164: Young Blood Can Rejuvenate Old Brains with Dr. Tony Wyss-Coray

In this episode, we are joined by Dr. Tony Wyss-Coray to discuss his groundbreaking research on brain resilience and aging.

He explains how systemic factors, particularly proteins in the blood, influence cognitive function and the aging process.

The discussion covers the role of proteomics, machine learning, and the potential of parabiosis and plasma infusions in developing therapies for age-related diseases like Alzheimer's.

Dr. Wyss-Coray emphasizes the importance of understanding the biological markers of aging and resilience to create targeted interventions for healthier aging.

Learn more about Dr. Wyss-Coray:

https://brainresilience.stanford.edu/

https://www.verobioscience.com/

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Download Dr. Buck Joffrey's FREE ebook, Living Longer for Busy People: https://ru01tne2.pages.infusionsoft.net/?affiliate=0

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Transcript

Disclaimer: This transcript was generated by AI and may not be 100% accurate. If you notice any errors or corrections, please email us at phil@longevityroadmap.com.

  What was even more striking is if we just looked in the healthy people between younger and older people. There were very prominent changes, so age related changes in the composition of the blood, and we focused on protein measurements, and that's really the beginning of all this work that we did to try to understand the role of the blood.

Welcome everybody. This is Longevity Roadmap with Buck Joffrey and, uh, today got a really cool show. I love this one. Uh, it reminds me, um, if you remember this show, uh, called Silicon Valley, uh, which is just, I mean, if you haven't seen it, you gotta go back and watch it. It was like one of. Uh, one of the funniest shows, um, I've seen in a long time, uh, which is basically, you know, is sort of a, does this, uh, thing on, on Silicon Valley, kind of makes fun of it.

Like, you know, sort of the oddities of the individuals there and stuff like that. One of the premises was that, um, there was, uh, I guess, you know, one of these billionaires who walked around with his, um. His blood donor, like a young man basically who, who basically would do transfusions with, uh, to, to get his young blood in his body.

Well, as it turns out, uh, some of that stuff is not, is not, uh, uh, just a, a joke. It's actually kind of real. And so in this show we're gonna talk about, you know, the science behind. Essentially Parabiosis is what that is called. This isn't necessarily entirely about Parabiosis, although we do reference it, but it does talk about the real data behind this kind of phenomena of, you know, people having older blood versus younger blood blood that is diseased with, uh, Alzheimer's disease blood that is, uh, from, uh, someone who is older, who is completely full intact, and the differences and the potential that creates.

For therapeutic intervention. So, um, anyway, fascinating show. Uh, and we will have that conversation right after these messages. Hey, longevity enthusiast. It's time to take it to the next level. I've been fine tuning my longevity regimen for years, and I look better and feel better than I did a decade ago.

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That's longevity roadmap.com. Welcome back to Longevity Roadmap. Today my guest is Dr. Tony Wyss-Coray. DH Chen, distinguished Professor of Neurology and Neurological Sciences at Stanford, and director of the Phil and Penny Knight Initiative for Brain Resilience. He's one of the world's leading researchers on how systemic factors, particularly molecules circulating in your blood, govern the aging process in the brain.

His lab's ground making discovery that young blood can rejuvenate old brains. Help redefine aging as a reversible body-wide process. And as translational work has inspired a new generation of potential therapies to preserve cognition and extend health span. Welcome, uh, Tony. How are you? Thank you. Thanks for having me.

I'm good. How are you? I'm good. This is fascinating stuff. Um, but let's just jump right into it. Uh, you know, so your lab's early work showed that old mice exposed to young blood. Regained cognitive function. So what was the key difference you found between young and old blood that produced these kinds of results?

Yeah, it's a great question. And it really started actually with humans. So I, I trained as an immunologist and uh, was really interested in, um, understanding the immune system in the brain and, uh, started to work in models for neurodegenerative disease. Most, mostly Alzheimer's disease. And the frustrating part about studying the brain in humans is that we don't really have access to the tissue.

Um, right? Mm-hmm. We, we can do cognitive testing, we can do structural measurements, mri, and, and, and so forth. But it's, it's not really possible to get a biopsy except if you get spinal fluid. Maybe that's sort of a, you know, relatively close to the brain. So we told with the idea that we could potentially get blood samples from patients with Alzheimer's disease and healthy controls and find immune molecules that would differentiate the, the two groups or that would even allow us to.

Predict who gets the disease and who doesn't. And the reason why we wanted to do this with focus on the immune system is because people have, uh, been showing increasingly, uh, in, uh, you know, 10, 20 years ago that the immune system seems to have a role in the disease and there's this inflammation in the brain.

So that's actually how we started. We, it was very difficult at the time because most, uh, neurologists, so brain doctors did not collect blood from patients, um, because they thought this is a brain disease. But we got our hands on, uh, a couple hundred samples and. Did indeed find differences in proteins between healthy people and patients with, uh, Alzheimer's disease.

But what was even more striking is if we just looked in the healthy people between younger and older people, there were very prominent changes. So age related changes in the composition of the blood, and we focused on protein measurements and that's really, uh. Um, the beginning of all this work that we did to try to understand the role of the blood, the role of the blood in aging, because age is the key risk factor for Alzheimer's disease.

And then all these, uh, biomarker tests and organ aging and things that we did. So what we found is, again, that the composition of the blood change between younger people and older people. And the question was then, is this cause or effect?

Mm-hmm. Yeah. So, so you've turned to, uh, I guess, um, we can define this, but, uh, proteomics, right?

And, um, tell us what you're kind of looking at there. What, just so people have an understanding.

Yeah. So initially we focused on. Immune mediators. These are like hormone like substances, uh, that the immune system uses to communicate with each other. So we call them cytokines, chemokines, interferons. Um.

Tumor necrosis factor, TNF, uh, which we block with, uh, some very, um, uh, well-known drugs, um, to, to block inflammation in arthritis and things like that. Um, so we measure these types of proteins, but then over the years, um, more and more, uh, proteins became. Uh, detectable and we actually use now mostly companies that offer panels of proteins.

They measure, um, and they can now detect in just a drop of blood. They can detect thousands of proteins very reliably reproducibly. And this is really, um, generating sort of a. A revolution in the field that goes beyond genetics, because in genetics we could sequence our genome, our DNA blueprint, but now we can measure on top of that, we can measure proteins very reliably, and these proteins give us more information than just the genes.

So this is what's called proteomics.

What, what kind of proteins are, are they, are they largely related to the immune system or are they other types? No, they're not way

beyond. Um, mm-hmm. So it, and you know, one, one of the companies measures 10,000 proteins, so that's half the genome, if you will. Now there there's some caveats because proteins come in different forms, but even so, we can measure at least one form from half the genome, uh, half the proteins that are encoded in our genome.

And so they cover anything from transcription factors to structural proteins, hormone like proteins, cytokines, uh, immune factors, but really anything, um. These, um, panels now cover any aspect of biology really. Um, you, you can, you can imagine.

So I, I would imagine that, you know, probably, um, you know, uh, machine learning and, and, uh, AI is really probably a big part of this.

So essentially trying to, I mean, I'm envisioning maybe, maybe I'm, maybe this is not accurate, but I'm envisioning creating, um, sort of fingerprints. You know, for different, uh, expressions.

Is that exactly, is that right? That, exactly that. So that's what people do now. And, um, most applications, uh, use what we call machine learning.

So this is not really sophisticated ai, but it basically tries to find, so let's say you have a disease. A person with a disease, you have a person who is healthy and then you measure a thousand proteins in, in, uh, all the individuals. And now what the machine learning tools are trying to find is, um, is there a protein that is different between the two groups?

And it will first rank the one that is the most different, and then it will take the next one and the next one and the next one. And so. You can imagine that maybe there's a dozen or sometimes 50 or several hundred proteins that are slightly different. If you take them all together, you get a pretty good model of what makes somebody or describe somebody with the disease compared to a person who is healthy.

Um. You know, I'm, I'm, I'm trying to tie this together with some of the things we, you know, we think of, we read about in, in longevity space right now, specifically, you know, what, why is it that these protein changes? And the parallel to me when I think about that is, you know, uh, changes to the epigenome, right?

Uh, changes to the expression of various genes. As we age, which we know it happens in part because of changes to the, uh, epigenome, is, is that kind of, uh, indirectly what we're in, uh, what we're measuring with the proteomes?

Absolutely. We are basically measuring the expression or the translation of the epigenome.

Now the next question is then of course, why does the epigenome change? And, you know, most aging researchers think, um, this is really, um, sort of just. A result of exposure of an organism to the elements, if you will. And I often compare it to a car, right? You have a car coming off the, um, you know about the lot and you know, they're all built with the same blueprint and should, should all be the same.

But you get sort of. Over age. Um, you know, the, the cars will start to break down in different parts in different cars, even from the same model, even from the same that were built on the same day. And this is, in a way, it's the result of exposure of that car to the elements, how you drive it, how, um. You know, how you treat it, how you, uh, service it, but also probably to some extent, to randomness, stochasticity, we call it.

Mm-hmm. And, um, and, and it seems in, in organisms such as in humans, you have sort of the same thing you have with age. Everything starts to deteriorate. And we don't think there is a, there's a program or there's a purpose in us. Disappearing except maybe that evolution needs us to reproduce and go to a next generation to make ever better models of ourselves, if you will,

in terms of, um, brain disease, then I would think that if you are coming up with a series of fingerprints, then you might in theory be able to predict like who's at higher risk.

Future brain disease is, is, is that, is that kind of what you're able to do now or,

absolutely. Yeah. So that's, and and that's really, um, a very exciting and, um, ever-growing field right now because of these tools that we can now reliably measure. Thousands of proteins, but at the same time there's also, um, sort of healthy aging cohorts or sometimes they were, uh, they were, um.

Developed or, or, um, funded to study heart disease or diabetes or whatever. Sure. And so now you have these cohorts with thousands or tens of thousands, sometimes hundreds of thousands of people. Most famously the UK Biobank, which is 600,000 people that are recruited into these studies. A blood sample is taken from them, their whole medical history, and then they're followed over decades.

Sometimes the UK Biobank has now 17 years follow up. You can now use these types of, uh, studies. For example, in the UK Biobank, we have, uh, data from 50,000 people, 3000 protein measurements at time zero. And then you have follow up over 17 years from all of these people. So you can now start to make models and you can say, okay, um, what are.

Differences in protein concentrations in people who will later develop Alzheimer's disease or who will develop, you know, kidney disease or heart disease and so forth. What are proteins to predict how long they live mortality? And people are, you know, working with this and playing with this. And it's, it's, it's really amazing.

And the other, uh, really. Terrific part about this is because we know these proteins, we know the name that makes up these models, right? We discover new biology and potentially new drug targets. So if you find a protein that is a very strong predictor of somebody having, you know, lung cancer. Then you might ask, what is the biology of that protein?

How does it cause lung cancer? And you can potentially then go into an animal model and see, can I model this? And, and, and I think it's really adding a, a completely new angle to how we study disease because we can now go from humans to animal models rather than the other way around how we often have done.

Um, how do you begin to. Disentangle correlation versus causation. In other words, we know that in, uh, somebody with a certain, um, uh, you know, somebody who's got Alzheimer's disease has a certain fingerprint. If proteins, how do you, how do you look at that and try to figure out, is it because they have Alzheimer's, that they have this fingerprint, or is the fingerprint.

The causation of the Alzheimer's.

Yeah, that is of course key. Now, it's not necessarily. Um, that important. If you just want to monitor somebody, right? Or if you want to see whether a drug has an effect, a correlate could still be fine. Uh, but for drug development, uh, to nominate something as a target, you want to know causation and the way you can do that.

There, there's different ways. One, sort of not the strongest way is again, to look in people. When they're healthy way before they develop a disease, right? So if something changes very early, it's unlikely going to be just. Um, a reflection of a disease process, but it may be more likely a driver, but still no guarantee.

Uh, what people can do with genetics. If you know the, the genome of people, uh, you can do something that, um, people call, uh, interference where you, you use sort of a genetic tool from large, uh, population based genetic studies to see whether. If you then randomize, uh, the proteins, whether they might be causative or not, uh, it's a complicated model that people now increasingly use.

Mendelian randomization is the term. Um. That, that gives you even more confidence that something might be causative. But then ultimately, um, you want to model it either in, you know, cell culture models, animal models, and then finally you need to test it with a drug that targets whatever you decided might be a cause and prove that it has an effect on the disease in a clinical trial.

You know, it, it makes me think though, in terms of, you know, how you attack this kind of stuff. Uh, it makes me think of, um, that, that show Silicon Valley with, uh, when, when they do pair, you know, you have this guy, this older, uh, uh, billionaire who brings around his young, uh, young, you know, his blood donor basically to do parabiosis, right?

He's essentially infusing. Uh, the younger man's blood into himself. I mean, this, this has a lot of that flavor. Is, is there, is there data behind Parabiosis in and itself that suggests that might be a, a legitimate approach to this? Because now you're not dealing with, um, specific targets per se. You're dealing with, you know, just.

Creating a a a new profile of proteomics for an individual.

Yeah, that's right. Yeah. So in, in, in mice, um, where, you know, we do parabiosis, we don't do it in humans. So parabiosis is really where you join the circulate, the, the circulation of two different animals. And it was actually invented more than a hundred years ago.

It led to the discovery of, for example, leptin. This factor that, uh, is a mediator of obesity. Sex hormones were described with this because you can, you know, sort of induce sex differences from males to females. Um. But what we've found and and many others in the field now, is that indeed there are factors in the circulation that can change the aging process.

So in other words, as you said earlier, blood from young mice, and specifically the liquid part of the blood, not the cells. We don't need the cells. The plasma. Right? The plasma. Plasma. The plasma. Plasma. Right. Yeah. If we transfer that, uh, from young mice into old, we can rejuvenate many different cell types.

And with rejuvenation we mean they look at a molecular and functional level, more like young cells. That's the term people usually use for it. Rejuvenation. And we can do this in very unbiased ways. So we treat the mice and then we take all the cells out and we profile them and we can show they look now younger.

What we also discovered is different cells respond in different ways. Some benefit much more. Stem cells, for example, benefit more from young blood. Um, specifically the stem cells of the immune system. Um. Liver cells also are very responsive, uh, blood vessel cells, endothelial cells, and then others show much less changes.

Um, and it may be in part how well these cells have access to the blood, uh, but also, uh, the receptors that mediate some of these factors, effects and so forth. But then the quick question is, how does that translate to humans? Right?

Yeah. Yeah, because the idea, you know, in my mind is, well, why, why can't we just, you know, why can't we.

Uh, do plasma infusions into, you know, older people. Uh, we, we can,

we can, yeah. And that's indeed what we did. So we, we started a company, alca has a while ago and worked together with one of the biggest plasma companies in the world, Grifols. They approached this actually from the angle of there, there are these proteins in Alzheimer's disease that accumulate, um, called amyloid.

Mm-hmm. And they said, what, what if we. Removed the blood from patients with Alzheimer's disease, would that bring out the amyloid from the brain sort of as a sink? And there were some studies in mice that supported that, that uh, if you removed the blood. And replaced it with, um, you know, just albumin, which is the main protein in, in, in mm-hmm.

Our blood. Uh, would that lead to an improvement in these people? And they did indeed find they had, uh, several hundred people. That they benefited overall from this treatment. And, uh, with our company of our startup, we then systematically look at what parts of the plasma might potentially be beneficial.

So these companies collect plasma from thousands of donors. They fractionated into different products that, um, are, uh, used in the hospital. That you as a surgeon have used all the time, right?

Yeah, yeah.

Sure. Um, but also, for example, antibodies, what we call IVIG is one of the main products that now everybody who has a transplant needs on a regular basis.

Um, so we tested these fractions and found some of them are really very beneficial. To slow down or reverse this aging process in mice. And so we used then some of these fractions under phase two trials in Alzheimer's and Parkinson's disease. And, um, that showed they're safe. And we had some positive signs that, you know, people may, uh, benefit from this.

So the next step is to run large phase three trials and mm-hmm. Um, you know, that requires substantial financial, financial resources and. I hope we're, we are still going in that direction, but, um, that's, you know, that, that takes some time. But overall, I think the field, um, agrees that there are beneficial factors in young blood that can slow or reverse aging and there detrimental factors in old blood.

So some people now pursue this idea of what is called, um, uh, plasmapheresis, um, mm-hmm. Uh, and or TPE. And, uh, just remove the old factors, uh, because that could also be helpful in itself. And then typically you give back. Um. Uh, small amounts of albumin to just make up the, the blood volume. And by the way, that albumin always comes from young donors because the, the donor population in these, uh, big collection centers is usually younger people.

Uh, and then also usually they have to give antibodies so that you're not immunodeficient, but there's now companies that offer this actually as a service.

But the, the albumin only approach seems to be like, you're essentially subtracting, but you're not really adding. Right. Because you've got That's right.

Yeah. You're missing, you're, you're missing all of those potential, uh, beneficial, yeah. Uh, proteins. Yeah. So why, why would they do that? Why, why not? Just, why not just, you know, supply full plasma, full plasma. Yeah.

Yeah, I could do that too. Um, it's. Probably a bit more expensive and in the, in the manufacturing process, that plasma is used for other products, uh, most importantly making antibodies.

Uh, but, uh, it's also important to, to notice that. The albumin fraction contains a lot of other factors, and con contains actually growth factors because albumin is the sponge that, uh, actually carries a lot of factors around. So even if you just have an albumin infusion, it contains other factors that might be beneficial.

What kinds of other next generation treatments, uh, are kind of emerging from this work? You know, biologics, small molecules, other approaches?

Yeah. What's been a bit frustrating from the research side is to figure out what are the key factors, um, because you could imagine, well, what if we just identify what these factors are that are beneficial?

And, uh, we make them synthetically and we have a drug. Right. But it turns out that it's many different factors and that makes sense. If you think about it, you know, different cells in our body have different requirements, um, and it has been very hard to figure out. What are the key critical ones? Because you need to do this in a living organism as soon as you take it out into a dish.

The cells have different requirements and they, we can culture them often, but if we can't really test whether that affects aging. Most cells, if you put them in culture, they have a very useful. Signature. They basically look like, almost like embryonic cells or like cancer cells. But we can't mimic age in a dish.

So we need really these animal models to test aging effects and to test, um, the effects on whole organ physiology.

Uh, you focus, um, you focus on the brain for the most part. Obviously, these things are applicable to. Entire body. But when you look at, um, what different differentiates people who maintain cognitive sharpness late in life versus those who decline early.

Do you, do you get a sense, I know you're, you're measuring a lot of proteins, but do you, do you have a sense for what kind of patterns or what, what kinds of things that determine those who. Have these two different pathways of either, you know, not having mental, you know mm-hmm. Uh, decline versus those who do

Yeah.

Yeah. Sort of resilience, right? Yeah. Mm-hmm. So we did studies to look specifically at, um, so one of was actually with, with, um, with spinal fluid where we had access to three and a half thousand people, spinal fluid. And these people had different levels of cognition. And again, we had follow up over 15 years.

So we can look, uh, based on the composition of the spinal fluid, who is at risk to declining cognitively, who is gonna be resilient. And we looked specifically independent of the classic pathology of Alzheimer's disease. We were interested in finding something new. And what turned out is that. Proteins that make up synapses were the best predictors.

And we, we came up with a ratio of just two proteins, which are a very strong predictor whether people are resilient or will decline. Um, now, you know, you can't go out there and now collect everybody's spinal fluid that's very invasive. Mm-hmm. Yeah. Um, but we're trying to find similar signatures in the blood and we found the signatures that, again, was made up with, uh, proteins that are involved in making synapses.

Uh, that, uh, seem to be a good predictor. Not as strong as the one from the spinal fluid, but I think it's a matter of time until we get this. And so we started a new company, Vero, um, that is trying to commercialize some of these, uh, discoveries that allow us to estimate the age of an organ, the age of your brain, the age of your kidney or heart.

Mm-hmm. And these are very good predictor, whether you will get. A disease of that organ. So in other words, if, if your heart shows, um, to be older than you actually are, you're much more likely to have, um, atrial fibrillation or a heart attack. Same for the brain. Um, and interestingly, the brain age is actually the best predictor for longevity.

So those people. Out of the 50,000 that we measured also in the uk Biobank, those with the youngest brains live the longest. And uh, those with the youngest immune system and the brain have the best predictor of longevity. People with the oldest brains live the shortest and have a high chance of developing Alzheimer's disease.

So this is still research material right now, but we want to translate it to. Um, really to, uh, a clinical setting, uh, in the next, in the coming years. Work very closely with clinician to interpret the findings, right? I mean, there's lots of companies out there that, you know, you can do a test and then it says, okay, you're five years older or five years younger, and that's it.

Yeah, yeah. Nobody tells you what to do with it. So I think what we really need is, first of all, we need detailed information, not about your age in general. But about the age of your organs or the age of your cells. Yeah. So that we can have specific interventions that are tailored to that organ and what we already know in standard clinical practice.

What would you do if you, if it shows you are at high risk to have heart disease, um, or high risk to get, you know, lung disease, uh, what would you do? And so working with. The clinicians, um, and giving them this new tool that you are at risk because it seems your organ is accelerate, shows accelerated aging, um, that hopefully will sort of, uh, trans, you know, transform how we, um, really assess, uh, health, um, and, and disease in the future.

When you look at those cohorts, so those different fingerprints that are le leading to different outcomes, do you, um, do you have access to, you know, understand what, if, if various lifestyle differences, uh, led to those different fingerprints, is that something that you guys look at?

Yes, absolutely. I mean, the, the, there, there's a bit of a caveat because most of these lifestyle factors are self-reported.

Sure. So they're not as well controlled, but some are better than others. Like, for example, uh, postmenopausal, uh, uh, um, estrogen replacement. You know, if people report I, I I I took estrogen replacement, they probably know. Um, yeah. And so there you get, uh, actually very good, um, data, I think where you can show that, uh, some of the organs are clearly younger with estrogen replacement.

Interesting. We also find, you know, people who eat. Um, fish, um, you know, they have younger organs. People who smoke have older organs. Excessive alcohol is associated with older organs. So there, there, there is growing data from these, you know, population based studies. And then I think the next stage is really doing controlled trials where, you know, people have an intervention and you have before and after, and you measure it with these new tools.

Show that you have now an indicator first, a predictor, but then also a response to your intervention.

You mentioned estrogen. I'm just curious, I mean, did testosterone, uh, in, in men, uh,

did you have that data? We didn't have the, we didn't have that data. Okay. Um, it might be in there, but often even in 50,000 people, the numbers might be too small and then, you know, the statistics is not really holding up.

Sure, sure.

Well, um, you, you now lead this, um, uh, Phil and Penny Knight initiative for, uh, brain Resilience at Stanford. What's the broader mission of the program and, and how does it fit into the future of aging research?

Yeah, that's really an incredible opportunity and, you know, this generous donation that we got, um, we basically, uh, have these funds to support research around, um.

Trying to understand why some people, you know, live to 90 years or even a hundred and their brains are completely intact and they just function perfectly fine. Mm-hmm. And then other people, um, you know, show these early cognitive changes and develop Alzheimer's disease and really get to understand what are the mechanisms behind that.

Um. Support, um, studies at all levels. I mean, it's a Stanford focused initiative, but we also want to understand just how. Does the human brain change with age, for example, we don't have really molecular information how the brain changes. So we're, we have, uh, large, um, sort of profiling efforts underway where we, uh, have people, uh, who died.

We got their brains from 20 to a hundred, and we try to understand. How does the cha the brain change at a molecular level? And then look at people who were clinically healthy, clinically normal at old age compared to those who had Alzheimer's disease or other degenerative diseases. And the goal is really to build sort of, um, an atlas of how the brain ages and becomes susceptible or resilient and derive new, uh, therapeutic targets that.

If you understood why somebody is resilient, what is the key why they didn't get the disease if they're a hundred years old? Yeah. If you could figure that out, you could potentially develop a drug and give this to every one of us, right? That, that we could all experience this resilience. Yeah.

Fascinating stuff.

Uh, Tony, I do appreciate you being on the show today. And, you know, if people are just curious about, you know, the, the work you're doing or some of these companies, what, what, what resources should we turn to?

Um, so the Knight Initiative has a website. Um, um, Vero has also a website, uh, Vero Biosciences. Yeah.

And yeah, just stay tuned on, uh, the Yeah, absolutely. The papers that come out. Yeah. Thank you so much for your interest. Yeah. Yeah. Thank you, appreci.

Thanks for listening. A quick reminder that while I am in fact a surgeon, nothing I say should be construed as medical advice. Now, make sure to include your physician in any medical decisions you make, and also, if you're enjoying the show, please make sure to show your support with the like, share, or subscribe.