Dr Sandra Kaufmann - The Kaufmann Protocol: A Systematic Solution For Cellular Ageing
7:40AM Sep 9, 2024
Speakers:
Leslie Kenny
Dr. Sandra Kauffman
Keywords:
mitochondria
cell
proteins
dna
tenant
agents
people
age
called
senescent cells
dna repair mechanisms
histone
important
aging
good
protocol
body
category
work
exercise
Perfect. So I'm Dr Sandra Cal from those of you who met me know that I'm an extremely informal Miamian. So I'm Sandy. Call me Sandy, as Leslie said. I started out as a cell biologist. My dad pointed out years ago that cells don't pay bills. I went to med school. I'm a practicing anesthesiologist, and I do I travel a lot doing anesthesia for various ages of people. The question is, why is any of this important? It is important because the Kauffman protocol is based on the fact that you age because your cells age, but Miss practicality. Drug oriented anesthesiologist decided that I was going to figure out what to do about all of those problems, and that's what the protocol is. So the first part of this is, why blue age, followed by, how are we going to fix it? So I love to start with this diaper, because every face the audience always goes, Oh, this is going to be a terribly boring talk, because this is what people think of Asian athletes. This is accurate. It's beautiful. I didn't make it. It was put out in 2021 but no one has ever looked at this diagram and said, Oh, I get it now. I know what to do, right? It's never happened. It's nine user friendly. So as a consequence of this, years ago, I came up with what I call Leslie, referred to the seven tenets of aging. Why seven? Because people can remember seven things. That's why phone numbers, once upon a time, had seven numbers, and other people like the hallmarks of aging, the hallmarks of aging. It's a fantastic list, but that's what it is. It's a list. You can't do anything with a list. The hallmarks, I'm sorry, not the hallmarks, the tenants. It's an organizational scheme, and it's a tool, and you're going to understand why that is as we go on. All right. So what are the seven tenets of Asian if you think about a cell as a factory, a lot of this makes more sense. I'm going to go through them. So for the scientists in the room, think science. For the non scientists, think factory. All right, 10 of one is DNA alterations. What goes wrong in your DNA? Many things do. We're going to touch on details as we go through. Two is mitochondria. You need energy if you have energy failure, if you fail. Three is cellular pathways. There are four big pathways we're going to concentrate on a little bit of one today, repair mechanisms. Lots of things go wrong in our factory, right? So our DNA breaks, our proteins break. We have to fix it. When you can't fix it, recycle items. That's going to be autophagy. That's all I do. For five is going to be your immune system that turns into your inflammatory system. Six is individual cell names. I like to pretend that all cells are the same. Clearly they are not, so that that tenant recognizes the fact that maybe you want to get rid of some of your senescent cells, maybe you want to be really kind to your stem cells, but a red cell is different than a brain cell versus a liver cell. That's what that category entails. And then the last one is waste management, right? You have to take out the trash or things don't work this diagram, notice all the circles are overlapping. And they are overlapping to remind us that all of these things are, in fact, entangled, much like in the first picture. But our greens don't work that way. There's no way we can think of that many dimensions at one time. So I separate them and talk about them as if they are different, knowing that they do overlap. Okay, so tenant one, DNA alterations. What happens to your DNA? Nothing good, right? We know telomeres get shorter over the course of time, replicated senescence. Every time a cell divides, it gets a little shorter. Also gets attacked by oxidative stress, glycation stress, et cetera. You will go to many longevity summits, and they will talk about telomeres. So I'm not going to bore you with that. Epigenetics is a big one. We heard a lot about epigenetics already, right? We know that those changes occur, but what you don't really hear about is changes in chromatin structure. So I thought, Aha, here, I can throw this in for some time, sis, perhaps, and give everyone something to take away from this lecture. So chromatin. Anyone here hear about chromatin recently? Maybe a little bit fantastic. So this is a close up of a cell. The red on the outside is the outline. That's the nuclear envelope with the lamina. The blue is going to be our nucleolus, and the rest of it is the nucleus. And the green and the gray, hopefully you can see that color. That's what the chromatin is. That's your actual DNA, and we differentiate between euchromatin and heterochromatin. Reason that's important is the euchromatin is the stuff you're actually using on a daily basis. So if you look at the picture on the bottom, you see that it's sort of not so compacted, right? It looks more like Christmas lights. You get a little bit of a tangle, and then you have a strand and a tangle and a strand. And the reason it's not entangled is because proteins and such can get in there. Use that DNA to process it, to make real proteins, right? Heterochromatin, on the other hand, is very condensed. It is protected. It is smashed together. You're not using that DNA, and you're not using it for good reason. Okay, so why do we do this? Well, there's a lot of things in your DNA you don't want used transposons, satellite sequences. These are really, really malignant to your DNA. You want to keep them tightly bound down. They're sort of a remnant of. Of where we came on just through evolution. We want to keep them contained. When they get loose, they lead to cancer, so we don't want them getting loose. The second thing is that it limits the repertoire of something, a cell that's already been differentiated. So for example, you take a cell that's a nothing cell turns into a kidney cell. Well, you don't want expressing the proteins of a brain cell or a different type of cell. So that information is packed densely in your heterochromatin. We don't want that information getting out as well. When it's densely packed, you have less DNA damage, and you protect it against oxidative stress. So having heterochromatin contained is extremely important, and when you sort of lose control of it. You lose genomic instability, and of course, this leads to advanced aging. How do we control it? And I promise it won't all be as detailed as this. I just kind of fall in love with heterochromatin recently. So here it is. So we control it with something called the heterochromatin protein one, right? And it's actually a family of proteins, alpha, beta or live in your heterochromatin area. Gamma lives in your euchromatin. Not really all that important. What is really cool is the way that this is sort of built and how it functions. So each protein, if you can see on the top right, is a single piece with two domains and then a linker the top domain. See if I can that thing the top domain looks at the circle allows it to stick to another one of its friends, so it heterodomerizes, right? So it works in conjunction of two at a time. The bottom piece looks like a claw. See the claw? That thing recognizes methylation groups on your histones, and it has to be a special trimethylation on specific histone threes. So what it does is, when these two proteins come together, it acts like a clothespin, and the clothespin actually draws your histones together, and this is what compresses your DNA and keeps your heterochromatin nice and tight.
So what happens when you age? Two bad things in this category, number one, because of epigenetics, you are less likely to have trimethylation at histone three, so there's less things for these little grabber proteins to grab onto. Secondly, the HP one protein is less produced, so there's less grabbers. So because of these two things, your heterochromatin falls apart. So all of the bad things that I mentioned earlier are more likely to occur, right? The good news is we can actually fix a lot of this stuff, which is why I hate to always sound negative at the end. We fix it. But this, there's lots of models of aging, or theories of aging, and this one is called the blossom heterochromatin model of aging, and it's just one of a zillion. Okay, moving on, mitochondria. This is tenet two, and I promise the most of these tenets will not be as lengthy. So what happens to your mitochondria? Lots of bad things happen to your mitochondria. We're having this conversation at lunch. There are seven categories in which things go awry. Structure. Your mitochondria fall apart. The DNA falls apart. Mitochondrial dynamics. Your mitochondria fizz. They fusion, make more. That's mitochondrial biogenesis. You also recycle them. That's mitophagy. Your electron transport chain doesn't work as well because you don't make the sun units cardio stasis, just like in the rest of your cells, true in your mitochondria. You're sure two, ones, three, four and five live in your mitochondria. They fell over time, as well as micronutrient deficiencies in your mitochondria. The biggest one, of course, is NAD. Just as a random aside, I thought I would pick one bit of structure that most people are not familiar with. So again, everyone gets to learn something. This is the mitochondrial permeability transition core. If you are a true geek, you've heard of this. That's sort of a self identifying factor. So if you look at a mitochondria, I'm a geek, so it's okay. If you look at mitochondria, it is a standard organelle, right? And it has a lipid bilayer. The outer layer actually comes from our cells. The inner layer comes from a different type of cell, because we inherited mitochondria. We actually brought them in. We engulfed them many, many years ago. So the proteins or the lipids in the inner layer are different than the lipids in the outer layer. Anyway, inside, in the matrix, is where the toxic menu of all the biochemicals are from the Krebs cycle, pieces of subunits, et cetera, et cetera. And normally speaking, the inside of the mitochondria is separate than the rest of your cell. And it's separate for a good reason, because this stuff is toxic. It's like little nuclear reactors in there. There is, however, this pore, and this pore goes from the inside to the outside, and when you are young, it's nice and closed every now and then it sort of flickers, opens up every now and but we don't really know why. But in general, when you're alone, inside and outside are very well contained when you get older. However, this fails, it opens up a lot. We think, we don't know. We think that it's due to increase in free radicals and an increase in the calcium in the matrix of the mitochondria. But what happens when it opens bad things happen, right? So things that are supposed to the outside come in and vice versa. So fluid comes in and it causes edema in the mitochondria, and it destroys the electron transport chain, so you're not making energy as well. All the toxic stuff on the inside flows out, NAD flows up. The thigh ion flows out, and the most important thing that flows out is something called cytochrome c. This is part of your electron transport chain, and when it flows out to the rest of the cell, it's a signal for absolute cellular apoptosis. So if you can control this pore, you can actually control if a cell lives or dies under stress. And thanks to Leslie, I can tell you that spermidine is one of the agents that controls the support. So again, very important things to think about aging pathways 10 and three. I have four big pathways here. Obviously I'm not going to talk about all four. There are these seven millimeters, which we'll talk about in a second. There's the amp kinase pathway and the mTOR pathway. These are the pathways that measure how much energy you have and respond accordingly. And then I put the circadian pathways in there recently, because they control up to 40% of all of your genome. But we're just briefly going to talk about sirtuins. Sirtuins are histone deacetylase agents. Not that anyone really needs to know that, but what they do do is they control all cellular homeostasis. They are shortened around the cell. One, six and seven live in the nucleus, 345, as I said, live in the mitochondria. You start becoming sirtuin deficient by the time you're 43 is actually a little bit sooner they think that we start losing that by the time you're 35 this is when real agent kicks in. This is my laundry list of things that they do, and the list is just infinitely long. So I took the big ones so they sense energy. They monitor your metabolism, telomerase activity, gene expression, blah blah blah circadian rhythms is huge. In this one, people always say, why can't I sleep? And you go to sleep, experts and like, oh, turn your light off. You know, don't look at your computer. Blah, blah, blah, blah, blah, Oh, no. This is all biochemical. You make two proteins that turn on and two proteins that turn off sleep. And if you don't make those, I don't care how many, like blue lights you have on or off. You're not sleeping. Life is biochemical, okay, but we're going to focus quickly on sir. Two and 713, and six, historically, are associated with longevity. Seven is my new pet project, because it's associated with heterochromatin that I obsessed about a few minutes ago. It lives in the nucleus and the nucleolus the only one that does that, and it does two important things for your DNA. Number one, it actually tethers the heterochromatin to the nuclear envelope, so it maintains nuclear structure, and it also organizes DNA repair mechanisms. And with all of the other ones, it declines with age. It's NAD dependent. So you really need to think about, when you create your protocol, worrying about sirtuin seven, tenant four, quality control. This is the idea that you have a factory. Things are broken, you must fix them. So this is DNA repair mechanisms. This is proteostasis, and this is autophagy. I'm just going to talk a brief minute here about DNA repair mechanisms because every day, every cell, you have 10 to the fifth errors. Think about that, 10 to the fifth errors per cell per day, that is a ton Your body knows this. It's pretty smart. So it has two major mechanisms to fix single stranded errors and two major mechanisms for double stranded and then there's mismatches of sort of its own category, right? But these mechanisms, of course, fail with age. You have more DNA damage. With age, without more likelihood of sene cancer, of the single stranded base excision is more common, but nucleotide is the one I wanted to just briefly mention, because this is why you get skin cancer. UV radiation literally melts your DNA together, specifically the thymine residues. That's not the point. It melted together in something called cyclobutane dimers, and you could measure this. So people say, how much time you spend in the sun, like not a whole lot. The good news is there are drugs and chemicals that you can repair this faster, and you can reduce the incidence of it, not just lotions and such. There's actually biochemicals you can put in your body, and that's part of the protocol. But the important thing is to know what you what you're getting when you're out in the sun. Okay? Immune System. This is 10 at five. We're just going to do this really briefly, because I could talk about this one for absolute hours. Your immune system does two essential things, and it does it via two different mechanisms, right? You've got your innate and your adaptive mechanisms. What's important is what it does, does all of two things. One, it protects you from the outside world, and two, it monitors and gets rid of your own cells that have gone awry. That's it. That's all it does. So when it doesn't work, what happens? Number one, ignore the fact that that's not completely blended. Number one, you're more likely to get disease if you can't fight infection, right? That's it's a primary job. You're going to have more infections. And we see this. People in nursing homes are always getting urinary tract infections or pneumonia or et cetera. Two, increased risk of malignancy. Why? Because your job is to clean out your bad cells. If you can't clean them out, you're going to get cancer. That's just what happens. Three all the infections that you have in your body, they're sort of tucked away. The latent infections are going to be reactivated, tuberculosis, shingles, all of those things. They come back because you can't control them anymore. And maybe the most important, while. This is systemic inflammation. We all know that this becomes inflammation over time that leads again to cancer, cellular dysfunction, blah, blah, blah, blah, blah,
clearly a big problem. All right, individual cell requirements. This is a huge category, so we're just going to be brief here. And this is the idea that all cells need to be treated slightly differently, senescent cells. We've heard about that a bit. These are cells that have gone awry. People call them zombie cells. I think of them as fat old man cells, because if you've ever been to a company, there's like the fat guy in the corner who's been there forever, kind of globular. Just exudes negativity that is a senescent cell. Unless you guys are listening to me, that's a good sign, right? And senescent cells exude something called the exist something called the SASP which is an inflammatory set of cytokinins and chemokines. And that's like the old grumpy guy, right? He's in there just whining and whining and whining, and eventually everyone around him is going to be equally as negative. That's what senescent cells do. That's paracrine influence. The other end of the spectrum, of course, are stem cells. We want to take care of our stem cells as much as possible, right? There's a whole way of doing that. Again, too much for this lecture, waste management. This is the last tenant, so we're almost there. In case you guys are bored, in this category, you have to take out the trash. And in this world, most of the trash is glucose issues. And then here's your glass accumulation of lipofusion glucose is key. Why? Because glucose and other reducing sugars bond with proteins under certain conditions, ie oxidizing and with metal catalysts to create something called an age. This is my favorite acronym, because AG, es cause you to age. Thank you, everybody. Yes. What the other key thing is, most, if not all, diseases of aging have to do with age. So if you can minimize this, then you can reduce relative risk of all disease. How does this happen? Well, in a non enzymatic process, it's six or seven steps, depending on how you count them. And this is important, it's non enzymatic happens all by itself. First three steps are reversible, and that's important because that's where we put our therapies in. The second steps are non reversible, so that's important, right? But these things sort of rearrange, and they become ages, and there's 20 of them, and they do horrible things around yourself. But we're going to take one step backwards and say, well, is glucose really that bad. Everyone's like, on a low glucose diet, the answer is, glucose is bad. However, fructose is 10 times as bad. So everyone that's like, you've heard these people that like, run only for fruit diets, that's like, the worst thing in the world, fructose is worse. And ribose, it turns out, is 500 times more glycosylating than glucose. So by relative standards, glucose is actually not that terrible. So What do agds do? Why do they so bad? Three basic things. Number one, molecules work proteins, especially by three dimensional structure. As soon as you change that three dimensional structure, it doesn't work anymore. So you've spent all this time and energy your cell has made this perfectly beautiful protein, and it's got its little chaperone protein, and it's off to do its job well, now it gets glycated and it's no good. So you wonder why diabetics have failed systems. It's because everything is glycated, and we measure it in terms of hemoglobin, A, 1c, but there's one molecule that we are measuring, and in fact, all of them are getting glycated. So think of yourself as getting slowly caramelized over the course of time. The next thing that they do is they cause proteins to stick together. They cause this thing called cross linking, right? So self cross linking is completely normal, and we need this is not that type of cross linking. This is bad cross linking. And the best example is collagen. If you take a cloth napkin and you put a drop of superglue in it, and you slide it around and break in all the collagen, that's what it does in your body. This is why your skin droops. This is why your bone is fragile. This is why you have cardiovascular which is why you have congestive heart failure without coronary disease. And then lastly, they're very inflammatory. All right, so if you accept that these are the seven tenants of aging, rather than the hallmarks. They're very organized, and it has to be in this order. Why? Because I rate them. Every agent that someone has said is good for you or not good for you. I spent a lot of time reading about it. And in every tenant, right? It gets a number. So if it does absolutely nothing in that tenant, it gets a zero. If it does something in a test tube, in a culture, or it's just a really damn good idea, it gets one if there is non human evidence mammals, some people do quail research, some people do course research, there's good evidence and that, it gets a two. And if we've good, solid evidence, it's a three, right? So this is evidence based numerical system, and it's conservative, because if we hadn't tested something, we don't know if it does it or not, so numbers can only go up. Okay? Based on that, I have charts and charts and charts of numbers, right? I don't not saying you need to take all of these. What I'm saying is this is your New Encyclopedia of what does what you don't need to take a picture of this because it's on my website. You. I've waited 50 non pharmaceuticals and 10 pharmaceuticals. The pharmaceuticals are not on the on the website, because I don't people killing themselves by accident. I know everyone's here and see natural stuff and do yoga. I love drugs. I made what I do for a living, right? I give people drugs. I is what I do. So as a consequence, you go natural. You go not natural. It doesn't matter. They're all molecules. But this is the system to help you determine what to do. So this is someone's stereotypical longevity protocol. So now it will make sense, right? But the seven tenants at the top here are agents here, here's our numbers, and you can add them together. And the cool thing about that is it tells you how well you are addressing every aspect of agent. So if you looked at this, for example, you say, well, wow, 10 and two, we're doing really well. We're at 17 points, great. Maybe we've got enough agents in that category. We were to add something, we'd go, Ah, this three's a little minimal. Next agent I'm going to add, I'm going to look for points in that category. So this is meant to be a simplified numerical algorithm for determining your longevity protocol. All right. So the only other thing I want to add on since my last slide is to think of longevity as the pyramid. There are things you do every day, there are things you do every week, last week, every month, et cetera and so forth. And it's designed after the horrible food thing that we learned in the fifth grade, at least in America. I don't know if they did it here or not, but that's up in the corner. Right? Foods that you take every day, you mask with the body, things that less frequently go at the top. So oral ages, this is what we just talked about, right, diet and exercise, fantastic breathing, fantastic light therapy, fantastic peptides. You can sort of, you know, move that around depending on how avidly you are into peptides. Every month I do have monthly exosome infusions. I do monthly senolytic infusions, all sorts of fun stuff. As you go further and further up the chart, obviously, sort of more interesting. And then my final thing is, I always put cryogenics at the top, because once you freeze your body, I think it's game over, like you get to do that once. Anyway, that is all. Thank
you so much, Sandy. No, no, no, we do have time for questions, so it's fantastic that you showed us the tenants. We will soon have another presentation on the hallmarks, so you'll be able to compare them. But let's take some questions for Dr Kaufman, anyone here in the back? I think that's Miranda Paul. If you could go all the way to the back, you
I'm Vivian, by the way.
I'm sorry that's a bit hard to see.
So talking a little bit about this last slide, I want to discuss a little bit about access. Because, for example, you said on the daily things, there's like, all the stuff that you take and they're very expensive, and red light therapy, if you're gonna do it every day, there's not that many options of how you can achieve that for the rights, the rights of technology. So what do you think is gonna write first, like, better technologies that are cheaper and more accessible, or like or like, or there are other things that everyone can be doing that are cheap enough, you know that like the access. So basically, it's like access to things versus price. There's a
very excellent question. So the answer is, diet and exercise always win, because they're the cheapest. It is super cheap to go outside, run down the block, right? Eating? Well, you could argue that you know it is or is not. In the molecular agent department, you just have to pick and choose. Some things are pennies a pill. Other things are dollars a pill. So for example, aloe vera, dirt cheap. Fantastic epigenetic modifier. It's full of ketones, does amazing things. It is dirt cheap versus, Oh say, ta 65 that's a, you know, dollar a pill spark against perfectly in the middle. Is that a good plug? In terms of light therapy, you know, you can pay a zillion dollars and go to spas. We have, like, the full light panels, etc. You know, I have a little two by two by one foot panel, a couple 100 bucks. You know, the more you use it, the cheaper it gets, by definition, and it just sort of depends. There's many things you can do, like, obviously, exercise are expensive, plasma plasmapheresis is expensive, but starting with simple agents, it can be extremely cheap. I mean, people do not care if they spend seven bucks at Starbucks, but tell them to take a pill for a quarter and they freak. I mean, like it's just, I think it's about establishing what's important to you as an individual, and going down that route, not sure that's what you want before.
Um. Um. Dr Elliott,
thank you very much for the talks. We've actually see it from that perspective. You mentioned them when we kind of got the pricing of things about exercise and obviously, without giving away your IP, I guess, in terms of kind of kind of the protocols you get people on, what are your big movers in the exercise world to help people kind of live longer and better and healthier?
Six, I'm sorry, with those big movers in terms of exercise protocols that you Oh, I'm not an exercise physiologist at all. I'm actually, I partner with a friend of mine who is an ex Olympic gymnast, and if you want to exercise, I send it to him. I run, I rock climb, I mountain climb, I swim, I fry my body in a catalyst suit. But everyone has to choose their own exercise, like you know, some people, everyone needs some form of resistance for muscle, and everyone needs some sort of cardiovascular what you do is on your own. Some people like to go salsa dancing. Some people live in the gym. I'm not going to dictate any of that. It's obviously, it's important, but we're all different.
Yes, the woman in front of Dr Elliot, are there
any likes, hello. Are there any supplements that you would recommend that really seem to work across the board for everyone when it comes
to anti aging. Oh, yeah. Oh, absolutely. So I caught it. So after the age of 40, I created this silly thing called the panacea. And the reason it's called the panacea is because the letters start to spell it out, and then it tapers off. And I'm like, good enough. So the panacea is paterosilbane, because it's one of the strongest sirtuin activators. You can change it up for resveratrol, as long as it's bioavailable, it's bioavailability, bio availability, excuse me, Resveratrol is very poor. So one of those two things, they're molecular cousins. Two is astaxanthin, because it's a free radical Scavenger. And there are odd people here that like are nodding their heads, I love astaxanthin. Three is some sort of NAD precursor. We're all NAD deficient by the time you're 40, so that's crucial. Four is some form of a bioavailable curcumin. I use something called meta curcumin. It's in a nanomyceae for just improved activity, but any sort of that sort of genre, because you need anti inflammatory. And then five on the list is carnosine. It's an extremely inexpensive dipeptide. It's a transglycosylating agents. So the combination of five things is the biggest bang for your buck. And I'll tell you that everyone loves it. After three months, people go, Oh, my God, I feel amazing. Now. What do I do when you write a dog? It is written in my book, on my website, it is everywhere. So if you Google, it is everyone asks. So if you go to Kaufman protocol.com, and you go to protocols, it'll say panacea. And there's a bunch. There's one for inflammatory. There's one if you have a sweet tooth that has a glycation issues, essentially. And if you want to create your own, all you have to do is identify which tenant to you is more important. If you're pre diabetic, for example, pick everything out of tenant seven. If your energy levels are low, pick everything out of tenant two. This is designed so that anyone can look at this list and go, oh yeah. These are the things that are important to me, because one size does not fit all.
I'm not sure we've got one time for one more question. Okay, any more questions? One over here? Zora bonamu, thank
you so much. Yes. So thanks so much for a great presentation. I've been following you for a long time, and I always love what you have to share, and I do read your books, and I I'm a supplement queen, so I tried, yeah, I've got the panacea going now. What is there anything new in your own personal regime that you discover? Because you're always on the cutting edge and learning about new, new, new, I don't want to say supplements, but new agents. So
my two new favorites, so dihydromerisitin, for heard of that one yet. Okay, so it's some Chinese vine tea. What dihydromuric does is it specifically upregulates sirtuin three in your mitochondria. And just by doing this, I'm convinced that you can change all of your lipid panel, because it's basically by selecting what type of fuel your mitochondria you're going to use, you will selectively, basically optimize your lipid panel, and you won't get hangovers, which is really kind of cool for anyone that drinks in the audience. No one here is going to admit it, so by up regulating the mitochondria after you drink, or if you take it all the time, you will not get a hangover, and you will not kill your mitochondria. So dihydromursidism on the drug side, I'm newly enamored with something called selvaps, and it is a Japanese FDA regulated medication for gastritis. But the cool thing about it. Is this actually a heat shock protein activator? So instead of sitting in the sauna for half an hour every day to activate your heat shock proteins, you can take this little pill, and it reduces all relative risk of neurologic disease. Because most neurologic disease, Alzheimer's, Parkinson's, etc, they're all proteinopathies. So there's an easy fix for you. So those are my two favorite newbies.
Fantastic. Thank you so much. A round of applause for Dr Sandra. Thank.