Podcast from: bengreenfieldfitness.com/plasma
[00:00] Introduction/About Mark Urdhal & Thomas Ingoglia
[05:52] What is Young Blood Institute
[12:14] About Heterochronic Parabiosis
[22:15] The intricate means of testing used on mice
[29:10] he risks of these plasma exchanges
[34:51] biomarkers Mark is tracking at the Young Blood Institute
[46:15] The lowest hanging fruit for people to track
[50:20] What a biological aging clock is
[54:45] The anti-aging booth that Mark and Tom will be operating at a conference called RAAD Fest
[1:00:30] Whether NAD actually gets absorbed into a cell via injections or IV
[1:14:30] How to use technologies such as Vielight and exosomes to address Alzheimer’s
[1:33:45] How senolytics works as a therapy for aging and Alzheimer’s
[1:26:11] End of Podcast
Ben: Hey folks, it’s Ben Greenfield and you’ve no doubt heard of this by now that in an attempt to live a longer time, there are some crazy anti-aging enthusiasts out there who are getting themselves injected with the blood of young humans via process that goes by a whole bunch of different names, but there’s one form of this called plasmapheresis. Plasmapheresis. And my first guest on today’s show is named Mark Urdhal. He is a technology entrepreneur from the Silicon Valley. He’s got a bunch of patents, he’s worked in big data and he began his career at IBM’s Medical Instruments Subsidiary that pioneered this process of plasmapheresis. He went on to found something called the Young Blood Institute which actually does this plasma exchange therapy to rejuvenate the body, stem cells and restore the immune system and prevent the onset of a whole bunch of age-related diseases.
So we’re going to talk about that just a bit with Mark today, but it gets even better because I have another guest on today’s show and he’s been on the show before. I had a podcast a couple of years ago called “The Next Big Anti-Aging Drug: Everything You Need To Know About NAD”. And in that podcast, believe or not, we talked a whole bunch about this stuff called Nicotinamide Adenine Dinucleotide or NAD. And as you learned in that episode, my guest Tom got very sick when he was in Costa Rica and he was prescribed a bunch of antibiotics, he suffered some pretty adverse reactions and was told he’d have problems especially gut issues, things like that for the rest of his life. He developed a whole bunch of food allergies, insomnia, anxiety, muscle pain, chronic fatigue syndrome. We went into his whole back story in that podcast episode that I’ll link to in the show notes for this episode which you can access over at bengreenfieldfitness.com/plasma. That’s bengreenfieldfitness.com/plasma.
Anyways though, through Tom’s eight-year battle, he got prescribed a whole bunch of different pharmaceuticals and he eventually turned to this stuff called NAD. Wound up long story short completely curing him and getting him off all these medications he was on, and I’ve hung out with Tom and he just like this, I would describe him as a ripped beast now. So he’s definitely come a long ways and we race a Spartan race together down in Las Vegas and he’s definitely come a long way since using this NAD therapies and he’s actually a guy who I can talk to who’s way on the cutting edge of anti-aging and longevity. And that’s why this podcast is about a lot more than just young blood and NAD, we’re going to talk about biohacking Alzheimers, and we’re gonna be talking about reversing biological aging, different biomarkers you can track and test, how to measure biological age, the biggest obstacles to age reversal, how you can get more involved in the anti-aging community, a whole lot more. And again, I’ll link to everything. All the studies we talk about, all the previous podcast episodes, everything if you just go to bengreenfieldfitness.com/plasma, P-L-A-S-M-A.
All right, so, let’s go ahead and jump in. First of all, gentlemen, welcome to the show.
Mark: Thanks, Ben.
Tom: Great to be here, Ben.
Ben: And that second voice that you heard, that was Tom. So Tom, you had the idea that both Mark and you are on at the same time, so tell me what it is that we’re gonna be talking about on today’s show.
Tom: Well, I think we’re gonna be talking about… you know, Mark can do a very good job talking about young blood or heterochronic plasma exchange. We also wanna talk about the different ways you can measure biological age and that’s becoming more important as new types of therapies developed and sort of explosion of information out there about all these different therapies that may reverse age. So we need to find metrics that could monitor where we’re at. And then we also wanna talk about Alzheimers. Alzheimers seems to come up because the number one risk factor for that is age, and then I do wanna like just sort of dust the conversation with all these other different ways that we can potentially reverse age and I think we’re gonna have a little debate about NAD. [chuckles] That’s unavoidable. So you know, yeah!
Ben: All right. Cool! We got a lot to talk about but, I have to admit that the thing that intrigues me the most right now from everything that you just listed off is this idea of replacing your blood with plasma, and I would love to hear from you Mark, exactly what this whole Young Blood Institute thing is. And I do know and I’d love for you to mention this as well that there’s another company in San Francisco called Ambrosia, some kind of a blood exchange and I’m curious what the Young Blood Institute is and how it’s different than this other company Ambrosia that’s doing from what I understand young blood exchanges and how this whole plasma exchange treatment protocol works. So, can you jump in to how we can inject young blood into ourselves and walk around looking like 13 years old?
Mark: [laughs] Well I don’t know if we gonna get to 13 but we could try. First of all, the Young Blood Institute is a 501c3 non-profit, okay. So, we got kinda humanitarian research mission to conduct clinical trials in what we call heterochronic, you know, big word for different ages. Heterochronic plasma exchange is basically removing the old plasma, replacing it with young plasma like young purified plasma component. So, yeah, obviously a lot of people have been discussing the concept for a long time. Other people out there that are trying this in different forms. Ambrosia folks as far as I know and I could be wrong, I understood from one of their MDs in Florida that I’ve met, and what they are really doing are infusions. They’re not necessarily getting rid of the old stuff.
Ben: Infusions mean that they’re taking blood from healthy, young donors and infusion that in to other people.
Mark: Yeah, plasma.
Ben: Okay. So just for people listening in, when you say plasma, is that the same thing as blood?
Mark: No. Plasma is the kind of the straw-colored liquid that’s 95% water but it’s 50% of your kinda blood volume is plasma roughly, that’s what carrying all of your red cells, white cells, platelets, immunoglobulins, proteins, etcetera throughout the bloodstream, as well as all the cytokines and signaling molecules and so forth. The primary components of blood are plasma, red cells, white cells, and platelets. There’s a lot of detail below all that but those are the primary components.
Ben: From what I understand, correct me if I’m wrong. Plasma is like about half of our blood volume. It contains the protein, fibrinogens, the antibodies, and basically all the good stuff that you would find in blood.
Mark: Bingo! That’s it.
Mark: Yeah. And so, you mention this I think in the beginning, I actually started my career of all things with IBM Biomedical Systems who had invented what we call back then the blood cell processor. Way before my time back in the 60s, there was an IBM engineer named George Judson who had a son with leukemia…
Ben: George Jetson? Like the Jetsons?
Mark: Not Jetson. Judson.
Mark: J-U-D… yeah, but it’s easy to remember. He had a son with leukemia that needed regular white blood cell exchange, leukapheresis as we call it. And at the time they have a manual process to separate blood, you know, all the blood component with specific gravity. It’s kinda like oil and vinegar, oil and water, etc. and I mean, you put blood on the shelf and it’ll stratify. But basically he invented this machine to draw the blood out of one arm and spin it around in a centrifuge which would [09:37] ______ gravity. While it’s spinning around it’s inside this little disposable plastic, that would allow him to essentially extract as things kinda layered up any particular component he wanted which could be white cells, red cells, platelets, plasma.
So the first application for the blood cell processor was leukapheresis motivated by the fact that his son had leukemia and he’s trying to figure out how to kinda automate the process and donate blood once a week instead of donate a component of blood once a week as opposed to whole blood every two months. And so, he got a leave of absence from IBM and they got a grant from National Cancer Institute and sometime around I think ’65, ’66, they basically created this machine, and then IBM who’s got kinda history of what we call entrepreneurial ventures created a business unit out of it. A lot of people know that IBM actually helps with a Harvard professor created the first heart-lung machine back in the 40s and they’ve done interesting little sci projects but they basically decided to create business unit out of this concept basically and that’s the business I joined when I got out of school at UC Sta. Barbara. And kinda by accident but I gone down for an interview with the computer guys and I got there and they told me there’s a hiring freeze and there’s no job. But there might be this opportunity over in this little business unit called Biomedical Systems and so I joined it and kinda got my crash course in medicine. They hand me tables, medical encyclopedia and I’m literally the head of the open heart surgery because they used our products in open heart surgery like my second month on the job watching the whole thing. And within the year of me joining, they sold the business unit and they re-deploy this into the computer group where I intended to go in the first place. And it really wasn’t until a few years back when I started reading about the mice research exchanging the young blood and I thought, “Man, this would really can do in humans.” Why are they spending so much time with mice and so…
Ben: What were they doing with mice? I mean, when you talk about the mice research, some people may not even be familiar with mice research. What exactly is going on with that?
Mark: Well, there’s a fancy term they called heterochronic parabiosis which in a nutshell…
Ben: Parabiosis, yeah, that was the other word I was looking for. That’s basically the word I see throwing around more than this plasmapheresis – parabiosis.
Mark: Yeah, look, let me tell you what they’re doing. They’re slitting open the sides of two mice, they’ll stitch them together and they’re measuring the effects of the complete exchange. They call it the systemic milieu. Basically meaning it could be blood, it could be all sorts of stuff that’s kinda float around but essentially it’s like they’re creating Siamese twins out of mice that were the opposite of… separate Siamese twins like creating a Siamese twins in mice. They basically stitched together- an old mouse and a young mouse, and measure what happens.
Ben: They’re not actually taking the blood out of the old mouse and transferring that to the young mouse. They’re actually connecting the two mice together?
Mark: Well, the first range of experiment sort of started in 2005, stitching the mice together. Now, in the last couple of years, they developed some devices that essentially allow them to deplete blood out of one mouse or the other and then independently inject it. It’s a very difficult problem with mice ‘cause they’re very small and their veins are incredibly tiny. And so, it’s not a very sophisticated process, let me say that, compared to humans.
Mark: I mean, they did this for humans for 50 years. I mean, we are…
Mark: Oh yeah. Since the 60s. Yeah, I mean there are millions of procedures of all sorts of what we call aphaeresis every year primarily for autoimmune diseases which is the big indication if you will probably, half of the treatments in the world today are plasmapheresis and the majority of those are used for autoimmune disorders. Things like multiple sclerosis, [14:42] ______, there’s a whole list of, kind of a dozen rare diseases where they’ve found what we call therapeutic plasma exchange which has a beneficial effect in removing [14:59] ______ factors, ridding the body of auto antibodies- the antibodies that attack themselves, regulating T cells disorders, things like that.
So, and that’s where we made the connection. I realized very quickly, I met a lot of the mice research people, let me say that, and they are all good people but most of them don’t have a lot of experience with human medicine. So when I set up the Young Blood Institute, I did so with recruiting some of the best immunologist, endocrinologist, nurse practitioners, MDs, etc. that have got really experienced in real medicine, and in particular with plasma exchange. So most of our nurses have been doing this for like 30, 40 years, I mean, typically. And so we’ve got institutionally a lot of experience with that and because I realized that what we’ve really gonna do is explore these new indications that are plausible because we’ve done a sort of connect the dots between autoimmune disorders or autoimmunity, and immunosenescence which is essentially the [16:28] ______ of the immune system. It turns out that autoimmune disorders and immunosenescence have three fundamental things in common: the presence of auto antibodies, the presence of T cell disorders, and the presence of pro-inflammatory conditions. So, the interesting possibility is the use of essentially an old technology to a new indication which is aging, associated with disorders that are caused systemically by immunosenescence.
Ben: Okay. So basically when you’re putting the plasma from a healthy young donor into somebody who comes in there to the Young Blood Institute, primarily what you’re going after is a stronger immune system?
Mark: Yeah, that was our original and kind of the base core hypothesis is that we could reboot the immune system just kind of like reboot your computer, right, that the majority of subjects are gonna be on a path of immune system decline. And we basically dive immunosenescence and you know, the immune system craters and the craters, we become vulnerable to all sorts of different age disorders.
Ben: Okay. So what exactly happens when somebody comes in there?
Mark: Well, first of all what we do is we partner with guys like Tom. So Tom has a clinic in San Diego.
Ben: Yeah. The NAD Injection Clinic.
Mark: Right. And so we have a network of really doctors and clinics across the country and we partner with those clinics to host the trial and sort of provide the oversight of facilities, the local MDs, etc. We run the what’s called an internal reboard- the IRB study protocol, we provide the nurses, the protocol, the equipment, very specialized and then we deploy in the East location and we kinda share the responsibility there, qualifying the subjects, overseeing the procedure generally, and then we’re providing the actual… we come in and kind of turn-key provide the plasmapheresis service for the subjects in these locations.
Ben: Are there any kind of risks to this? Like if I was gonna go down and do something like this because I wanna track my telomeres and see what happens to those, or if I want to get a stronger immune system, I mean, is this the type of thing that just anybody can wander and do?
Mark: Well, millions of procedures are done in a year, okay. And we started with what is arguably the safest protocol possible where we used purified plasma components because plasma is 95% water. So there’s a multi-billion industry that basically collects plasma donations and usually they have plasma collections in universities and places like that. They then distill out the water, they take the key ingredients which are primarily the albumin, the immunoglobulins, and the fibrinogen and they pasteurized it, which means they heated up, wash it, purify it, and it goes through decades of old FDA regulated process. And it’s kind of frozen lemonade, I mean, shipped around the country, add water, got plasma. So, it’s a very safe protocol. There’s about a 4% risk of a transfusion reaction and the transfusion reaction risk is a bit minor and it’s not really that much different than if you went and donate blood at the blood bank. You know, for flushing or thinking or things like that which usually after someone goes through the process you just make sure that they sit down for a little while and have some water, maybe a snack or something like that. It’s considered to be a very, very safe procedure. It’s probably one of the safer procedures in the medical world today.
Ben: When somebody comes in and does it, do they get multiple plasma exchanges or you just do one plasma exchange and that’s it, you’re done?
Mark: Well, in our protocol, at least our first protocol, you go through six exchanges which is different than let say an infusion protocol, and the reason being that is we’re using specialized equipment to remove the old plasma. And the fact is if you’re drawing blood out of one arm, you’re spinning it around, you’re extracting the old plasma, you’re putting the other blood components back in the other arm and then you’re adding the new plasma. After awhile, you’re producing drawing the old plasma with new. It’s kinda like trying to change the oil in your car while it’s running and you didn’t drain the open. And so you can only get two-thirds of the old stuff out roughly, plus or minus 5% but before… you know, I mean, that’s kind of a max and so you’ve got to wait, let it settle, come back within a week or so and then do it again. And there’s a curve that’s in our website but there’s some sort of mathematical, this is called a history from the 12th edition of Hematology that basically demonstrates mathematically that it really takes six treatments to get rid of, let’s say, 98% of the old stuff.
Ben: Is that six days in a row? You’re coming in six consecutive days or do you split those up?
Mark: Six weeks in a row.
Ben: Six weeks in a row. Okay. Got you. So do people need to travel to Silicon Valley or the Young Blood Institute to do this or like you mentioned you’re partnering up with clinics so people can go to these clinics at their town?
Mark: Yeah, that’s why we’re doing it because if they live in San Diego, okay, go to town. If they live in Raleigh, North Carolina; we’ve got a doctor there. You know, if you live in Florida, we’ve got docs there, I mean, we’ve got doctors in Texas. And because of our model, it’s relatively easy for us to add any location. So if we have somebody who lives in hey, Spokane, Washington, and they want to undergo the treatment, kinda the first question is, who’s your MD? And they be understood in hosting the procedure and becoming what we call a sub-principal investigator because they actually are a part of the study. You know, grant a space in these guys where we integrate them because they have a lot of wisdom and they kind of a human biomarker, right. We identify all the data from a study sampling but a doctor and a nurse frankly can make observations that get recorded into… the record for the treatment. So maybe they know somebody that after three treatments is skipping and jumping, there’s a relative fact that we wouldn’t capture the blood test.
Ben: Okay. So when people are looking for a place to go and do this, can they just go to the Young Blood Institute website and do a search for practitioners or where do they do this in a local community?
Mark: Yeah, we don’t really have the list of practitioners in the website but they can submit an inquiry and we can work with them. The bottom line is we’re flexible. If we have a doctor in the area, great! If we don’t and they’ve got a doctor, well that works too.
Ben: Alright, gotcha. So when people are doing this, what exactly are you measuring? What is it that you’re looking at to see if this plasma exchanges are actually working, like are you tracking biomarkers or tracking specific data points?
Mark: Yeah, I think that’s probably the most significant thing we’re doing, and actually to be honest because we’ve probably got more technology, testing capability than Stanford, John Hopkins and Harvard combined. I mean, we have sort of gone to the mat with respect to rolling out the most advanced, sophisticated, scientific test technology on the planet.
Ben: Like what?
Mark: Well, one of the key technologies is called time of flight mass cytometry which provides extremely comprehensive understanding of self-phenotypes signaling ways it really enable what’s considered to be system cell biology at a single cell resolution. It’s called single-cell proteomics- the large scale of study of proteins basically. And it’s a very advanced method to measure in phenotype cells that can generate significant details about cells and roughly small sample, and it’s sort of a successor to what’s called flow cytometry for the last 30 years where we’ve been measuring immune systems and immunology and so forth. So we’ve got literally semi two biomarkers just in that alone. Then we’ve got some ELISA Technology, enzyme-linked immunosorbent assay which has been along for a time and we do a few test using the old ELISA technologies ‘cause we can’t get it on the new ELISA, but there’s a new technology called Digital ELISA which is really…
Mark: ELISA. E-L-I-S-A.
Mark: Stands for enzyme-linked immunosorbent assay. And the digital ELISA is anywhere from a hundred to thirty-five hundred times more sensitive than the traditional ELISA, and that enables detection quantification of biomarkers that previously where almost impossible to measure and it gives us also automated results so we can minimize operator variation, and give us very sensitive accurate detection of cytokine proteins, all sorts of assay. We got about 24 biomarkers there. Then we’ve got mass spectrometry assay for Alzheimers that’s noble and unique, and one of our investigators basically is the inventor of this assay. And it’s clinically proven in Japan back in like 2012, 2013 to be an accurate measurement or roughly the equivalent of a PET scan in detecting amyloid beta plaque in the brain. But detecting which considered to be the least evidence of not the cause of Alzheimers using only a blood sample. So, the problem with Alzheimers is that typically when the time you get diagnosed, it’s too late. You get diagnosed because people are observing problems. You may not remember those problems, you get in to get the diagnosis and the disease has already taken its grip. So that’s the big challenge because it’s not necessarily obvious until it’s too late. So what we’re trying to develop is essentially with all of these things actually not just the Alzheimers but essentially serious early detection of biomarkers that would allow us or enable us to prevent the onset of a number of diseases before they actually begin to occur or become significant.
So, along the lines of colon cancer, breast cancer, early detection regimens that have been very successful, we’re also trying to essentially develop a kind of a next generation of early detection techniques revolving around the immune system, neuro immunology, neurological disorders, etc., and then we also have incorporated DNA methylation markers, and general markers and other kinda newer more nascent types of “biological aging”. The differences are we’re not using those as kind of the key measurement, we’re actually working with the methylation companies to look up all of the detailed sub-data underneath so that we can collate it with the other data we’re collecting. One of the many things we’re doing is getting a significant variety of different types of biomarkers and biomarker testing technologies that we can then correlate to get kind of the whole elephant, if you will, right? Like if anyone test or anyone approach- yeah, you might be looking at the trunk, you might be looking at the tail, you might be looking at the leg. You get the whole picture and so in order to do that, we’re getting as many test as we possibly can including a new one. We just added relatively recently, I mean, just half as we get started but we didn’t discover it until then but we’ve got a new one on blood [31:09] ______ which turns out to be kind of interesting.
It turns out that as blood ages, it thickens. And there’s an interesting curve that shows that past age 60, [31:24] ______ thickens, and so there’s been a lot of historical measurements in let’s say, research settings but it really hasn’t been translated to the broad populace. And yet, it kinda make sense that if your blood is turned to sludge, it’s kinda hard for your heart to push it around. And what we’ve noticed in some of our treatment therapies is they’re getting rid of the old stuff, some which may look a little thicker than in a young person that after a few treatments it starts to thin out or normalize. And we’d had people report, “Wow! I had the best sleep I’d ever had in my life.”
Ben: After getting a plasma exchange…
Mark: After getting, yeah, one or two plasma exchanges. And if you look at the output plasma in those cases… and different people have different kind of experience, let me say that, and because we cryo freeze the blood, we measure all at the future point time all at the same time, we don’t have all our data yet, but just experientially what we’re kinda seeing and observing that there are different characteristics of plasma that are coming out of people and those attributes are normalizing after several exchanges.
Ben: What do you think based on all the different anti-aging biomarkers that you just listed off, people should be tracking and what would be the lowest hanging fruit because I mean, you know somebody can’t get in to Young Blood Institute ‘cause you’re tracking a lot of things there, what would you say would be the lowest hanging fruit for people to actually track if they just wanted to kind of do this on their own or talk to their doctor about running certain test or doing like a telomere length analysis to something like telo years or something along those lines. What would be the best anti-aging biomarkers in your opinion to track?
Mark: Well, that’s a pretty tough question because to be honest with you, we’re probably less concerned about “age” as a human constructed in Roman calendar, I mean, ourselves don’t know about age, right? Ourselves don’t know that there are 24 or 48 or 94, so we’re focused really more on the function of the body, and I will just say on the telomere point, we are cryo freezing the blood and we hope to be able to test it at future point on telomeres but the problem with current telomere testing is that they typical access the telomere lengths on the total, what we called purple blood cell blood mononuclear cell population- PBMCs derived from whole blood. Basically, PBMCs have a mixture of cell sub-populations that have dramatically different telomere lengths. So like naive versus effector T cells for example or T cells versus NK cells. And T cells can have the longest telomere lengths.
So, you could come in the morning and we can do a blood draw and you may have 30% total T cells and you know, things look pretty good, and later that day we do a blood draw, and we only get 5% T cells, and by age 10 years. So the whole methodology around telomere testing is sort of froth with complication, and we’re looking at methods of possibly spinning down the cell population subsets so that we could look at the differences in those specific cell population subsets. For example, naive CD4 cells, CD8 T cells, etc. We compare apples and apples. And even so, we’re still not sure, I mean, they did a little study on this. It’s not clear there is absolute correlation with “age” but, it is of interest in terms of its correlated value to us. So, we’re not really kind of the biohacking community, I mean, we worked with people who are biohackers obviously in the sense of dialogue collaboration, discourse, etc. but we’re kinda trying to get to the bottom line, what’s working, what’s not, and the answers; we don’t know. I mean, there’s a line out there and just understanding which says matter is the whole important part of the equation.
Tom: You’re going to get you know, whatever test you do, there’s always gonna be someone that’s gonna poo poo it because there’s so many different theories of aging, and there’s some few scientists that like to poo poo the telomere length. And so really the approach is to find multiple ways to measure aging markers and biological aging clocks.
Ben: What’s a biological aging clock?
Tom: So, biological aging clock, if you want to study aging and you’re using Farris therapies, you might have to wait 50 years to see what the results are, or you could do your study in 75, 85-year olds and then it has something with certain statistical power in order that you won’t have to wait as long. Or you have something like telomere length that spits out a particular age and that would be another means to determine whether or not the therapy is any good. So the telomere length is one and then Zymo put out this DNA methylation and at aging test they have a few now.
Ben: What’s a Zymo?
Tom: Zymo is a laboratory and they’ve worked with scientist Steven Horvath who sort of a biostatistician and he’s looked at DNA and he has seen a pattern statistically from methyl groups, they’re attached to a certain part of the genome. So at various points in your life certain molecules attach and detach to the genome and based upon that it’s phased out a high correlation of age. And so out of this high correlation, there’s even sort of starting to think that perhaps some of aging is coming from the way in which the methyl group attached to the DNA.
Ben: Okay. Alright, got you. So, as far as this biological aging clock and how to reverse it or how to slow it down, are there any other things that you found, Tom, as far as whether you can track biological aging or slow the rate of this biological aging clock?
Tom: Well you know, I don’t have the access to some of the machines that Mark does unless we partner together, and we’ve talking quite a bit since we met at this cocktail party in Florida where he presented this and yeah, we said yes, this definitely worked together because we’re so passionate about aging and just to come now with this Alzheimers. What we’ve done in our non-profit and at NAD Treatment Center is we’ve looked at some of the more popular inflammatory markers and we’ve also looked at part age which is measuring arterial stiffness, brain age which we use CNS vital signs to compute a brain age and then long age, we’re using spirometry- how much air you could breathe out and then we use cutometry to detect the age of skin elasticity. So those are some of the things that we’re doing and then also we’re gonna be using a new instrument out in the market called Age meter that will be at RAADfest which is a conference which can be held in San Diego on September 20. So we’re gonna have one of the largest booths if not the largest booth at RAADfest in doing IVs of NAD, and exosomes, and also we want to…
Ben: When is this RAADfest? September 20th?
Tom: September 2oth.
Ben: Oh that soon.
Tom: That is soon. I hope you can get the podcast out.
Ben: Yeah. I think this podcast comes out like the week that you’d be doing this RAADfest. So tell me more about RAADfest and tell me more about this anti-aging booth.
Tom: So, Mark is gonna be there. He’ll be able to talk more about plasmapheresis and also what we wanna do is we wanna really encourage people to get their aging clocks done and we’re using a system called PhysioAge that calculates the aging clocks and you’ll spit out an age. You know, at the end of the day, it’s the more data that you can get, the better. There’s always not gonna be enough data to calculate age and aging markers but I’d really love to have maybe if legally possible have sort of a contest where people can sign up and calculate their age and then maybe in the next RAADfest we could figure out who’s made the most progress or whatnot. And yeah, so RAADfest is something that I’m very excited about. I think it’s an amazing conference and it’s very different than some of the other conferences.
Ben: What is RAADfest stand for?
Tom: So, RAADfest is Revolution Against Aging and Death. It’s the biggest conference on radical longevity and it’s a place where you can go and hear about studies that people are doing, trials, make investments, have dinners with scientists and doctors, and it’s a social gathering and it’s a non-profit, so it’s pretty inexpensive just a few hundred bucks to go and get a ticket there. And I think Mark and I will have a side room to talk about… maybe doing some other case studies. I know Mark and I are very interested and looking at other ways beside this very promising plasmapheresis and so, for example, I had lunch with a scientist two months ago, Greg Fahey. He wanted to talk to me about an NAD test that he was working on and he said this was a huge game changer. So, he wanted to maybe have some sort of partnership and figure out how we could help each other. Little do I know, I find out later, he’s developing a therapy for thymus regeneration and because if you lose your immunosenescence, then you could be healthy like Jack Lalanne and catch pneumonia in a few days later, you’re dead. So, that’s one of the things he’s working on and the foremost authorities on cryonics or cryonic vitrification which is taking cells or organs and cryonically preserving them. So, I had no idea who I’m talking to and then these are people that I’ve met at RAADfest the last couple of years and it’s just a great environment to see people who are passionate about longevity.
Ben: You guys are obviously… you’re talking about things that I haven’t heard anybody before talk about when it comes to aging and longevity, but one thing, just to clarify here, what are the different parameters you’re measuring at this booth? Just list them off again because it was very interesting. It was about long skin… What are some of the other parameters here?
Tom: So, heart age, arterial stiffness, I think that’s called [45:45] ______, brain aging, we’re going to use old standard CNS vital signs, and then you’ve done those air tests, spirometry where you blow as much air out of your lungs as you possibly can. Then, there’s a skin test that uses a laser to measure the skin elasticity of your forearm and produces a skin age. So, looking at all these different parts of the body, you’re able to get a better handle on what your age is. And of course DNA methylation and telomere age, they’re even better when they’re all measured together. And, we’ve got a couple other ideas for aging clocks as well. I’m going to be speaking there, so I’ll speak a little bit more about the aging clocks that we’re doing and I’ll be encouraging people to get involved and to see if we can make changes in life expectancy because our life expectancy has dropped three years in a row and our health span is declining as well. So, this is something that I get really excited about.
Ben: Interesting. You guys are going to be measuring a lot of things. So, RAADfest. I will link to that in the show notes over at bengreenfieldfitness.com/plasma. Kind of last minute, but if folks want to get over to that and check it out, it’s in San Diego. Right?
Tom: It’s in San Diego. Yup.
Ben: Alright. Gotcha. I mean, one of the things I talked with you the last time I had you on the show about, Tom, was this concept of NAD and we haven’t talked a lot about NAD, but one kind of the elephant in the room I should address while I have you on the show, is this idea that was mentioned by Dr. Charles Brenner the last time I had him on the show. We talked about nicotinamide riboside or NR and he has this supplement called TruNiagen. ChromaDex, Thorne has one. Elysium Basis is another one. A lot of these folks are saying that compared to NAD, that NR is far more absorbable and a much better way to boost your NAD levels, and we know that NAD to NADH ratios are really important as a way to control aging and to enhance mitochondrial health and overall health in general. I personally, I take NR, but I do these NAD injections. I’ve been down to your clinic and I’ve done an NAD IV. I do right now on a weekly basis, I do an NAD push IV self-administered. It’s one of those things that are controversial though because a lot of people, including Dr. Brenner, will say that NAD can’t enter the cell membrane like NR supposedly can. What are your thoughts on that?
Tom: How do you feel when you inject NAD versus taking NR? I’m just curious.
Ben: Well, absolutely amazing but I’m wondering if part of it is because the injection process sucks so much and you get so nauseous and your gut feels like it’s on fire. I wonder partially whether or not it’s due to just extreme relief that the actual injection is over- I feel like a million bucks. Subjectively, all joking aside, I feel amazing when I do my NAD injections and I can’t say I feel the same immediate, noticeable effect when I take NR. Again, there are a lot of confounding variables: I’ve got a needle in my arm, I’m getting this stuff injected, you have that rush of adrenaline from the injection itself. I mean, I’m more interested in data than my own subjective feelings.
Tom: Well, yeah. I’m too afraid to do the fast injection. I’m not sure I want to encourage people to do it.
Ben: It’s uncomfortable.
Tom: Yeah. That’s like being run over by a steamroller or something like that.
Ben: I have to do box breathing the whole time. It takes me about 15 to 20 minutes to push it all in and I take out a trashcan so I can puke if I need to from the nausea, but then it’s over! And I save myself six hours and a flight to San Diego, baby.
Tom: Okay, alright, fair enough. You know, many NAD scientists usually say that NAD does not cross the plasma membrane. The sort of consensus is there, and I personally disagree with that. You just sent me an article that I haven’t had the chance to read, but there was also a journal – Brazzoni – there was an Italian group in 2001 that showed that NAD can cross the plasma membrane at the 3T3 fibroblast which are mouse embryonic fibroblast. So they used something called protium liposomes and they figured out that NAD crosses the plasma membrane. The hemidesmosome protein called connexin 43. So if you disagree with that, then one could always go on to Sigma-Aldrich website and buy 3T3 fibroblast for $400 and they’ll be shipped to your door and you can run the experiment. I really liked the research that was done at the NAD Conference that I held last January where Ross Grant, who you interviewed talked about the uptake of NAD. I’m not sure if or when that’ll ever get published, but Naty Braidy showed that increase in [51:53] ______ activity and SIRT1 microRNA expression. Some of that research is trickling out and what I’d love to do is… I was just talking with an NMN, nicotinamide mononucleotide scientist and he’s also an MRI expert; he was trying to sell some technology to the government to detect lies with his MRI but he wants to use the MRI much like a Hubble telescope goes out and peers out into the stars. He wants to use this MRI to peer into the brain before and after NAD treatment and actually count the molecules of NAD in the brain. The hypothesis is that not only is NAD in the brain, but it’s also crossing the cell membranes. He asked me to sponsor that, he wants to look at that for NMN and NAD and I said “sure, let’s give it a go”.
There’s a bit more information and we’ll just show that on the show notes, but it’s kind of neat to see the controversy and the debate, but I really do feel like to really debate too extreme is really unhealthy. The FDA thinks that we should decide which is the safest and best vitamin B3 therapy. Whether it’s NMN or NR or niacin or what-have-you, and they’re misinterpreting the law called the Drug Quality and Security Act which goes far beyond NAD. There’s 453 ingredients that the FDA’s pharmacy compounding advisory committee have reviewed, and that they refused to review 390 ingredients and PCAC has further rejected 71% of the 49 ingredients that they’ve reviewed to-date despite a long history of safe use and patient need. So, what you have is a number of things that you love, Ben, okay, and then a lot of our listeners love, are being threatened of being taken off of the market. It’s pretty sad.
Ben: What do you mean? Why is it being threatened to be taken off the market?
Tom: Compounds like glutathione, for example. That for example of glutathione push, that’s being threatened right now. There’s a review, it’s almost like a court hearing, and people are going to argue for and against glutathione, and they usually give about two or three weeks…
Ben: They would want to take it off the market?
Tom: For compounding pharmacies. Yeah. This means that veterinarians, ophthalmologists, dermatologists…
Ben: Okay. Not that many people. The general public though, not than many folks are using glutathione in that form, right? The compounded form?
Tom: Well, I mean, if you go to a functional doctor, that’s a pretty common IV. It doesn’t end there. There’s alpha lipoic acid…
Ben: I was thinking most people were just ordering off of Amazon like liposomal glutathione or whatever.
Tom: But the uptake is not necessarily that good. People have digestive problems and there’s other things too like thiamine, curcumin, selenium, resveratrol, magnesium glycinate, vitamin A, zinc picolinate. All those vitamins I just mentioned, are vitamins that we use that we want to be using in Alzheimer’s study that we’re doing where we’re combining Bredesen Protocol with IV NAD. We’ll be doing a lot of that stuff orally, but those are vitamins… Who knows? There’s lot of Parkinson’s patients that rely on glutathione. There’s vegans who want methyl B12 and there’s a real risk that that could go away.
Ben: I don’t understand how it’d go away. Why would they want to do that?
Tom: [laughs] Well, I have my own reasons, but the reasons that they state is that safety is a concern. But, the reality is that there’s no money involved in proving the safety of these vitamins that doesn’t actually have any intellectual property. And so if there was then essentially as soon as that occurred then the price of these vitamins would go up, and so health care costs would go up, but basically not only do you have a sort of threatening to naturopaths and functional medicine doctors, but it’s also threatening to the cost of health care itself. This is sort of what’s going, so I don’t think that a debate about NAD is necessarily a healthy one. There was a girl the other day that called up the center and she said, “I’m hallucinating”, and I said, “why?” and she said, “well I took Levaquin and I have massive anxiety and I’m hallucinating.” “Oh! Hang up and dial 911 and go to the ER.” And she said, “I just came from the ER and they just kicked me out and I was just googling around and I found you and what should I do?” And I was like, “Well, I’m not a doctor, but there’s based on some information I got from [58:29] ______, he’s prescribing 600mg of NAC which converts the glutathione and magnesium 400mg or a gram, and he’s able to stave off some of the problems of adverse reactions to Fluoroquin antibiotics.” So, lo and behold, she goes out and she takes that. I tell her to go see a doctor of course, but we were communicating and she said, “Now, the hallucinations aren’t as bad as they were. They’ve really have calmed down my anxiety, my insomnia.”
And so doctors need to… there really should be some freedom with doctors and compounding pharmacies, and patients when they’re really desperate and they don’t have anywhere to turn to. For example, the silver IVs are an alternative to these antibiotics and that’s being threatened to come off the market. The myrrh from the three wise men, they’ve taken myrrh, the FDA wants to go after myrrh. What did myrrh do?
Ben: Poor baby Jesus.
Tom: Little baby Jesus. There is really just a threat to all the other potential NAD therapies out there that are making end to health care costs and I think the FDA is really the biggest obstacle to longevity. That’s what I think so.
Ben: Interesting. I want to get into Alzheimers here in a second because I know you’ve been looking into that quite a bit and both of you guys have some pretty big thoughts on a multi-modal approach to Alzheimers and what we can do about Alzheimers, but before that you briefly mentioned that article I sent to you, Tom, about NAD uptake and this one I will link to in the show notes over at bengreenfieldfitness.com/plasma, but it does show that most mammalian cell types can transport NAD across what’s called the plasma membrane from the extra cellular medium and into the cell. And it does actually show a pretty significant amount of NAD uptake despite the people that sell the NR supplement which I’m nothing against in this NR supplements and how they work. But a lot of folks will tell you NAD can get absorbed and I just over and over again I see data like this and you just leave it to, Tom, and it shows that it does, so that whole debate I think we could probably put a nail on that coffin and say that NAD does actually get absorbed. And again, for those of you who wanna look at the research, we’ll put some over at bengreenfieldfitness.com/plasma.
But I know you have been using NAD to fight Alzheimer’s disease, I know you guys have been using something called the Bredesen Protocol, so tell about what have you been doing when it comes to Alzheimers?
Tom: Well you know, I’ve heard about Bredesen Protocol when I talked to a lot of functional medicine doctors, they just lied up when they talk about Dale Bredesen and what he’s been up to with Alzheimers, and there was a speaker at my conference who talked about how he was combining NAD with Bredesen Protocol and he was seeing very good anecdotal results, and by the way, Ben, we’ll be selling those videos with the discount and we’ll put those in the show notes as well. So if you’re listening to this podcast and you wanna watch the videos, and then we’ll also just bundled that with the next NAD Conference that we’ll gonna be putting on in February 2 if you want to go to that as well.
Tom: But you know, Alzheimers is a five-hundred-billion-dollar disease and it’s the 6th leading cause of death, and it’s part of that 5% of society that makes up 50% of the cost of healthcare. And so we think that looking at everything that we can to reverse Alzheimers, the risks are outweigh by the potential of looking at a lot of different therapies. So, when you’re looking at some of the things that Bredesen does, with Bredesen Protocol he talks about using a metaphor where Alzheimer’s disease is like a roof with 36 holes in which if it’s raining, you’re gonna have 36 leaks. And each holes need to be filled in order to achieve the best outcome and he claims even reverses Alzheimer’s disease. So, the 36 holes represents 36 metabolic imbalances in the brain and while previous Alzheimer’s drugs are successful at filling one or two holes, his protocol addresses all 36 holes.
So, he sort of breakdowns Alzheimers into different subtypes: inflammatory markers- glycotoxic which happens to deal with high carbohydrate, sort of diabetic, and there’s atrophic that has to do with sort of hormone related, and there’s toxic which has to do with things like microtoxins and heavy metals, and there’s cardiovascular and traumatic which is brain injury. So, people like the poo poo say it’s sort of like, he seems to bring out a lot of things that he brings up like ketosis, and using MCT oil, and it’s just fits well with me. Doing intermitted fasting, he has this sort of 12 hours off intermitted fasting and eat 3 hours before going to bed, doing low carb diet, these sort of things, it’s a lot of these stuff you’ve talked about for a very long time and so, it’s exciting to see sort of the cross pollination of what you see in biohacking world and Paleo world and what’s happening here. So we’ve been looking at filing to do the NAD with his protocol and we’ve actually been wanted to throw in the Vielight, so I first stuck the Vielight up my nose.
Ben: A lot of people don’t know what a Vielight is. That’s the photobiomodulation, basically the laser light for your nose and for your head that they’ve done some interesting research behind. I’ve had a whole podcast on it, but essentially it’s like photobiomodulation like infrared therapy that you put on your skull like a helmet. I have one sitting here beside me. It’s right next to me right now ‘cause I wear it about 48 hours and it causes an activation of mitochondria, neural tissue, causes the release of nitric oxide. It’s a pretty powerful little headset.
Tom: Yeah. And the manufacturers doing the study with Alzheimers right now out in Toronto, when you’re going after Alzheimers, you just wanna throw everything that you can if it’s seems like we think it’s a rather safe therapy to combine. There’s a ton of precursors that have been sort of… there’s been a lot research that has been linked between NAD precursors and Alzheimers, and Bredesen uses resveratrol, nicotinamide riboside because anecdotally what you see in functional medicine practices, you see pronounced cognitive changes with the IV NAD, we think we hypothesized that potentially using a pure NAD is going to be promising to reverse this nasty disease. So we talked to Nady Braidy about it. He wrote a book about NAD and neurodegeneration, and aging and he saw it was a great idea. So he is our primary investigator and he’s the first scientist to show that NAD levels decline with age. So, it’s a pretty good wind to have him on board.
Tom: There’s so much out there and that’s would get us excited. That’s would Mark and I get excited. I mean like, maybe even the potential of using these exosomes that you’ve been talking about for Alzheimer’s disease.
Ben: Are you guys using those as well? Exosomes? And you would use them for Alzheimers?
Tom: Yeah. There’s a protocol that Kimera has for Alzheimers.
Ben: What’s Kimera?
Tom: Kimera is the of the labs that’s producing sort of this undifferentiated broth of MSC placenta-derived exosomes. So gosh! It’s a big term but basically I’m not the best at explaining what exosomes are. You probably better maybe. Their extra cellular vesicles that sort of messages in a bottle that communicate between cells…
Ben: Yeah, that’s vesicles… back when I was taking Exercise Physiology. They chose these photos of cells with these diagrams of cells that have these little tiny circles getting released from them, and people just thought that they were essentially almost like junk that the cell was releasing. But it turns out they’re actual signaling molecules and they have specialized functions like not just into cellular signaling but like waste management, and blood coagulation, and they can also when combined with stem cells or even in the absence of stem cells, it appears actually allow for better trafficking of certain, I guess, like nutrient signals, etc. from cell to cell. They essentially are like the carriers like taxis from cell to cell so that it influenced the immune system, and the immune response to pathogens, tumors and again, when I got injected with stem cells, they are almost uses a way to upgrade my stem cells and yeah, pretty fascinating what they all can do and this came from this lab, this Kimera lab that you just refer to.
Tom: Yeah, I mean, they take stem cells and then they treat them in such a way that they shed off these exosomes, these messages. They might be proteins, RNAs, micro-RNAs and they’re coming from rejuvenatory sort of placenta and they’ve been using them for a number of different issues. I mean, you and I know… we have a common friend who have a spinal cord injury and he… you should probably put that in the show notes, I have him sign a release, but he seems to have a significant improvement in his spinal cord injury where he’s able to bend down more, and he’s been able to have improvements in tone and spasticity from the spinal cord injury and it’s just those moments that makes you wanna go further and see how exciting sort of cutting edge science can do. The cool thing is that these exosomes have their homing capability, some are anti-inflammatory immune modulating. I was talking with the lead scientist there, not only that their exosomes have the GDNF and PDNF, these are sort of neuronal RNAs but it also has this GDF11 microRNA which is like the RNA that produces the protein that has real potential.
The interesting thing about talking to people from RAADfest is like, this one lady that I spoke to and she’s claiming that her biological aging clocks have gone from her 70s to a 30s. So, Steve Perry is gonna be speaking at RAADfest and he’s gonna be speaking about these hundred individuals that have took it upon themselves to inject themselves with GDF11 but exosomes have the RNA for GDF11. So it’s like this copy machine for GDF11.
Ben: So you could get this GDF11 which is like a DNA repair molecule that would act on stem cells to make them active again, and I know a little bit about GDF11, it’s got some pretty potent cardiac and muscular and neural effects but what you’re saying is that exosomes would allow you to get the same effect as GDF11 or enhance you GDF11 availability?
Tom: Potentially. I mean, no one really knows. A lot of these stuff is so new. At least I don’t know what potentially it could come out, but you hear sort of these stories and I hear more stories from the people who have taken the GDF11 and seen improvements in like an injection. It’s a very very small dose and they’ve seen improvements in sex drive, and they’ve seen improvements in hearing and smell, sight, things like that.
Ben: Interesting. Do you guys do injections down there at the NAD clinic?
Tom: No, but we’d like to. I mean, there might be some legal hurdles to go through in order to make that happen. So, we’ll be looking into that. You’d have to find a way to procure it. It’s just a really exciting part of longevity right now, it’s this GDF11- it’s a hot topic.
Ben: Okay, interesting.
Mark: It’s been a hot topic for a long time and the bottom line in all these biohacking is kinda fine, cool and interesting, but how do you actually measure results? And a lot of people got stories but the real fundamental question is, where’s the data? What data supports what result? And that’s what we’ve been kinda focus on. Okay. We’ve kind of built a platform to test it and so I would say, Tom or Ben, anything you guys come across you think, as merit really, we’re in. We’ll test it. Beecause we’re looking for a common yardstick to sort through the myth of the stories, the hearsay, and all that to get to hard data that says, “Hey, we saw this changes in the cellular cytokine panel, or we saw the stem cell project or panel change, or whatever.” How people feel, what their kinda anecdotal sense of things is, kinda interesting but the most primary question is, are you detecting a potential problem and preventing it? You know, are you rejuvenating something that you can measure a change. Can you measure myogenesis- growth in muscle cells, neurogenesis- growth in brain cells as a result of some treatment therapy. And so, that’s kind of the most fundamental issue I think in the anti-aging world right now is the crazy copy of characters and if we’re all going to benefit from this, at the end of the day, then we need a common yardstick or common yardsticks. And Tom’s got a lot of cool stuff. He’s add to the mix and we’re kinda testing it and I mean, taking anything that is of merit worthy. But we’ll be equally critical of tests that aren’t merit worthy.
Telomeres, that’s kind of the low on the list of having any merit. It kinda feels good but it could change day to day based on the random blood draw. So we’re trying to get to a place where we can get more definitive certainty around cause and effect of associating all of these stuff. So we could all save time, I mean, it’s just as valuable to figure out what’s not working and what’s working.
Ben: Yeah. One of the other things I wanted to ask you guys is about this idea of senolytics because I think it was Tom I heard talking about senolytics, this idea of senescent cells. Can you guys get in to senolytics a little bit and how that works?
Mark: Can I just say one more thing about Alzheimers and then before we transition over there?
Mark: I just wanna say that there’s a study that’s been going or that concluded last year or the last 4 years using therapeutic plasma exchange to treat Alzheimer’s patients. It hasn’t been published yet. There’s been some results published in 2016 and they’re on our website. There’s a link to it in the reference section. But out of the line is we hired 11 nurses that were on that study, and they saw recovery, real recovery first-hand. These are not newbie nurses just out of nursing school. These are like nurse practitioners with 30, 40 years of experience who can tell you actual stories of actual people who actually recovered as a result of treatment therapies.
Mark: And so, we’re probably gonna have a whole separate branch or arm that really create that’s gonna be more Alzheimers or neurologic specific. Right now, we’ve kind of the big net for anything and everything anti-aging. Including the minimal base of ultimate blood test. We’re probably going toward this year and beginning next year create a protocol that more or less mimics the protocol that was used by Grifols over the last 4 years over hundreds of patients and thousands of treatments that hasn’t yet been published but have pretty word that it worked. And we’re pretty confident and I bet what some of the principal investigators as well, so we’re pretty confident that when they do publish those show with positive results, as the result to the treatment therapy. The cool thing is, it’s like, Hey, I think we’re gonna find out, I mean, the Bredesen stuff is great, a lot of folks are working on diet and neurological disorders and so forth, which we would like to test by the way, a real form of clinical trial. But it may be a combination of these things and I tell people that we can change the oil but if we keep putting garbage on the tank, you’re gonna screw up the engine again. So, there may not be one right answer here, but the key is getting the data around this and we’re going to have the most advanced, most definitive, minimally base of blood test in the world for Alzheimers that will objectify some of the answers here.
Ben: Wow! That’s fascinating that you guys have gotten those kind of results with Alzheimers. I remember heard of it being reversed to that extent and that’s gonna be very interesting for a lot of people.
Mark: Well, these are right now in a category of nurses’ lore because it hasn’t been published but it was a very rigorous clinical study. We do expect they will publish their results within the next 6 to 12 months and we just need to jump on it because we just hired a few nurses that happened to be on duty administering the treatment.
Ben: Wow, wow! So what about this senolytics thing?
Mark: So yeah, unlike plasmapheresis that has so many years and it’s been used so many times, and senolytics is a newer technology. A broad term to describe, small molecules which selectively induced death of the majority of senescent cells. So, a senescent cell are basically like zombie cell that live in your body and as you age you accumulate more of these zombie cells that don’t really help out the rest of your body, and they excrete chronic inflammation, increased risk of cancer, and secrete pro-inflammatory cytokine, chemokines and extracellular matrix proteases that contributes to aging and cancer. So, there’s companies like Unibio Technology- they’re out there but I’ve spoken to some people, on some of the folks there that are at, they’re be at RAADfest about how they’re experimenting with some of these therapies and some of them don’t even wanna talk about because they’re so new and they are risk apparent to them. But the idea is to get rid of some, but not all of these zombie cells ‘cause apparently you need to have some of these cells to keep healthy. You don’t want to eliminate all of them, but I mean, right now Life Extension I think did an article and I’ll post that in the notes where they’re recommending taking 150mg of tocotrienols– a vitamin E spectrum per day and then 500-800mg of quercetin per day as a way of minimizing the damage from senescent cells. It’s really exciting because it’s this anti-aging therapy that I’ve heard people talking about how they’ve got more energy and more of an indepth sort of more knowledgeable explanation at RAADfest.
Ben: So quercetin would be a supplement that you would take to actually stave off of the development of these senescent cells?
Mark: Yeah, quercetin which is found in onions and then…
Ben: Yeah, you found that in apples too.
Mark: Apples, yeah, that’s right.
Ben: You would take somewhat a supplement to get a lot more than you can get from say, onions and apples.
Mark: Yeah. I think so.
Ben: Interesting. I mean, a lot of these stuff people are just unaware of like GDF11 injections, NAD IVs along with the reverse of Alzheimers from things like plasma exchange therapy or this quercetin and took tocotrienols to decrease senescent cell formation, I mean, there’s a lot here and I realized that we’ve only really scratched the surface. I know, you’ve sent me a ton of studies I need to dig through, and add to the show notes, Tom, and I’m gonna be doing all that and carrying some pretty robust show notes for you guys who want to take a deep dive over at bengreenfieldfitness.com/plasma.
I know, it’s kinda science-cey during today’s show and my apologies. Hopefully everybody’s was able to kinda keep up with some of the stuff we were chatting about. But, I would recommend that for any of you interesting in kinda keeping your finger on the pulse of all these that you check out the links we’ll be having in the show notes, and you follow what Tom is doing, and you follow what Mark is doing because I do talk to these guys and they’re really are on the cutting edge of a lot of these stuff. I would recommend that you follow them, follow their clinics and again I’ll link to everything. I also link for those of you who want the last minute going to this RAADfest. I’ll link to RAADfest in the show notes and perhaps to those of you who wants to plan things out and plan your conferences in advance, I’ll also link to this NAD Conference that’s gonna take place in February for those of you who wanna get down to that, I’ll probably go to that one myself. I don’t think I’m gonna make it to this RAADfest but I’ll probably at the NAD Conference.
Tom, Mark, anything else you guys wanna bring up before I let you go?
Tom: Great job, Ben.
Mark: Thanks, Ben.
Ben: Awesome. Well, thanks for coming on guys and again folks, if you want to take a dive in any of these stuff, just go to bengreenfieldfitness.com/plasma. That’s bengreenfieldfitness.com/plasma. I’ll put links to all these conferences, all these studies, pretty much everything that we talked about in the show notes over there. Until next time, I’m Ben Greenfield along with Tom Ingoglia and Mark Urdhal signing out from bengreenfieldfitness.com, have an amazing week!
You’ve no doubt heard of it by now…
In an attempt to live longer, some anti-aging enthusiasts are getting themselves injected with the blood of young humans, via a process deemed: plasmapheresis.
This podcast is about several age reversal therapies. It’s also about biohacking Alzheimers. It’s about all these therapies (senolytics, exosomes, gdf-11, etc) that scientists have been talking about for age reversal as well as biological aging clocks and biomarkers to measure them. You’ll learn about ways that you can biohack Alzheimer’s disease, how to measure your biological age, how to reverse aging, what the biggest obstacle to age reversal is, how to get more involved in the anti-aging community and more.
About the Guests
Mark Urdahl is a technology entrepreneur from the Silicon Valley. He has numerous patents and has worked in big data. He began his career at IBM’s medical instruments subsidiary that pioneered plasmaphoresis. Mark founded the Youngblood Institute to advance new uses for well established therapeutic plasma exchange therapies which have recently evidenced a previously undocumented potential to rejuvenate the body’s own stem cells, restore aging immune systems, and prevent the onset of many age-related disease condition, so that we might live healthy as we age and ultimately live longer lives.
Tom Ingoglia first appeared on this podcast in the episode “The Next Big Anti-Aging Drug: Everything You Need To Know About “NAD”.” As you learn in that episode, Tom is a private investor with a master’s degree in finance. In the midst of trading, investing in technology and developing real estate in Costa Rica, Tom became very sick. He was initially prescribed antibiotics, suffered from an adverse reaction and was told that he’d have stomach problems for the rest of his life. In the years that followed, Tom also developed severe food allergies. His symptoms worsened, and he next began dealing with insomnia, anxiety, muscle pain, tendinopathies, joint pain, chronic fatigue syndrome, altered and clouded cognition and headaches. He finally had a mental breakdown in 2008. After a prolonged period of taking antibiotics, Tom began experiencing tendonitis throughout his fingers, hands, wrists and ankles and feet, so he started taking pain medications to relieve this pain. He had to give up his career in trading because his sole focus for the next eight years would be on finding a cure to his growing symptoms.
His life consisted of working with physical therapists, going to the gym, going to new doctors, and trying new foods to see if it would help. Throughout Tom’s eight-year battle, he was prescribed consistently and persistently more medication. For six years, he was taking excessive amounts of Hydrocodone and Tramadol every day. Tom became obsessed with researching symptoms and treatments and learned about the NAD+ treatment. He visited a clinic, and on Day 7 of his treatment, “It hit me. I started feeling better. I felt amazing. There was a calm that came over me. I felt safe. I just had no cravings for drugs or pain meds. There was no need for them. I just didn’t have the excruciating pain that I had before. I felt eight years of pain melting away.” Tom has nearly fully recovered, using related treatments to NAD+, and has engaged two cofounders to assist him in building out a facility to help bring this treatment to others in similar situations.
In my conversation with Mark and Tom, you’ll discover:
-The history of The Young Blood Institute and how “heterochronic plasma exchange” works…16:00
- Heterochronic plasma means simply removing old plasma and replacing it with “young” plasma.
- Others are experimenting with this concept.
- What Mark does is different from a plasma “infusion.”
- Plasma is approximately half of our blood volume.
- Mark began with IBM Biomedical Systems, who had invented what we now call the “blood cell processor.”
–The intricate means of testing used on mice…22:15
- Basically creating “siamese twins” with mice by stitching them together.
- Similar procedures have been conducted on humans for over 50 years.
- Mark wanted to recruit the best medical professionals to the Young Blood Institute. Many of them have been doing it for 30-40 years.
-What, if any, are the risks of these plasma exchanges…29:10
- Roughly a 4% risk of a transfusion reaction, which is akin to what you might experience donating blood.
- One of the safer procedures in the medical field today.
- You go through 6 exchanges as part of a protocol.
-The network of doctors that Mark and Tom have built to do a plasma exchange…32:42
- There are medical professionals all over the U.S. that can do the procedure.
- Submit an inquiry on the Young Blood Institute website to find a doctor that is near you.
-What anti-aging biomarkers Mark is tracking at the Young Blood Institute…34:51
- They have more technology testing capability than Stanford, Johns Hopkins and Harvard combined.
- Key technology: time of flight mass cytometry. Single cell proteionomics.
- They are trying to develop early detection biomarkers that enables them to prevent the onset of diseases before they become significant.
-The lowest hanging fruit for people to track…46:15
- The YBI’s concern is the function of the body, rather than the age.
- Your cells are not aware of your “age”.
-What a biological aging clock is…50:20
- Zymo is a lab that has worked with Steven Horvath. Zymo DNA Methylation Aging Clock
- Looked at DNA, and seen a pattern from methyl groups attached to certain parts of the genome.
-How can we track biological aging, or slow down our biological aging clock?…52:30
- Inflammatory markers, heart age, brain age, lung age, skin elasticity.
-The anti-aging booth that Mark and Tom will be operating at a conference called RAAD Fest…54:45
- Revolution Against Aging and Death
- Want to have a contest where people calculate their age, and track their progress.
- Mark and Tom have one of the largest booths at the conference.
-Whether NAD actually gets absorbed into a cell via injections or IV…1:00:30
- How does Ben feel with an injection? Answer: Incredible.
- Tom doesn’t recommend the injection due to the level of discomfort.
-Why compounded formulas such as glutathione and Vitamin B could be taken off the market soon…1:07:30
- There’s a review similar to a court hearing, where people argue for and against glutathione.
- Taken off the market for compounding pharmacies.
- Tom “has his own reasons” for why this could be deemed unsafe.
- Core problem: the vitamins don’t have any intellectual property. Could affect the costs of healthcare.
-How to use technologies such as Vielight and exosomes to address Alzheimer’s…1:14:30
- Alzheimers is a $500 billion industry; the 6th leading cause of death.
- A Vielight is basically a laser light for your nose and head; photobiomodulation on your skull.
-What GDF11 mRNA is and how it works to improve hearing, smell and sight…1:25:30
- GDF11 is a DNA repair molecule; makes stem cells active again.
- Patients see improvements in sex drive, vision, smell, hearing, etc.
- Legal hurdles to being able to administer it.
- “Unofficial” results are very positive.
-How senolytics works as a therapy for aging and Alzheimer’s, and the importance of quercetin and tocotrienols…1:33:45
- Describes small molecules that lead to the death of “zombie” cells that don’t help the rest of your body.
- Life Extension article “Natural Compounds that Remove Aging Cells”
-And much more…
Resources from this episode:
–Beyond NAD Conference – Use discount code “BenlovesNAD” at check out
–Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-γ coactivator 1α regulated β-secretase 1 degradation and mitochondrial gene expression in Alzheimer’s mouse models
-Book: The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline by Dr. Dale Bredesen
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