Full Transcript Introduction and Research Background 0:00 Welcome back to the conversation. 0:01 I am now joined by doctor Dale Bredesen, M.D., 0:04 who is an internationally recognized neurologist with specialty expertise 0:08 in the mechanisms of chronic neurodegenerative diseases. 0:11 He is the senior director of Precision Brain Health at the Civic 0:15 Neuroscience Institute, and the chief scientific officer at Apollo Health. 0:19 Doctor Bredesen has contributed significantly to medical knowledge 0:21 and literature over the 30 patents and nearly 250 papers. 0:25 Notably, he put much of his findings in research 0:28 into the 2017 New York Times bestseller The End of Alzheimer's. 0:32 Doctor Bredesen, welcome. 0:34 Thank you so much, Jason. Great to talk to you. 0:36 Yeah. 0:36 And I guess we're going to have to add to that list, 0:38 because you have a new publication that I'm really excited to dive into. 0:42 But for those who may not know your name, I first heard about you, 0:46 I think in maybe 2010 when I think your original paper came out, 0:50 if I remember correctly, detail or maybe 2014 something, or in that range. 0:55 The first paper was the first report of reversal of cognitive decline 1:00 in people with Alzheimer's we put out in 2014. 1:03 So yeah, great memory was 2014. 1:06 I actually saw the first patient in 2012 and in 2014 wrote up the first ten. 1:12 But we've come a long way since then. You know, 1:14 we had a paper with 100 documented improvements in cognitive decline. 1:18 Then we had a proof of concept trial that was published in 2022. 1:23 And then doctor Heather Sanderson published a confirmation 1:27 she did her own trial and got virtually identical to results to what we had. 1:31 And then what I'm excited about is we just finished a randomized controlled 1:35 trial at six sites around the US, and we had the best results ever published. 1:39 So this is now in peer review. 1:42 But the preprint is already available and had over 14,500 downloads. 1:47 So very excited about that. 1:49 And also, I have to say, I'm honored to work with the six clinicians 1:53 who were involved with this Doctor Kat Toups, Doctor Anne Hathaway, 1:57 Doctor Christine Burke, Doctor Craig, Tonio, Doctor Nate Bergman 2:01 and Doctor David Haase and really fantastic results 2:04 with the people in this particular randomized controlled trial. 2:08 So very excited. 2:09 And we saw improvements in their in their composite memory, improvements 2:14 in their executive function, improvements in their overall neurocognitive indices. 2:18 So very, very enthusiastic about that. And yet. 2:21 Of course, in the trial, 90% of people showed some improvement. 2:25 Now some of them dramatic improvement, some of them modest improvement. 2:29 And then, of course, there are the 10% that didn't show improvement. 2:32 So we want to understand 2:34 why did some people do so well and some people not respond. 2:39 Typically what we've been finding is the ones that don't respond 2:43 are the ones that simply aren't doing the protocol, 2:46 or the doctor really hasn't looked into what are the critical drivers 2:50 of the process? 2:51 I mean, this, this all this work all came out of 30 years in my lab 2:55 looking at all the things that drive this change and what we found. 3:00 You know, Jason, what we found is really fascinating. 3:02 Just as you go from sleep to wakefulness. 3:05 So you have this mode switch. 3:07 You know, a whole set of things, hormone changes and of course, gut changes. 3:10 All these things that are changing 3:12 as you go from sleep to wake from the ceiling, 3:13 your peristalsis is changing all these things. 3:16 What happens is you have a connection mode 3:20 where you have your tau is not phosphorylated. 3:24 You're not making these prions that are damaging the brain. 3:28 You're not making a lot of amyloid. 3:30 You're literally focusing on connection. 3:33 Your amyloid precursor protein is cut 3:36 at a single site, and you're making things that make new synapses. 3:40 So you're literally in connection mode. 3:42 On the other hand, when you have these various insults, leaky 3:46 gut viruses coming up, your virus or bacteria coming up your vagal nerve 3:51 and into your brain stem, which changes in oral microbiome, 3:55 chronic sinusitis, tick borne illness, toxin exposures. 3:59 You literally have this beautiful biochemical switch
From Drug Discovery to the ReCODE Approach 4:02 that takes you from connection to protection. 4:06 And what's amazing is you can follow the molecular 4:09 biology, the change in phosphorylation of tau, the change in neuronal signaling, 4:15 the change in synaptic versus synaptic classic signaling. 4:20 It is remarkable to see. 4:21 And when you look at Alzheimer's, all it really is, it's 4:25 put you it's a chronic situation where you're in that protection 4:30 mode and away from the connection, so you're not making new connections. 4:33 And in fact, you are sacrificing the connections that you have made 4:38 in order to protect your brain 4:41 against these various pathogens, toxins, metabolic change, gut leaky ness, 4:46 all these sorts of things. 4:48 So we're really understanding the biochemistry 4:52 of what happens in your brain. 4:53 And what's important 4:54 is that this really comes back to just brain health in general. 4:58 So you can see that, you know, if you are having metabolic syndrome, 5:04 if you've got a poor gut function, if you've got a, you know, 5:08 an abnormal microbiome, these things are all giving you brain 5:12 health compromises, even if you're not all the way to having Alzheimer's yet. 5:16 So there's a lot we can all do. 5:19 We have a guy recently who went from those guys out working 5:22 usual, you know, normal person, 5:24 but he scored 10th percentile on his memory studies. 5:28 We put him on the program. 5:30 Turned out he had some especially some metabolic 5:33 abnormalities, horrible insulin resistance. 5:36 For example, 5:37 five months on the program, he's now scoring 91st percentile on his memory. 5:42 So, you know, all of us can do better with our cognition. 5:46 That's remarkable. 5:47 I mean, you know, and I'm going to go back to that kind of 2012 time timeframe. 5:52 I think what's fascinating to me is, you know, 5:56 you've been looking at neurodegeneration. 5:59 Yeah, most doctors, especially in the the research world, really 6:03 look at it from a perspective of how can I find a drug to address these things. 6:09 What was it for you that kind of really 6:12 I mean, look, you're kind of a renegade, I guess, in the medical world 6:16 to kind of look at diet, lifestyle supplements, nutraceuticals. 6:21 Very. 6:21 You know, when I saw this, your original work, I said, 6:25 yeah, this this makes sense. 6:27 This is amazing, you know. 6:29 So in one sense, it was like, I guess, kind of obvious in a sense. 6:32 But on the other side, it was it was revolutionary in the field of 6:36 neurodegeneration because at that time, at least as far as I was perceiving, 6:40 there was a general acceptance of dementia and Alzheimer's. 6:43 It's a one way street. 6:44 This is how it goes. At best, we can manage. 6:47 Try these drugs. 6:48 Yeah, sure. You know, change your diet maybe, or sure. 6:51 Try to get some sleep and exercise. 6:53 We all know that's good, 6:54 but there was no real intervention and certainly no plan in place 6:59 to to actually come up with a trial or a study to look at this stuff. 7:02 So what was it for you that, like, really drew you into pursuing that 7:06 in a very research minded way? 7:10 Yeah, a great point. 7:10 And of course, then every expert said the same thing. 7:13 There was a standard tag line and you could actually see it 7:16 on the Alzheimer's Association website, and it said there is nothing 7:20 that will prevent, reverse or delay Alzheimer's disease. 7:24 Like that's it. 7:25 If you got it, got it still persists, right? 7:28 Like even with your work, 7:29 this is still the prevailing paradigm in the medical community. 7:32 And I would say largely in the in the general population. 7:36 Yeah, it's actually amazing. 7:38 So what we were doing at the time was what just what you were describing. 7:41 We were looking for drugs. 7:42 And so we had discovered in the lab that there was this switch back and forth. 7:48 We were just looking at a tiny little piece of it, which was app signaling. 7:52 So you have this amyloid precursor protein. 7:54 It sticks 7:55 through the membranes of your neurons and to a lesser extent, other cells. 7:59 And it's especially at synapses. 8:01 And it's clear that is the parent of the amyloid itself, 8:05 the little, little peptide. 8:07 And so we were looking at this switch. 8:10 And so we said okay let's look for drugs 8:13 that keep you away from the amyloid side and put you on to that sap alpha, 8:19 that side that seems to be associated with anti Alzheimer's effects. 8:24 And we were screening through these drugs. 8:26 And so 8:26 we actually had one very interesting one that we identified called tropism Tron. 8:30 It was available in some other countries for other things not for Alzheimer's. 8:35 Nobody had ever looked at. So it would be a repurposed to drug. 8:38 And we thought, okay, we need to set up a trial for this. 8:41 As I was sitting, I was actually sitting in my office looking at the whiteboard. 8:45 We were 8:45 putting all the stuff down for the trial and I thought, well, wait a minute, 8:49 that doesn't get it. All the pieces. 8:51 I thought, you know, maybe we should add like brain training, because professor 8:54 Mike Merson was the is the godfather of brain training 8:58 and the one who developed brain HQ, which still has by far 9:01 the most data associated with improvement in cognition. 9:05 And I started thinking, well, each of these things alone is not perfect. 9:10 I thought, well, now what if we started adding, you know, 9:13 what if we started adding like some exercise? 9:15 And then of course, after about 3 or 4 of these, the light bulb went off. 9:18 And I thought, now why would we withhold anything 9:22 if we're talking about this network insufficiency, 9:25 which is what we realize in the lab, if you if you graph out, 9:29 if you look at all the molecular species, you know, there are over 9:32 25 molecular species that just interact just with AP alone. 9:37 It's a it's an integrator of all these different things. 9:40 And, and you can literally follow the molecules. 9:43 You can see estradiol 9:45 binds its receptor goes into the nucleus, it changes hundreds of genes. 9:49 And one of the ones is the one that cuts the app to go toward connection. 9:54 So you can literally see this beautiful ballet playing out in front of your eyes. 9:59 And so I thought, well, if this is if we really believe and if the 10:04 if all the data are showing that this is a network insufficiency, 10:08 you don't take a hammer to those things and whack them and say, 10:11 okay, just do one thing and everything's going to work. 10:13 It's kind of like trying to fix a country or a company. 10:17 You've got to tweak here and tweak there, and you got to look at all the things. 10:20 What actually drove this problem. 10:23 So we started saying, oh, okay. 10:26 And then of course, Patient Zero came to see me in in April of 2012. 10:32 And she was from the CIA, actually, and was ready 10:36 to commit suicide because her mother had died of Alzheimer's. 10:39 She'd watched her mother die. 10:41 And then she was she had now been to her doctor, and her 10:44 doctor said, you've got the same thing your mother had. 10:47 There's nothing I can do. 10:49 And then I got a call from her friend who happened to be near 10:52 where our institute was and said, you know, 10:55 you were going to do this trial, but it got turned down by the 10:59 by by the IRA that we were
Key Drivers of Cognitive Decline 11:01 the trial was actually supposed to be done in Australia, 11:03 because that's where you could get easy access to trapeze Tron. 11:07 And it was going to be trapeze Tron alone versus placebo. 11:11 And then the whole set of things with or without trapeze tron. 11:16 So the idea was, could we see this additive effect 11:19 of the drug candidate with these various other pieces? 11:23 And the IB said, no, you can't do something that has that many pieces. 11:28 It just has to have one thing that's and you can kind of 11:32 just see the people who were on the IRA after they turned it down, 11:37 contacted us and said, can you help us do this in our own patients? 11:41 And we said, guys, let us do the trial, please. 11:44 So, you know, this has been as you said, this has been a real slog 11:49 because I r BBS and medical 11:53 standard of care is to do one thing. 11:56 But these diseases, like Alzheimer's and other complex 11:59 chronic illnesses are not one thing diseases. 12:03 They are multifactorial. 12:06 And so you really do have to chase down, although there's some basics 12:10 that everybody can do. 12:11 You've got to chase down the things. 12:13 If this person has a tick borne illness like Babbage or Bartonella 12:17 or beryllium or Erika or Anna plasma, you got to chase it down. 12:21 You got to treat it. 12:22 And by the way, Doctor Richard Horowitz, the lime expert, as a remarkable case 12:27 recently, someone who had chronic Lyme and the Alzheimer markers went up. 12:32 P t is the classic one p tau 217 as he treated the chronic Lyme, 12:38 the cognition got better and the Tao came way down. 12:41 So it goes right back to what we've seen for so long. 12:45 There are multiple things that contribute, and you've got to identify them 12:50 and you've got to go after them. 12:51 The typical thing we see is severe metabolic dysfunction, damage gut health. 12:56 And then on top of that, some toxin exposure. 13:00 When you address those things, these people, one 13:03 after the other after the other get better. 13:05 And it's really great to see. 13:07 Yeah. It's interesting. 13:08 You know I in the work that I do, I, 13:10 I kind of phrase this to my clients and students that there's basically 13:14 the body knows how to be healthy and there's these blocking factors. 13:17 Right. 13:18 So we have our habits right, which we can all control. 13:21 Right. They may be difficult. 13:22 They may be difficult to change, but that's under our realm of control. 13:25 And then we have these blocking factors that are kind of getting in the way 13:29 of, as you said, this sort of connection, right, versus versus protection mode. 13:33 Right. And that's really what we see, the nervous system level. 13:35 We see it even at the mitochondrial level. 13:37 We have these kind of two modes of operation in. 13:39 The body's always going to choose survival first. 13:43 Right. 13:43 And it's going to stay sort of stuck there or remain there or be conditioned there 13:47 until we can get these blocking factors out of the way and restore 13:51 some of this healthy function. 13:52 But again, I'm kind of I want to go back to this for you. 13:55 So you're whole breeds and protocol, which I really 13:59 that's what everybody calls it, you know. And we can call it that. 14:01 Was it the recode. 14:02 Was that what it is? 14:03 Yeah. We could for reversal of cognitive decline. 14:05 Yeah. 14:06 Which is a great name. 14:07 But I think people just say, oh, this is breathable 14:09 because because it was so revolutionary. 14:10 What are some of the key factors for in the British and protocol 14:13 that I guess made this so revolutionary in the medical world? 14:17 Yeah, I think the key was that this actually is what fits the research. 14:22 If you actually look at the idea of anti amyloid antibodies 14:26 sucking the amyloid out of your brain, it makes no scientific sense. 14:31 It was you know, it was 1990s thinking. 14:34 And it just took a long time to develop the drugs. 14:36 And they're actually been over $40 billion put into this now. 14:39 But it doesn't make your cognition better. 14:42 That's been shown again and again and again. 14:45 So the idea is we want to look at the common things and we want to figure out. 14:50 So the bottom line is you have assessment and then you have treatment. 14:54 On the assessment side you want to look at three key groups. 14:59 So anything that reduces your energetics you saw what happens. 15:04 You've got 500 trillion synapses in your brain. 15:09 You have the ability in your brain to store more information 15:13 than over 200 home computers. 15:18 It's incredible actually. 15:20 So you've got all these, you've got all this 15:22 incredible ability to store information. 15:26 And what's happened is that as you now decrease the support, so energetic. 15:31 So it's sleep apnea. 15:33 Very common contributor to cognitive decline, poor blood flow, 15:38 sedentary lifestyle, poor mitochondrial function reduced oxygenation. 15:43 So I check every morning I check and see okay, how is my oxygenation? 15:47 When I was sleeping last night or sleep? 15:49 Another great one. 15:50 Another common one. 15:51 So energetics number one. 15:53 Number two is anything that induces inflammation. 15:58 So what happens is the inflammation 16:02 can come from, as I mentioned earlier, tick borne illnesses. 16:05 We see it all the time from bio toxins. 16:07 We see it from a leaky gut. 16:10 Maybe that's the most common of all. 16:12 We see it from poor dentition. 16:14 We see it from chronic sinusitis, which often patients and their doctors 16:19 ignore. Yeah. 16:19 You know, I've had a little sinusitis for years and years. 16:22 Well there is it's been shown now that there is tremendous interaction 16:26 between what's going on in the oral cavity, in the sinuses and in the brain. 16:31 And in fact, you can literally trace as these things go back. 16:35 And in fact, there's a normal brain microbiome. 16:38 And that that's the opposite 16:39 of what I was taught in medical school was supposed to be a sterile organ. 16:42 Well, that turned out to be wrong. 16:43 And what do you find in the brain as a normal microbiome? 16:47 A lot of stuff from the oral cavity. 16:50 So it's common. 16:51 So, you know, period. 16:52 On Titus, a gingivitis, you know, a deep abscesses that you may need 16:57 to pick up by convict of course mercury another big one airway issues. 17:03 So the oral cavity is a huge player in cognitive decline. 17:07 So anything that is inflammatory that's the second piece. 17:11 And then the third big piece, which really surprised me because I wasn't 17:15 taught this in medical school or in neurology residency or fellowship. 17:18 And that is toxicity. 17:21 And so, you know, there were some you know, there was a question about 17:24 aluminum and questions about mercury, but nothing about bio toxins. 17:30 They turn out to be so common, so important. 17:33 Nothing about microplastics, of course, nothing about anesthetic agents, organics. 17:39 So we think of the toxins, then the toxin exposures as three different types. 17:42 It's the inorganic air pollution has turned out to play a big role. 17:47 Second one is the organics toluene, 17:51 benzene, anesthetic agents, as I mentioned, microplastics. 17:54 And then the third group is and maybe the worst of the three is bio 17:58 toxins, incredibly common trichomes scenes. 18:02 Okra toxin a interestingly, is one that is particularly damaging 18:07 to the hippocampus, the very area that's so important in memory 18:11 and so important in Alzheimer's disease. 18:13 And so we see this all the time. 18:15 And of course, not only do you get the toxic effects of these things, 18:19 but you also get this pro-inflammatory effect. 18:22 As Doctor Richie Shoemaker described years ago, 18:25 this is a as he called it, chronic inflammatory response syndrome. 18:29 So it is an inflammation that is been driving anything 18:33 that is driving inflammation in your brain. 18:35 And that includes things like mast cell activation, various 18:39 chronic infections, again, leaky gut, all these sorts of things. 18:42 This will enhance your likelihood of developing cognitive decline. 18:47 So that's a lot of things you've got to be careful about. 18:49 And you just have to find them and address them and people again 18:53 and again and again 18:54 we see these miraculous improvements or things that were years ago, 18:59 miraculous people with cognitive decline actually doing better. 19:03 Now, of course, as you can imagine, as you lose more 19:06 and more synapses, you got a longer and longer way to come. 19:09 And now then the idea of removal, optimizing things and then rebuilding, 19:14 resetting and rebuilding the rebuilding becomes a bigger and bigger issue. 19:18 And then you're looking at, you know, stem cells and hormones 19:21 and all these sorts of things and trophic factors and, and all these 19:25 sorts of things that you have to do to kind of get back to where you were. 19:28 But this is why if you come in relatively early, there is so much that can be done. 19:35 You know, if when you develop Alzheimer's, you go through four phases. 19:38 There's the pre-symptomatic phase and the great news we can pick that up now 19:42 with simple blood tests, you can get literally go to get a brain scan 19:47 and pick and get this up. 19:49 I just had mine check my tau 217 checked a couple of months ago. 19:53 If from between 35 and 60 check it every five years. 19:56 You don't need to do it often. 19:57 If it's just like hemoglobin A1, C for the brain. 20:01 So it's telling you are you headed in the wrong direction here 20:04 so that you can catch it before their major problems? 20:07 The second phase is CI subjective cognitive impairment by definition. 20:12 You know, there's some problems. 20:14 You may have some trouble with things like coming up 20:17 with the right word at the right time, things like that. 20:19 But you're still able to score normally on cognitive testing. 20:22 That's called CI. 20:23 And by the way, it lasts about ten years. 20:25 So you really have a tremendous window. 20:27 Those first two phases 100% of people get better.
Assessment, Treatment, and Early Intervention 20:31 The third phase is called MCI mild cognitive impairment. 20:35 And as one patient said there's nothing mild about it. 20:38 So that is something where by now, by definition, you do have trouble 20:43 with your cognitive testing, but you still able to take care of yourself. 20:47 And then the fourth and final phase is dementia, where now you're having 20:50 trouble with activities of daily living, balancing your checkbook, 20:54 driving home, taking care of yourself, all that sort of stuff. 20:57 So we don't want to wait until that fourth phase, right? 21:00 We want to get it, preferably in the first two phases. 21:03 In our trial, we only took people in the third and early 21:06 fourth phase simply because that's what the same time as the drug trials. 21:11 So we're looking at does this work better than worse than whatever. 21:14 And what we found, in fact, is that this was 21:17 this had the best outcomes of any protocol to date. 21:20 This is a precision medicine approach where you actually address the things 21:25 that drive the problem, and we get better outcomes than anything else. 21:30 Well, look, I followed your work for quite a while, 21:33 I guess fairly loosely, but but, you know, I'm good friends 21:36 with Heather Sanderson, too, so this type of stuff. 21:39 But I didn't realize how much we are on the same page. 21:42 Like you're speaking my language here and not enough, in my opinion. 21:45 Not enough people are really aware of this, 21:47 primarily what you mentioned in the mouth and the nasal passage and I run 21:51 I frequently run tests for, for nasal swab. 21:54 And what I find is Markham's, which is multi antibody resistant, 21:57 coagulated negative stuff, I find mold, I find Klebsiella and other. 22:03 I mean there's so much going on in the nasal almost nobody's looking. 22:06 And look it's got a direct line to the brain right. 22:09 It's like right there dysregulated the immune system creating inflammation. 22:12 And then the other area that I send people to and make them aware of is, 22:16 is their mouth and really advise them to go to a biological dentist 22:20 if they've had crowns or, or root canals in the past that weren't properly done, 22:25 or they have some suspected issues going on there, and of course, mouth 22:28 breathing at night. Right. 22:30 Which is kind of that sleep apnea changes the oral microbiome. 22:34 Right. Creates that elevated inflammation reduces sleep. 22:36 So I mean to me like these, these two areas that you mentioned 22:40 that you kind of lead with are dramatically underrepresented 22:43 or under discussed in the realm of, of really immune function, 22:48 brain health and overall health like that is so critical that you mentioned that. 22:52 So just to kind of recap, we got the nasal passage to to to look at 22:56 opportunities, nasal passage, the mouth, the gut microbiome are huge. 23:00 Your habits. Right. 23:01 And looking at those blood sugar regulation metabolic health. 23:05 Right. 23:05 Which we've we've kind of there's loose loose sort 23:08 of descriptions of Alzheimer's and dementia being type three diabetes. 23:11 Right. Which is kind of colloquial discussed. 23:13 But but really the part of it invading the message. Right. 23:16 Which is to say that blood sugar is really important to, to overall 23:19 health and particularly the brain health in this regard. 23:22 Anything I missed in there that's like a primary opportunity. 23:25 And of course, metals and cleaning up and facilitating good detoxification. 23:30 And for me, I don't like to aggressively go after things like heavy metals. 23:33 I think they're a huge problem. 23:35 But really, I like a more gentle approach and helping the body to naturally 23:40 let these things. I mean, they're really significant, right? 23:43 If we've got lead stored in the bones, if we've got aluminum, 23:46 which kind of takes the place of calcium in the gut and other places, this 23:50 we don't want to move these into the system aggressively. 23:54 That's really disruptive. 23:56 The body has a natural sort of pacing with this stuff. 23:59 And I think 23:59 that that becomes an important thing, but super critical to get them out. 24:03 Absolutely. 24:03 No doubt to get them out 24:05 slowly, as you say, one of the things that was fascinating to us 24:08 when I started looking years ago at subtypes of Alzheimer's. 24:12 So we see a more inflammatory subtype 24:14 and we see a more atrophic subtype, and we see a more toxic subtype. 24:18 What we found is that many, many people, and it was typically women 24:23 who were presenting in their early 50s around the time of menopause 24:28 and perimenopause with this toxic subtype of Alzheimer's. 24:32 And we realize this is this is during that so-called 24:36 osteoclast burst, where you're now rereleasing 24:40 some of these toxins that have been stored in the bones for years. 24:44 And so you have essentially sequestered them, and now they are reappearing. 24:49 And it's the same 24:50 sort of thing that does happen if you are overly aggressive with detox. 24:54 So, as you said, you want to move out slowly. 24:56 And we talked about the testing. 24:58 They put that into a therapeutic approach. 25:01 We have the seven basics and the two specifics. 25:04 So the seven basics are plant rich mildly ketogenic diet, exercise, 25:09 sleep, stress, brain training, detox and some targeted supplements. 25:14 The two specifics are what are the chronic infections? 25:17 You have changes in your oral microbiome, changes 25:20 in your gut microbiome, all those infectious related things. 25:24 And then what are the various toxins that you have? 25:27 Do you have scenes at a high level? 25:30 Are the is that what's moving the needle for you? 25:33 What what is changing you over from that connection mode to that protection mode. 25:38 And this sort of approach is what has worked better. 25:40 Then on top of that, all the things coming out great, but people will often 25:46 try to do one thing and ignore the basics, and there's no question it works best. 25:51 And there are so many great new things. 25:53 You know, photo bio modulation has worked really nicely. 25:56 Some of the some of the magnetic stimulation. 26:00 There are things coming out with plasmapheresis and new columns 26:04 coming out like MT 100 that very, very promising. 26:08 So, you know, blood scrubbing instead of actually exchange. 26:12 There's so many new things, all the stem cell stuff that's coming out. 26:16 And again, there are stem cell trials, but it stem cell with nothing else 26:21 is like trying to rebuild a house as it's burning down. 26:26 It makes no sense. 26:28 Now the fire first, then 26:31 you know, you got to send out the fire. 26:33 It's the same analogy. 26:35 Yeah, I love it, I love it. 26:37 I use this all the time because this is kind of what happens if we and the things 26:41 that are adding to the fire, the gasoline, so to speak, could be a certain food, 26:45 but what have you. And then we blame the gasoline, right? 26:48 And my whole thing is like, great, take away the gasoline. 26:50 House is still on fire. 26:51 Gotta put that out first. So I love it. 26:54 Yeah. 26:55 So talk to me about this new research that you, you kind of alluded to. 27:00 What what's so new about it and what did you guys find it. 27:03 Yeah. So much interesting stuff. 27:05 Because as we're now able to see this disease in a way that we didn't 27:09 before, that was unknown before some really exciting things pop out. 27:13 And I mentioned the randomized controlled trial. 27:15 I mean, we had the best results in history. 27:17 So very enthusiastic about that. 27:19 It's out as a preprint, as I mentioned earlier. 27:21 Now we can now take this and say, okay, if we understand these molecular drivers 27:26 of this neurodegenerative disease, Alzheimer's, we can start looking at 27:30 are the drivers the same or different for others. 27:34 So there's Louis body disease. 27:35 There are million Americans with Louis body disease. 27:38 We're seeing improvements in the Louis body disease as well. 27:41 But you can see already it's got different drivers. 27:44 It is more on the organic and bio toxin. 27:48 It's really a toxin related Alzheimer's. 27:52 And so real quick what is the sort of clinical distinction 27:55 like how do you 27:55 or I guess what's the presentation. 27:57 How does that look different in 27:58 in in the patient or in the, in the real world. 28:01 Great point. 28:02 So Louis body disease is if you took someone who's developing Alzheimer's 28:06 and you added a little Parkinson's, 28:08 so they have some trouble with their movements as well. 28:11 They often have visual hallucinations because they have dysfunction 28:16 where they are dopamine and they're still choline. 28:19 Both go down astill choline more about memory. 28:21 Dopamine more about movement. 28:24 What's low in Parkinson's. 28:26 But it's also about visual hallucinations. 28:28 Dopamine up in schizophrenia with hallucinations.
New Findings Across Neurodegenerative Diseases 28:31 So what happens as these two go down in Louis body? 28:34 If the acetylcholine goes down much more than the dopamine, you end up 28:39 with visual hallucinations, which is common presentation 28:42 with people with Louis body disease, they'll have a lot more change. 28:45 They'll go up and down a lot. 28:47 So so-called Showtime, they're very good. 28:49 And then they're really affected. 28:51 They'll often have some delusions. 28:53 They'll often have some autonomic symptoms that you see more on the Parkinson's 28:59 and what's called MSA multiple system atrophy. 29:02 So you can start to tease these things apart. 29:04 First case of reversal of posterior cortical atrophy, 29:09 which is a about 5% of Alzheimer's patients 29:12 present with that just recently published by Carrie Rutland. 29:16 And what we saw there with that is this person 29:19 did have tick borne illness and mycotoxins. 29:23 On the other hand, 29:24 a different presentation, cortical basal syndrome, published by Doctor Craig Tonio. 29:29 That one was much more like Parkinson's, had the organic toxins 29:33 as the drivers, not the bio toxins, not the Lyme disease. 29:37 So you can start now 29:39 picking these apart and looking at what are the things driving. 29:43 Why would you get Alzheimer's? Lewy body? 29:46 Why would you get ALS? Why would you get these? 29:49 And so I do think we're in an era where neurodegenerative diseases 29:53 are going to become increasingly well understood and treatable. 29:58 One of the ones I'm particularly interested in, I think 30:01 is an important concern right now is called late. 30:05 Late, which means limbic 30:08 age related TDP 43 and cephalopod. 30:12 That's a mouthful, but this was just described 30:14 a few years ago by Doctor Nelson from University of Kentucky. 30:18 And what they found is that many people 30:20 and this is turning out to be a relatively common problem 30:24 for especially for people who are older in their 80s and 90s. 30:28 We haven't seen it a lot in the 40s and 50s and 60, 30:31 whereas we're seeing more Alzheimer's in the 40s and 50s than ever before. 30:35 That's well documented, published by epidemiological groups. 30:39 But what's important about late is that the TDP 43 30:44 is a response to a number of viruses, including Covid. 30:48 And it's been clear that if you've had Covid, 30:50 you're at increased risk for cognitive decline. 30:52 And it looks like some of these cases are going to turn out to be late, 30:56 so-called late. 30:57 So we're looking at that right now to see, okay, 31:00 how do we is this going to be more of a long Covid issue. 31:04 Is this going to be more because it's Covid plus immune changes? 31:07 You know, we'll see. 31:08 But again, this is an era where everything is opening up. 31:12 It's not this old idea of you had a protein that misfolded 31:16 and therefore you got this disease. 31:18 It's about what are the drivers? 31:20 And really we need to focus less on pathology and more on physiology. 31:25 As you've alluded to multiple times here, it's the physiology. 31:29 What is your body doing to try to protect you as it's producing 31:35 amyloid phospho two or TDP 43 or alpha synuclein or things like that? 31:42 Yeah. 31:42 You know, I think what's really interesting, 31:44 I think when you came out with that first sort of published research and book, 31:48 you know, about a decade ago, I think what was people loved the protocol. 31:52 Now, what I'm really feeling 31:54 with kind of your research and where your whole mind is going 31:56 is like, no, no, no, we're going to actually look 31:59 at the functional mechanisms and the drivers and the solutions. 32:03 Right? 32:04 Because then then it starts to become I can see it, I can feel it. 32:07 It's like it all becomes clear, 32:09 like you're starting to create distinctions 32:10 between what's driving what's happening and what to do about it. 32:14 Right. 32:14 And that becomes and I think as that picture continues 32:17 to emerge, there will be further insights into the differences. 32:20 Right? 32:21 Like that's what gets I don't know, I'm kind of excited hearing you 32:24 kind of parse all this out, because I can really see that the future 32:28 that that, that work you did a decade ago 32:31 became the critical sort of inflection point in how we're approaching this. 32:36 Right? 32:36 Because, as you said, it was like, okay, 32:38 we're looking at things that are happening and providing drugs now. 32:42 It's a completely different direction, right? 32:44 That is opening up that I'll allow a deeper understanding 32:48 and how to prevent these things, 32:50 what's driving them, so we can target these specific things. 32:53 And then the solutions, as you recall, just recently, Ted Turner, 32:58 who is the entrepreneur who founded CNN and had the idea of CNN years 33:02 and years ago, just passed away from Louis body disease. 33:05 And what's amazing, you can go right down the list 33:08 here and see what Alzheimer's, what the response is. 33:12 And Louis body. 33:12 And just as one example, 33:14 the amyloid from Alzheimer's is a response to herpes viruses. 33:18 So when you are exposed to these herpes viruses, you're making that amyloid 33:23 which surrounds, sequesters and inactivates the herpes viruses. 33:28 Well, when you get Louis body, you're making alpha synuclein, 33:32 which is a different prion, a different immune response. 33:37 That thing targets RNA viruses 33:40 instead of the DNA viruses, the herpes family. 33:43 So you can see the difference here. 33:45 In fact, one of the things that targets, for example, is West Nile virus. 33:49 So you can just go right down the list and you can see how the body saw different 33:54 insults with the different genetics, epigenetics and various responses. 33:59 You're now having different responses for different things 34:03 and ending up with conditions which again, in the past we just said untreatable. 34:07 We don't know what causes it. There's nothing to do. Now. 34:09 We can really start getting to the crux of these and understanding, 34:13 and that will allow us to treat all of them. 34:16 And we've actually had some interesting results already with age related. 34:19 Macular degeneration is another one. 34:22 So all of these things are degenerative conditions that have at their basis 34:28 a network insufficiency with different subnetworks that your brain has set 34:33 in, your nervous system has set up, and you can now start to look at 34:37 what actually happened and do something about it. 34:41 Yeah. 34:42 You know, it kind of reminds me of of years ago 34:44 when we blamed cholesterol, you know, for heart disease. 34:47 And, you know, 34:48 then we were blaming tau protein and beta amyloid and alpha synuclein. 34:52 We're blaming these things as the problem. 34:54 But in reality, what it sounds like is that these are the 34:57 these are the firefighters showing up to the fire. 34:59 And we're just calling them bad because there's association that okay. 35:03 Well, if the firefighters are there, they must have set the fire to the house. 35:07 But the reality that we now know is there there as the solution to the problem. 35:12 And sure, that causes issues, right? 35:15 Just like a firefighter spraying your house 35:17 with tons of water, it's going to cause water damage and flooding. 35:20 But the deeper problem was the fire, right? 35:23 And we got to get to the solution. 35:24 So this again, I'm just sort of saying that 35:26 because just to make it very overt here, that there's a deep recognition
Future Directions and Resources 35:30 that for somebody dealing with these cognitive decline issues, 35:34 that we got to really be mindful, not to blame the Tao, not to blame 35:39 the the actual proteins that are there, that they're there for a reason. 35:42 And it's important that they're there. 35:43 And we need to understand why they're there and also how to 35:48 help them do their job, 35:49 which is to clear this stuff that they're trying to, to, to deal with. 35:53 Yeah. Exactly. Right. 35:54 And these things have all turned out to be antimicrobial proteins 35:59 and peptides dealing with they are trying to protect you. 36:02 Unfortunately we have things like mitochondria that descended from microbes 36:07 and they are particularly sensitive to these same things. 36:10 So yeah. 36:11 And again just like as you mentioned, 36:13 you know, the fire same sort of thing with the police. 36:16 If they're shooting, they're going to be some strays that are going to hit people. 36:20 And so they blaming the police when there's been 36:23 all sorts of crime, it's not the right way to go. So 36:28 where is this going? 36:29 Where do you, where where in the future do you see this going. 36:32 Like where do you have your eyes on. 36:34 Where's your mind going now with all this latest research and what you guys 36:37 have uncovered in the past, where do you feel like this is? 36:40 I mean, look, we're kind of 36:41 you can bring this in or not, but, you know, it's always crossing my mind. 36:44 AI is kind of here, and it's going to continue. 36:47 There's some perhaps opportunities there. 36:49 Where is this going in the future with brain research? 36:52 Oh, no doubt AI will play a key role. 36:54 And we have now data on over 10,000 people who've been on the protocol. 36:58 So we can start having AI sift through this and look and see 37:01 what are the things that work best and worst. 37:03 So there are three things. Three places is going. 37:06 One is to make it simpler to say, okay, 37:08 there's lots to do here, but we can now start to prioritize. 37:11 If you can just do these three things so that we'll now start to make it simpler. 37:16 And bringing in drugs so that we have some tremendous drug candidates. 37:20 Now that we understand 37:22 what should be drugged, that doesn't mean you should forget all the insults. 37:26 You still have to do the right things, but we're now going to be able to develop 37:30 much more effective drugs, much more, you know, new generation drugs. 37:36 The second place is a global reduction in neurodegeneration to have programs, 37:41 just as we had a reduction, you know, a simple one. 37:44 We had a reduction in smoking. 37:45 Then we see a reduction in lung cancer, same sort of thing. 37:49 We have a reduction in metabolic syndrome. 37:51 We have a reduction in exposure 37:53 to microplastics and exposure to these various toxins. 37:57 And we have fewer water damaged buildings. 38:00 We're going to have less neurodegeneration. 38:03 And then the third piece is, 38:04 as I mentioned earlier, now 38:05 extending this to all the other neurodegenerative diseases 38:09 so that we understand what's driving each one. 38:12 It is different. 38:12 Each one has its own fingerprint profile, but there is overlap in 38:17 things like metabolic damage, gut health really really critical for this. 38:22 So we're going to understand better and better about what's driving what. 38:25 And we should be able now to treat all of these successfully. 38:29 So that's what I'm really enthusiastic about. 38:31 Amazing doctor. And this has been fantastic. 38:33 Tell people where they can find if they're, you know, 38:35 if they're helping somebody with Alzheimer's or dementia 38:38 or they're kind of in that early cognitive decline, 38:40 or maybe they just want to find resources to, to protect against cognitive decline. 38:44 Where can they go? 38:46 Yeah. 38:46 So any of the books that I wrote, The End of Alzheimer's, 38:50 the End of Alzheimer's program, the First Survivors of Alzheimer's 38:53 and The Ageless Brain, which is more for everyone's brain health, 38:56 how to get this out there. 38:57 And then you can go to doctor Reticent. 39:01 Also, everyone 39:02 should check there's a free check for your cognition. 39:05 My CQ test CQ is cognitive quotient. 39:08 So my test. 39:10 Com and then as I said earlier, everybody should know what their status is 39:14 with 217. 39:16 Just like hemoglobin A1, C and the most 39:19 sensitive one was developed by a group called neuro code. 39:22 And you can get that at get a brain scan, 39:25 get a bra in scan. 39:30 So any of those things will give you information. 39:32 And really this is becoming an optional problem. 39:36 Cognitive decline should not be so common. 39:39 It is now the number one cause of death in the UK, if you can believe that. 39:44 It just shouldn't be nearly as common and we can have a dramatic effect 39:48 on reducing this if we all work together. 39:51 Beautiful. 39:52 And I couldn't agree more that it's really worth your time 39:55 and investment to get things checked, to start to implement some of these things. 39:59 Doctor reticence books are super practical, by the way. 40:02 They're not. 40:02 I know he's very advanced in some of his research and technical terms, 40:06 but the books are really, really easy to understand, great to put into practice. 40:11 Right. 40:12 So they're not just a mental exercise, although that's good to, 40:15 I guess, for the brain, but the really, really practical. 40:18 So I just want I just want to put that in there 40:20 that they kind of belong on everyone's shelf. 40:22 So doctor, thanks so much for coming on today and sharing your time. 40:25 Appreciate it. 40:26 Great to talk to you. Jason, thanks so much.
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