Transcript
Speaker: We used to be the original palm readers. You know, you can say splinter hemorrhages. If somebody has splinter hemorrhages, guess what? There's something wrong with their heart. If they have bruising, unintentional bruising, something can be wrong with their hematology. Now, some really cool research is showing that there could be these zombie cells that live on our skin that can actually get into your lungs and heart. So it's a bi-directional street and it's a very much a living organ.
Speaker: This is the Home of Health Spam podcast, where we profile health and wellness role models, sharing their stories and the tools, practices, and routines they use to live a lively life.
Speaker: Dr. Sayac, welcome to the Home of Health Spam podcast. Thank you for having me It is a conversation I've been looking forward to for a while. And before we get into why I've been looking forward to it, how would you describe yourself?
Speaker: I describe myself as a curious researcher, father, builder, who loves turning deep, learning ideas into meaningful impact and conversations. And everything I do is centered about growth, purpose, and the desire to leave an lasting impact and really change the world for the better.
Speaker: Fantastic. Yeah. And we'll talk about all you've done to date and are doing to to do exactly that. You know I grew up in a household with a pediatric cardiologist and a pediatric hematologist where there was always a fight of what's more important, the heart or the blood, right? Going back and forth. But today we're talking about our largest organ, our skin.
Speaker: And i think there is a misconception with a lot of people of, oh, that's vanity where no, I mean, it it is a marker of health. People who look younger are healthier and it's hard to tell direction, but as someone who goes deep into the science of longevity, as well as in into the science of skin and and dermatology, what do you see as that connection there? Yeah.
Speaker: Yeah, I love i mean, the first of all, I love that you said your parents were both, you know, hematology, cardiology. I always tell to my patients, I'm like, listen, skin always loses. And for one main reason, you know I'm like, yes, it's the biggest organ, but two, we can almost always fix your skin, you know, whereas with the heart, it's hard, you know, sometimes the damage is permanent.
Speaker: Whereas with the skin, we can generally fix it. We used to think that with sun damage, that's irreversible. We call it a permanent permanent chemical, permanent damage. But some cool research has really come out showing that even that's not true.
Speaker: I love that you're also saying that it's people think of it as a vanity organ. When you're you know when you go to the gym, Nobody questions it. Nobody says, like, oh, you're just trying to look vain and have big muscles. They they know there's also a big health component.
Speaker: um But whereas with the skin, we don't have that. People just assume, many, many people assume that if you've got if you want to take care of your skin, that you're just vain. And there's some really amazing research showing that the opposite is actually true, that the signal not only can tell us about your internals,
Speaker: We used to be the original palm readers, you know, and and you know you can say splinter hemorrhages. If somebody has splinter hemorrhages, guess what? There's something wrong with their heart. If they have bruising, unintentional bruising, something can be wrong with their hematology.
Speaker: So that was the original. We used to think it was a one-way mirror, but now some really cool research is showing that there there could be these zombie cells that live on our skin that can actually get into your lungs and heart. So it's a bi-directional street and it's a very much a living organ.
Speaker: And treating your skin properly, not just surface. You know, there's a lot of products that are very, very surface oriented, but actually truly healing your skin can actually also impact your longevity.
Speaker: Okay. And that's what I'm really excited to to dive into. So I think some of our listeners know I've had multiple malignant melanoma aggressive. I was a distance open water swimmer, lots of time outside.
Speaker: um And there seems to be some disagreement on is it sun exposure? Is it other things causing this damage? And even my parents kind of debate and go back and forth on what's in my mom's had her own skin cancer issues.
Speaker: Where does that come out? Because on one side, the research I've seen, that says, hey, of all the things you can do, the one that is unequivocal is sunscreen is going to help protect your skin. like that's That's the one thing that has been true.
Speaker: ah But are we risking something on vitamin D on the other side of that? I love that you asked that. So the the jury's still sort of out. There is a study that just came out. There's all the studies up until now suggest that sunscreen on itself is not enough to stop vitamin D production.
Speaker: Okay. There was a study that just came out recently, sort of said the opposite and said, ah, no, no, no. All of those previous studies were SPF 15. We wanted to see if it's SPF 30, what ends up happening? And their argument was that, yes, it can slow down production. But There were design flaws in that study. So that's always the issue. You know, when you talk in Instagram, to TikTok, all of that stuff, it's very surface level. So it's like reading that, you know, the article in the news, it's like, you know, the Mars is falling on earth. You're like, oh my God, we got to go in bunkers when Mars is falling on top of us. And then you find out, no, no, no, Mars is like,
Speaker: moving one millimeter closer to Earth every 200 years so that in a billion years, Mars will hit Earth. you know So you're like, oh, like that doesn't make a difference to me. So that's the issue. People read the headlines and and that the way news information is designed is you got to sort of grab them in a second. So if I tell you like, listen, Andrew, like,
Speaker: it doesn't really make a difference. You're you're not gonna tune in, but if I say vitamin d could be impacted by your sunscreen and your doctor is lying to you, you're gonna listen, you know what I mean? And then I'll say, well, no, actually, if we look at the study, and you might tune out.
Speaker: So the study that I was talking about showed that it was a five nanomole difference, okay, per liter. with the sunscreen versus without. And if you look at it, the baseline is 50 nanomoles per liter. So it's at best a 10% reduction. And if you look at the study population that they looked at, most of them were actually already like very close to being vitamin D deficient.
Speaker: That's the main thing. In our society right now, I'm seeing at least 30% of people are vitamin D deficient. When they come, we also run a testosterone clinic, male health, you know, overall HRT, even women's health.
Speaker: People come in, they're, well, I want testosterone, I want estrogen, I want progesterone. and I'm like, let's check your vitamin D levels first. And 30%, third, are deficient in it. So can sunscreen impact it? Yes, I think at best is maybe five, 10%.
Speaker: So it doesn't really, the biology doesn't, like if you see yourself getting a little bit of a tan, that is vitamin D production right then and there. So if you're wearing sunscreen, generally we think outdoor exposure here, arms, 15 minutes in midday sun, that's enough even if you have sunscreen or not. If you're wearing sunscreen, increase it to 17 minutes and you're good.
Speaker: Okay, yeah that that was gonna what I was going to ask for the practical. So for skin health, probably still put on the sunscreen, just get a little more time in the sun. Like take take a 20-minute walk after lunch and you'll probably be good.
Speaker: You got it. And and that's the thing. I think we are shifting. We used to say absolutely zero sun. You know, go or like especially someone like you, if you've had melanoma, I'm like zero sun. And to go back to your question, is it the only cause? we We are finding out now there are, it's like most things in life, it's multifactorial. There's no one thing.
Speaker: One of the analogies I used to say is like, you know, for guys, they say, if you're watching sports, I can give you the best goalie in the world. If you don't have other players on the field, it doesn't matter. You're going to lose, right? So your sunscreen really is the goalie. You know, if you don't have a goalie, you could have the best strikers, the best defenders. You're going to lose pretty much every game.
Speaker: for For women, I usually say, because, you know, not as many watch sports. I mean, if they watch sports, it's easy analogy. What I say is if you go to, the for example, the opera, you know, what what what made the opera special? Was it the singers? Was it the dancers? Was it the orchestra? Was it the environment?
Speaker: It's all of it, you know? So it's really all about, you know, for me, I hate looking into like what individual thing is. is It's all about stacking the right environment for you. And the reason I say that is we are finding that complete avoidance of the sun goes beyond vitamin D. It's not just vitamin D. It's nitric oxide. It's endorphins. It's, you know, synthesizing your diurnal stuff.
Speaker: People who are not exposed at all in the sun are actually having much higher rates of cancers. They're having higher rates of heart disease and higher rates of depression. That's why we call it seasonal affective disorder. Sad, in the winter, things go awry, right? So we need some sun, but it needs to be, you know, not high UV index. You do need to wear your sunscreen.
Speaker: We are getting in an era where you can actually track these things. There's new technologies that we can track the health of your mitochondrial DNA on your skin. We can test the ah oxidant pro-oxidant level with something called the PAOT test.
Speaker: So there are ways for us to sort of more safely say, okay, what is your risk? what's How do we mitigate that risk? Yeah. And I mean, a couple of things on that One of the the reasons my father and others had just been skeptical. It's, it's all sun damage is the amount of malignant melanoma you see in between toes or on your bottom on, on parts of skin that aren't in the sun. A prior podcast guests, unfortunately, this was a conversation after we stopped recording, had his own cancer and everything. He said, you know, they, they'd found marathon runners had higher than normal, uh,
Speaker: melanomas. um And so they assume, oh, it's because they're out in the sun too much. And then they they held that controlled and it like had absolutely nothing to do with the time in the sun. It was lack of blood flow to the skin, which I think makes it more susceptible maybe to those damaged cells reproducing, doing other things. I said, okay, well, that's actually really interesting because, you know, I would swim 25 kilometer races, which is back-to-back marathons. And No matter if I'm in Bermuda in the summer when it's a billion degrees, by the end of my swim, I'm cold because all the blood flow going to my organs. And my parents would comment on, wow, you were white as a sheet after a race because all your blood flow is going in. i said, well, if it is that, that makes a lot of sense why I got this because there have been many, many times in my life almost each week where I'm doing that to my body.
Speaker: And so, as you said, it's no single thing, but there are all these things at play. I absolutely agree with that. So whether it's blood flow or not, i mean, it's again, it's, you know, you also want to look at one study if it's repeatable. So sometimes you can get these things. We call it, there was a Harvard study where it showed like, I i forget which zodiac sign, but let's say Capricorns were much more likely to get bowel perforation. There were 200 times more likely to get bowel perforation, right?
Speaker: It ended up being that if you test, so your statistical significance, the you know, N95, 0.005, 95% confidence intervals, that means one in 20. But if you look at 20 random things, completely random, you're going to find one that's statistically significant. So that's why I'm like, we need to repeat these studies. Yeah. But I do agree, you know there are other things we're seeing. like you know We are seeing, there are evidence mostly in mice, but there are some emerging studies that diet plays a huge role. So again, is it the blood flow? Is it that you're running out and you don't have enough fuel to fuel these things?
Speaker: But really for melanoma, especially somebody that's had repeated melanoma like you, I would say genetics. Genetics is the biggest, biggest driver of anything. And it goes back to that validation component where you got it if you got this, we should I don't know if you've had yourself checked out,
Speaker: I do every three months. Yeah. Genetics, genetics is look at, think of it like height, you know, if like Shaquille O'Neal, basketball player, seven feet tall, he could have eaten popcorn, desserts and and whatever, you know, and he might've not gotten seven feet, but he would have still been six foot five, you know, he, so that's, you know, where you get two, three inches and it's same for for melanoma. If you have a gene mutation that's driving this,
Speaker: you're gonna be at an increased risk. Now, the goal is, well, how do we minimize minimize that risk while still keeping you you? Because you know if you stop swimming, you're probably gonna go into depression. This is you.
Speaker: So one, sunscreen, yes, you know there can be on the toes. Again, that's more more likely. Could it be vascular? Maybe. Could it be genetics? Maybe. But it's all a combination of things. And the sun is yet just yet another. We know it causes that DNA damage. So if you already have damaged DNA, we want to reduce that risk as much as possible. Like, you know, we know from tanning beds, one, one session. Now the newest data, we used to think it was like 40, 50%. Now it's like 200% increase, right?
Speaker: With a single session. Single session increases, right? So so that's that's kind of the the data that we're looking at. Doesn't mean, you know, never do it. No, but you have, like for the tanning beds, no, never, right? Sunscreen, same thing. If for you, that's the single best protection you can do with sunscreen, right?
Speaker: The problem is not, like people always look for problems. It goes back to that issue of like, they wanna be heard, they wanna be the experts. Like everybody's now an expert on Instagram. I'm like, one, look at their credentials. Like why is a chiropractor talking about putting sun in weird places? Like and there's, it's a trend. They're like, oh, expose this part of your body to the sun.
Speaker: I'm like, what's your credentials, man? What's the, like, what is going on? And then they always go back to the toxicity. Sunscreen is toxic. They're giving you this toxic stuff. Look, there's this one study that showed it in a Petri dish. I'm like, well, how does that apply to humans? Like, humans, yeah.
Speaker: Anyway, but it's it's it's sad. And there's so much misinformation. And because people are vain, of people are, I mean, it's what you show to the world. You know, it does tend to resonate a lot when people are talking about the skin and spreading misinformation.
Speaker: So you started off talking about there are things we can do for the skin, not just the service level, but truly caring for it, taking for care of it. And we started with sunscreen. But what are some of these other things that you recommend do with your patients and your clinic?
Speaker: So some of the best data right now is laser treatments on highly exposed areas. So neck, face, we know so now CO2 laser, there was a study, randomized control trial, first of its kind. We had tons of studies even before that. Dr. Fitzpatrick and his group in 2007 showed that ablative laser retrospectively looking at patients, 90% reduction in skin cancer when compared to matched controls.
Speaker: Study in 2021 out of Dayton, Ohio showed that um fractional laser, Forearms over three years, those that were treated also had a 90% reduction. This was a randomized control trial. So a landmark study.
Speaker: We've replicated that and we just published in Brazil, we had a med student present this data. Facial skin, we needed three sessions. After one session, we couldn't quite achieve 90. And it goes back to your blood vessels. So I do think there's something there. you know So facial skin, we needed three sessions to achieve that 90% rate over three years. So it wasn't enough with one and we need we needed it to go deeper as well. Is it every 12 months? So when you say three sessions, what was the frequency over that period?
Speaker: We generally do it every month. So we do, it we can stack it sort of thing. We did it every month, or every four to six weeks. And then after those three sessions, we were able to reduce future pre-cancer skin cancer by 90%. Could you give us a bit of a primer on on the different kinds of lasers? Cause there's ALO and MOXIE and BBL and yeah.
Speaker: Yeah, so there's, first of all, we call them ablative versus non-ablative lasers, right? So ablative just means if we look at the skin, you know, so this is your top layer, this is your bottom layer, it leaves this top layer intact and really does all the damage here. And it really is. Everything with laser is some type of damage. It's control damage.
Speaker: but we're targeting a certain sort of what we call a chromophore. So what does the laser see? So some really cool studies show, like for example, if you go and you look at balloon, white balloon versus red balloon and fire a laser, the white balloon does not get damaged, the red one will.
Speaker: You know why? Because it's detecting that red. So certain lasers like pulse dye laser, XLV, evolution light, you know, a lot, there's many, but really what they're targeting is the the the peaks where the red is it's at the highest, you know so 1064, 595, 755 to a lower extent, but those target the reds, right? So that when people are going after red spots, that's the laser and that's a non-ablative full beam laser, okay?
Speaker: The ones you were talking about are more, the they and those lasers, the ones I just talked about, there's no real data that they do anything for like health of the skin. They might maybe build a little bit of collagen as mandarin, but they don't do anything for true ah skin cancer prevention. Now, things like long pulse and the ag laser can because basal cells specifically have a lot of blood vessels in them. So if you starve those blood vessels and you get rid of those blood vessels, you can actually cure basal cell to a certain extent there, right? It's not the first thing we go to. We generally go to surgery, but it can cure basal cells, but it doesn't do preventative. Now, we're going to what you said, Moxie, Fraxel.
Speaker: We have basically, those are fractionated lasers. So if you think of and they target basically um tissue. They target tissue, water. They target water, so the water in the tissue, they target and they evaporate the water. By evaporating the water, they create a column of damage in the in the in the tissue. So they superheat the water and then it creates that channel.
Speaker: So full beam lasers, we used to have ablative, fully ablative, you hear about that, fully ablative CO2 laser means it just, just like if you have your pointer, you know, and you see the laser, it just, everything in its path is what people typically think of when they think of a laser, it cuts a hole through a wall, right? yeah that's That's direct beam, not doesn't split the beam. And I talk about it, that's like power washing your driveway. It's full beam of water,
Speaker: Fractional laser we figured out is we if we put a type of shower head on it where we can split that beam and so we go from like a fist to like this, where it looks like a shower head, yeah much less damage, much less pain, we can achieve similar results and much, much faster recovery.
Speaker: So then you have that split beam, fractionated, that's where it says fractionated, because we fractionated that beam and created a shower head. We have non-ablative stuff where it bypasses the top layer of the skin, goes down on the bottom.
Speaker: That's things like Fraxel, Moxie, that don't damage the surface layer of the skin. Then we have, they on the other end, Erbium YAG and CO2 that actually do the full column. So they damage the top part, they damage the bottom part, and that's that's why they're ablative, because they're damaging the top part as well, not just the bottom.
Speaker: Now, why that's important for patients is especially if you want true skin health, you want to do that preventative, you want to decrease the future risk potentially of skin cancer. Fraxel, the best data suggests that it too can do it, but about 50% reduction over 18 months
Speaker: ablative fractional lasers, 90% over two to three years, right? So something about that damage on the actual, the top layer as well, seems to be very important physiologically as well.
Speaker: Okay, that's that's really helpful. And then the last part is the depth. So there's a really cool, exciting research. We used to do, there's something called chemotherapy cream. It's also trending on Instagram, chemo cream, and they they they look like they've had laser, but it lasts much longer, about six weeks. You look like raw hamburger meat.
Speaker: The question was, well how come this doesn't really prevent skin cancer? It does it temporarily. Like you'll you'll get a reduction for about six months to a year, and then it all comes back.
Speaker: We're like, why? I wipe the field. We call it literally field therapy. We treat it the whole area. We're treating even the ones we don't see. Why does it come back? you know We just found out. There's ah a group that found out there's a second hibernating focus in the actual dermis, that bottom layer. Remember that when I said there's two layers? So Effudex targets this, gets that damage.
Speaker: There's a second layer here that actually sends these zombie senescence-associated secretory proteins and peptides phenotype that actually starts remutating. And they saw the mutation started happening right above that. So these collection of zombie cells start impacting the epidermal cells right on top.
Speaker: The main difference, and this is what our research found out that we published in Brazil, we need higher energy. So so forty is we need to go to around 400 to 600 micron depths to really eliminate that focus.
Speaker: And it it matches the studies from Queensland, Australia, where they also saw that we can actually decrease mutation load, but it was dependent on getting to that about 600 micron depth. Most corporate wellness programs overwhelm employees with too much, or they offer too little to be useful.
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Speaker: The outcome? A healthier, happier workforce. A measurable impact for your business. Visit Alively.com to see personalized wellness in action. You just, in a totally different context, but just mentioned buzzword that I think a lot of people are going to be curious about, and the peptides. And so I'm curious on peptides or even repomycin, some other less known treatments. People can do it, GHKCU, other things when you when you start talking about skin health.
Speaker: What are you seeing in that? Even if, look, the research hasn't caught up yet, but we're seeing it clinically or anecdotally, and maybe there's promise here. So I'll start with the skin peptide GHKCU, copper tripeptide, right? So we've known about this for like 20 years on the skin. It helps with wounds, it's it's great. We have it like, um I think it's a great peptide. I use it, we formulate, we make our own products. It's it's in a lot of my products.
Speaker: What we don't know is the latest stuff where people are sort of just injecting it into themselves, right? We just don't know. And you have all these people like, look at my skin before, look at my skin after. And then the lighting's all different. I'm like, you got to have standardized photography. Like, I don't know if you airbrush this. I don't know what's happening there, right?
Speaker: You know, and people kind of go like saying like, well, it's a naturally occurring peptide. So I'm just going to inject it. Well, you know, what else is a naturally occurring peptide? Insulin. Arsenic. Hemlock. like there There are a lot of naturally occurring substances you have to You know, i like like growth hormone, testosterone is natural. You know i mean? I'm like, we know all kinds of stuff. So problem is, you know, one, we don't know any short-term stuff.
Speaker: People are sort of saying like, well, I'm not seeing any issues. I'd love to see registries, like, you know, where people are, It's HIPAA compliant. There's no judgment. There's not gonna be any government kind of coming in and arresting you. Like I'd love to see physicians create this where it's a registry where people can come in. And so if you're, ah I look at it like smoking, like i we've been talking about smoking for the last like 100 years, like don't smoke, it increases lung cancer. Guess what? The number, the rates of smoking are still like 20, 30%. There's a subset of people that are just like, you know what?
Speaker: Big middle finger to the air. I'm gonna do whatever I want. I'm tough. I'm gonna prove I'm tough. I don't care, right? yeah So, but how do we at least give those people the information of like, here's what it is. So registry trials is that they're amazing. They have these ah other countries are much better. Like the the Scandinavian countries, UK, they have the UK biobank where whatever you tell your doctor, they record it. It goes into a central sort of station and it's anonymized. you can't really tell, but you can say, listen, we've had 500,000 people in this biobank in the last year.
Speaker: and We should keep that up on the blockchain. Like that seems like such a huge win. I know, that's what I'm saying. But then you can say, hey, we've seen 10,000 people on peptides, copper tripeptide. Guess what? I don't know, 90% of them said it was useless. They stopped after six months, you know? Because that's the thing. Are you going to continue?
Speaker: We don't have dosing. I'm like, well, so when do you stop? Like, are you going to do it for three months and then you stop? And then is it all going to go away? Are you going to get worse? Is there going to be a rebound effect where you're worse?
Speaker: We have no idea. It's a black box. So like if people are doing it anyway, I'll say, well, yeah, I mean, I'm happy to follow you in my clinic, like no judgments, but like I don't know, let's at least do something. Let's like measure. We have high-resolution cameras. You can probably see it behind me. evil Where we can sort of see, is there things being are you building more collagen? Are you building more elastin vascular? like we have This doesn't measure that, but there's other tools we can use, corniometers that can tell us what's happening. So if if it is changing, great.
Speaker: But again, is it placebo? we it's It's just an unknown box. um And then I'd like to classify the other peptides that you mentioned, I'll dive into it briefly. So there's like the 14 to 19 that, you know, RFK has talked about, like, let's just release them to the world and see there's low risk of sort of maybe human issues.
Speaker: They were before, you know, category one, they were moved to category two. Now he's like, well, I mean, you know, why are we putting him in the category two? There's no signal that it's bad, you know? So, So that's the thing. And then a lot of physicians will say like, well, it's it's bad. I'm like, ah okay, you're evidence-based.
Speaker: What's the data that it's bad? you know So we also don't have that. So we're in this weird Goldilocks zone where we just don't know. And there are some that I think, BPC-157, tons of data in mice. There's 200 papers.
Speaker: Have you heard of something called the LD50? Have your parents ever mentioned that? No, LD50, no. So it's a research term where it's a lethal dose, 50%. fifty percent So if I give this dose to mice, it's measured in mice, 50% of the mice will die.
Speaker: So that's a standard measure of toxicity, right? So people sometimes also talk about Botox. They're like, oh, Botox has an LD50 in mice and you're giving this toxin. I'm like, no, no, no, no no listen, the toxin, the dose makes the toxin. like In humans, we have like, it's number it's literally the McDonald's of skincare. Like we have a billion patients served, you know, and we are not seeing deaths if it's used from the right source. You will every once in a while see like, oh, 10 people with Botox admitted it to the hospital. I'm like, what?
Speaker: And I look, oh, great. Guess what? Gray market Botox, right? Because it's research grade. So that's the issue is there's so many of these, you know, Chinese factories where they're like, oh, I went on Yanosec and I checked and it's all HPLC purity. I'm like, yeah, but one batch, what about the next batch? They're they're not CGMP certified.
Speaker: I don't know what's happening, but getting back to LD50, BPC-157, can you guess what it is for BPC-157? I mean, I don't know the the units and everything. So...
Speaker: It doesn't exist. They couldn't they couldn't give enough. There's no dose that, they so they tried, they couldn't do it, but that's again, that's mice. Mice you know live live in their own feces and stuff. So they have a different immune system, right? So that's why whenever whenever they say, like a lot of influencers, are they'll say like, oh, it's super fine in mice. They live 20% longer. I'm like, but mouse only lives two years. Like and what happens at year 30?
Speaker: But we think things like BPC-157, we're like, it doesn't really, there's now, there's three studies now. I mean, same group, Dr. Edwin Lee published sort of like, you know, some studies there and it seems safe. There was no side effects. Most of them sort of had maybe a little bit of an improvement. So we're like, okay, you know, maybe this one, if as long as your doctor tells you and as long as you followed and they say, listen, this is an experiment. i I have no clue what's happening, but if you want, if you're already doing it anyway,
Speaker: Let's monitor and see what happens, right? So that's that. And then there's like, yeah, the other ones that sort of, the one I don't like is Epitalin. People talk about It's a big popular one. i don't know if you've heard of that one. Yeah, yeah, yeah. They talk about longevity. The main thing is they talk about the Talon.
Speaker: Telomeres, yes. But telomeres are again like height. So it's me like telling you, hey, Andrew, how tall are you right now? I don't know, let's say you say 6'1". I'm like, this will make you six foot three. I'm like, well, is that gonna change my health? Like, what does it do?
Speaker: So telomeres are really only important if you're extra super short. So if you're if you're in the middle and you increase it by like 10%, I'm like, it doesn't do anything. Like you're just, I mean, great. You feel better because you have a test now.
Speaker: But that test is like literally saying like you went from six, one to six, three, unless you're a basketball player, you're probably not gonna care that much, right? So, you know, that's the kind of the honest stance on the peptides. Like I'm all for, I hope they work, you know, but we need a better system.
Speaker: Yeah, we just don't know yet. We don't know, and I hope we can all come together as a group that's interested in this and just say, let's create registries that are anonymized. So I i don't know if you're taking it I'm taking it, you know, the FBI or whoever, FDA is not gonna come after us, but we can actually start generating these safety and efficacy signals to see if it's actually working or not. I mean, that's what happened during COVID, because we didn't know, we didn't,
Speaker: There was like minute to minute, one day we're like, oh, shoot, the new the newest data suggesting it's bad or it's good, it's bad. So we had to adjust on the fly. So I think if we can take that sort of approach of like, if people are doing it anyway, like I'm going to say, listen, ah there's no data, don't do it.
Speaker: But if you're doing it anyway, let's at least find a way to record this data safely, effectively, and anonymously so that people, you know, can do it and not lie about it. Yeah, I love that idea. I hope somebody listening to this does create something, gets's with some Reddit groups and we have a blockchain. It seems like it could be an interesting business there.
Speaker: What about other, so outside the peptide realm, other maybe less well-known NMN or rapamycin or senolytics? What are other things that you see when you talk about really taking care of, not just surface level skin health?
Speaker: Yeah, so there's what we, I think we're very close to discovering true, real anti-aging stuff. And something, I mean, I look at LeBron James and I'm like, whatever he's on, ask him, like, you know, once he publishes his memoirs, whatever he's taken, do that. Cause like, I mean, to be 41 and dunking like he's doing, that's like, honestly, that's unheard of, right?
Speaker: Well, part of it's, I mean, he spends eight hours a day recovering, right? Like he treats recovery as a job as well. And so we know like with the glymphatic system, if you're not getting enough sleep, you are going to be inflamed. You are going to have puffy. Like, so I think a lot of it isn't just what he's doing.
Speaker: It's what he's not doing, which is overtaxing. And that's what I say. So we have our longevity. I mean, if if your listeners, clients want this stuff, we can put, ah you know, we have a longevity stack where we talk about, listen, this is actually validated based on sort of parameters. The true one we have is actually true diagnostic does a, I'm not affiliated with them. I don't have any, you know, royalties of people get true diagnostic.
Speaker: But it's ah it's a test where you can actually measure your epigenetic age, your dundene pace, which is the pace of aging. So NMN does have some data. you know There's and a product called Novos Labs specifically. They've actually tested it at MIT Harvard venture where it's a multi-component thing. And really what you wanna target is the 12, we call it the 12 hallmarks of aging. So proteostasis, zombie cells, cell-to-cell communication, stem cell exhaustion,
Speaker: 12 of them, okay? Inflammation, ah reactive oxygen species. So what I think is right now, we're sort of taking the shotgun approach where we're sort of saying, well, let's just target all of them, right? The issue is always individual variability. Like for you, maybe you need out of those 12, maybe you need like number 12, number three, and number eight, and I need like number two, seven, and nine, you know, to really optimize.
Speaker: So right now, it's also a bit of a crapshoot. Rapamycin, I think it has some really good data, but it's sort of the opposite. you know One of the big you know peptide stacks that people talk about, Tessa Morel and Ipamorel and CJC, right what what does it do? like do you know I'm sure you've heard of it. like Stimulate the human growth hormone. Yeah, and IGF-1. Guess what rapamycin does?
Speaker: stomps on IGF-1. exact ah Exactly. mTOR inhibits it. So the exact opposite. So I'm like, so at the at the very least, like you might be like, you know, the acid-base chemistry, like, oh I'm taking an acid for, you know, this. And then I'm taking a base for that. And like, at the end of you, get some salty water. You're getting saline. You're literally getting saline. I'm like, you're you're literally placeboing.
Speaker: So I think that's the issue is that we don't really know how these things interact, but I think, yo, rapamycin does have potential. I was on it personally for a little while. I was tracking through it. didn't really work for me.
Speaker: And then I was getting a little bit, and one of the side effects is sort of you can get mouth sore. So personally, I was getting some of those. I'm like, ah, Maybe not for me. you know Metformin has some maybe data. Again, it's all about that sugar processing.
Speaker: So I think you know along that line, we're gonna start probably, I'd love to see the newest data. And and there is some newer data on GLP-1s actually decreasing all microdosing. But again, what does microdosing mean? It's gonna be different for you, for me, right?
Speaker: For me, i'm one of the there's actually newest data that there's these super responders that just like even of with, they put some out. um I was one of them, you know that I was on trizapatide, even 2.5, I had massive migraines migraines for three days. wow So now I'm on like a third of the dose, so like 0.8 milligrams, and that seems to be okay for me, and I'm seeing sort of the benefits. So it really is gonna be patient to patient dependent. And when you say the benefits, are you tracking, is it like fasting insulin? What what are you looking to try to improve when you're doing that?
Speaker: Yeah, so I mean, one body composition, I think that's number one. If you have extra fat, especially around the belly, that's number one thing that's gonna be killing you. you know I think it's probably, to some extent, based on the studies, even worse than smoking. So you know carrying too much weight around the midsection especially, having a A1C level that's high, you you know poor intake of food, so you you know you want you need to make your micronutrients. So I'm like, unless you're doing all that, forget peptides, forget anything else, forget GLP-1s, you gotta to get that in order.
Speaker: Now, there are people, it's metabolic. It's like me saying, why are you wearing glasses? Just squint harder, you know? Again, it comes to genetics. Some people, it's they just have this insatiable drive to eat.
Speaker: And that's where, you know, you turn down that volume with a GLP-1 and you can really help them out. so So that's kind of that. So I think GLP-1s are really starting to take over that whole like longevity. But again, we have to track it with something. what What are we seeing? So fasting insulin, are we decreasing homocysteine levels? Are we looking at like LDH? Because again, if you're fixing your diet, you're going to help your LDH. you're going to look at apolipoprotein, you know, B and stuff. So those are going to those are going to be your best ones. And then HSCRP, like inflammatory markers.
Speaker: so Yeah, C-reactive protein. Yeah, C-reactive protein is going to be very key. So those are going to be the things you're going to do. And then again, you got to track it. It might not be able to sort of fix that specifically.
Speaker: To give you the best example, we do phase one through phase four research on a lot of autoimmune conditions like hedronitis subvertiva, some of the highest CRPs out there. And even when we treat them with medications, it doesn't really come down. And we know these patients, if it uncontrolled HS, they live 15 to 20 years less than people then that don't have HS, right? Psoriasis, about five to 10 years less than people that don't have that inflammation.
Speaker: So really inflammation, you know, metabolic patterns, we really have to improve on and we have to really track it. The issue is like another thing that people say like, well, how much does diet help? And that this is the one thing, there is this movement where, oh, don't take any medications. I'm like, why does it have to be one or the other? Why can't we just? Social media is not good at nuance. I need a big headline that's going get clicks, yeah.
Speaker: Exactly. So i'm like, why am I picking between mom and dad? Exactly. What if I want a little bit of both, like a little bit of medicine? Maybe I can decrease the dose of medication that I'm on by doing the diet. So just giving you example of a diet. So they'd finally have that research and they're like, doctors never talk about diet. I'm like, what do you mean? yeah Every consult, I say, I say, see a dietitian. I'm not going to be the one to go through it You know, just like exercise, I'll be like, go see Andrew, man. The guy swims 25 kilometers. Like, why am i talking to about swimming? It's important. It's great on your joints. You're not gonna need, oh wait, well, maybe shoulders, but you know, go see Andrew.
Speaker: It's important. But let's talk about what I actually prescribed here. We're gonna spend the majority of the time. They have finally a look at the diet. So one of the best ones is intermittent fasting. you know so So looking at that, there's and there's different ways you know that you can intermittent fast, right? So is it the 18-hour window? Is it Monday, Wednesday, Friday where you're only doing 600 calories? right So many different ways to call it intermittent fasting.
Speaker: So that can help with psoriasis, but it's about equivalent to what we call methotrexate, where 35% patients will get 75% or better. Wow. Yeah.
Speaker: wow yeah yeah But back to that super responder group, right? You said 35%. 35% get pretty clear, okay? But with the best medication, something like Skyrizi, for example, or Bimzilex or Brodalumab, we can get 90% of people getting over 90% better, right?
Speaker: So I'm like, so why are we missing out on that? And if you're if you're not one of the 35, because the ones that respond, the super responders, They're gonna be loud and say, look at me, I cured myself with just the food. I'm like, dude, you're just the super responder and you don't have bad genes.
Speaker: Why are we then shaming people that actually need the med? you know Yes, do both. Maybe if you do the food, it'll decrease it. So maybe you need a lower dose of the actual medication. That's always the goal.
Speaker: Yeah. Dr. Sayesha, there's so much in here, so much to unpack. I know we could go a lot longer. There's so many other topics, but I really appreciate your work and and how deep you went with us today on so many of these topics. Thank you.
Speaker: Hey, it's absolutely my pleasure. Thank you for having me on. I mean, it's, this is what it's about spreading that message, getting people to understand the nuance that, yeah, maybe you can hook them for three seconds. ah I sometimes say outlandish things to hook them to. And I'm like, listen, go listen to my podcast for the full information, you know?
Speaker: Yeah. Those that want to follow you, learn more, get more information about everything you're doing, where can they find you? And we'll make sure to put in the show notes. The best thing is just my first name, last name, MD at Instagram. So we're we're there.
Speaker: we have ah If they want to see me in clinic, we have now clinics in Toronto, Brentwood, California, soon to open up one in West Palm Beach area as well. So if they want to in person. And then we also do virtual consultations as well if if they feel like could benefit.
Speaker: Amazing. Well, Dr. Saeed, I really appreciate you again coming on today and enjoy a lively day. Thank you, too. Thank you for joining us on today's episode of the Home of Healthspan podcast.
Speaker: And remember, you can always find the products, practices, and routines mentioned by today's guests, as well as many other Healthspan role models on Alively.com. Enjoy a lively day.
