409. Keeping Death at Bay | Dr. Adeel Khan

[0] Hello everyone.

[1] So today I have the opportunity to speak with Dr. Adil Khan.

[2] Adil is a physician that I've worked with.

[3] He offered Tammy and I a treatment, a couple of different treatments.

[4] The treatment for her was particularly successful.

[5] It helped her deal with chronic osteoarthritic condition in her forearms and was quite remarkably successful.

[6] And so that's very interesting.

[7] And it deals a young Canadian physician, very very, very sharp character, seems to be on the cutting edge of the expanding field of regenerative medicine, which is, what would you say?

[8] It's developing not precisely in opposition to, but in parallel to standard allopathic medicine that's more symptom -based in its approach.

[9] So the regenerative medical types are attempting to get to the root cause of chronic health problems and to address them.

[10] And so there's much advance being made on that front.

[11] And so we're going to talk through the potential of these new treatment protocols for depression, chronic pain, degenerative diseases like osteoarthritis, multiple sclerosis, fibromelgia, and a variety of chronic pain conditions.

[12] We talk about gene therapy, stem cell usage, and tissue engineering.

[13] So stay tuned if you're concerned about your health and about, you know, living happily and healthily.

[14] even just living.

[15] Well, thank you for coming in, Dr. Kahn.

[16] You treated Tammy and I a while back, and so maybe you could start by telling everybody who's watching and listening what you did and why.

[17] And then we'll talk a little bit about what you do more generally and about who you are and the way we'll go.

[18] Yeah.

[19] So in your wife's case, she had a very common issue, which is chronic pain.

[20] Chronic pain is something that the medical industry has grappled with for years, and traditionally they've used cortisone, which is an anti -inflammatory drug.

[21] They've used narcotics, opioids, and then if that doesn't work, surgery.

[22] So what we do is we identify that there's a gap where people don't get better necessarily with just cortisone and therapy, and they don't always want surgery.

[23] And so this is kind of that gap of patients who are just suffering or living with chronic pain.

[24] and taking pain meds, as we know, Oxycontin and so many other pain meds, what they can lead to with addiction and all these risks.

[25] And so what we do is what's called regenerative medicine.

[26] So we use different types of regenerative molecules, whether that's stem cells, PRP, exosomes, which we'll talk about, to repair the tissue back to a previous state.

[27] So in your wife's case, she had what's called ostearthritis, which is degradation of the joint, cartilage loss, and you get inflammation.

[28] and then she also had some small tears in the tendons around the joints.

[29] And it bothered her for 10 years, as you know.

[30] And she couldn't garden, and she left the garden.

[31] So what we did is we used an ultrasound, as you saw, and we go directly into the tears and into the joint where the inflammation is to repair the tissue back to a previous state.

[32] And so that's how we got rid of her chronic need.

[33] When was the ultrasound for diagnosis?

[34] Diagnostic and intervention.

[35] And intervention.

[36] Yeah.

[37] So how does the ultrasound intervene?

[38] Because it allows us to guide the needle directly into the area of damage.

[39] Right.

[40] And how can you see what's damaged?

[41] Because the ultrasound, and that's the skill.

[42] So it's telling gray from gray on ultrasound.

[43] And that's the steepest skill set.

[44] To give you an example, I treated Mohamed Olivar.

[45] He's the guy who owns the Birch Khalifa and the six tallest buildings in Dubai.

[46] So he had a shoulder issue for 15, 20 years.

[47] And he did an MRI.

[48] MRI was normal.

[49] So they just did cortisone.

[50] He was living with chronic pain for 15 years.

[51] And he's arguably the most, he's the wealthiest man in Middle East.

[52] And he's a very well, renowned businessman.

[53] So he's access to any doctor in the world.

[54] Right, right.

[55] And so he found me, and I flew down, I did an ultrasound, and we did, and we found some small tears that were missed on MRI, and then we injected him similar to what we did with Tammy, and we fixed it.

[56] But the principle is the same, which is that sometimes you need to do diagnostic, dynamic ultrasound to find the issue.

[57] And that's...

[58] How did you learn to distinguish, as you said, Gray from Gray, and are the AI image systems getting good at that?

[59] We're training.

[60] We're developing a machine learning neural net to do that, but that hasn't been developed yet.

[61] That's actually something we're...

[62] doing because we're kind of set the standard for it.

[63] Because my mentor, Dr. Anthony Gallia, he was the first one in the world to do this stuff.

[64] He did it for Tiger Woods, Alex Rodriguez, a lot of A -list athletes.

[65] So he was the one who taught me all this, and he was the one who pioneered this field.

[66] So I learned from him, and I was fortunate because I got to learn from the best.

[67] And because of that, I was able to kind of take it and translate it into my own patients.

[68] How much exposure to image data did you have to undertake in order to start to be able to distinguish?

[69] Thousands of hours?

[70] thousands of...

[71] Yes.

[72] It's not...

[73] The learning curve is so steep.

[74] Yeah, right.

[75] And we have ultrasonographers, as if you remember, I brought her with me at the time, who are specially trained by us, and they're the ones who actually guide us.

[76] Because there's so much nuance between telling what's a tear and what's not a tear that you really need a specialist.

[77] And unfortunately, most...

[78] Yeah, and a really trained specialist who actually knows what they're doing.

[79] I know there's huge difference in radiologists, for example, in their diagnostic accuracy.

[80] I know on the AI front...

[81] that they have trained AI systems now from what I understand to be able to be pretty good at distinguishing like lung cancer lesions, for example.

[82] Yeah, they're pretty good at x -ray and cancer, but musculoskeletal is still a big gap.

[83] And so that's what we're developing, because that's our specialty, is we're going to develop a machine learning neural net using what's called supervised and reinforcement learning to teach the machine learning algorithm to detect what's a tear and what's not a tear and then guide the physician on how to do it.

[84] So that's kind of how we're going to scale what we're doing.

[85] And how do you get the data set up properly because you need a training, if you're going to reinforce the proper response, you have to be sure that the material that you're training the machine on is actually accurate.

[86] Exactly.

[87] So how do you solve that problem?

[88] Because we have a brilliant radiologist on our team who's going to be training the AI on what's not a tear and what's a tear.

[89] And then you have normal.

[90] You have to first get this.

[91] Is more than one radiologist?

[92] No, we're just going to use the one who's specially trained by us, who does our MSK interventions and diagnostics.

[93] and she's obviously exceptional at what she does.

[94] And she can train the AI to say, but the AI needs thousands of normal before it can recognize abnormal.

[95] And that's the data sets that you have to build into it first.

[96] And then she has to train it over time to say, hey, this is a tear and this is not a tear.

[97] And then eventually it learns.

[98] Right, right, right, right.

[99] And what did you inject Tammy with?

[100] So we use something called exosomes.

[101] So the way I explain exosomes, imagine if you're going, so let's talk about stem cells first to explain exosomes.

[102] So most people have an intuitive concept of stem cells.

[103] They understand that they rebuild tissue or they repair tissue.

[104] So they can come from umbilical cord.

[105] They can come from fat.

[106] They can come from the bone marrow.

[107] They can come from amniotic fluid.

[108] There's so many different sources where we can get them.

[109] We use something specifically called mesencomal stem cells, which is just an embryological term to explain their origin of where they're being derived from.

[110] And the reason we use mesencomal is because they're easy to access.

[111] So, for example, the most easiest place to access is after birth, right?

[112] You take the umbilical cord tissue, or you take the amniotic fluid, and you can isolate the mesenchymal stem cells, or stromal cells is technically the right word.

[113] But anyway, most people call stem cells, but MSCs for short.

[114] And so what you do is you isolate those, and then you can grow them in a lab for three to four weeks.

[115] Why are they an umbilical cord tissue?

[116] Why?

[117] Yeah.

[118] Because there's a, is there just a rich source of, uh, repair and regeneration of the mesocimal stem cells from that.

[119] So meaning the umbilical cord tissue is just rich in MSCs.

[120] So why are they rich in MSCs?

[121] Well, I read that the babies actually send stem cells into their mother's body to help the mother repair her own tissue.

[122] Right, yeah, there is that mechanism built in.

[123] So I think a lot of it is probably that cross talk between the placenta and the mother, right?

[124] So I believe, and the cool thing is your body has stem cells too, right?

[125] and you have stem cells in your bone marrow and in your fat.

[126] And they're basically cells that are undifferentiated that can turn into any tissue?

[127] So there's different types of stem cells.

[128] If you have embryonic stem cells, which is from the fetus, then they can turn to any type of tissue.

[129] But as you know, embryonic stem cells during the Bush era and everything, it was controversial, right?

[130] And the reason for that was because they were saying, are we going to be harming fetuses?

[131] Obviously, that becomes ethical issues.

[132] And so that never really took off.

[133] But luckily, we figured out, hey, wait a minute.

[134] minute, we have something that's almost as good as embryonic stem cells.

[135] Not as good, but it's called pluripotent, meaning it has ability to turn into many different types of tissue, but not every type of tissue.

[136] So they're slightly farther down the developmental chain?

[137] It's not totipotent.

[138] It's pluripotent.

[139] And so those pluripotent stem cells, mesencomal stem cells, are pretty ubiquitous.

[140] You can get them from dental pulp, you can get them for fat, umbilical corals.

[141] As you talk about bone marrow, there's a lot of different sources.

[142] And so they're easier to harvest and easier to source.

[143] And because of that accessibility, that's where the research really took off in the last 10 to 15 years is with the MSCs.

[144] So are there variants of cells, like is it a continual variant from the cells that are omnipotent?

[145] Did you say the ones that can turn into anything?

[146] And then there's the ones that are, what was the next level?

[147] Pluripotent.

[148] And do the totipotent cells turn into the pluripotent cells?

[149] Is that the developmental sequence and then into specific tissue?

[150] Yeah, exactly, yeah.

[151] And that's kind of how it can differentiate down the line.

[152] And so the cool...

[153] What's the difference between a stem cell and a cancer cell?

[154] So a cancer cell has some similar properties because it can essentially, it loses a signal, or in a sense, it gets kind of hijacked, and it loses the ability to stop killing itself.

[155] So meaning it stops apoptosis, so it keeps replicating.

[156] Right, right.

[157] And it has an infinite amount.

[158] It can keep going.

[159] Right.

[160] Right.

[161] And it's undifferentiated.

[162] to some degree too.

[163] Right.

[164] And so that's why there's actually something called cancer stem cells.

[165] And so if we can target cancer stem cells and stop that process, so that's an active area of research.

[166] So they're not all stem cells are good, right?

[167] Because people think, and that's the problem with stem cells.

[168] Well, undifferentiated tissue in the wrong place could be a real well, that's about cancer.

[169] And that's actually the problem with embryonic stem cells too.

[170] They're too strong, they have too much stemness, meaning they can keep replicating and grow into tumors.

[171] Whereas mesencomal stem cells, they have a finite ability to grow.

[172] So they don't keep growing, which is why they're safe.

[173] And so when we grow the mesancomal stem cells, the soup that they grow in, so imagine the...

[174] How do you say that?

[175] MZancomal.

[176] How do you spell it?

[177] M -E -S -E -N -C -H -Y -M -A -L.

[178] Yeah, wow.

[179] It's going to take me a while to get that one, right?

[180] Yeah, no, it's an embryological term.

[181] So just call them MSCs.

[182] MSCs.

[183] Okay, I'll do that.

[184] When they're grown, imagine the MSEs are the chicken meat and the soup, the broth, is the exosomes.

[185] So the broth has all these nutrients and cytokines in there, but there's no actual stem cells.

[186] And why is that important?

[187] Because those exosomes can send all the signals, which are the proteins, the cytokines, and growth factors, to reduce inflammation and repair tissue without the risk of having cells, which sometimes can not survive, or it can cause reactions in certain people.

[188] So that's what you used on TAMI was exosomes.

[189] And that encourages the cells that are already there to what?

[190] To repair themselves?

[191] Exactly.

[192] It's a signal.

[193] It's a signal that says to your body, okay, start repairing this tissue.

[194] So send signals to your endogenous stem cells.

[195] So does it essentially signal to the body that something's wrong?

[196] It sends to the bodies to start healing and regenerative pathways.

[197] Well, I know that, for example, can correct me if I'm wrong, but part of the reason that your face skin doesn't repair itself when it wrinkles is because your body doesn't actually note that the damage has occurred.

[198] And I know that some of the therapies that regenerates skin, like intense pulsed light, produce enough damage so that damage is now signaled, right?

[199] Your body has to figure out, so the cross -linking that occurs as a consequence of sun damage is so subtle that it can accumulate across time with no indication of damage.

[200] And so the exosomes signal to the body that something needs to be fixed.

[201] Exactly.

[202] And that's what this really is all about.

[203] And especially the first generation of stem cells, we'll talk about second generation.

[204] But first generation of stem cells is really about paracrine signaling, which is basically signaling to the local tissue, hey, there's something wrong here.

[205] Start fixing it.

[206] And that's really what it is.

[207] And so exosomes, in the case of Tandy's case, they send a signal to reduce inflammation.

[208] And then they sent growth factors to help repair and regenerate the tear.

[209] So, and then you can actually see if you do a follow -up ultrasound, which we do all the time, that they're tissue is actually repaired and regenerated.

[210] Can you do that systemically?

[211] Yeah, exactly.

[212] So intravenous stem cells or intravenous exosomes are being used a lot for a variety of neurodegenerative conditions, autoimmune conditions, chronic pain, chronic inflammation.

[213] There's so many different things that are being done for.

[214] There's a recent trial done for inflammatory bowel disease, which is a really terrible condition.

[215] And right now, the only really medications are like methotrexate or immunosuppressants.

[216] Carnivore diet?

[217] Yeah, carnivore diet.

[218] It does work, actually.

[219] But not everyone's going to stick to it.

[220] Yeah, right.

[221] It's a hard diet.

[222] And a lot of doctors don't really know about it, so they're not going to recommend it to their patients.

[223] So patients have to self -educate, right?

[224] And so instead of just suppressing your immune system, what the intravenous stem cells do is they do what's called immunomodulation.

[225] So they actually reset or repair your immune system from a pro -inflammatory state to an anti -inflammatory state.

[226] And is that the exosomes or the stem cells per se?

[227] It's more the stem cells.

[228] The stem cells have a strong immunomodulatory effect.

[229] Xosomes don't have a strong immunomodulation.

[230] That's why you have to do intravenous stem cells if you want to treat something systemic autoimmune conditions.

[231] And there's trials where patients have actually gone into remission.

[232] And that's incredible to see because...

[233] Yeah, you've treated MS?

[234] We have, but MS is much more tricky because it's not just...

[235] There is an autoimmune component to it, but then there's also...

[236] There's a lot of other components to it.

[237] And that's where it becomes you have to take a holistic approach.

[238] So the way we're going to treat MS, which we're working on, is we're going to have the second generation of stem cells.

[239] So what that means is instead of just using umbilical core stem cells, we create what are called gene -edited stem cells.

[240] So we can actually take, so this is what Professor Yamanaka in Japan, he won a Nobel Prize in 2014 for what's called discovery of induced pluripotent stem cells, IPSCs.

[241] So what he discovered was that you could take any somatic cell in your body, like a muscle, a skin cell, and you can reprogram it using genetic reprogramming and turn it back into an embryonic stem cell state.

[242] So that's sort of revert to an earlier form, essentially.

[243] So I like to call it the Yamanaka stem cell.

[244] And basically, it's a pretty crazy discovery if you think about it.

[245] The fact that your body has this almost innate ability to go back to like an infant state.

[246] But you just have to overexpress certain transcription factors to do that.

[247] And so that discovery was pretty incredible.

[248] You know, the immune system does that too, eh, is that when it's mutating, when it's adapting to the presence of a new virus or a bacteria, it'll produce more and more accurate gripping mechanisms at the cellular level, but it stores representations of the ones that were part of the developmental sequence.

[249] So it can imagine that an immune cell is trying to get purchase on a bacteria.

[250] It'll sort of go like this first, right?

[251] It's not doing it very well, but it'll stick a bit.

[252] And then what sticks a bit varies, and then it'll stick a bit better.

[253] And then that'll vary, and then it'll stick a bit better like that.

[254] Well, then it's the thing mutates.

[255] This grip might not work, but this one might.

[256] And so that the information is still stored.

[257] And if this one doesn't work, well, this one might.

[258] So it stores that developmental.

[259] So there's more early variability and less fine accuracy.

[260] There's a trade -off, right?

[261] And it sounds like the same thing is happening with the standards.

[262] cells is that they'll differentiate into their final form, which is specialized, but that the possibility for earlier forms with more potential is reserved.

[263] Exactly.

[264] Yeah, you know, the same thing seems to happen with regards to junk DNA.

[265] So I had a friend tell me, for example, if you breed fruit flies and you breed them so that they don't have eyes, you can do that, you can alter them genetically so they don't have eyes, and then you take the blind fruit flies and you let them breed amongst themselves for seven or eight generations, the eyes will come back because the genome takes information out of the junk DNA and rebuilds the eyes.

[266] And so even in the DNA itself, there seems to be additional information stored so that the system can revert to an earlier stage of development and then progress forward again.

[267] And that's really what I believe is you have 3 .2 trillion cells or so in your body, and I believe they're working for you.

[268] But we have to figure out and give it the right signals so that you can heal disease.

[269] And that's what regenerative medicine, the promise of it is really about, which is that we can use, customize cell and gene therapy to restore your body back to a previous state.

[270] And that's the era we're finally in.

[271] It took a while to get here.

[272] But you see how there's all these interesting, almost clues from fruit flies, from the immune system that tell us that maybe this is possible.

[273] And now we're just trying to put piece that together using next generation cell therapeutics.

[274] So can you distinguish, let's speak more generally for a moment, if you can distinguish between regenerative medicine per se and medicine as it's commonly practiced.

[275] And it sounds like the regenerative field is much newer and you're obviously at the forefront of that.

[276] But how do you distinguish what you do from what physicians typically do?

[277] Well, I think the big narrative shift, hopefully going to happen is instead of giving pills for chronic disease, we want to be giving cells.

[278] And what that means is we can make customized cells now to treat chronic disease.

[279] Traditional medicine is amazing when it comes to acute care, right?

[280] If you get a fracture, you go to the hospital, phenomenal.

[281] Our surgeons are amazing.

[282] They're so good at that.

[283] But when it comes to chronic disease, unfortunately, we've been told by regulatory bodies and by guidelines that giving prescription drugs is the best way to manage them.

[284] And the reality is those drugs don't really treat the root cause.

[285] They're just kind of symptom.

[286] Symptom maskers.

[287] Exactly.

[288] And so, but now, and it was fair.

[289] It was not an unreasonable solution, but now we're kind of at this place where we actually have real solutions to get people better using these specific cell therapies and put them into remission or actually, I don't like to say cure, but at least remission, where there's diseases controlled.

[290] And so they don't necessarily have to be on pain meds.

[291] And so I think people need to, and this is, I'll give an example, like lupus is a terrible condition.

[292] And again, the only way they can traditionally manage it, it's an autoimmune condition is usually some sort of immunosuppress it.

[293] Right.

[294] Which brings with it all sorts of other risks, like chronic infection of other sorts.

[295] Exactly.

[296] And so many other risks with it.

[297] And so there was a trial done in Germany where they used something called gene -edited CAR T cells.

[298] So what they do is they take your T cells out of your body.

[299] They add a chimeric antigen receptor, which basically allows these T cells to hone in and kill B cells, which become hyperproliferative in lupus.

[300] And so it's called CD CAR -19.

[301] It's just, it's a specific type of antigen that they add on to the T receptor.

[302] The gist of it is that what it does is just makes it hone in on the problem.

[303] So it's really, it's really fascinating because you're, you're gene editing, you're making these bespoke cells almost that are specifically designed to do a task.

[304] And these cells, they actually put everyone in the trial into remission.

[305] And even a year follow -up, even though their B lymphocytes went back up, patients were still doing well.

[306] Their symptoms didn't come back.

[307] So that just shows you the power of these next generation therapeutics.

[308] So is that a widely used treatment now?

[309] So CAR -T is approved by FDA.

[310] However, it's $500 ,000.

[311] And why is it though expensive?

[312] because of pharmaceutical companies, a lot of them just, unfortunately, because it's patented and all this stuff, they just charge a lot of money.

[313] And so what we're doing is we're using our technology, which we can talk about, to create our own car tea and hopefully offer it at one -tenth the price.

[314] And that's kind of the goal that we want to take, because it's just, it's not, like, very few people can afford that, obviously.

[315] But the point is you can make these customized cell therapies for different chronic diseases.

[316] And there's so many, it's going to be autoimmune conditions, cancer, and, you know, Everything in the next few years is going to shift towards gene and cell therapy to actually cure people or put them in remission as opposed to just giving them pills for everything.

[317] How far along is regenerative medicine in relation to the treatment of cancer?

[318] So a variant of car tea is used for different types of leukemia and lymphomas, and it's successfully been used for several years.

[319] So that's one type of gene that is cell therapy that's being used.

[320] And then there's also something called natural killer cells, which are part of your innate immune system, as the name suggests, natural killers.

[321] They go there, they kill things that don't belong.

[322] So what you can do now is you can actually gene edit those natural killer cells with that car antigen I was talking about.

[323] So you can create something called car nk.

[324] And that car nk with that antigen onto it can hone in and kill the cancer.

[325] So there's trials being done now where they're using car nk for.

[326] different type of solid tumors as well.

[327] And there was also very promising.

[328] It's still early stages, but again, this is where the, I think, cross -cultural medicine becomes really important.

[329] So when I worked in Japan earlier this year, I learned that they've been using these type of cell therapies to treat cancer for over 10 years.

[330] But in the U .S. is completely new.

[331] So it just shows you that there's this disconnect.

[332] Why is there a 10 -year leg?

[333] Exactly.

[334] So it's a loaded question, because the problem is there's the biggest problem by far is regulatory bodies.

[335] And unfortunately, the regulatory bodies in North America are making it very difficult for cell and gene therapies to be approved.

[336] Whereas in Japan, they set a framework.

[337] It's called PWDA, which is just a framework for regenerative medicine regulation, which started in 2014.

[338] So it's almost nine years.

[339] So they actually approved different type of cell therapies nine years ago.

[340] whereas in the U .S. it's technically still illegal to do certain types of stem cells.

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[356] So why do you think that is?

[357] Is it merely a matter of, I mean, nine years is long in terms of, nine years is a long time if you happen to be suffering from cancer, but on a historical time frame, it's a blink in time.

[358] I mean, obviously there's going to be some resistance and lag in every system to the introduction of new innovations, and perhaps some of that's useful because some innovations cause a lot more trouble than they solve.

[359] But why do you think it is that there is a lag in the United States, which is generally a very dynamic place with regard to innovation on the regenerative medicine side compared to Japan?

[360] I think it has to do, unfortunately, with the pharmaceutical companies because a lot of them have lobbyists that influence...

[361] Yeah, seven for every member of Congress and senator in the U .S., seven lobbyists.

[362] Right, so plenty.

[363] And I think they control 75 % of mainstream television advertising.

[364] I think it's something like that, and I think it's actually higher for news broadcasts per se.

[365] And they actually spend more money advertising to doctors than they do to even consumers.

[366] So then doctors are inundated with these pharmaceutical reps and with this information.

[367] And if you're, if you're a busy, doctors have really challenging lives.

[368] Yeah.

[369] As you, I'm sure you know.

[370] And so they're busy working.

[371] They're in clinic.

[372] They're trying to just help their patients.

[373] They don't really have time to check everything that's going on outside of, and they don't have time to travel.

[374] Don't have time to look at what's going on in the whole world.

[375] Or read the journals.

[376] And they're not trained very well to do that to begin with.

[377] No, they're not.

[378] And they're basically told what they're what they're trained well to do is follow guidelines.

[379] And those guidelines, where do they come from?

[380] From specialists who have industry sponsors or ties to pharmaceutical.

[381] Well, it's a tricky business, right?

[382] Because the pharmaceutical companies are within their proper purview to attempt to educate physicians about their new products.

[383] But drawing the line between that and marketing per se and unethical marketing is very, very tricky.

[384] And I mean, it's the same with regards to high prices for novel medical interventions.

[385] I mean, it can take a lot of time and money to develop a new drug or a treatment, and it's not surprising at all that to begin with, it's expensive, because everything that's introduced into the market to begin with that's novel is expensive.

[386] Hopefully, then it gets widespread enough, so the price starts to come down.

[387] I mean, it's easy to damn the pharmaceutical companies, and I'm highly inclined to do that under certain circumstances, you know, because I think, I don't know, it seems to me that maybe a line was crossed when the pharmaceutical company, got the okay to advertise directly to consumers, that seemed to have warped the system pretty badly, and that was about 20 years ago, if I remember correctly.

[388] I think they moved from, what would you call it, scientific research enterprises to marketing machines at that point, and it doesn't look to me like the consequences of that were particularly good.

[389] No, and the reality is that if you're a physician, most of your continuing education comes from once -a -year conference, conferences that are given by specialists who are considered the top in their field from institutions who are usually have some sort of ties with pharmaceutical companies.

[390] So where are you getting your continuing education from?

[391] And it's really difficult for them to get out of that system.

[392] And so the only reason I think I was able to get out of that system was because I always looked at prevention and I always looked at finding cures.

[393] That's just the way I was taught because of functional medicine.

[394] And functional medicine is this whole concept of trying to repair your body and trying to heal it.

[395] There's before cell and gene therapy, a lot of it was just focused on supplements, lifestyle.

[396] Like you've obviously, you know, like carnivore, like those type of interventions can be very powerful.

[397] But there's no education on the physician side on that stuff.

[398] Well, it's also hard to transform them into something that generates profit.

[399] And this is, you know, it's easy to be cynical about that, but that's actually a big problem.

[400] I mean, I know there are a lot of off -the -shelf pharmaceuticals that are essentially free that can be used effectively for treating various conditions.

[401] So there's a lithium, I'm not, this is not medical advice, by the way, for everyone watching and listening, but there's a lithium variant called lithium orate, which is dirt cheap and has virtually no side effects that appears to be reasonably effective in the treatment of manic depressive disorder.

[402] And you can buy it on across the shelf for virtually nothing.

[403] And everyone asks, well, why isn't this more widely known?

[404] And the answer is, well, if the chemical is widely available and essentially free and no one can generate a profit from it, no one has the incentive to market it or educate people about it, right?

[405] You see the same thing for treatments like, what's the precursor, the precursor to serotonin, 5 -hydroxytryptamine, 5 -hydroxytryptamine, which is a good precursor for serotonin.

[406] It's also extremely inexpensive and, by all appearances, relatively harmless.

[407] And you might say, well, why isn't it more widely known?

[408] And again, it's the same problem.

[409] If there's no market, there's no impetus for the distribution, of the product or for education about it.

[410] So they just fall by the wayside.

[411] And so it isn't merely a matter of the profit -hungry, you know, vampires of the pharmaceutical industry.

[412] It's actually a very troublesome technical problem.

[413] When you're making dietary recommendations too, it's like, well, you know, how do you do that?

[414] And at the same time, or any form of prevention, for that matter.

[415] It's hard to even get credit for prevention, right?

[416] Yeah.

[417] Now, if you're very good at prevention, then the thing that you could be rewarded for just never happens.

[418] And so that's great, but it's very difficult to reward and to note.

[419] So how did you get interested in regenerative medicine and why did your educational pathway diverge from the typical physician?

[420] Before I went into med school, I was a personal trainer.

[421] So as a personal trainer, my job was to get people moving, exercising.

[422] And a lot of times, you actually see them come off their medications, diabetes, high blood pressure, just by exercising.

[423] So then intuitively I knew, I was like, wait a minute, exercise can solve so many chronic disease problems.

[424] And then it turns out in the literature, 80 % of chronic disease is preventable.

[425] Right, right.

[426] With lifestyle.

[427] Right.

[428] And so it's very hard to get people to make lifestyle.

[429] Exactly.

[430] And it is.

[431] So I was always fascinated by that.

[432] And so even in medical school, I was kind of like, why aren't we learning more about nutrition?

[433] We had one lecture on nutrition in all of medical school.

[434] One.

[435] And it was the can of...

[436] And it was probably wrong.

[437] It was wrong.

[438] Yeah, no doubt.

[439] It was the can of food guide.

[440] Oh, great.

[441] Yeah, yeah.

[442] Which is what?

[443] It was sponsored by dairy, by, you know, it's just, it's like you have to have grains.

[444] Like, it's just ridiculous.

[445] But during, but then what happened was I got exposed to this whole like alternative medicine world.

[446] Because even though I was studying allopathic medicine, I was simultaneously studying functional and integrated medicine.

[447] Distinguished those for the people who are watching.

[448] Allopathics.

[449] Right.

[450] So alopathic medicine is traditional medical doctor.

[451] You get a doctorate of medicine, and that's a traditional, you know, drug -based, surgical -based interventions that we learn in medical schools, which is great.

[452] So disease treatment.

[453] Disease treatment.

[454] Yeah, yeah.

[455] But then functional medicine and integrative medicine is taking naturopathic stuff.

[456] That's evidence -based that has actual signs behind it and lifestyle measurements to intervene and treat chronic disease.

[457] So, you know, I went to the temple of a sclepy.

[458] in Greece recently.

[459] Yeah, it was extremely interesting, a very large compound.

[460] And at the Temple of Asclepius, there were rooms where you could, they actually had people sit and dream in rooms full of snakes.

[461] Right, and God only knows what the reason for that was.

[462] My daughter used to have snakes as pets, and she said that she would often have nightmares as a consequence of having the snakes in a room, and I suspect it had something to do with their order.

[463] So God only knows what dreaming with snakes would produce in terms of visions.

[464] But anyways, there was a place set up where you could have a healing vision.

[465] But there were also theaters and stadia there and places for massage and for saunas essentially.

[466] Like it was a compound that was devoted to health that was multidimensional, right?

[467] And so, and there were theaters there because part of the healing process was drama and part of it was exercise and part of it was vision.

[468] And when I went to that temple, I thought, these people were more sophisticated than we are in their approach to disease, right?

[469] Because they were, it wasn't merely a matter of, I know there are modern medical miracles and certainly surgical bone setting and that kind of thing.

[470] Hip replacements and so forth.

[471] Some of the things that can be done are absolutely miraculous.

[472] But our notion of what constitutes health and how to progress towards it, I don't think, is it's certainly not as sophisticated as what the ancient Greeks managed at their heights.

[473] No, and I believe in 30 years we're going to look back on this era and be like, wow, we did a lot wrong.

[474] And the reason is because, just as I was saying, we realize now that the system is broken.

[475] The U .S. spends more money per GDP on capita than many developed countries, but they don't have better health outcomes.

[476] And they're just drowning in debt because of how much their health expenditure is going up.

[477] And the reality is like you were saying, people aren't going to, yes, I think the concept of people promoting exercise health and healthy living is great.

[478] But the reality is it's really hard to get people to change.

[479] And the environment is obisogenic, meaning it's set up, let's be honest, it's set up for failure because of just the accessibility of processed foods and the way the environment...

[480] Massive calorie foods, you know.

[481] And the advertising...

[482] Well, yeah, 1 ,500 calories.

[483] You know, in I think Netherlands, they banned direct -to -consumer advertising of sugar to children, which is great.

[484] It's a great start.

[485] And Japan, I think, did that as well.

[486] So there's starting to be finally this notion that, hey, process -refined foods like sugar, it's really, really bad for you, and it can lead to food addiction.

[487] And what are the obesity rates in the U .S.?

[488] It's 40%, I mean, I think overall, some states are higher than others, yeah.

[489] Yeah, it's stunning.

[490] It's absolutely stunning and catastrophic.

[491] Yeah, so I think the reality is it's going to be really, really hard to get people to change unless there's huge policy changes, which probably won't happen anytime soon.

[492] So what we're doing is we're trying to build resiliency in people's body so that they can get the benefits of healthy living without necessarily doing healthy living.

[493] So it sounds kind of crazy, but that's what gene therapy is all about.

[494] Well, it's kind of crazy, except, you know, I mean, people also hand -wave about the pathology of pill -taking.

[495] But one of the things you learn as a behavioral psychologist, perhaps above all else, is that behavioral changes are very, very difficult for people to make, even what you would think of as small changes.

[496] And everybody kind of knows this because they have their New Year's resolutions, and they decide they're going to go.

[497] to the gym and they go for like a week and then they quit and people revert back to their old habits and you might say well people should behave better it would be better for them but then you think well how often do you take that advice for yourself and so one of the things you learn as a behavior therapist is to help people make behavioral changes very gradually and incrementally but that's very labor intensive right and it's also difficult for the people themselves to do especially if you're dealing with someone who imagine that they're quite ill and they're in crisis, maybe economically, not least as a consequence of the illness, then to ask them to make a radical lifestyle change is maybe it's even necessary, but the probability that they're going to do that on top of everything else they're struggling with is very, very low.

[498] So it's a tricky, it's a very tricky thing to get right.

[499] It's called social determinants of health.

[500] Basically, if you're low social economic status, that's the best predictor of health, long term.

[501] So if you're, unfortunately, if you're poor and you don't have access to much capital, then you're more likely to have obesity, more likely to have chronic disease, and then helping those vulnerable populations...

[502] You're going to get cheap, fast sources of calories?

[503] So how can you tell people, yeah, you just need to exercise more and eat less.

[504] It doesn't make any sense.

[505] Well, and people also won't do that.

[506] The literature on diet's pretty damn clear, is that if you put someone on a diet that actually requires food restriction so they're chronically hungry, they may diet successfully for a while, lose some weight, but as soon as they stop dieting, they're going to revert not only back to their original weight, but generally gain weight on top of that.

[507] And so any diet, it seems to me that any diet that involves protracted periods of hunger is actually doomed to failure.

[508] And that's what the fitness industry promotes the people, so they're set up for failure because they see all these people online who are doing these extreme diets, but they're doing it, A, as a profession, and B, a lot of times are enhanced, using other things.

[509] Yeah, right.

[510] But so the regular person sees those people, and then they wonder why it's so hard for them.

[511] Well, and those people are actually specializing in doing that, right?

[512] Because maybe they make a living doing it so they can put the time of effort into it.

[513] One of the advantages of a ketogenic diet or a carnivor diet is that you don't have to be hungry.

[514] Exactly.

[515] That's a big deal.

[516] Because protein is very satiating.

[517] And you can eat as much as you want.

[518] So that's a massive improvement over diets that involve like chronic calorie restriction.

[519] because there's no way.

[520] The other thing, too, you see people develop eating disorders this way, too, is like if you get in a fight with the systems that mediate hunger, you're going to lose because those systems are very, very powerful when they're overactivated.

[521] And you see this with people with eating disorders.

[522] They get into a war with their hypothalamus.

[523] And like, no one wins that war.

[524] No, you're going to be set out for failure.

[525] Or you develop a very unhealthy relationship with food.

[526] Yeah.

[527] So it's developing a healthy relationship with food, which means you're eating it for nourish.

[528] and not for coping with emotions or stress or so many other reasons why people use food for.

[529] And developing that healthy relationship is really what, it takes a lot of therapy, actually, and it takes a lot of work, which is cognitive behavioral therapy, right?

[530] CBT.

[531] And CBT is one of the few evidence -based therapies out there to help people treat obesity, right?

[532] And so, but it's not, but it's a lot of work.

[533] It is a lot of work and a lot of attention, a lot of strategic planning.

[534] And it's expensive for that reason, too.

[535] And time -consuming on the part of the people who are being treated.

[536] So, all right, so how did you, you said that you worked as a personal trainer, and so you were already interested in lifestyle modification.

[537] And then you, and how long did you do that?

[538] And why did you decide to go to medical school?

[539] So I was basically doing that from undergrad like three, four years, and then I got into medical school.

[540] But the reason I decided to go to medical school was mainly because intellectual stimulation.

[541] Because obviously being a personal trainer, there's only so much you can do, and it kind of becomes repetitive very quickly.

[542] And so I wanted to learn more about how I can help and heal people, and being a doctor naturally seemed the best way to do that.

[543] But what I didn't realize was when I got into medical school, I was a little bit disillusioned because I realized that a lot of these things just don't resonate with my belief system, which is that I don't believe just giving pills to people.

[544] It just never resonated with me. And so I was always kind of trying to learn more about how can I actually get to the root of this.

[545] And that was just a question I always wanted to ask myself.

[546] I did like surgery because surgery, it's very gratifying because if you have a trauma, if you have someone, you know, you can fix them, you get them on their way and they're done, right?

[547] But then you realize even in surgery, most of what you're treating is the end stage of chronic disease.

[548] Like hip replacements is osteoarthritis.

[549] Like ophthalmology, a lot of it is cataracts and that's related to diabetes.

[550] And so many other surgical specialties are actually vascular.

[551] Like a lot of it's just chronic vascular disease, heart disease.

[552] Like these are just end -stallitis.

[553] stage of lifestyle stuff.

[554] And so the reality is if you look at even most surgical specialties, a lot of them are just doing what could have been prevented.

[555] Yes, exactly, mop up.

[556] And so that's why I ended up not going into surgery.

[557] And then I kind of got into this whole world of, I naturally, because of personal training, I like sports medicine.

[558] So then that's where I went to sports medicine with Dr. Anthony Gallia.

[559] And that's...

[560] And was that a post -medical school?

[561] Yes, after residency training.

[562] After residency training.

[563] Then you do sports medicine with Dr. Gallia, who's kind of the pioneer of the plate -lip -rich plasma injections.

[564] Yeah, sports medicine is the medical domain that probably overlaps most with cognitive behavioral therapy, as it turns out.

[565] Interesting.

[566] Yeah.

[567] Right.

[568] Well, that would make sense.

[569] Yeah.

[570] And so, interestingly, I've had professional golfers I've treated using some, we do something called a vagus nerve injection, which helps with their nervous system to help performance -based anxiety.

[571] So, but anyway, so when I went to sports medicine, I got exposed to Dr. Galli, and kind of the pioneer of platelet -rich plasma, which is where you take your blood, you centrifuge it, you concentrate the platelets in the plasma, and those platelets release growth factors that stimulate healing.

[572] This is kind of like a lower version of the exosomes we were talking before.

[573] If you were to compare PRP to exosomes, the cytokine profile is about 10 times weaker.

[574] PRP is the platelet -rich plasma.

[575] So PRP is still good for like muscle tendon tears, like acute injuries.

[576] It's not great for chronic wear and tear.

[577] So that's where exosomes and stem cells are more superior.

[578] But when I work with Dr. Gallia, obviously I got exposed to all this kind of alternative stuff.

[579] But then I realized he's treating some of the most high -profile people in the world.

[580] I'm like, there must be a reason they're coming to him.

[581] So why would these people who can go to any doctor?

[582] Right.

[583] So is it alternative or is it cutting in?

[584] Exactly.

[585] Exactly.

[586] And the media used to print it as though he's, you know, there's a lot of negative stuff out there about him.

[587] So it's hard to discern.

[588] Yeah.

[589] It's like what's really the truth?

[590] And then you realized quickly, once you're in there, some of the most important people in the world come see him.

[591] And so I realized he's obviously doing something right.

[592] And then that's when I got into regiative medicine.

[593] The regiative medicine, PRP was a great starting point, but now it's evolved into cell and gene therapy and tissue engineering.

[594] How did you learn to read the relevant scientific literature?

[595] I had to just make Google Scholar alerts and just for everything regenerative medicine based and just reading primary literature sources.

[596] And then just reading Was that something you did fundamentally on your own?

[597] Yes, yeah.

[598] Yeah, because one of the, correct me, if you think I'm wrong, but one of the things, I did a fair bit of research with psychiatrists, especially back at McGill when I was doing my PhD.

[599] And one of the things I learned very rapidly was that there was a big difference between physicians and scientists in that.

[600] So if you're trained as a Boulder model, clinical psychologist, you're basically a research scientist who does clinical work.

[601] So you're trained to evaluate.

[602] the scientific research.

[603] You're trained to learn how to do statistics and to understand them and to write scientific papers and to evaluate them.

[604] And I thought the same was true of physicians, but I soon discovered it wasn't true at all.

[605] And even the psychiatrist that I did work with, they often had statisticians do their stats.

[606] And I thought that was so unbelievably Well, you know, even the peer -reviewed process, do you know how that works?

[607] The doctors don't actually review the data.

[608] They just get the primary and that's, and then no one vets it to them.

[609] Right.

[610] They just go through it and they're just like, yeah, it looks good.

[611] Yeah, well, it's very, well, it takes a long time to learn to evaluate scientific research.

[612] It's not a, this is why I was wondering how you managed to do it, because it's a very intense training process.

[613] Even to, to understand the jargon that surrounds the statistical analysis, that's years of work.

[614] And now the medical literature is doubling so fast.

[615] And from 1900 to 1950, it took 50 years for the medical knowledge domain to double.

[616] Yeah.

[617] Now it takes 73 days.

[618] It's 73 days.

[619] For the medical knowledge literature.

[620] Yeah, I can believe that.

[621] You know, I've been reviewing some of the psychological literature pertaining just recently to discuss sensitivity, which is a neurologically based, partly gastrointestinal, partly emotional response, but it has implications for all sorts of things you wouldn't expect.

[622] So, for example, societies that are, what would you say, characterized by higher levels of infectious illness are much more likely to have authoritarian forms of local and national government.

[623] Like, way more likely, not a little bit.

[624] There's a massive connection between disgust and authoritarianism, as it turns out.

[625] Anyways, I was reviewing that literature, and I haven't looked at it for, you know, five years, and I was just absolutely stunned at the proliferation of new papers.

[626] It is essentially impossible to keep up, and so, but it's also extremely exciting because there is so much knowledge being generated constantly.

[627] And so the big, I think the key takeaway is you have to be able to look at it from a bird's eye view because there's too much.

[628] So you have to look at trends and you have to look at where is a science headed.

[629] And that's the tricky part where life is for sure.

[630] And that's the problem with current medical system is that everyone's in silos.

[631] And then you have scientists and you have doctors who are in their little silos, but they're not stepping back and looking at, hey, where is medicine headed?

[632] And how can we take the best of what the science is presenting to us and bring it into patients?

[633] patients.

[634] Well, or into public policy.

[635] Exactly.

[636] And so a lot of that, and there's a huge, what's called the clinical translation gap of 15 to 20 years.

[637] So meaning that there's data out there to support the use of certain treatments, but a lot of regular doctors don't put it into their treatments for 15 to 20 years, which is crazy, right?

[638] And so patients aren't getting access to the best treatments available.

[639] And it's very unjust because a lot of people are living with chronic disease and suffering when there are options for them.

[640] And that's really what got me super motivated to get into this field because I saw people suffering with chronic pain, especially people don't realize how hard it is to live with chronic pain.

[641] It is one of the most challenging things.

[642] It leads to mental health issues, at least to disability.

[643] And in fact, chronic musculoskeletal conditions have a greater cost to society than any other disease, meaning the total cost of there's billions and billions of dollars because of missed work days and because of the disability burden.

[644] Yes, heart disease kills more people.

[645] yeah but quality of life and economic burden of musculoscleedal is the highest so it's a very important problem and that's why i was so motivated to get into this field because i saw these people not getting better and i and i've been able to help a lot of people that no one was able to help so it's well let's talk about that a little bit so when you when you first see someone now you're the regenerative medicine practices that you engage in that's an element and aspect of lifestyle medicine so you're looking at sleep and exercise and stress, a broad sort of, I would say, a behavioral analysis.

[646] So how do you move from the general behavioral analysis through the diagnosis to the recommendation of the therapies that you can provide?

[647] And what they're, like, how do you step along that?

[648] How do you decide who's, how do you, well, that's what I mean.

[649] How do you lay out the diagnostic process and determine what treatments are appropriate?

[650] If someone came to see you, what could they expect?

[651] Yeah, no, I have a team who are kind of health coaches and biochemists who can work with the nutrition and lifestyle stuff.

[652] So they try to optimize that as much as possible, but sometimes that's not enough, right?

[653] And that's why they're coming to me because they've already tried the traditional things.

[654] A lot of them have already seen multiple specialists.

[655] And so the most common thing I see by far is osteoarthritis, right?

[656] Osteoarthritis is just like we're talking about, it's cartilage wear and tear, is chronic inflammation.

[657] But now we realize that osteoarthritis isn't just chronic inflammation.

[658] There's all these hallmarks of aging.

[659] There's 10 hallmarks of aging.

[660] And as you probably know, aging and longevity is a huge hot topic.

[661] Because if we can cure aging, we can pretty much treat almost all chronic disease, because they all have the same 10 hallmarks.

[662] So I'll list a few of them.

[663] There's a genomic instability, mitochondrial dysfunction, loss of proteostasis, stem cell proteostasis, which is protein regulation, like homeostasis of protein regulation.

[664] And you get malfunction of proteins and they build up and that can lead to cell dysfunction.

[665] And then there's also like stem cell exotuses.

[666] chronic inflammation and senescence.

[667] There's all these different hallmarks.

[668] So there's about 10 of them.

[669] And now we realize those 10 hallmarks of aging actually govern most chronic diseases.

[670] So even osteoarthritis, what happens is those chondrocytes, which are the cells that line the joints, they have all these different hallmarks of aging.

[671] So they get those epigenetic alterations, the mitochondrial start becoming dysfunctional.

[672] All those things start happening at a cellular level, which can happen years before the doctor picks it up.

[673] Right, sure.

[674] And so that's part of the problem.

[675] Well, I know with neurological conditions, often you don't see any overt symptoms till 95 % of the underlying tissue is being destroyed.

[676] And so that's why diagnostics is becoming advanced too.

[677] In fact, they're using exosomes, which can be a biomarker for a lot of these diseases, because these cells start releasing these different biomarkers, and you can detect them using exosome technology.

[678] So it's becoming, and even the diagnostics is really far behind now in traditional medicine because they're not doing any of this stuff.

[679] But anyway, so to the point, So if you have someone, let's say a knee, that's really bad officer, it's right, like stage four.

[680] They've been told by their regular doctor, they want to get a knee replacement, and they want a second opinion.

[681] So that's usually why they come to me. And they want to look at the alternatives, and they've tried, you know, the lifestyle stuff.

[682] And so what we do is we assess their x -ray MRI, we do an ultrasound examination, and then we see if they're an appropriate candidate for our procedure.

[683] And the way we do that is based off MRIs.

[684] So you have to have, you have to have characteristic findings, for example, like Bonadie.

[685] which is inflammation in the bone, that's something we can target and treat with stem cells because they're very anti -inflammatory.

[686] And then we also have to make sure their bone isn't too deform.

[687] So for example, because this is a problem with my field, if you Google regarded a medicine doctor, there's a thousand of them in the U .S. And there's so many of them not doing things properly.

[688] And the problem is because of the lack, because there is almost a black market where there is a lot of people doing it illegally in the U .S. because the FDA can't keep up with shutting down all these clinics.

[689] There are so many stem cell clinics, even though stem cells are technically illegal in the US.

[690] So it's become a weird place because it's hard for patients to kind of figure out who's actually telling the truth and who's just selling them a lie.

[691] And that's the biggest problem with the whole stem cell field.

[692] You see the same thing with plastic surgery?

[693] Exactly.

[694] Exactly.

[695] It's the exact same thing.

[696] Yeah, well, it's a Pareto distribution problem, which is that in every field, only a tiny minority of people actually know what they're doing.

[697] Right.

[698] So you always have a signal to noise detection problem.

[699] It's like, who are the people who actually, and then of course, often the people who don't know what they're doing genuinely think they know what they're doing.

[700] The Dun & Cougar effect.

[701] Yeah, absolutely.

[702] It's really problematic, yeah.

[703] And that's exactly what happens.

[704] And - So why should people trust you?

[705] Because I'm a Canadian physician.

[706] And in Canada, we were never taught about money.

[707] We were never taught about the business side.

[708] We're always taught about patients first and making them better.

[709] And I think that's, being on the global stage, stage as I am now, we're in traveling and treating people around the world.

[710] My focus is never on the monetary stuff.

[711] And I always focus on treating the patients first.

[712] Yes, some of the treatments are expensive.

[713] And that's just because the market price is expensive.

[714] But as we talked about earlier, anytime there's just a new technology, over time, the price is going to come down.

[715] And there's always going to be early adopters.

[716] And over time, we want this to be accessible to the average person.

[717] In fact, we want it to be covered by insurance, which in Japan, it is.

[718] So if Japan's doing that already, I think eventually there's going to be an impetus for this stuff to move over here.

[719] It's just going to take time.

[720] Yeah.

[721] But I think that's because I went into medicine generally to make a difference and help people, that's always been my motivation.

[722] It has never been anything more.

[723] And the big thing, too, is honestly, if a lot of patients who see me, they can tell, I'm pretty, like, I'm honest and I'm transparent.

[724] And I don't promise the moon.

[725] Like, there's certain things that we can fix, certain things that we can't fix.

[726] Stem cells aren't a magical cure for everything.

[727] But the next generation of cell therapy like we were talking about like the genital cell therapy that really will be allowing us for custom cell lines for almost every medical condition like diabetes cancer dementia there's Parkinson's disease there's a clinical trial done this year those IPSCs i was talking about earlier and they are IPSCs are the induced pluripotent stem cells the yamanaka stem cells so they created what are called ipSC dopamine producing neurons oh yeah and then they transplant them surgically into the areas where they lose those dopamine neurons, and then they did a one -year follow -up, and so many of the patients basically go into remission, their symptoms get so much better.

[728] And they actually regrow new neurons that produce dopamine.

[729] This was a Blue Rock therapeutic clinical trial.

[730] So this shows the power of IPSCs.

[731] And this is just the beginning of IP.

[732] This is what I'm going to call the IPSC revolution.

[733] There's going to be so many different IPSC cell lines that are going to allow us to treat specific medical conditions.

[734] So in the future, people will think about cells to treat their conditions as opposed to pills.

[735] Let's go back to osteoarthritis because that's a very interesting place to dive into because generally when people have rheumatoid arthritis and use anti -inflammatories, you can slow down the degenerative process, but often when you see people in late stages of osteoarthritis, they've already suffered a tremendous amount of loss of cartilage, for example.

[736] And so you evaluate people using MRI, and you said there are times when their joint damage is too far gone for you to be able to intervene.

[737] But so at what level of severity can you intervene and what sort of responses have you seen and how widely generalizable is that?

[738] Yeah, so even for, so there's four kind of stages of osteoarthritis.

[739] And so we can even treat stage three, stage four, which is the more advanced one, as long as their bone, like I was saying earlier, if their bone is actually deformed where they need some sort of alignment or corrective, where the problem is mechanical.

[740] If it's mechanical, then stem cells aren't going to fix that, right?

[741] They need some sort of surgical correction.

[742] So, but if it's more inflammatory base or if it's more based off like the cellular dysfunction we're talking about, then that's something stem cells work really well for.

[743] So for example, people who have chronic daily pain, night pain.

[744] it's affecting them all the time, that's very inflammatory base.

[745] And that's where stem cells work really well for.

[746] And even MRI, we can correlate if they have inflammation in the bone, then we have a specific target.

[747] So it is generalizable because if we have patients like that, we know it's going to work.

[748] So it brings down the inflammation.

[749] And it can help to regrow a little bit of cartilage.

[750] Oh, yeah.

[751] This is the first generation of stem cells, which are the umbilical core stem cells.

[752] Now we're transitioning over the next six months, actually, we just licensed it.

[753] We just have this technology now.

[754] It's the second generation of stem cells.

[755] So they're the Yamanaka stem cells, but specifically for osteoarthritis.

[756] So they're the IPSC -derived MSCs.

[757] So they're mesencomal stem cells, but they're IPSC derived, and they're gene -edited to overexpress certain transcription factors to target osteoarthritis.

[758] So see how specific the cells are getting is becoming a really cool technology because it's not just like, okay, stem cells.

[759] It's like, no, this is a very specific IPSC -derived MSC product for osteoarthritis.

[760] So that's the era we're in now.

[761] So you can treat muscle tears and damage and tendon, tears and damage, and you can treat osteoarthritis.

[762] What other conditions do people suffer and come to you for that you have had success in treating?

[763] I've had, I get a lot of, so because of the online world, I get patients from all over the world, and most of them are chronic complex conditions.

[764] So a lot of them are like fibromyalgia, which is just like chronic pain everywhere.

[765] There's chronic fatigue syndrome.

[766] There's people with toxic mold who don't get better.

[767] There's people with rheumatoid arthritis who just have chronic inflammation and joint pain everywhere, and they've tried all the meds, inflammatory bowel disease.

[768] So we're getting a lot of chronic complex conditions, and now we're building out a team of specialists.

[769] So these are long -term systemic dysfunction.

[770] Exactly.

[771] And so it's about restoring your immune system and getting it to be functional again.

[772] And that's kind of what we can do with the combination of the systemic intravenous stem cells and with the different peptide protocols we have.

[773] And even where now we're manufacturing and we have our own what are called fecal microbial transplant pills, FMT pills.

[774] But basically FMT, as you know, is to repopulate the gut bacteria.

[775] And the gut is where most of your immune system is stored.

[776] And so if we can restore the immune system, we can treat a lot of chronic diseases.

[777] Even Parkinson's...

[778] So tell me what you're doing with those...

[779] So we have our own process to manufacture FMT.

[780] We have a human microbiome.

[781] Is this in Canada?

[782] No, Mexico.

[783] In Mexico.

[784] So we have a manufacturing plant there.

[785] That's where we do the stem cell manufacturing.

[786] Is that product available already?

[787] It'll be available in the next few months.

[788] Oh, yeah.

[789] And so our scientists, her name is Dr. Caroline Gannibus, great Ph .D., human microbiome specialist.

[790] And this is her specialty, and she has her own proprietary process on how to manufacture these pills, select for the donors, and give them to patients.

[791] And the beautiful part about these treatments are only one week long, and they can have a huge impact on your body.

[792] And who do the fecal transplant pills work best for?

[793] So you can use them for even anti -aging and longevity because in mice, FMT has been shown to extend lifespan by 30%.

[794] So I think there's going to be a lot of people who are just going to use it for long -dress.

[795] And that's a consequence of gut biode proliferation.

[796] Because the gut microbes produce so many different metabolize and help with processes, so many different cellular processes.

[797] They're not just...

[798] And that can be used post -antibiotic treatment as well, right?

[799] Yes.

[800] And so we're going to make one for children as well because a lot of toddlers and a lot of young kids, unfortunately, get antibiotics like crazy with their gut.

[801] Yeah.

[802] And there's actually...

[803] Well, and cesarean birth actually is a problem, right?

[804] Do you want to explain that?

[805] Yeah, because you don't get exposed to the vaginal flora, which is the bacteria.

[806] So I recommend anyone who gets a C -section, just take the stuff down there after your baby's born and rub it on their face.

[807] Right.

[808] And just get them that exposure to the good bacteria.

[809] So the reason is because...

[810] That's a good example of just how bloody complex things are.

[811] Because who the hell would have ever guessed that a cesarean birth would cause post -birth trouble years later.

[812] because there wasn't the proper trip through the vaginal canal.

[813] Man, that's unbelievably complicated.

[814] It is.

[815] And that's why, what we got to learn are principles.

[816] What's the principle of the human body?

[817] Immune dysfunction is one of the most important principles that governs so many different chronic diseases.

[818] So if we can train your immune system properly at a young age, I always say like your immune system's like a teenager.

[819] If you don't train it properly, it's going to misbehave when you're older.

[820] So now we're learning how to train it properly, which means you have to get exposure to certain, bacteria you have to be played with pets you have to play with soil you can't be afraid of germs because that actually leads to more issues older and antibiotics too much cleanliness too much cleanliness yeah and we know that antibiotics for every antibiotic course that children take it increases the risk of autoimmune disease by 1 % so it can become a cumulative is that right yeah and so it become like it was NIH research that's interesting because I was chronically treated with antibiotics for recurrent tonsillitis right probably 20 times So, and I think a problem, and we talked about the beginning of an interview what we did for you, I think you have a component of immune dysfunction, which is why we're going to be doing these different cell therapies to get your immune system functioning again and get you out of this chronic, pro -inflammatory state.

[821] Now, you've also treated depression.

[822] Yeah.

[823] Yeah, so let's talk about that a little bit, because the first thing people who are watching and listening should understand is that there isn't any such thing as depression.

[824] There are multiple medical and physical conditions that produce decrement and mood, and And some of those are lifestyle associated, and some of them are a consequence of not having a functional life, and some of them are pure consequences of physiological malfunction.

[825] So there's a lot of evidence, for example, that chronic depression is an inflammatory condition, and there is evidence as well that part of the reason that SSRI's work is not directly because of their neurochemical consequences, so on serotonin function, but because they're actually anti -inflammatory, right?

[826] And there's a big overlap between...

[827] That's like statins, too, by the way.

[828] Oh.

[829] Yeah.

[830] Oh, so, no, I don't know that.

[831] So statins for people who don't know are cholesterol -lowering drugs.

[832] But the reason they actually have an effect on mortality, we believe, is because they reduce inflammation.

[833] Uh -huh.

[834] So what's the underlying cause?

[835] Chronic inflammation.

[836] Where does that come from?

[837] Chronic immune dysfunction.

[838] Right, right.

[839] And where does that come from?

[840] Your gut.

[841] Right.

[842] Well, there's a huge overlap, too, between depression and immunological problems.

[843] Exactly.

[844] And so, okay, so what have you done with regard specifically to the treatment of so -called depression?

[845] So let's come back to the fundamental principles of what causes depression from a cellular level.

[846] It's neuroinflammation, there are some chemical imbalances, and then there's a gut brain access.

[847] You have more serotonin receptors in your gut than you do in your brain, right?

[848] And so it's looking at this from a holistic approach.

[849] And so for me, as an interventional physician, what we can do is we can reduce neuroinflammation by using intravenous exosomes, they cross the blood brain barrier, they reduce inflammation in the brain, and then we can also help with the nervous system.

[850] What are symptoms of brain inflammation?

[851] If you look at this data out there, if you go to the literature, almost every neuropsychiatric disorder is linked to neuroinflammation.

[852] It's hand in hand.

[853] It's almost kind of like autoimmune conditions and intestinal permeability or leaky gut.

[854] Right?

[855] You've heard of leaky gut?

[856] I know there's Michaela interviewed a psychiatrist at, what's the big hospital, McLean's, claims in Boston who's been using dietary manipulations to treat like schizoaffective disorder.

[857] Right.

[858] And I think it's very probable that the really catastrophic neuropsychiatric diseases like schizoaffective disorder or schizophrenia, we're going to find out they have a physiological basis.

[859] Exactly.

[860] And so we're starting to learn.

[861] Depression, too, manic depression.

[862] Exactly.

[863] And so we're starting to learn about those physiological basis, and that's what we intervene on.

[864] So the way we do that is reducing neuroinflammation.

[865] And that's with exosome treatment primarily.

[866] Yes, intravenous exosomes.

[867] And then what we do, because we know so many mental health disorders are rooted in unresolved emotional trauma.

[868] And a lot of that comes from, do you know Paul Conti?

[869] No. He's a psychiatrist.

[870] He wrote a book about this, but he talks about how many depressive and anxiety disorders are rooted in this unresolved emotional trauma from childhood.

[871] And sometimes it's in the unconscious mind and they don't even know it.

[872] And so what we do intravencially basis, we actually do something called the stelly ganglion block and injecting to the vagus nerve because the stelic ganglion interferes into your sympathetic nervous system.

[873] And a lot of times your sympathetic nervous system is overactivating it's overdraft that's chronic chronic fight or flight yeah exactly and that's also because of that unresolved emotional trauma and then the vagus nerve the vagus nerve is kind of this master nerve regulator of your parasympathetic nervous system and that's the one that helps you to relax and calm down but a lot of people what that happens in neuropsychiatric disorders is they can't relax yeah they're just they're just jittery they're just irritable yeah you tell them to relax it's like telling it's like telling an obese person to stop eating to eat less or someone on cocaine exactly it just It's not helpful.

[874] Yeah.

[875] So it's just telling people who are anxious and depressed to relax is not helpful.

[876] And so what we do is we're trying to intervene.

[877] And so what we actually inject directly into the stella gang down, we inject something called peptides and anesthetic, which calms it down.

[878] And then into the vagus nerve, we inject peptides and actually some exosomes, which helped to remodulate the signaling of the vagus nerve.

[879] So this can have a dramatic effect on their nervous system, make them more calm, make them more resilient, and deal with stress better, and just make it.

[880] their bodies.

[881] Until you help with parasympathetic activation.

[882] Exactly.

[883] And so I have a diagnostic question for you.

[884] Yeah.

[885] One of the things I noticed when I was practicing as a clinician in concert with physicians who were prescribing SSRIs, I had clients who showed like miraculous response to SSRIs on occasion where they would be chronically depressed for months or even for years and they'd start a course of antidepressants and if they were fortunate, their symptoms would remit in like, well, between three days in a month.

[886] And it's not supposed to remit that quickly.

[887] But there's a neurochemical effect as well as the neurophysiological effect.

[888] But here's one of the things I noticed.

[889] I want you to tell me what you think about this.

[890] So as we already discussed, there's a lot of different disorders in the depression bin.

[891] And one of the things I would do with my clients is do an evaluation of the dimensions of their life.

[892] So imagine this.

[893] Do you have a long -term partner?

[894] Do you have friends?

[895] Do you have a job that you enjoy or that at least is functional and providing for you, you know, economically.

[896] Are you, do you have plans for your education?

[897] Do you take care of yourself physically?

[898] Do you have an alcohol or drug or other, like, abuse problem, et cetera?

[899] So multidimensional analysis of functionality along all these different, well, dimensions of life.

[900] Now, now and then I'd have a client who had no problem with any of those, but was depressed.

[901] Right?

[902] And, those were often people who showed a stellar response to an antidepressant, as opposed to the people who, well, they didn't have a partner, they didn't have any friends, they didn't have, like their life was just an absolute bloody catastrophe.

[903] Then you could imagine two different forms of depression.

[904] There's many different forms, but two classic forms.

[905] One would be, you're not depressed.

[906] Your life is an absolute shambles, and you're miserable because nothing you're doing is working.

[907] And then there's another person, it's like, oh, no, like you work hard, you're well -educated, you have goals, you have a partner you love, you have friends, but your mood is just absolutely dysregulated, you're worse in the morning.

[908] Something's wrong with those people physiologically.

[909] So I'm wondering if when you do your diagnostic process, if you look at, because I could imagine that there's a subset of people whose lives are in functional order but are suffering dreadfully for whom a physiological intervention like exosomes would work particularly well.

[910] And those are the ones we're primarily treating.

[911] Yeah, okay.

[912] And so why are those the ones that you're primarily treating?

[913] Is that just the people who end up coming to you?

[914] I was going to say, I think it's just selection bias.

[915] Yeah, probably.

[916] Probably.

[917] I think the people who seek me out are generally those type of people.

[918] Right.

[919] They have the wherewithal to do it.

[920] Exactly.

[921] Unfortunately, the people in the other category probably don't even know I exist.

[922] Right, right?

[923] Because they're just going to a family doctor and they're just that and that's the means, that's all they have.

[924] Yeah.

[925] Well, and it's of course the case.

[926] If you have a chronic illness long enough, it's going to start to affect your function in all these other dimensions of life too.

[927] So it's It's not a clean cut, but I often think, too, that the research literature pertaining to the effectiveness of antidepressants would be a lot cleaner if the diagnostic categories were set up properly.

[928] It's like, well, are you depressed, which means that your life is functional, but your mood is disregulated, or are you just merely suffering the consequences of having an absolutely dysregulated life?

[929] There's no way that a pharmaceutical intervention is going to fix that.

[930] I mean, I didn't see some of my more seriously affected clients on the behavioral side.

[931] now and then they'd take an antidepressant and it would decrease the probability they would commit suicide, which isn't nothing.

[932] And maybe it would help them a little bit garner enough energy to start to improve some of the things they could improve, but it couldn't be a magic bullet because an antidepressant isn't going to give you a life partner, for example.

[933] No, and for us it's about restoring the cellular processes as much as possible so they have resiliency to deal with the life stressors.

[934] Right, right.

[935] Yes, yes.

[936] And that's why we take this approach.

[937] And so we're talking earlier, and because the intervention that we're doing is so powerful, we actually have the Canadian military wanting to cover this for their veterans.

[938] And that was for specifically which treatment?

[939] For the vagus nerve and the stella ganglion block, the combination of that.

[940] Because I'll give you an example.

[941] Any downside to it?

[942] No. I mean, for me, it's a five -minute procedure.

[943] I've done hundreds of them, and it can have such a big impact.

[944] I'll give you an example.

[945] Yeah, I'll give you an example.

[946] So I had a special forces operative.

[947] he has a world record for the longest sniper in the world.

[948] He's 3 .2 kilometers, which is crazy.

[949] So he's, but he's, so he's this high level special force operative in Canada.

[950] His mid -40s, really, really bad PTSD.

[951] He's a point that he tried every medication, tried every psychiatrist, psychologist, and he's basically told that you can do maid, which is medically assisted suicide, essentially, right?

[952] In Canada, that's now allowed.

[953] and oh even recommended it's honestly it was heartbreaking because he has four children and the fact that this was the only option that our government is giving to him was really it just made me devastated and so I actually wasn't even into mental I mean I'm a sports medicine doctor by trade right so I this was actually one of my you know one of my friends friends so I so he asked me is there anything I can do and so that's how I started getting into this whole interventional mental health stuff and so that's how I came up across these procedures, and I talked to some of my friends in the States.

[954] And so he came down.

[955] We did the procedure for him, the steli ganglion, and then the vagus.

[956] And what do you do to do that, exactly?

[957] So, yeah, so we use, so in the steli ganglion, we're injecting something called bupivocaine, which is an anesthetic, and we mix it with certain peptides.

[958] And what the combination of peptides and stalagin do is they suppress that sympathetic overdrive.

[959] And then the vagus nerve, we inject some exosomes and peptides, and what that does is it modulates and so you do both of those?

[960] At the same time.

[961] At the same time.

[962] Oh, yeah.

[963] And then we do, usually we try to do dual.

[964] We do both sides.

[965] Oh, yeah.

[966] And so afterwards, he said, like, he literally said a weight has been lifted off his shoulders.

[967] And he started crying.

[968] Wow.

[969] Oh, yeah.

[970] It was the most dramatic thing I've ever seen.

[971] I don't say this happens to every.

[972] How long did he cry?

[973] How long?

[974] Yeah.

[975] 10, 15 minutes, with his wife was there too.

[976] And he just said he was, and he gave me a coin, which they usually don't give to anyone who's not in the military.

[977] So that was, like, a huge honor for me. And I felt, I just felt very privileged to help someone like this.

[978] So it was that fast, hey?

[979] It was that fast.

[980] And now he's doing pretty good.

[981] He's, he's back to playing hockey.

[982] He's feeling better.

[983] He's just, it's, it's hard to explain because there's so much emotional baggage and unconscious reservoir of these different traumas are built inside of your body.

[984] And you can't.

[985] I think they, they lock themselves into something like a positive feedback loop, eh?

[986] Yeah.

[987] Because, like, once you get anxious to a certain point, every little thing makes you more anxious.

[988] Right.

[989] And then you can start to become anxious about the anxiety itself.

[990] And like, I actually think that most of the things that we regard as psychiatric disorders are positive feedback loops that have gone out of control.

[991] So, for example, let's say your mood starts to fall and then you isolate, right?

[992] And then you start performing worse at work.

[993] Well, obviously, if your mood is low and you isolate and you're performing worse at work, your mood is going to get lower and then you're going to isolate more.

[994] So it loops.

[995] With panic disorder, what happens is people get anxious, right?

[996] But then they start to avoid, and that makes their anxiety worse.

[997] And so then they're in a loop.

[998] And with alcoholism, what happens to people is they start to see that if they drink, it cures their hangover.

[999] Well, obviously, that's going to generate a positive feedback loop.

[1000] And so many of the things that we see as conditions, I think, are positive feedback loops that are self -sustaining and inspiring other control.

[1001] Exactly.

[1002] And so for us, it's creating an intervention that breaks that spiral positive feedback loop.

[1003] Yeah, yeah, yeah.

[1004] So how many people have been treated with this particular treatment?

[1005] At this point, I've done hundreds, including panic attacks for young girls.

[1006] Like, it's been incredible to see the changes that one intervention can have on people.

[1007] Is it for everyone?

[1008] No, but there are a lot of people it can help.

[1009] Yeah, and so how do you decide who can be helped and who, like what are your inclusion and exclusion criteria for the treatment?

[1010] I mean, the biggest thing is a lot of them, if they say yes to, have you heard of Gabbermate?

[1011] Yeah.

[1012] So his, you know, ACEs, adverse childhood events, he has his questionnaire.

[1013] So a lot of them, if they're positive to that, that's giving me an indication that they have some sort of unresolved childhood trauma.

[1014] And almost, I would say, it's crazy.

[1015] Almost 90 % of them say yes.

[1016] So many of them have these issues that they've just kind of buried in the past.

[1017] And they're dealing with depression or anxiety, but they actually have something that triggered that maybe when they're they were younger.

[1018] So that's a good indication that this.

[1019] Classic Freudian analysis.

[1020] Yes.

[1021] So that, to me, is a big indication that these treatments will work.

[1022] And for a lot of people who just have anxiety, it can be very helpful too.

[1023] So like panic attacks or low stress resilience and day -to -day irritability, then that's an indication where they just need some - Do you ever do personality assessment on your clients?

[1024] Well, here's something, this would be a very good thing to do on the research end of things, is that before you do your intervention, have them do a big five personality inventory and then have them do it six months later and see if you get decreases in trait neuroticism right yeah right because if you did that would be absolutely fascinating yeah we are going to start a trial so i will include that because you bet use the big five aspect scale yeah because it gives you more differentiated analysis but if you could show that you could decrease trait neuroticism with a physiological treatment like that that would be a major that would be a major discovery yeah no i think that's great so what we're doing that's a resilience measure essentially, right, an emotional resilience.

[1025] And I get that feedback all the time.

[1026] My patients say that I have more resiliency.

[1027] What used to stress them out, doesn't stress it out anymore.

[1028] And so I see that anecdotally, so it would be great to quantify that.

[1029] Absolutely.

[1030] Well, and it would be quite the miracle if you could produce a transformation in a personality trait because neuroticism is actually very stable.

[1031] Right.

[1032] Right.

[1033] And so, and very difficult, well, difficult to ameliorate, goes along with stable.

[1034] But, you know, there is, there are other indications that such things are possible.

[1035] So, for example, a single dose of psilocybin that produces a mystical experience produces, I believe it's a half standard, you know, it's a one standard deviation increase in trade openness a year later that's permanent.

[1036] Exactly.

[1037] Right.

[1038] One standard deviation.

[1039] I know.

[1040] You just, well, you just took the words out of my mouth because I was going to say, we call this procedure the V shot, the Vegas nerve shot, and basically we combine it with psilocybin assisted therapy, a macrodose.

[1041] And so that combination is so powerful to kind of reset their...

[1042] Which do you do first?

[1043] We usually do this first and then send them off to therapy afterwards.

[1044] The psilocybin therapy?

[1045] No, we do our injection first, calm down the nervous system.

[1046] And then afterwards they go off to therapy and do psilocybin.

[1047] Yeah, so they do the physiological intervention that decreases stress reactivity first.

[1048] Right, so that would also increase the probability that the experience they have with a hallucinogenic would be positive.

[1049] Exactly.

[1050] Because their nervous systems are calmed down.

[1051] Right, because set matters, right?

[1052] So if you're in an anxious state and you take a hallucinogenic, the probability that that state will be magnified into something approximating a bad drip is very high.

[1053] Yeah.

[1054] And so we're going to start hopefully a phase one trial sometime next year for this intervention so we can actually get some real data behind it.

[1055] Yeah.

[1056] Yeah.

[1057] Use the big five.

[1058] Use the big five.

[1059] Right.

[1060] That's great.

[1061] That's really powerful because if you could show...

[1062] Big five aspect scale.

[1063] Yeah.

[1064] Right.

[1065] No, it makes perfect sense.

[1066] Yeah, yeah.

[1067] Well, that would be really remarkable if you could manage that.

[1068] All right.

[1069] So you, and what sort of, what sort of effects have you seen with the people that you've treated for depression?

[1070] We've talked about anxiety more specifically, so...

[1071] Yeah, no, depression, I think the big thing with that is combining it with some sort of psilocybin or some sort of psychedelic assistive therapy and the combination of that with everything else that we do has been great.

[1072] And so it can help people who are even, like that better now saying, who was PTSD, who was suicidal, and it shifted him from not being suicidal anymore to basically not being suicidal.

[1073] It actually changed his life.

[1074] And so it's been super impactful, on people like that.

[1075] But he's also the right candidate because he has severe PTSD.

[1076] And because of that PTSD.

[1077] And he has a life.

[1078] He has a wife.

[1079] He has kids.

[1080] He has all that other stuff.

[1081] So it may not be for everyone, but I think there are a lot of people who fall into that category where they have this trauma and they have these issues that they haven't dealt with.

[1082] And this intervention can actually make a big difference on their life.

[1083] And how do you protect yourself against over, like, you know, people say anecdotes are not data.

[1084] And that always bothers me because anecdotes might not be.

[1085] data, but they are definitely hypotheses.

[1086] Yes.

[1087] So, but how do you protect yourself against over -interpreting the positive consequences of your interventions as a consequence of this plethora of anecdotal information that you are receiving?

[1088] I mean, for me, it's all about getting the patient, it's all about clinical outcomes.

[1089] As a doctor, my job is to improve my patient's health or quality of life.

[1090] And at the end of the day, if they're feeling better and they're getting, then they tell me that, that to me is what matters.

[1091] is the most.

[1092] And the way I achieve that often is multimodal, meaning that you have to use multiple interventions.

[1093] And the problem with traditional randomized control trials is they only want to look at really one intervention for one.

[1094] Yeah, right.

[1095] So there's a conflict.

[1096] But that's not how the body always works.

[1097] Well, it's also a conflict with the immediate necessity of medical treatment, right?

[1098] Right.

[1099] Because it's lovely if you can just change one thing.

[1100] But if you're dealing with people who are absolutely bloody desperate, you're going to be tempted to throw, you know, everything and the kitchen sink at them.

[1101] And that's the reality of the patients I see.

[1102] the refractory to the traditional medical system, so they're looking for alternatives.

[1103] So it's not often just one intervention.

[1104] I often have to do multiple things to get them better.

[1105] And that's why the trials we're going to be doing are going to be multimodal.

[1106] We're going to have multiple things that we're using to intervene.

[1107] And when you say trials, like are these actual research trials?

[1108] Yeah, clinical trials, yeah.

[1109] So, for example, we already, we're starting a clinical trial for a phase two trial for a gene therapy, which we haven't talked about yet, but basically we're going to be looking at, It's called pholostatin gene therapy.

[1110] So it's basically the world's first reversible plasmid gene therapy.

[1111] So traditionally viral vectors were used for introducing a foreign gene into your body.

[1112] But what we've developed is a plasmid, which is just a circular strand of DNA.

[1113] It comes from E. coli, but there's no actual live bacteria in there.

[1114] And the plasmid, the beautiful part about the plasmid is it can target any protein or peptide up to 10 ,000 base pairs with 100 % accuracy.

[1115] What do you mean by target?

[1116] What does it do exactly?

[1117] meaning it can tell your body to whatever gene of interest to produce more of that.

[1118] So, for example.

[1119] Whatever gene of interest?

[1120] Yes.

[1121] Oh, yeah.

[1122] That's promising.

[1123] Yes, it's very promising.

[1124] And it's what's called an epizomal vector.

[1125] So it's non -integrating.

[1126] So it's not going to go into your genome and make you like a translocate or have those risks that viruses may have.

[1127] And it's also because it's not a virus, you don't have to take immunosuppressants.

[1128] It's not immunogenic.

[1129] So there's all these cool benefits to it.

[1130] So is it temporary?

[1131] And that's the beautiful part.

[1132] It's reversible because it's E. coli origin, so you can take a tetracycline if you want it out of your body, so it has that safety mechanism, and it lasts for about one and a half to two years.

[1133] So you can repeat it as needed.

[1134] Whereas viral vectors, you cannot repeat them.

[1135] Once you do them, you do them, and you can't really get them out of your body.

[1136] Right, right, right.

[1137] So this technology is really beautiful, and we did our phase one already, so we're doing our phase two.

[1138] Targeting what conditions?

[1139] So sarcopenia, because that's the loss of muscle as you get older.

[1140] Oh, really?

[1141] Which is probably the biggest driver of aging.

[1142] Because as you lose muscle, your body to protect itself and regulate your immune system and vitality goes down.

[1143] You become frail.

[1144] And that frailty, we know, is such a big predictor of mortality.

[1145] Like falls.

[1146] And even in COVID studies, they found that people who had more muscle mass had better outcomes.

[1147] Well, you know, one of the best predictors of lifespan is grip strength.

[1148] Exactly.

[1149] Yeah, yeah, which is quite remarkable.

[1150] Which is just a proxy, right?

[1151] Yeah, it's a proxy for muscular integrity, essentially.

[1152] Yeah, and so if you look at it, if we can preserve muscle, that can be one of the best ways to have anti -ease.

[1153] Oh, yeah, that's a huge deal.

[1154] So pholostatin is a peptide that's naturally made in your body, and as you get older, your fallostatin levels decrease.

[1155] And so what we're doing is we're just delivering this through a gene therapy form, the plasmid vector, and it increases your fall of statin levels for one and a half to two years.

[1156] And it's completely reversible if you want to have your body for whatever reason, and it wears off on its own.

[1157] Well, what happens if you increase fallostatin levels?

[1158] So it inhibits myelstatin, which is kind of the enzyme that's, sets a limit on how much muscle you can put on.

[1159] So it makes it easier for your body to put on muscle.

[1160] It also increases...

[1161] So why does it decrease with age?

[1162] Because the aging process is cruel.

[1163] And so so many different peptides as you get...

[1164] So you think it's just a consequent, another element of degeneration.

[1165] Exactly, degeneration, exactly.

[1166] And so...

[1167] Entropy.

[1168] Yeah.

[1169] And so if we can restore it back to your levels, your youthful levels, not only will you inhibit myelstatin, which makes it easier for your body to put on muscle, it'll also activate what's called FOX -O3 pathway, which reduces systemic inflammation.

[1170] So it has this, and so we showed in our phase one trial that patients over the age of 60, on average, reduce their intrinsic biological age by 12 years, which is actually incredible.

[1171] Wow.

[1172] At 60.

[1173] Yeah.

[1174] And there was actually some hyper responders who had biological age reduction of access of 60 years, which was crazy to believe.

[1175] So does that mean they're going to leave 60 years longer?

[1176] We don't know that yet.

[1177] Well, probably not.

[1178] Probably not.

[1179] There's probably multiple dimensions, but still.

[1180] But their telomere length, which is a proxy.

[1181] We also set a world record for that as well.

[1182] You showed telomere length increase as well in that patient who was a hyperresponder.

[1183] And so we're actually applying.

[1184] Wow.

[1185] Yeah, so it's pretty powerful.

[1186] It's as a network.

[1187] Another animal studies that have been done with this already?

[1188] Yes, false stat and gene therapy has been around for a while in animal studies.

[1189] And what does it show with animals?

[1190] Similar, 30 %, 32 % life extension in mice.

[1191] But actual life extension, not just the markers.

[1192] No, exactly, like extension.

[1193] And so.

[1194] When people fast, I mean, I know animals that are starved to like 75 % of their body weight, they'll live 40 % longer, something like that.

[1195] Does that have anything to do with them?

[1196] Yeah, because it activates similar pathways, which are anti -inflammatory pathways, regenerative pathways, pathways that help with cellular synestis, like all the hallmarks of aging that we talked about.

[1197] So whenever you think about any intervention, think about how is it affecting the hallmarks of aging.

[1198] So now we have an understanding of biology, because in physics, we always had first principles, right?

[1199] Like Newton's laws.

[1200] Like we understand first principles, right?

[1201] In biology, we never had first principles until recently.

[1202] Now we understand there are, we're called fundamental principles which govern chronic disease and cellular distinctions.

[1203] And are those associated with those 10 markers for aging?

[1204] Exactly.

[1205] Those 10 hallmarks govern.

[1206] So that gets you to, it gives you a foundation on how to interpret data and how to figure out if an intervention is actually going to do something for you.

[1207] And so where are you with this trial?

[1208] So the phase two trial is going to start in spring 2024 in Canada.

[1209] We have tentative approval.

[1210] We're just getting the funding together to start it.

[1211] And so So the phase two trial is to look at false statin gene therapy.

[1212] It's going to be randomized controlled trial with the placebo group.

[1213] Yeah.

[1214] And basically to look at sarcopenia, osteopenia, and then different inflammatory markers.

[1215] How old are your client?

[1216] You'll have anyone from age.

[1217] It's going to be open to age from 30 to 80.

[1218] So it would be really interesting to see what it does with people who are particularly old.

[1219] Yeah, exactly.

[1220] And that's where it's the most powerful.

[1221] But even in, I mean, younger people don't need it as much, but a lot of them just do it for the gym.

[1222] Like I've done it myself.

[1223] Yeah.

[1224] Just for the benefits of more energy, more strength.

[1225] strengthen the gym.

[1226] Because obviously, by inhibiting myelstatin, it gives you more...

[1227] Downside?

[1228] To date, there hasn't been any adverse effects.

[1229] So, that's a beauty of it.

[1230] Yeah, it's been studied for...

[1231] Hard to believe.

[1232] I know.

[1233] It's been studied for over six years.

[1234] And we haven't seen any adverse effects.

[1235] To add some credibility to it, we are backed by Peter Thiel and Sam Altman.

[1236] Those are our two seed investors.

[1237] And they're both well -known names in the world.

[1238] And I think the reason they backed us is because they understand that this has...

[1239] has a potential to revolutionize a lot of gene therapies.

[1240] Because if you think about it, the only other real big gene therapy competitor is CRISPR.

[1241] Right?

[1242] And CRISPR, but the problem with CRISPR, yes, it's more powerful than minisercle, our technology, but it also has off -site targets.

[1243] So meaning it may hit, it may do something that's unintended.

[1244] And that's the risk with CRISPR.

[1245] Whereas with the mini -circle vector, it's not as powerful, but it's going to, whatever vector that we want to do, it's going to do that with accuracy.

[1246] And that's the beauty of this plasmid vector technology.

[1247] Well, that's ridiculously exciting.

[1248] It is.

[1249] So I wanted to also ask you about, let me see, I'd just check my notes here too.

[1250] Yeah, tissue engineering.

[1251] So we were talking about earlier, can we regrow cartilage, for example, in osteoarthritis?

[1252] So with the first generation, no. The second generation, what we can do now is we can combine those IPSC MSCs that we're talking about.

[1253] They're engineered specifically for osteoarthritis, and then we can use a 3D bioprinter.

[1254] and we can embed them into a scaffolding, basically a scaffold.

[1255] And then you can implant those arthroscopically, and then that can regrow new cartilage.

[1256] Uh -huh.

[1257] So that's the scaffold?

[1258] The scaffold with the embedded stem cells.

[1259] So that's called, that's the intersection of gene therapy, cell therapy, and tissue engineering.

[1260] Is that specifically for cartilage, or can you do that with other organs?

[1261] No, you could do it.

[1262] And that's the promise of it, right?

[1263] This is just the beginning of tissue.

[1264] And how far is that advanced?

[1265] What are you doing specifically?

[1266] So for cartilage, there's already trials being done.

[1267] is Dr. Farshad Ghaliak in University of Washington.

[1268] He's already been doing trials in humans with the similar technology.

[1269] And then so we're just starting to do our own trials with that this year.

[1270] And who's we?

[1271] The regenerative medicine community.

[1272] Okay, I see.

[1273] I see.

[1274] But you also have people that you're working with who are involved in these specific trials.

[1275] Yes.

[1276] I have my own group and we have our own company and we have our own researchers and scientists we're working with.

[1277] And where's that company located?

[1278] So we have our mini -circle technology company, that's an Austin, Texas.

[1279] That's in Austin.

[1280] And then we also do research in Mexico.

[1281] Why in Mexico?

[1282] Because, so you can do phase one trials a lot quicker offshore.

[1283] Yeah.

[1284] And then you can get the approvals and move things along quickly.

[1285] And then we can move onshore for the phase two.

[1286] So that's kind of our strategy.

[1287] That's kind of our strategy.

[1288] Because if you just go through traditional health canon FDA, it's going to take 10 to 15 years to get anything done.

[1289] Yeah, yeah.

[1290] That'll just kill you.

[1291] Exactly.

[1292] So we figured out kind of a disruptive model where we can do phase once quickly, get our trials done, collect our patients, collect our data, show our safety.

[1293] Risks in that?

[1294] Are there risks in doing it that quickly?

[1295] Do you think?

[1296] I mean, the technology we're using already has really good basic signs behind it and has lots of animal data.

[1297] So there's already safety data there to, and we're not doing it without unreasonable justification.

[1298] So there is mechanistic basis for what we're doing as well as good safety data in animals.

[1299] So the next logical step is put it in humans.

[1300] Someone has to do it.

[1301] So So it's, and that was the same thing with the plasmid technology.

[1302] It was just we were the first ones to do it in humans.

[1303] It was done in animals for a long time, but then we were the first ones to take it into humans.

[1304] When did that start to happen?

[1305] About six years ago.

[1306] Wow, that's ridiculously exciting.

[1307] Yeah, it took six years of R &D to get it into commercial product.

[1308] But now we have a first commercial product, and we're doing phase two, but we're also offering the fall of stat and gene therapy in approved regions, like Mexico, Prospera, Dubai.

[1309] We have approvals in certain areas where we can do it.

[1310] Do you enjoy the business side?

[1311] Because it sounds like you do.

[1312] I enjoy helping people and creating scalable technologies allows me to help more people.

[1313] And that's really what I mean.

[1314] Yeah, well, fair enough.

[1315] But that's the intelligent integration of the business vision into the medical practices, right?

[1316] If you set up an organization properly, then you can move faster.

[1317] You can do more things and you can scale.

[1318] Exactly.

[1319] I can only help so many people one -on -one as a musician.

[1320] But if I create technologies and do trials that are large scale, eventually we can help millions of people.

[1321] The dream is, imagine you go to your family doctor, let's say, 20 years from now, and you get these gene therapies, you get these cell therapies, and you keep every two years, and it keeps you healthy, and you never get sick.

[1322] That's the world I want to see.

[1323] Yeah, yeah.

[1324] Where we just eradicate chronic disease.

[1325] Now, you're going to treat me for something tomorrow, as I understand.

[1326] So exactly what are you planning to do to me?

[1327] Well, as you have talked about publicly, you have toxic mold.

[1328] You've been exposed to it, right?

[1329] And I think in Florida.

[1330] That's the theory.

[1331] Yeah, that's the theory.

[1332] And so what happens with toxic mold is it kind of hijacks your immune system and makes it difficult for your immune system to function properly.

[1333] And so what we did for you the first time was we did intravenous stem cells, which is to help your body to build some resiliency and to strengthen.

[1334] And that was different than the excess.

[1335] Tammy did that as well, but she also did the exosome treatment, which I didn't do.

[1336] Yes, yeah.

[1337] Because your problem's more systemic.

[1338] And so what we're going to do now is we're going to do we're called intravenous natural killer cells.

[1339] And natural killer cells, as we talked about earlier, are the cells.

[1340] in your innate immune system that can kill chronic, it can kill cancer, it can kill chronic fungal infections, which is kind of what happens with mold.

[1341] So it's basically giving your body the...

[1342] What do you make of that sick building syndrome literature?

[1343] I think it's very underappreciated because a lot of physicians don't test for mold and they have a lot of patients with chronic illnesses that...

[1344] Well, the literature is horrifying, you know?

[1345] I mean, I was reading about the state of military accommodations across the United States and the unbelievably high levels of mold toxicity that military personnel are exposed to.

[1346] It's absolutely horrifying.

[1347] In fact, you can't read it.

[1348] I guess it's about as bad as the discovery that asbestos was causing cancer.

[1349] I mean, asbestos was used everywhere.

[1350] And all of a sudden, it was like, oh, we're killing like lead and gas.

[1351] I mean, these things have happened before.

[1352] No, and there's a new theory on cancer.

[1353] It's called cell suppression theory, which now is getting a lot of traction, is basically that the idea that fungal spores are hijacking the cells, and preventing cell opaptosis.

[1354] So they're preventing the cell from functioning properly.

[1355] So then they're saying that the root cause of cancer is actually potentially fungal infections.

[1356] In addition to everything else that happens with genomic instability.

[1357] But this is one of the potential risk factors.

[1358] Because we all get exposed to funguses all the time.

[1359] It's part of living in a bodily environment.

[1360] Most people's immune system can deal with it, but some people's immune system can't.

[1361] Well, especially if they're in a place where they're being chronically exposed to levels that they can't actually tolerate.

[1362] Exactly.

[1363] So how do we build a resiliency in your body so you can deal with those fungal infections?

[1364] We give you the cells to do that.

[1365] And that's what the natural killer cells are going to do.

[1366] And eventually we probably give you the FMT as well so we can give you your...

[1367] And FMT is the fecal microbial transplant.

[1368] Oh, yes.

[1369] Because then your body, again, restrengthening your immune system and we're building resiliency for you to deal with these chronic infections in your body.

[1370] So it all comes back to first principles.

[1371] And that's the biggest, I think, takeaway for people to understand is biology is moving at this point, at this alarming pace almost where we're understanding down to a single cell function how cells can operate and target those make very specific targeted interventions as opposed to just being like take this pill and hopefully hopefully your disease doesn't progress right right okay so if people are interested in the listeners are interested in falling up with such things learning more about it what should they do I think scientists are the best people to learn from.

[1372] Unfortunately, online, a lot of the people who are the loudest aren't usually academic scientists because they just don't get a lot of attention.

[1373] So my favorite podcasts on these topics, if you're interested, they're very dense, but there's one called the stem cell podcast, and there's one called the immunology podcast.

[1374] And there are academic scientists who are top tier, who go bring on different scientists on their show, and they talk about these different topics.

[1375] And that's where I learn from.

[1376] And I think that's where you have to go to.

[1377] You have to go to the scientists who are doing the hard work to make this a possibility for patients to get access to one day.

[1378] And I talk about it a lot online.

[1379] I try to take that information and disseminate it in a way where people can understand it.

[1380] Because it is complicated and there is a lot moving at a fast pace.

[1381] And so my job, as a clinician, scientist, is to take that information and simplify it and make it digestible so people can access it and hopefully give them hope that there is a brighter future of medicine ahead of them.

[1382] Right.

[1383] All right.

[1384] Well, that's, unless you have something else, you'd like to tell people who are watching and listening, that's probably not a bad place to close off.

[1385] Is there something that you wanted to cover that we didn't discuss yet?

[1386] I like to tell the world that we're in the world of Medicine 4 .0.

[1387] And so Medicine 4 .0 is essentially using cell and gene therapy that's targeted to allow for more longevity, which means a broader lifespan and health span where you can do what you want and live a high -quality life.

[1388] So instead of just saying exercise, eat well, we can use these gene therapies like phallostatin to allow your body to get all these benefits, even if you're not exercising of longevity.

[1389] And that's where the era of medicine we're headed towards, and that's what we want to really share with the world.

[1390] Okay, well, thank you very much for all the information that we walked through today.

[1391] That was much appreciated and very enjoyable.

[1392] And to everybody watching and listening, thank you very much for your time and attention.

[1393] I'm going to talk to Dr. Kahn for another half an hour on the DailyWire Plus platform.

[1394] I think we'll go over, well, some of the topics that we've gone over already, but I want to also, as I usually do on that platform, delve into the development of his interests.

[1395] And so we'll go a little further down that road.

[1396] And if you want to join us there, please feel welcome to do so.

[1397] Otherwise, hopefully you'll tune in again in the relatively near future.

[1398] And thank you to the DailyWire Plus folks for making these conversations possible.

[1399] Thanks again, sir.

[1400] All right.

[1401] Thank you.

[1402] You bet.

[1403] You bet.