results,

13:09 we didn't quite believe our results and we tried to look and and see,

13:13 yeah, were more people exercising in the placebo group?

13:16 Um you know, were they taking more of the study drug?

13:19 But no, it overall between the two groups, they were actually roughly similar.

13:22 We were quite lucky with the participants that we had um that they were,

13:26 you know, quite adherent to this protocol.

13:28 So, you know, ultimately at the end of the day,

13:30 what you found is that that in this particular small subset of of information,

13:36 you have people who who basically didn't gain as much muscle,

13:40 but we don't really know about any life,

13:42 you know, actual longevity that comes with that.

13:44 Do you think that one of the this could ultimately be about trade-offs?

13:48 Like, some people maybe rapamycin extends life, but at the cost of muscle?

13:54 Yeah, it's a tricky one because in the lifespan mice studies,

13:58 so they're in a lab, they don't they don't have to run away from predators,

14:01 they don't have to try and hunt for food.

14:03 So, some of the criticism is that even

14:07 if these mice are frail and living longer,

14:09 that doesn't that isn't going to translate into humans because

14:12 obviously we don't want to be frail as we get older,

14:14 and that's one of the, you know,

14:15 big things that I see in the clinic is, you know,

14:17 my older adults when they start to lose their muscle strength,

14:20 that's when they start to need to go into rest homes and private hospitals.

14:22 And again, that was one of the reasons why I wanted to set

14:24 up the study because I wanted to try and prevent that from happening.

14:28 So, the the truth is we don't we don't know,

14:32 we don't have that data, so all of this is kind of speculative.

14:35 What I suspect is that I think we did overdose with rapamycin.

14:40 I think that if yeah, I think that if we spaced out the doses,

14:46 so for example, instead of dosing every week,

14:48 maybe if we dosed every 3 weeks or every 6 weeks,

14:51 maybe then we would have a different result.

14:53 Or maybe it is that rapamycin simply doesn't

14:55 have a role to play in in healthy aging.

14:58 Again, I'd I'd love to do more studies over

15:00 a longer time horizon to actually answer some of these questions.

15:03 Dan, do you think that would happen?

15:05 So, one of the things that's just so fascinating about how this came out, right?

15:09 Is rapamycin sort of showed up in the public

15:11 consciousness for this for longevity somewhere between 2011 and 2018,

15:17 depending on like how you want want about who was talking about it at that time.

15:22 And then the biohackers sort of got on board, right?

15:25 Peter Attia started be I think in 2021 was when Peter Attia was like, "Hey,

15:30 everyone should take rapamycin." Or I had Sorry,

15:32 he said he was going to take rapamycin cuz he thought it was worth it.

15:36 And then, you know, thousands and thousands of people followed suit.

15:40 But we're doing this sort of, you know,

15:42 on a whim because we're like cuz as you mentioned,

15:44 the mechanisms are really promising, you know?

15:47 You know, even mTOR, which I find this so fascinating is

15:50 mTOR really just means the target of rapamycin.

15:54 So the actual pathway is named after the drug.

15:57 This is how like down into the weeds we get here.

16:00 Um I mean what is the calculus that that that that that goes

16:06 on here between excitement about pathways versus let's go do this stuff.

16:12 And then how do we validate it?

16:14 Yeah, I think people have got different risk thresholds.

16:16 So some people will see, you know,

16:18 something exciting in mice and they don't want

16:21 to wait for human clinical trials because they will take,

16:23 you know, years and years.

16:24 So what they'll do is they'll say, you know, I only live once.

16:27 I'm going to try this experiment and, you know, fingers crossed it works.

16:32 And if I need to change my strategy later down

16:35 the track as more human research comes in, then I can,

16:38 you know, change my decision.

16:40 The I I think that the caveat to that is that you Sorry.

16:44 People sometimes think though that the there's no risk

16:48 and that there's only going to be potential upsides.

16:50 And I think that's sometimes where people get tripped up.

16:53 So for example, with metformin,

16:55 metformin was one of the darlings of the longevity community

16:58 at one stage because in certain mice studies it was extending lifespan.

17:03 Now some of those studies have been redone

17:07 in a slightly different way and that lifespan effect is gone.

17:10 But that didn't stop people from starting to take metformin.

17:13 Again, thinking that it's widely prescribed today.

17:16 There's virtually no downside, so it was thought.

17:18 So, you may as well take it because if there is a benefit,

17:20 you know, wonderful, you can make the most of it.

17:23 The trouble is, as more research came in, we found that, you know,

17:27 metformin it lowers testosterone levels.

17:30 Much like my study in rapamycin, if you take metformin every day,

17:34 it also blunts the positive effects of exercise.

17:37 Um, so, you know, those are two real

17:39 downsides to taking metformin for otherwise healthy individuals.

17:43 And then you had the diabetes prevention program who ran

17:46 a decades-long study uh that was placebo-controlled and it was in non-diabetics.

17:52 And what they found is that there was no benefit for cardiovascular disease.

17:55 There was no mortality benefit.

17:57 Um, there was no cancer benefit, either.

17:59 So, when you actually look

18:01 at the human research around metformin for non-diabetics,

18:04 I'd say that there's no evidence

18:07 of benefit and there's probably evidence of harm.

18:09 So, that's where I think we just need to be careful about,

18:13 you know, people who are taking uh yeah,

18:16 who are extrapolating mice research um to their own health because,

18:20 again, there are risks uh to doing that.

18:23 So, when you funded this, uh this When did the crowdfunding start?

18:28 Was it Was it 20 2001?

18:31 Sorry, uh 2021?

18:33 yeah.

18:34 5 years ago.

18:35 come about?

18:35 Because you crowdfunded it.

18:36 Like, tell me exactly how that pro That's not how you usually do this stuff.

18:40 So, how'd that happen?

18:41 No, so, generally, it's because it's a drug, generally,

18:44 it's big pharma that will come um and come to the party and and fund the drug.

18:48 The trouble is, rapamycin it's off-patent.

18:51 It was discovered in the 1960s.

18:52 So, there's no money to be made here.

18:55 Um, now, when I crowd when I initially started crowdfunding,

19:00 I made two fatal errors.

19:02 I didn't realize how much how expensive these studies are.

19:05 I thought, you know, this is a 40-person study over a 13-week time horizon.

19:09 At worst, it's going to be a 100 grand.

19:11 And, you know, surely would be able to to fundraise that.

19:15 So, that was the first mistake.

19:16 The second mistake is that I massively overestimated my reach on YouTube.

19:20 So, at this at the time, I had about 30,000 uh YouTube subscribers.

19:25 And I was thinking that, you know,

19:26 surely there'd be a couple of big whales who would who would

19:28 be able to come to the party and and fund the study.

19:31 Um now, credit to the YouTube community, we managed to raise $36,000,

19:36 uh which is wonderful and I'm incredibly grateful because all

19:39 of that uh allowed us to get the study um over the line,

19:42 but it it wasn't nearly the 720-odd thousand that we

19:46 needed uh to to get the study actually done.

19:49 So, um you know, we we then had

19:53 funding from uh a crypto organization called VitaDAO.

19:57 Uh we also had a couple of supplement companies come in, um but the the big

20:01 one was when uh there was one

20:03 particular big whale who wishes to remain anonymous.

20:07 Um he funded half of the study.

20:09 So, we So, we were almost there and then but we still had this, you know,

20:14 quite large shortfall.

20:16 Um and I I tried for about a an extra

20:19 year to try and get funding for uh for, you know,

20:23 uh to try and plug that gap, but it just wasn't working.

20:25 And that's when I realized, you know,

20:26 I was taking a couple of supplements that I

20:28 was convinced um based on the human clinical research,

20:31 uh you know, had benefit to the human body.

20:33 So, I was taking those and I kind of figured,

20:36 well, if I combine all of those supplements into into one,

20:39 uh and then, you you know, offer it to my community,

20:42 maybe we could use that to plug the gap uh in funding.

20:44 And that's what we managed to do.

20:46 So, yeah, it cost us, yeah, 720,000.

20:49 It it took us about 3 and 1/2 years to fundraise,

20:52 but again, now we've got the results.

20:54 That And that's crazy.

20:55 And and you know, you you just released your video here on YouTube.

20:59 Uh and I think your title, last I looked,

21:00 was something like, I spent $724,000 to test metformin.

21:06 I I The title is has that number in it.

21:09 And I saw also that your video only had 28,000 views, which is criminally low,

21:13 which makes me think that you actually did the most

21:16 the lowest ROI on a YouTube video ever because of that.

21:22 Yeah, yeah, I think I'd have to set some sort of a record there.

21:26 But again, I didn't do this for views.

21:28 I did it out of scientific curiosity because I

21:30 think these are important questions that needed to be answered.

21:33 You know, if again, if you have a look at the preclinical world,

21:37 rapamycin over and over again extends lifespan.

21:40 And I think unless we did something radical like like what we did,

21:44 I just couldn't see you know, the human clinical trials being done.

21:48 So again, I'm just so grateful for YouTube to be able to you know,

21:53 crowd fund something like this and and get this underway.

21:56 What would you say like this is a real problem in medicine right now, right?

22:00 We have a clinical trial, I mean, 10 years ago,

22:03 I the number I would quote would be a billion dollars for clinical trial.

22:06 It's actually gone up since then.

22:08 For to get for from an idea from a drug idea to release on the market,

22:13 it could be 1.5 1.5 3 billion dollars to get a drug out.

22:17 Why first, this is a two-part question.

22:20 Why do clinical trials cost so much in the first

22:23 place because now you have experience with that.

22:26 And and two, the second part of this question is will it

22:29 ever be possible to do longevity medicine research in the clinical trial system?

22:38 Yeah, so I I think there's a couple of things to say.

22:41 It's different if you're testing a supplement

22:43 compared to if you're testing a drug.

22:44 So if you're testing a supplement, the regulations and rules,

22:48 they're a lot more relaxed compared to a drug.

22:51 So since we were testing a drug,

22:53 it automatically bumps up the cost because of all

22:55 these extra hurdles that you have to jump through.

22:57 So in in terms of the the costs for us, so yes, I crowdfunded the study,

23:04 but you need to make sure that the the sponsor of the study,

23:07 so in this case it was me, doesn't interfere with the data collection

23:10 and and the actual running of the study.

23:12 So, so there's a a wall that that that can't be breached.

23:16 So, it in my clinical study,

23:19 we got Auckland's hospital to actually run the the study for us.

23:23 So, I had nothing to do with actually,

23:25 you know, discussing with patients or prescribing rapamycin.

23:29 And again, that just means that the data is clean.

23:31 But, you can't just rely it because it's a drug trial,

23:35 you can't just rely on that on that hospital

23:38 or that study organization to actually make to get the data correct.

23:42 What you need is a third-party auditing company to to come

23:47 and actually make sure that everything is done correctly.

23:49 So, you you've got the the data collection by the study nurses,

23:53 and you have to have someone to actually prescribe the drug,

23:57 you have to have data oversight committee,

23:58 you have to have a third-party auditing committee,

24:00 then you have to clean all of the data.

24:03 So, yeah, that's it it again, it's a lot more expensive compared to what

24:08 I was anticipating when I first undertook this venture.

24:13 Yeah, it it feels to me that so obviously

24:15 there's so many critiques of big pharma out there.

24:18 At the same time, I also want to say that big

24:19 pharma has done some great things and has created miracle medicines,

24:22 and that's awesome because they've created these sorts of clinical standards,

24:25 which, you know, involve a whole industry of CROs, which you mentioned,

24:29 which would run these things and validate data who are independent.

24:32 And you're like, oh, I can, you know,

24:34 you're you're you're fixing a lot of conceptual problems

24:37 in data with this huge and expensive industry that comes in.

24:42 The problem, of course, with big pharma is that you need also

24:46 immense profits to make this whole thing run.

24:50 And one of the things that goes on with longevity medicine, in my, you know,

24:55 interpretation of it, is that one,

24:59 your clinical endpoints are often a little weird, right?

25:02 If you're if you're testing longevity, like again,

25:05 you you you have to be studying someone for 80

25:07 years to really get a longevity understanding, or at least 20.

25:11 You maybe you start at 50 to see how they go on after that.

25:15 And it it it's just one just very, you know, complex to do it,

25:20 but also there's just no there there may not even be money in it,

25:23 because with longevity, like what are you treating?

25:26 Is Is dying Is getting old a disease?

25:28 Like that's not clear to me at all that get aging as a disease.

25:32 And And And so then to create an industry that studies this and validates it,

25:37 which is what we all want, right?

25:39 We What you did was heroic, right?

25:42 Even though your results didn't weren't what you what we wanted,

25:44 what you did was heroic,

25:46 because you're applying the scientific method and these things

25:49 that is and you raised a ton of money.

25:51 Um but it's also clear that we need to do what?

25:54 10 other studies like this to even get a real answer to the rapamycin question.

25:58 So, you know, what are your feelings about about this?

26:02 Yeah, I think setting up a lifespan study uh that that's a non-starter.

26:07 Uh it's again it's going to be super expensive.

26:09 You're going to need hundreds and hundreds of patients to do it.

26:12 So, that's why I think you need to select a particular

26:15 endpoint that's going to improve someone's health span, if if you like.

26:19 Um so, it's a how healthy do they feel?

26:21 So, that's why we chose muscle.

26:22 But if you have a look at something like GLP-1 therapy,

26:25 so as in big for instance,

26:27 you know, that's now completely exploded because of um you know,

26:31 its weight loss effects.

26:32 And through its weight loss effect,

26:33 you can uh get patients off their blood pressure medications.

26:36 them off their diabetes medication.

26:37 So, there are all of these health metrics that do improve

26:41 um even if you don't yet have that that lifespan data.

26:44 So, that's where I think the longevity uh if you were trying

26:48 to set up a a study looking at a a so-called longevity molecule,

26:51 you do need to pick a particular endpoint that will improve someone's

26:54 life now rather than waiting to see if it will extend lifespan.

26:58 So, again, that's why we chose the 30-second chair

27:00 stand test for the primary outcome of our study.

27:03 Um but it, you know,

27:04 even popular supplements like creatine, for instance, um you know,

27:09 there's reasonable evidence that it does improve,

27:11 um you know, muscle power and performance.

27:13 There's now potential uh evidence that it

27:15 does improve uh aspects of cognition and memory.

27:18 So, I I don't think you need lifespan data uh on creatine before

27:23 someone can actually start or make the decision to start to take it.

27:26 And yeah, so that's where I see um you know,

27:29 the so-called longevity field going is looking at endpoints

27:31 that improve someone's health now rather than waiting for lifespan data.

27:36 So, I have been in general I'm very

27:39 skeptical of the entire supplement industry because, you know,

27:42 we have this this I mean, problem where where as you said the the validation

27:48 for supplements studies is is much lower, right?

27:52 And we also have people who just right across the spectrum

27:57 for supplements because you can just

27:58 basically start making marketing claims now.

28:00 Like if I wanted to tell you that this Earl Grey tea

28:06 makes my boost my energy and uh and will will sharpen my vision.

28:11 I could probably say that and get away

28:12 with that legally in America and make a million dollars.

28:16 Whereas, rapamycin, you you know, with with a drug it's it's very different.

28:20 And you know, you you mentioned creatine and I'm not at all

28:23 an expert on creatine supplementation or or or what those pathways are.

28:29 But when you start making these these claims that, you know,

28:31 you said that it appears that it improves cognition,

28:34 that you know, there's some evidence about muscle mass.

28:37 I really worry about the weight of that evidence.

28:40 I really worry about people's thinking that that those words

28:43 are more certain uh than they are.

28:45 And then when you add on to the the question of longevity,

28:48 we we get into sort of a sort of almost an existential question.

28:53 So, you're absolutely right that it is a minefield out there with the supplement

28:57 industry because not only do people make claims about a a particular molecule,

29:02 but often times you don't actually know whether the supplement

29:05 that you're taking actually contains that molecule or not.

29:08 So, it it is a complete minefield.

29:11 What what I would say is that for for certain supplements like creatine,

29:15 I think there is there is good

29:17 evidence for improved muscle power and performance.

29:19 And that's why, you know, for example,

29:21 the International Society of Sports Nutrition,

29:23 they do mention it within their guidelines

29:26 that that it does have some reasonable evidence behind it.

29:29 But I think, you know,

29:30 for antioxidant supplements for instance, and and, you know,

29:34 many many other supplements, resveratrol,

29:37 there is no good evidence that they improve any aspect of of health.

29:41 But they're still sold in in the millions today.

29:44 So, you're you're right to be skeptical.

29:46 And I think that's one of the reasons why I'm

29:48 such a fan of your channel is that you do take

29:50 a skeptical mind to this field because it is so easy

29:54 just to get caught up in the hype of these marketing claims.

29:58 Yeah, I just generally start off with the idea

30:00 that anyone who's talking to me is a liar.

30:02 And it's a really it's been a very useful way to go through life.

30:05 And it's just proven accurate over and over again.

30:08 I am also willing to be proven wrong with evidence.

30:10 Like I love actually being proven wrong.

30:13 But there's so much marketing, there's so much out there,

30:15 and there's so much incentive to over hype things.

30:19 You know, obviously you know, the grifters, that line of people who just like,

30:23 you know, people people who maybe said that resveratrol was so great, right?

30:28 You know, David Sinclair made a roughly a billion dollars

30:32 selling the idea that resveratrol was a great life extender.

30:37 And it you know, there's nothing really to it.

30:40 And and then we also see just like the whole world of wellness scriptures.

30:43 Open up your Instagram feed now and say gut health and just see what comes

30:47 up and you're going to be in a just a a hole of terrible information.

30:53 And then sort of weeding that out as we go forward,

30:56 you know, there are doctors who have some information.

30:58 Obviously you have great information.

31:00 You obviously have ethical standards because and you know,

31:03 for everyone who's watching this, you can tell someone's ethical standards

31:07 by whether or not they admit they are wrong about something.

31:10 And you just came out and said, well,

31:11 my hypothesis didn't turn out to be the what I dreamed that it would be.

31:16 And I promise you that Brad would be making a lot

31:18 more money if you fudged the results in the other direction.

31:23 But you're right.

31:24 I think I think a lot of people go

31:26 out there to try and prove their theory correct.

31:28 When actually ideally you want to be trying to prove your theory wrong.

31:31 And I think that's what we did in this study

31:33 at least at the dose that we tested.

31:36 Um Now you mentioned a couple of things for example

31:39 about gut health and This is one of the things

31:42 that that I get a little bit worried about I

31:45 suppose is the best way to put it is functional medicine.

31:48 So I think functional medicine is a byproduct of a failing of primary care.

31:52 So I'm a primary care physician and I know

31:56 how difficult it is for patients to see me

31:57 in the clinic in a timely manner and you've only

32:00 got a 15-minute window cuz that's just how the funding works.

32:04 And so you often don't give the best care possible.

32:09 And because of that gap,

32:10 that's where functional medicine comes in and they promise to treat you know,

32:13 the root cause of your health issues and they then they do

32:16 a bunch of different tests that don't actually have clinical validation like gut

32:20 health tests because the the actual it's interesting that there's been a couple

32:24 of studies looking at different ways to test you know, gut microbiome.

32:28 And all of the different tests they come up with different results.

32:31 And often if you use the same test on the same on the same person,

32:34 you'll come up with different results as well.

32:36 But that doesn't stop people from then trying to interpret

32:39 those results and then make clinical decisions around them.

32:41 So, I I I do I I I agree that primary care is underfunded.

32:47 It does have issues, um, and it does need to be fixed.

32:51 I I just worry that functional medicine is not the the the way to do it.

32:56 Yeah, functional medicine to me, when I when I when I look at it,

32:59 and I actually have This is I actually I have the book.

33:03 I have the actual basic functional medicine textbook,

33:06 the the one that they they that is taught in the functional medicine courses.

33:10 Gifted to me by a functional medicine doctor.

33:11 But, like the the thing that is the the idea behind it is good, right?

33:16 The idea behind we're going to get a lot of data on you.

33:20 We're going to get all the data,

33:21 and then we're going to try to like figure out what say,

33:25 um, a healthy person looks like.

33:26 So, you have to create a sort of similar

33:28 and a a platonic ideal of a healthy person based on statistics.

33:32 So, 40-year-old should have great testosterone,

33:34 and, you know, all of these other things.

33:36 And then you say, "Okay,

33:37 we're going to try to get all of your numbers into that that platonic ideal, uh,

33:41 and that is going to make you healthy or younger,

33:44 or, you know, that they're going to start defining what that means.

33:47 The problem is is that one,

33:49 we don't have the tools in general to move all of those metrics.

33:52 We can move some metrics, of course, but we don't we can't move them all,

33:56 and we can't really define what

33:57 that that what healthy means in terms of numbers.

34:01 We need to Disease is actually the word means dis-ease.

34:05 It actually comes from It is a symptom.

34:07 It's something you feel.

34:08 It's something, you know, you have symptoms, which are things you feel,

34:11 and you have signs, which are clinical identification thing.

34:14 I can look, and I, you know, the sign of a broken leg is that it's crooked.

34:18 So, okay, guy, we got We have this the clinical objective sign,

34:21 and the the symptom is, "Oh, man, my leg really hurts cuz it's crooked." Right?

34:25 And and these are sort of obvious things,

34:26 but when we start abstracting out of pathology,

34:31 out of a real problem, then you start inventing a disease.

34:35 And I think in my my problem with both functional medicine,

34:38 because it it invents tons of diseases, like you have a vague symptom,

34:43 we're going to give you some data to explain what your vague symptom is.

34:46 And in longevity medicine, it it it has this concept of a biological age,

34:50 and it defines aging as disease.

34:54 I find this all just ridiculous and like philosophically problematic.

34:59 Uh and I don't know.

35:00 I I I you know, usually interviews are supposed to ask questions,

35:03 but I think I just went on a diatribe.

35:05 So, sorry about that.

35:09 No, I completely agree with you.

35:10 And I think an analogy is useful here.

35:12 So, people don't play basketball to be tall.

35:15 It's, you know, people who are tall play basketball.

35:18 And it's um a similar thing with uh you know, functional medicine.

35:22 So, a classic example is vitamin D.

35:24 So, when you go into rest homes uh and you measure

35:27 the vitamin D levels of those uh rest home uh patients,

35:30 often their vitamin D levels will be quite low.

35:32 And so, people will extrapolate to say, well,

35:35 low vitamin D levels have caused um you know,

35:38 this person to become frail and weak and need a rest home.

35:40 Therefore, if you start supplementing with vitamin D, um you can uh you know,

35:45 be much healthier compared to you know, what these people are.

35:47 Whereas, it it's it's the opposite.

35:49 These people um because of their functional decline,

35:52 they haven't been going outside to see much sunlight.

35:55 Uh and that's why their vitamin D levels are low.

35:57 And that's why um you know, a a lot of the clinical what virtually all

36:01 of the clinical trials um of vitamin D have been largely disappointing.

36:04 It was hoped, for instance, that we'd see uh you know,

36:07 decreases in cancer, decreases in cardiovascular disease.

36:11 But the VITAL trial, which was a massive study, I think,

36:13 of about 25,000 people, uh that looked at omega-3 and vitamin D.

36:19 And it found uh with with vitamin D in particular,

36:22 it found no impact on cancer um or cardiovascular disease.

36:26 So, and and and if you take it a step um forward,

36:30 there's been a couple of other studies looking at um

36:33 bone density uh and also um falls as well.

36:36 And we we don't quite know why we see these results, but but here they are.

36:40 Um the it and and some of these studies,

36:43 the higher doses of vitamin D are associated with greater

36:47 bone uh mineral density loss uh and also worsening fall risks.

36:52 So, again, we don't quite understand why we saw those those results,

36:55 and it might be artifacts of those particular studies.

36:58 But o- overall, we didn't actually see improvements.

37:01 Um and so, again, I I just get concerned that a lot of people are doing tests uh

37:06 and then treating those tests with a particular supplement

37:08 or a diet or exercise protocol or whatever it may be.

37:11 But we don't actually have clinical validation that um

37:15 those tests are both meaningful uh and worth treating.

37:18 What do you think about the the the sudden rise

37:22 of the um what I'm going to call small pharma, right?

37:26 We have big pharma, which is Pfizer and Bayer, right?

37:28 All the big all the big guys who make the big drugs that that uh that you know,

37:32 are in pharmacies everywhere.

37:33 But now we have this new version of small pharma,

37:36 which I'm going to say is this sort of un- quasi pharmaceutical market,

37:41 usually around peptides.

37:42 We could say stem cells, regenerative medicine in general,

37:45 where we have things that are often legal to take because a peptide,

37:49 for instance, is just a fraction of it's

37:51 like a small amino acid, basically, right?

37:53 Um and a a small protein that made up of amino acids.

37:57 And and then and then there's all these people

37:59 that that look like they came out of the bodybuilding world.

38:03 Uh and and if you scroll through some of these websites,

38:05 you'll just see things like BP-147 or the Wolverine stack,

38:10 and GLP-1s, obviously, and all of this stuff.

38:13 How does How should a human right

38:17 now who's watching this video navigate that world?

38:20 Like, is there promise in that world, Or is that oh my god, that's horrible.

38:25 Yeah, I think this really started to kick off with the advent of GLP-1 therapy.

38:28 So, GLP-1 is glucagon-like peptide 1.

38:32 And I think that really caught the imagination of this, you know,

38:35 peptide community for what for want of a better phrase.

38:37 Um because, you know, there's a bunch of different peptides that um

38:41 have shown some promise in preclinical models,

38:44 but for whatever reason just haven't had the the human clinical trials for them.

38:48 And this sort of harks back to what we were talking about before,

38:50 that for some people their risk tolerance uh

38:53 is greater than than say mine for instance, where they would see um you know,

38:56 some positive results in preclinical models

38:59 and decide to to take a particular peptide.

39:01 But, the the concern is that we just

39:04 don't know the benefit versus risk ratio in humans.

39:07 So, we know a lot about the benefit versus

39:09 risk ratio for GLP-1 therapies because big farm has

39:12 come along and poured millions of dollars into doing

39:14 clinical trials so that we can actually um you know,

39:16 present these findings to patients

39:18 in in the clinic and have a evidence-based discussion.

39:21 Whereas, a lot of the, you know,

39:22 other peptides that that you can buy from, you know,

39:25 compounding pharmacies or or different peptide clinics,

39:28 they don't have that validation.

39:30 So, I would just be again,

39:34 concerned that we don't know if there is any benefits to any

39:37 of these particular peptides um and whether there's actually true harms or not.

39:41 So, the general advice that I give to my patients in the clinic is, you know,

39:45 don't inject these strange uh chemicals into your body because again,

39:49 we just don't know the benefit versus risk ratio.

39:51 And I think that's a reasonable place to start.

39:53 But again, other people will will have will have

39:56 different risk tolerances and just decide to take them.

39:59 And you know, their health, their decision.

40:01 But if they were a patient of mine, I would just urge caution.

40:05 I mean, I think that's well said.

40:06 And I also feel like a lot of people are daredevils, right?

40:09 Because as you said in the very beginning

40:10 of this, people don't anticipate negative side effects, right?

40:13 We anticipate the marketing spiel that comes at us.

40:16 Like things like the Wolverine stack that sounds so cool in terms of peptides.

40:20 You know, Andrew Huberman,

40:21 like many many people are are advertising various iterations of this.

40:26 And, you know, I know that I have gotten

40:29 two different peptide companies approaching me this week saying,

40:32 you know, will you sponsor our peptides?

40:34 I bet you you have gotten those offers recently as well.

40:38 Um you know, how you know, and I think that people like the marketing.

40:43 They like the idea that they can sort of take

40:45 control of their health where the medical system has failed them.

40:48 Uh but but but do we really, you know,

40:51 you're you're you've already said this, you don't know the risks.

40:54 Um you know, how bad is it?

40:55 Like, what what could go wrong?

40:58 Yeah, well, we just don't know.

40:59 Like, um there's one particular uh peptide

41:02 that can make your skin a bit more tan,

41:04 and there's a concern around cardiovascular

41:06 health that it may increase cardiovascular disease.

41:09 Um so, yes, you might be a bit more tan,

41:11 but you might be increasing your heart attack risk.

41:13 And that's just one example.

41:15 I think it a slightly different approach that that people might want

41:19 to take is that instead of paying money to inject these things

41:22 into your body and and you don't exactly know whether it's going

41:25 to be harmful or whether it's going to be beneficial, you know,

41:28 maybe set up a clinical trial or or donate to someone

41:32 who's actually running clinical trials looking

41:34 at these peptides because, you know, I I think one of the reasons why this area

41:38 has really exploded um is that big pharma companies,

41:42 they haven't really poured money into this area um and and had a proper look.

41:46 Like, uh BPC 157, I think, is one of the the more uh popular peptides,

41:52 but we don't have a lot of human research on it.

41:54 I think we've only got, you know, one one or two human studies.

41:57 And um so, I think if people really wanted

42:00 to know if there are true benefits or risks, you know,

42:03 maybe set up a a clinical study like what I did with rapamycin

42:06 and actually explore this um and take a scientific approach to it.

42:10 Because again, there there there might be something here,

42:13 but equally we we just don't know and we need those human studies to be done.

42:17 So, if someone wanted to to make a big difference for, you know,

42:20 not only their own health, but for the the world's health, you know,

42:25 maybe try and set up something like what I did with rapamycin.

42:28 What about Hey, hear me out.

42:29 This could be crazy,

42:30 but we have a lot of people who are willing lab rats in the world, right?

42:34 Who are just like, "Give me BP 157.

42:37 I heard it on a podcast and I believe

42:39 in it." And they're willing to inject themselves with it.

42:42 Is there a way to set up a clinical trial based on the lab rats own,

42:48 I think, poor decision-making,

42:50 where you actually collect valid clinical data from a bunch of these human

42:55 trials because they've willingly given hopefully informed consent to do it.

43:00 Is there a way to ethically collect that data off of these, you know,

43:04 you know, human lab rats?

43:07 You could potentially do an observational study.

43:10 But the trouble is observational studies,

43:12 they can only tell you about correlation.

43:13 They don't really tell you causation.

43:15 So, in a perfect world, you'd want a placebo-controlled study.

43:19 So, one group who are taking, you know,

43:21 BPC157 and and another group who is taking placebo.

43:25 Um and they're blinded, so they don't know which group they're actually in.

43:28 And then you can follow these patients up to see, you know,

43:31 what clinical endpoints um are are are um are affected by this.

43:36 Now, to do that, you do probably need to go through an ethics board.

43:40 Um you need to have funding.

43:41 You need to make sure that the again,

43:43 the sponsor of the study doesn't interfere with the data collection.

43:46 Um and I don't know whether BPC157 would be classed I

43:50 I'd imagine it would be classed as a drug, not a supplement.

43:53 So, again, you start to ramp up the the costs.

43:56 But since there's such excitement around peptides, um you know,

44:01 instead of just getting swept up in that hype,

44:04 you know, I I think clinical studies should be done.

44:07 Um and I think there's enough excitement

44:09 around it to hopefully build that community

44:11 to be able to crowd source something um that that moves the needle forward.

44:15 Cuz again, if if big pharma isn't going to do it,

44:17 it it's up to you know, it's up to the community to do it.

44:20 But you want to make sure that that's done safely and ethic and ethically,

44:23 not just people um you know, injecting strange things into their bodies without

44:28 knowing what the benefits or risks are.

44:32 What What future trials do you envision on rapamycin?

44:35 Like are you planning to do any more clinical trials on this or other drugs?

44:38 Is this going to be a model for you or you or or are you feeling like this was

44:42 a lot of work and I I I think I'm

44:44 going to just be a primary care physician and a YouTuber.

44:48 Um I I think this trial was really beneficial for, you know,

44:51 the the so-called longevity community because I I do

44:54 think we've got reasonable evidence now that once-a-week dosing,

44:58 which at the time was the most popular off-label strategy,

45:02 um I think that is too much.

45:04 I think that if if and this is a big if,

45:08 if rapamycin does have a role to play um for healthy aging,

45:11 I think that you do need to extend the inter-dose interval.

45:14 So, sirolimus, which is the version of rapamycin that we used in our study,

45:18 it's got quite a long half-life.

45:20 So, that just means that the drug sticks around

45:22 in the body for quite a long period of time.

45:24 So, one of the potential explanations for why we saw the results

45:27 in our study was that even though people were taking rapamycin on Saturday,

45:32 there was probably still some rapamycin in this system

45:35 by the time that they were exercising again on Monday.

45:38 So, that's potentially why it blunted some of the positive effects of exercise.

45:42 Whereas, if you dosed it every 3 weeks or every 6 weeks,

45:46 then the vast majority of your exercise uh

45:49 sessions wouldn't have rapamycin on board as well.

45:52 So, maybe then you truly would have

45:54 separate periods of time where you're switching mTOR

45:56 complex one down and then separate periods

45:58 of time where you're switching it back up again.

46:00 So, I would love to be able to do that study,

46:03 but it would be a three-arm study, I think.

46:05 You'd need a placebo group.

46:06 You'd need a group that's taking rapamycin once every 3 weeks,

46:09 and another group who's taking it once every 6 weeks,

46:12 and you'd you'd need to follow them up for about 12 months,

46:14 I think, to actually get um you know, some some reasonable uh evidence.

46:19 So, to run such a study,

46:22 um you you'd you'd probably want to have about 40 or 50 participants per group.

46:28 So, you know, between 120 and 150 participants in total over a 12-month period.

46:34 Now, that's a that's a lot more money compared to um you know,

46:38 my short-term study of 40 participants.

46:41 So, you know, it it would be and and I'm I'm ballpark figuring here.

46:44 It would be somewhere in the vicinity of 3 to 4 million,

46:47 maybe, to do such a study.

46:49 And I certainly do not have that financial firepower.

46:52 So, if if um if we were going to do such a study,

46:56 which I think would be very useful for the scientific community,

47:00 um yeah, we would need some some people with quite a lot

47:03 of money behind them who want to further uh further this field.

47:07 So, what I'm hearing you saying, Brad,

47:08 is that if a whale happens to be watching this and wants

47:12 to give you three or four million dollars to run this study,

47:15 you would be willing to do it?

47:18 Yeah, 100%.

47:18 It It's simply a a matter of money.

47:21 I I would love to do it because I I there are still open questions here.

47:25 Um I think if that if the follow-up study where

47:29 you're dosing it every 3 weeks or every 6 weeks, if that study failed,

47:32 then I think you could you could say with reasonable confidence that rapamycin

47:37 probably doesn't have a role to play in in otherwise healthy aging for humans.

47:41 Because if it does interfere with the benefits

47:43 of exercise over that time horizon,

47:45 and even though you've extended the inter-dose interval, um you know,

47:48 I personally wouldn't want to prescribe it to my older patients,

47:51 and I certainly wouldn't want my parents to be on it, either.

47:53 Um and I I think that that's where you could finally yeah,

47:57 turn turn the switch off of rapamycin and look elsewhere.

48:00 Um but until you've got that study,

48:02 there's still going to be that lingering hope that maybe

48:06 it maybe it will have a role to play.

48:09 And I think there's one thing in your study, which is an unequivocal result,

48:13 which is someone that we sort of knew about anyway,

48:16 but is a positive result, which is that rapamycin or not,

48:20 as you get older, if you do exercise, that is good for your health.

48:25 Because both the placebo arm and the rapamycin arm showed

48:28 that exercise as you get older is a pretty darn good idea.

48:33 Yeah.

48:33 And again, that was really pleasing to see

48:35 that both groups did improve um their muscle performance.

48:38 And you know, and the selection criteria to into the study

48:42 was that you had to be relatively sedentary.

48:44 And we defined that as no more than vigorous

48:47 um activity three times a week for about 15 minutes.

48:50 So so these people were relatively sedentary.

48:53 And they did see quite significant improvement in the 30-second

48:55 chair stand test during the 13-week time horizon, which really isn't that much.

48:59 And all they were doing was doing um that they had

49:02 the exercise bike three times a week for half an hour.

49:05 And that was it.

49:06 And they saw significant improvements in the 30-second chair stand test.

49:09 So yeah, out of uh the the main takeaway

49:12 is that you just can't beat exercise at this stage.

49:14 And anything that we do in this, you know,

49:16 so-called longevity field should stack on top of exercise.

49:22 I love it.

49:22 All right.

49:22 Well, Brad, uh thank you so much for all of the work that you do.

49:25 And for everyone who's watching this video,

49:27 if you came through my channel, go check out Brad's channel.

49:29 He's in the the contributor thing that down there it says Brad Stanfield.

49:34 Go follow him, too.

49:36 And if you came through his channel, you should follow me.

49:39 Uh and uh you know, thanks so much for being on the show.

49:42 And uh and you know, I love the work that you're doing.

49:44 And I will absolutely still be watching you.

49:46 And I really hope that, you know,

49:48 uh we can collaborate on something fun in the future.

49:50 Yeah, absolutely, Scott.

49:51 Thanks for your time.

49:52 Thank you so much to my supporters here on Patreon

49:54 and on Substack and even on YouTube who make this work possible.

49:59 It means the world to me that you're here.

50:01 And if you want to get your name on the honor roll,

50:04 all you need to do is sign up at the links down below.

50:08 From Foxtopus Inc.

50:09 in Denver, Colorado, this was Scott Carney Investigates.