Hunter Williams·Library
← all videos

Peptides & Longevity Medicine Explained by a Real Cardiologist | Dr. Abid Husain, MD

2026-04-30 · 1:11:13 · 7 min read

I sat down with Dr. Abid Husain, a triple board certified cardiologist who left the traditional hospital system to focus on what actually prevents disease. He now works at the Boulder Longevity Institute combining conventional cardiology with peptides, HRT, and functional medicine. We got into peptides, hormones, advanced cardiac imaging, and what he actually does for his own health. Here are the highlights.

From Hospital Cardiology to Longevity Medicine

Dr. Husain spent years in traditional cardiology in New Jersey before realizing the system was built for end-stage emergencies, not prevention. He kept seeing the same patients show up with problems that could have been stopped years earlier with the right information and tools.

So he retrained himself. Functional medicine first, then bioidentical hormone replacement, then peptides starting around 2015 when they were first becoming available.

His advice to doctors looking to make the same transition is simple. Start with education. Get certified, attend workshops, and learn the differences between conventional and bioidentical hormone replacement. No single organization has it all figured out, so build a diverse education and decide for yourself.

Why Cholesterol Alone Is a Bad Marker

When Dr. Husain trained 20 years ago, cholesterol was the only pillar. That has changed.

Cholesterol by itself is a poor indicator of atherosclerosis risk. You have to look at particles (ApoB), the shape of those particles (small and dense versus large and buoyant), inflammation, liver function, the thrombotic system, and what's actually happening in the vascular wall.

No single biomarker tells the whole story unless it's massively abnormal. Things like familial hypercholesterolemia are the exception. For everyone else, the biomarkers act as risk amplifiers. You stack them together to figure out where to focus treatment.

This is the same lesson cardiology learned with blood pressure and heart failure. Small doses of multiple medications beat maxing out one drug. Atherosclerosis treatment works the same way.

Calcium Scores Are Old News

I had a calcium score done recently and it came back zero. Good news, but Dr. Husain made it clear calcium scores are first-generation imaging.

Plaque evolves. It starts as soft, cholesterol-filled plaque with no calcium. Then it becomes mixed. Then it fully calcifies. The most dangerous plaque is the mixed, metabolically active stuff with little or no calcium. A calcium score misses all of that.

Generation two is a CT angiogram with contrast. You can see inside the artery wall and identify soft plaque.

Generation three layers AI on top of high-resolution scans. The software goes pixel by pixel and identifies calcium, soft plaque, and inflamed plaque. This catches the high-risk patients who would otherwise slip through.

Up to 50% of people who die of heart disease never make it to the hospital. These are sudden heart attacks from plaque around the 50% blockage range that causes zero symptoms. A stress test only catches blockages over 70%. By then you're already at the end of the line.

The Patients Who Look Perfectly Healthy

Dr. Husain sees plenty of patients who do everything right and still have plaque. Sometimes they're doing too much of the right thing. High stress, overtraining, aggressive fasting, mold exposure, Lyme disease. The overall load on their system is too high.

Lab tests don't always catch this. Advanced imaging often does.

The Testosterone and Heart Disease Myth

The claim that testosterone causes cardiovascular events came from three studies in the early 2000s. All three have been debunked. Some were retracted. Some miscategorized patients. That's where the FDA black box label came from.

Men with testosterone under about 250 have a 50% higher risk of dying from heart problems and much higher prostate cancer risk. Testosterone has a receptor in every cell in the body for a reason. It supports the vascular lining, nitric oxide production, glucose management, brain health, bone health, muscle health.

Replacement therapy targeting 750 to 1200 total testosterone is safe. There's no data showing that range causes heart disease.

The myths come largely from bodybuilders running 10x physiologic doses. That can cause hypertension, left ventricular hypertrophy, and premature plaque. Real risks, but in an extreme population that gets conflated with normal replacement therapy.

Hematocrit on TRT

Testosterone stimulates EPO, which increases red blood cell production. So hematocrit goes up. This is expected.

What people miss is that testosterone also increases PAI-1, which helps break down clots. So you're getting slightly more blood along with slightly better clot breakdown.

Mild elevations in hematocrit haven't been associated with increased blood clots in studies. If you push into the 55s, consider phlebotomy. Below that, you're not getting a clot from the testosterone.

Women's Hormone Replacement Has Changed

The FDA dropped the black box warning on HRT for women. The industry is finally accepting that the Women's Health Initiative used synthetic, non-bioidentical hormones at high doses and the findings don't apply to modern bioidentical HRT.

Women need estradiol, progesterone, and testosterone. The question is how to deliver them.

Oral synthetic estradiol can increase clot risk. Topical bioidentical estradiol is much safer. Oral micronized progesterone is not associated with inflammation or clot risk. Testosterone helps women with mood, libido, and overall well-being.

For older women starting late, go slow. A 77-year-old who hasn't had hormones in 20 years needs gentle introduction to avoid breast tenderness or spotting. Start low and increment up over a year or two.

How to Think About Peptides

Peptides have been around over 100 years. Insulin is a peptide. What's new is the manufacturing technology, the human genome project, and the scalability.

A lot of peptides are already FDA approved. Ozempic, Mounjaro, PT-141. Doctors getting started should learn these first, then move to peptides like BPC-157, TB4, TA1, and the growth hormone secretagogues like CJC and ipamorelin.

Each of these has cardiovascular applications.

GLP-1s and the Heart

The SELECT trial showed GLP-1s reduce cardiovascular events in non-diabetic patients, independent of weight loss and glucose control.

GLP-1s reduce inflammation in the endothelium. They reduce adhesion molecules that grab onto LDL and pull it into the artery wall. They can slightly relax the arterial system. There's data showing GLP-1s combined with maximum goal-directed therapy can help reverse soft plaque.

For the heart muscle itself, GLP-1s optimize fuel source switching. The heart is the only organ that shifts fuel sources based on output. In heart failure or enlarged hearts, that balance is off, and GLP-1s help re-establish it.

BPC-157 and TB-500 for Vascular Health

BPC-157 stimulates over 100 genes quickly. Its biggest effect is on nitric oxide production. It helps the genes that make eNOS, improves how your body uses nitric oxide, and modulates VEGF for controlled angiogenesis.

BPC is a modulator. Short-acting pulses. Your body checks the stimulus and decides whether to follow it. It doesn't cause uncontrolled growth.

TB-500 works on fibrosis, collagen deposition, and the actin cytoskeleton. It's anti-inflammatory and inhibits inflammatory cytokines.

Together they reduce vascular inflammation, support healing, and help keep LDL particles from grabbing onto the artery wall.

Growth Hormone Peptides vs. Synthetic HGH

These are two very different animals.

Synthetic growth hormone has a long half-life. Once injected, it stimulates your system continuously. Your body can't regulate it. Long cycles cause acromegaly, hypertension, organ enlargement, the big abdomen behind the six-pack.

Secretagogues like CJC, ipamorelin, and tesamorelin have half-lives around 20 minutes. You get a pulse of stimulation, then your body takes over. No uncontrolled growth. No enlarged heart. In fact, metabolic health improves.

Dr. Husain cycles them. Two months on, one month off. Constant use can desensitize receptors and bump cortisol.

Cancer Concerns with Peptides

For someone with no cancer history, check IGF-1 first. If it's normal, you're fine to start. These peptides are short-acting modulators of compounds your body already makes.

For someone with a cancer history, it depends on the cancer and whether it's active or in remission. Interestingly, tesamorelin in early HIV studies actually caused regression of Kaposi's sarcoma. Stimulating growth hormone produces IGF binding proteins that can be anti-tumorigenic.

It's still a gray area legally, but the data supports careful use.

Mitochondrial Peptides for the Heart

Dr. Husain likes SS-31. It improves cardiolipin, the structural protein that keeps the inner mitochondrial membrane folded properly. When the membrane flattens, ATP production tanks. SS-31 restores it.

He doesn't start with SS-31 right away. First he gets the membrane health right with omega-3s, omega-6s, urolithin A. Then SS-31 at around 20mg daily, which is high and expensive but effective.

Humanin helps autophagy and the endothelium. MOTS-c comes last. If you give MOTS-c to someone whose mitochondria can't produce energy well yet, you can actually make them feel worse. I've seen this with a lot of people who jump straight to MOTS-c and end up worse off than when they started.

Fix the engine first. Then push it.

SGLT2 Inhibitors for Longevity

SGLT2 inhibitors block reabsorption of sodium and glucose in the kidneys, so you pee both out. Sounds minimal. The downstream effects are huge.

They trick the body into a fasting state. They stimulate AMP kinase, the metabolic efficiency system. SGLT2 receptors aren't just in kidneys. They're in the heart, vascular system, brain, pancreas, gut, and some muscle tissue.

The gut effects recalibrate the microbiome and improve short-chain fatty acid production. The cardiovascular effects are well-documented in heart failure trials.

I think SGLT2s will make metformin obsolete once pricing comes down. The benefits are broader and the downsides are minimal.

What Dr. Husain Does Personally

Sleep by 10:30, up at 5:30. Gym six days a week. Mediterranean diet, high protein, high fat. Doesn't count macros.

Daily supplements and meds include baby aspirin, low-dose Cialis for vascular health, low-dose telmisartan (not enough to drop his normal blood pressure, just for the longevity pathways), tirzepatide, testosterone replacement, vitamin D, magnesium, and urolithin A. Spermidine for a week before any extended fast.

For peptides, he runs tesamorelin and ipamorelin regularly and cycles them. SS-31 and epitalon quarterly. BPC-157 and TB-500 are almost always in rotation for injuries.

My take

This was one of those conversations where every answer made me want to ask three more questions. Dr. Husain bridges the gap between conventional cardiology and the longevity world without losing the rigor of either side.

The big takeaways for me. Get a CT angiogram with AI processing if you can, not just a calcium score. Stop fearing testosterone based on debunked studies. Build mitochondrial health from the membrane up before reaching for MOTS-c. And SGLT2 inhibitors deserve way more attention than they're getting in the longevity space.

I'll have him back on soon. We barely scratched the surface.

JOIN THE PRIVATE COMMUNITY
Talk peptides with Hunter and the Axion Collective
Direct access, member protocols, and live discussions you won't find here.
Full transcript click any paragraph to jump video

you Hey everybody, this is Hunter Williams. I hope you're doing amazing wherever you are at in the world today.

which is the peptides and HRT space. So I'm really excited for one for me and myself just to get to pick his brain, but then also expose him to my audience as well because I think he has a lot of very valuable things to say in the realm of cardiology, especially as it relates to our world, like I said, I'm gonna read just his background real quick and we're getting into it. So Dr. Abed is a triple board certified cardiologist in cardiology, internal medicine and functional medicine. He spent years in the traditional hospital system in New Jersey before walking away to focus on what actually prevents disease.

I think that's one thing that we all focus today. And now he's at the famed Boulder Longevity Institute working with optimizers and other people to really dial in their health and he works on combining conventional therapy, you know, with peptides, HRT, and all the other things that we love to talk about in our world. Dr. Robert, thank you for being here today. And let's just talk a little bit about your background first. What got you into this world and how did you go from being a traditional doc to one in the longevity world?

Well, first, thanks for having me, Hunter. This is a real pleasure to be here. You know my journey into the world of practicing medicine, It's called longevity, we call it cellular medicine. You could also think of it as systems related biology where we're looking at everything and seeing how it all interacts. Conventional medicine is notorious for being siloed and just looking specific problems in isolation.

When I'm dealing with an emergency, when I am dealing people that are on life and death situations, yeah, you have to look at the specific problem because that's the thing that threatening their life at that time. But really, that's not the only thing that showed up. That's what showed at the end of the spectrum. What's leading to that is often a larger systems breakdown, and it's just showing up in that one spot. So when I kept on seeing people show up, in the conventional system, with the similar problems, yes, there was change that we were impacting there.

I just kept on seeing this shortcoming of, well, we could have prevented this if this person had just been given the right information early on, or they'd been giving the lifestyle changes, the medications early. These changes that were happening at the end of the spectrum as emergencies are largely preventable. So why is it that in modern medicine we can't do that? You know, the issue was that the medicine that we practice is hospital based and so is designed to deal with things when they show up at the end and it's

not optimal to look at things. When they're showing up as a slow percolating illness or issue and you know the training that I got in medical school residency and fellowship was all geared towards that. end of the lines, end-of-the-spectrum type of disease. So I realized I had to go back and retrain myself to understand what was going on from the other end. And when you look at what's going in the end, it's slow, chronic conditions.

Functional medicine is really suited for that. That's the type medicine that looks at those slow percolating diseases. I just didn't see that we had a lot of preventative tools. When I started practicing, it was 20 years ago when I finished fellowship, and the only tool we had was niacin and a statin, maybe some coli styramine or something like that. So there was very little teaching. And I'm an athlete.

I've, uh, you know, been fascinated with diet and exercise and performance enhancement all my life. And so I just knew that there was something that connected and I had to connect the dots myself. So it started with functional medicine, learning about root causes. What is it that creates chronic disease? What does it, that, where we can stop it. That led to hormone replacement therapy. and then advanced training in hormone, really bioidentical hormone replacement therapy.

Once I finished that, that's when peptides are really just at the beginning of being available. And so we're talking probably, you know, 2015. You know I started working with peptide and getting certified with early groups and just integrating that into my practice. So it's been an interesting journey and really educational and It's kept me an ongoing student my whole life. Yeah. I do want to ask this because I have quite a few doctors that follow me and I get questions from them a lot of time.

They're like, Hey, I might be in this one area of medicine, but I love the peptide world and love hormone world. Do you have any advice for doctors out there that are looking to transition? I actually just got a message from one earlier today. It's funny that we're talking. Um, do you ever any advise for doctor's out that kind of probably are like you like very into health fitness and actually helping people get well. You have an advice to them and kind making that transition. Yeah, it's got to start with education and it can be something as simple as a certification, a workshop, but they've got get their feet wet in understanding

the differences between conventional hormone replacement therapy, bioidentical, and the different ways to administer it because that's one of the challenges of this field. There's so many different ways to administer hormones and every single organization has their preference. There are some that have better data supporting others, supporting them versus others. But that's what you have to figure out and sort of tease apart on your own with certain educational systems.

There's no one that you should subscribe to completely. This is something where every practitioner should get a diverse set of education and really decide on their own because there is no governing body. And a lot of it's about what type of risk you're willing to take and being risk, whether it's medical legal, because this is still not something that's widely accepted, as well as, you know, what is the clinical risk that might be involved? So you got to know what to look out for. Yeah.

Getting into traditional cardiology versus what you would call you practice now. A lot of people, especially when they kind of come to the realization that, okay, maybe I'm in my forties and fifties, and I am going to get my blood work done. I will start evaluating some of these things and hopefully get on the right path. Let's say someone goes to a conventionally trained cardiologist is very much in that method of just more treating disease rather than helping someone be well versus you. Would you say there's maybe some pillars that you differ now based on your conventional training and how you approach the practice of cardiology?

Definitely. Yeah. When I was training, the only real pillar that I taught was cholesterol. Well, That's evolved significantly over the past 20 years. And cholesterol by itself is just a really poor indicator of what type of atherosclerosis risk somebody has. What we want to look at is particles. So that's APO-B measurements. That is one first differentiator.

The whole idea that cholesterol is the only arbiter of the athroscorosis is completely flawed. We've got to take a look from multiple pillars like you're saying. The particles are one of them. They do impart a risk. Are they associated with inflammation? How is the liver involved? how is it thrombotic system involved and what is he doing to the vascular system? That's how I think about it. Inflammation, we know, is part of the atherosclerotic process.

It will amplify risk that may or may not be there with elevated particles. When you look at the particles, you have to get more granular. Look at this shape of those particles—are they large and buoyant, or are they small and dense? Dense ones being the ones that cause more athroscorosis. If you layer that with somebody that's got some low-grade chronic inflammation, that somebody gets more prone to atherosclerosis. Then you look at the liver. Liver meaning that involves blood sugar or it involves the liver itself, because the livers where those cholesterol particles are being produced and where

a lot of the inflammatory particles of being. So, and then the inflator cytokines too. You've got to look at that liver is the crossroads for a of these systems. And then lastly, there's the thrombotic system, platelets, your blood cascade, you're blood coagulation. If that's off, they actually can promote inflammation on the vascular wall. And so putting it all together gives you me an idea of what's going on in the Vascular Wall.

So that's really, you know, the, cause the vasculature wall is a, is fluid. It's a it's got a layer that protects it. You know it has got enzymes that create compounds that protect it and then reduce inflammation. so you it is looking at what is involved in those, in all those little systems. Yeah. When you say ApoB and some of those other markers, obviously probably some people are more genetically predisposed to be skewed one way or the other and maybe on the higher end. Do you think it's much more, I guess, relevant?

So if we look at someone that let's say they're doing everything right, so they are eating right. They're training right at least they knew they do what they know they were supposed to do right And let's say they have, okay, maybe there are APOBs higher and some of these small particle numbers are higher based on whatever genetic predisposition do they'd have. Do you think it's much more important to evaluate that in the context of all those other things you mentioned like inflammation, liver health, uh, vascular health and all those things, or is it something that you have to say, Hey, you kind of got the, genetic short straw in this sense.

Do we now need to treat that? Um, I guess in isolation, Or is that much more important to look at all of those other things first before you end up going to just treating that and you know, whatever that looks like from a treatment standpoint. Yeah. Because there you were talking about different, different pillars and different layers. Things like particles, things like inflammation, and when we break it down in the biomarkers, they're like risk amplifiers. So no one thing really does it unless it's significantly abnormal.

If you have familial hypercholesterolemia, You know, then that's where those LDLs are sky high. They're in the hundreds, you know. In the two, three hundreds. Maybe more. You've got triglycerides that are significantly elevated. That's a system where the body just can't handle the amount of lipid that is going through it. Outside of that, in a case that you're talking about, we want to look at the other amplifiers. We want look what is doing on in those other systems because that tells me where to focus some of the treatments.

It's never really just one thing that we got to do. I mean, that's one of the lessons that has come out of what we look at when we looked at hypertension and heart failure treatments. In the past, it used to be that they would take one medication to the highest dose and then consider adding on medications. Well, what learned over the decades is that small amounts of multiple medications are far better and give us better outcomes. It doesn't feel great for a patient to have to take multiple medications.

So there is a psychological component to it, but the outcomes do much better when we give them multiple treatments. So when you apply that to atherosclerosis, it's very similar. Like there's not one thing. It's just going to be particles. We've got to look at the particle shapes. What are the risk amplifiers there are? Inflammation. Is the mitochondrial function off? What's oxidative stress look like? And this is not where the conventional cardiologist is going look because, number one, they're looking at the end stage emergency situation that needs

to be prevented and they don't necessarily have the training to do that unless they've sought it out. Yeah. I recently, and this was part of a company I was just doing a little bit of promotion for, I had a calcium score test done, came back zero. So I guess that's a good thing. But I would say with calcium scoring, do you weight that as something that is very relevant to this conversation? Or what are your thoughts around that? And is it something people should go and get done? Whether they're, you know, thirties, forties fifties and beyond.

Yeah, calcium, these calcium scores are the, the first generation of imaging testing for screening for heart disease. It's the first-generation, and we're probably on the third generation now. So doing a calcium score is a great, cheap, entry-level test, but we can do so much more right now, it really behooves us to do much. The problem with the calcium is that it detects, as it says, calcium.

When you look at plaque, it's got an evolution to it. It starts out as a soft plaque cholesterol-filled, no calcium. Then it turns into something that is a little bit mixed, calcium and cholesterol, and then it becomes fully calcified. That evolution, when it is soft, plaque and it starts to become mixed that's when the cholesterol underneath the lining of the artery becomes a bit inflamed. When it becomes inflamed, it triggers the immune system and then our body's desire to cool down the inflammation is why we calcify it.

All that to say that the most vulnerable plaque is the stuff that's mixed, metabolically active, that either got small amounts of calcium or no calcium and it's all soft. So when you do a calcium score, you miss that entirely. So generation two is doing a CT scan with contrast. And with that, we can then look at the inside of the artery and the wall and see where's the calcium, and then where is the space that's not calcium that

is probably cholesterol. Then it gives us an indication of how much actual cholesterol is in that plaque and how many plaque you actually have. The third generation is where they take that data, they acquire it with higher resolution now with better scanners, and then they upload it into AI based software. There's multiple companies out there that are doing that now. And what it does, this is amazing because this was one of the first applications of machine learning to medicine.

It takes those images that were super high resolution. goes through it pixel by pixel and is able to determine which ones of those based on density, you know, color density. Which of these pixels is either calcium, soft plaque, or inflamed plaque. And so with this new technology, we can actually identify inflames plaque and high risk patients. That's the biggest demographic of patients that we're still missing.

Up to 50% of the people that die of heart disease never make it to the hospital because these are the sudden heart attacks that were missing, plaque that is 50 percent-ish that doesn't cause any symptoms. That is the stuff that kills people. So when you get a stress test, you're only detecting stuff, that's 70% or higher. And that at the end of a line. So that whole, like a stress test, is an antiquated test to assess for how much atherosclerosis you have.

Sure, if you had chest discomfort, it's an important test differentiate if it is from a narrow artery. But when you're looking at it in a much earlier place, you know, much early time frame like in prevention, to see if its ramping up, that doesn't help, because it isn't going to show up if is lower than 70. That's why these tests like the CAT scan with contrast, and the ones that do this AI processing, that is where the real state of the art is happening right now.

Do you feel like with the AI processing alongside with contrast, is that providing a much, much better indicator of someone's actual state today of their cardiovascular health? Really than anything that we could probably see like on the old generation stuff, like the calcium score, or even some of those blood work markers, does it go way beyond informing what a lot of people would see on their just traditional blood tests that they're gonna get once or twice a year? Yeah, I think so. I mean, if you're coming to me, i'm going to do a really thorough panel on you and that will give me a much better idea about what plaque I may be able

to anticipate seeing on the scan. There's always surprises and I also want to make sure because What we can see in the biomarkers, oftentimes, you know, we still don't know everything about medicine, believe it or not. And so there is a lot that's lost in translation in what we think we know we see, in labs and what shows up. So we have the ability to bridge that gap now. When I have patients that come to me that are middle-aged, they're young and they wanna get screened, I feel like getting a CTA with coronary angi,

with CT of the coronal arteries with angiogram, with contrast, is much more important than doing a calcium score, especially early on, because that's going to identify who has that at-risk plaque. And when you're young, that is really important. If you get identified young then that a life that saved potentially. if you don't have anything, then it's great. You don´t need to do the test for another five years or more. But if have been identified as somebody with early plaque, then getting on treatment earlier is important because then you could prevent that event and

prevent maybe other issues that are associated with atherosclerosis. Yeah. Would you say with the people that you work with, obviously it's a little bit more unique than just would be someone that's going into their general practitioner's office? Would say a lot of the that maybe catch some of those things are, let's say they have it done and maybe they just look like a healthy fit, middle-aged person. Do you actually find that some Where the outside you might say, Hey, that perfect. If I saw him walking down the street, they look perfectly healthy to whereas you get that done and you are able to catch a lot of those things earlier.

Whereas like all outward signs would tell that person like, hey, I'm in, in pretty good shape. I have nothing to worry about. Yeah. It does, it helps to identify that population. You know, we have a, our society has got a high stress burden and there's a hi inflammatory burden. There's lot going on in the background with our metabolism and our ability to be resilient, to survive a lot of these small insults that happen to our

system on a daily basis. Lab tests don't necessarily pick that up all the time. And there are plenty of people out there that look healthy on the surface. They are doing all the things that they can be doing. In fact, they may be too much of the thing that I think they should be for their health. Because sometimes, you know, we push ourselves over into overdoing things. Whether it's fitness, or whether it is fasting, you know, or if you're just a high performing individual and your stress burden is high. These are the kind of people that show up and they have plaque that's more surprising than I would have expected because they're trying to do all the right things,

but the overall load that they had on their system is just too high, you now our liver detoxifies, our body derives to detoxify. That's a generic term, But it's true. We try to, quell, inflammatory stress. We try to reduce the amount of toxins our mitochondria make on a day to day basis. Well, if your mitochondrial are pumping out higher amounts of anti-inflammatories or energy to cope with a load of stress, a lot of maybe, you know, chronic inflammation.

Maybe you're living in a home with mold, maybe you've got Lyme disease, I mean, it comes from all over the place. So this world that we're in has a higher burden than in the past and that adds up. Yeah. Switching gears a little bit, because I know a lot of the audience is kind of waiting with bated breath to hear your opinions on some of these subjects. If we look at the TRT and HRT user population, a people that listen to my stuff or men or women that are in that, and a of them are the optimizers that

want to take everything to the nth degree and make sure they're doing it right. And I think if you look at users of HRT, we're seeing an explosion right now in people getting on hormones, which is a good thing. And with that comes a lot of caveats to make sure that people are doing it right and they're with a doctor and everything. When you looked at HR or BHRT in the context of cardiovascular health, one, can you talk about the myths that have been perpetuated for a long time And then like why some of those are wrong. Cause a lot of people know like, okay, like HRT is probably a good thing for me to do, assuming that I need it.

But I've heard all of these things in the past about I'm going to get heart disease or worsens my risk for heart diseases. Can you speak a little bit to kind of the, the passed mythology around that to where we have today? Well, let's start with men. You know, The classic myth is that testosterone has been associated with cardiovascular events. That's been largely debunked. There were about three studies that came out in the early 2000s, maybe up into the 2014, I think.

They were meta-analysis or there weren't even studies actually looking at cardiovascular outcomes, but they made claims that testosterone was associated with increased cardiovascular events. All three of those studies have been debunked and even some were tracked by the authors. And some of them weren t even doing basic statistical or data gathering accurately. Like they were miscategorizing people. So that is what prompted the FDA to put the black box label.

And that's where a lot of this myth comes from. Also, there's always been this question of why do men have more heart disease than women at equivalent age? And they thought that it was related to testosterone. That's not it either. When we look at the studies that look men with low testosterone, all right, When we look at the studies and the cutoff is a little varies, but let's say it's around on average 250. Men that have a testosterone lower than that, have 50% higher risk for dying of heart related problems.

And they have much higher risks for prostate cancer and aggressive types of prostate. So what we, you know, that and then a hundred years of of studies and anecdotal studies, case reports, and tell us that testosterone is vital for men's overall health. When we look at the experimental studies we see that it's vital to vascular health, really helps to maintain the lining of the artery, the endothelium, maintains the health maintains nitric oxide.

Testosterone is something that has got a receptor in every cell in our body for a reason. Brain health you name it, bone health muscle health, recruiting glucose, getting it out of our bloodstream faster. You name it, testosterone is beneficial. And as we look at the levels that people need, replacement therapies, within like 750 to 1200 for your total, that's shown to be safe and even a little higher.

There is no data that shows that elevated levels of testosterone in that range or using testosterone replacement therapy causes heart disease. In fact, it may be the opposite because it helps with improving the vascular lining and glucose management. There's many myths that are associated with testosterone use and cardiovascular disease, I think part of that comes from the bodybuilding community. I love bodybuilders because they experiment on themselves and They were using testosterone cycles at much higher doses.

So that gave us the information to know that, yeah, if you push testosterone to 10 times the physiologic dose, that's going to cause hypertension. That could cause, you know, left ventricular hypertrophy, heart enlargement. It can cause adverse issues, especially if do multiple cycles or you don't take breaks. It can adversely affect your HDLs and make you have premature plaque. So there are real risks, but it's in that extreme population.

But that extremely population gets conflated with the population that just wants good replacement therapy. Yeah. Speaking to that, one of the questions I get a lot of, especially around the men conversation, you don't really see this as much in women that are using testosterone therapy because it's such a lower dose. When you look at hematocrit and hemoglobin, obviously the reference range for hematochrit is usually the cutoff. I want to say it was like 49 or 50 for guys. And you have a guy, he starts testosterone three to six months in, and he feels amazing.

He's like, wow, this is the best thing that's ever happened. It feels so healthy. You get to somatic grip back on his first or second blood work, He has a panic attack because maybe the doctor is saying, oh, now we've got to go phlebotomize you. And we have this cascade of things that start happening. Can you talk about what's going on there, one with hematocrit and men on testosterone? And then maybe what is important to understand contextually for a guy that's on a testosterone that may be different for the guy? That's not around those numbers. Yeah.

When you're starting, so testosterone stimulates the EPO gene or the epo hormone epigen And epigen is what, you know, was used for blood doping to help increase your hematocrit. So this is a natural way to increase you hematic rate somewhat sometimes, but it stimulates your kidneys ability to make that, that increases your red blood cell count. Um, so taking testosterone and it varies at different, at individuals, the levels vary.

will stimulate some red cell production more than you might be doing normally. And this is why we keep track of it. It also gives us a gauge of where your system might being pushed with testosterone higher than we expect or lower. When the system is making the more of those red cells, it actually also increases production of things that break down clots. So PAI-1, that's what's involved with clot breakdown.

And so when we are making more testosterone, we're actually thinning the blood a little bit too. We're improving the the Blood's ability to break down blood clots. So when you see slight elevations, that is the, you're getting a little bit more blood in the system. That by itself doesn't necessarily, and has not been associated with any increased blood clots in studies. And then when we look at the experimental pathways of testosterone, we also see that you are getting little extra blood thinning.

So what ends up happening is, I say blood-thinning kind of loosely. What ends happening when you get to higher levels of hermeticrit and hemoglobin, say you up into the 55s, then that's a little bit high and you may want to consider getting a phlebotomized, but below that, you're not going to have a blood clot. And if you do, it's not from the testosterone, It's from something else. How do you, speaking of blood clots, I've been to several conferences and I kind of heard off the record, like when they're talking for their CMEs versus like,

when I'm just talking, for a question and answer, treating people that have had a history of flood clods. Say you had someone come to you with a story of a flood clot, what are your thoughts on that? Is that someone that is just not a candidate for testosterone or are there ways to approach that intelligently to maybe where you can help them optimize? Oh yeah, yeah. No, they are still candidates. It depends on what the situation is. And if they've had multiple blood clots, if there are blood thinners, that doesn't mean that testosterone is out of the question either. It really just means what was the situation and how can we mitigate the risk?

What else can I add, whether it's a pharmacologic agent or a supplement that can reduce the risks? So bloodclots are, they are something to consider for both men and women. And it is a great segue to talk about women's hormone replacement because when you look at what's one of the concerns for women's hormone replacement therapy is using oral agents if you've had a blood clot. So, women's hormone replacement, testosterone, estradiol, progesterone has gone through some major changes in the past year.

The FDA dropping the black box warning, the industry really accepting the mistakes of the Women's Health Initiative and the fact that women need hormone-replacement therapy to maintain health. just like men need testosterone, women need estradiol, they need testosterone, and they progesterone. And the question is, how do we deliver it to them? The studies looked at synthetic commercially made projestins, synthetic estridiols that weren't even human, you know, that's why they created inflammatory issues,

especially with the projestins. When you look at bioidentical hormone replacement therapy, it's a completely different story and a much safer way to give women back the hormones that they vitally need. So, you know, estradiol, when you take it orally can cause an increase in risk of blood clotting. And that was based on studies that looked at synthetic estridiol replacement, not bio identical. and they're different chemicals.

So, you know, they don't necessarily, there are apples and oranges. You can't, necessarily equate one with the other, but that's what's happening. Oral, bioidentical, estradiol, maybe we'd be cautious and use a topical. But that is not the case with progesterone, the oral micronized progeterones, not associated with inflammation or clot risk. And the same thing applies with women as I said with testosterone. Same thing apply to women.

It's vital for a lot of their function. Women respond a little better to testosterone with their mood, with libido, but equally vital to all of those sort of performance enhancement type goals and just general sense of well-being. Yeah. It's interesting kind of this explosion of just awareness about hormone replacement therapy. Obviously like just talking to people online, coaching a lot of people. I think it's almost easier now for a lotta women, especially if they're perimenopause or postmenopausal, to convince them that they need testosterone than

it is some men. They kind of have this type A, like I'm going to tough it out and do everything I can to naturally raise my testosterone. Whereas I think a lot of women are in a situation where a guy that's in his 60s or 70s, his testosterone is going be a little lower and he's probably going suffer, but he can grind and bear it a bit. I would actually say to that point too, I'd be interested in your take on this. I've seen a lot of guys like in their 60s and 70s blood work have higher natural testosterone levels than a lotta guys now that are in there 20s. And whether or not that's like an epigenetic thing of like lifestyle choices or history, I actually think it probably has a little bit more due to the

endocrine disrupting chemical exposure that some of the younger people have experienced. all the way from being in the womb to where they are now. But it seems like women are a lot easier to convince to go on testosterone because a lotta times they don't have a choice. You can have women, I've seen women that do everything perfect from a metabolic standpoint. They take care of themselves, they eat right. And they can be 62 and their hormones are still gonna be zero. A lot of times their only choice is to either suffer or to get on HRT.

It's kind of interesting. I hope as more and more people get exposed to information like this helps inform and form their decisions. It is amazing. And I had a 77 year old patient today who I talked about hormone replacement therapy with a year ago. After hearing about the FDA reclassification and acceptance of hormone, replacement, therapy for women, they're now willing to start hormone replacement

therapy and there's no age it's too old to star. It's just a matter of making sure that the risks are well assessed because especially when it comes to cardiovascular disease, the first six months for starting estradiol and some of these hormones, they did have an increased risk in the WHI trial of a heart event. Again, it's synthetic estradiol, and they're starting at a really strong high dose. So it was really simple. You just start low and then work your way up and the system adjusts very nicely.

Yeah. Actually, that actually sparks a question I have, because I've heard topics of conversation around this before. Let's say you have maybe a 77-year-old woman that's been through menopausal, maybe 15 or 20 years post-menopause. Do you approach treating them with HRT, assuming that they've never been on hormones at all? differently than maybe you would like a 53 year old woman who's newly been a puzzle that kind of for the first time is going through this hormonal fluctuation. Cause I've heard, you know, things talked about in the past of like, Oh, well you got to treat someone that has basically been devoid of hormones for a

lot longer than may be someone who is newly transitioning through menopause. Do you think about those differently at all? I do it much more gently and slowly with the older population. Once their system doesn't understand or remember the way hormones reacted to them, then they're going to be more prone to having side effects, especially starting estradiol, progesterone. I make sure we start low so they don't get breast tenderness or spotting.

I mean, a 77 year old woman does not want any of those kinds of things. No woman wants to deal with that. Forget about later in life when they thought that those days were behind them. So I warned them about that and then start really slow and just incrementally go up over the course of a year or two. Yeah. Shifting gears a little bit, let's talk about peptides, everyone's favorite thing to talk these days. Peptides are all the rage, obviously, and I think for good reason. Just kind of, I would say, before we get into the weeds and the nuances of stuff, how do you think about peptides through the lens of cardiology?

And is there something, as a cardiologist, you'd think if someone is new to the peptide world, Is there a way that you kind of like introduced them to this? Because obviously you can go down, there's hundreds of different peptides that people can use. How do you think about it? Let's say someone's never used peptide before, how do kind walk them into this world and explain what it's going to mean for their cardiovascular health? Yeah. The first thing I like to give is a contextual kind framework for that. Peptides, they've been around for more than 100 years.

Insulin's a peptid. That's one of our first ones. So we've been using, and pharmaceutical companies have been, using peptides for 100 years. They just haven't been able to get utilized well because peptide has been very fragile. It had a short lifespan to them and we didn't know how widely applicable they would be. So it's only taken, it has only been the convergence of pharmacy technology, the human genome project, and our scalability to be able to make these in

the past 10 years, where it's really been something much more available. So it is not something that's brand new and it something technology that we've been familiar with. And then the next discussion point is that peptides, when we talk about it sort of like this, are a lot of the maybe fringe peptides that conventional medicine doesn't really talk about. There's a whole host of those peptide that are mainstream medicine. You know, there's Ozepic, Monjaro, those are the two that're the most globally known.

So we have many of them that's FDA approved. PT-141 or Bromelanotide, that's FDA approved for sexual dysfunction for women. So there's a lot of FDA-approved peptides. If a doctor wants to understand how they function or at least be familiar with them, learn those or get accustomed to those. GLP-1s are everywhere and just about every doctor should know how to use those because everybody's going to be using them at one point or another.

Once they kind of get over that hurdle, then it's start talking about some of the other peptides that may be a little bit more on the fringe. You know, peptide that are considered research because they don't have a lot of human data. There's human on most peptids now. It's just whether it is randomized controlled trials or whether its data that's actually stateside and in English because When you look at peptides like BPC,

there are many studies that are from Russia, from the Eastern Bloc countries that just not in English, they never made it over to our databases. So the way to get them to start introducing or understanding is just take one peptide, take a handful of them that we know are safe, and just learn those. And that's basically what I did. I started with BPC, I start with TB4, TA1, and then the secretagogues, CJC, ipameralin.

Those are plenty to learn right there and each one of those has an application to the cardiovascular system. They help the vascular system more often than not. Things like BPC, they help that lining of the artery, regrowth, collagen, reduce fibrosis. TB4 similarly does the same thing. you know, get to know a few of the aspects of how these peptides are functional, maybe know how they work on a cellular level,

because peptide's really, their strength is how the interact with us on the cellular-level. And when you learn that, then you learned what it does in one cell. It does that in multiple cells. So that's a really good way to kind of expand your knowledge. But there's applications for each of these peptides that I mentioned in the cardiovascular system. It's just a matter of learning them and then I can lay it out for you now if you want.

Yeah. Let's do that. I was actually going to say, maybe let's just start with GLPs. Obviously people kind of think about those as a diabetic slash obesity medication, which they are. But what do you see, especially in the context of heart health that they're actually doing? Because even like some people that I've coached, like their blood work is kind actual lifestyle change that they introduced, which I think everyone should introduce lifestyle. Change. I'll just say this. A lot of people that watch like my father-in-law refuses to change anything and his lifestyle and I love him to death, but he's not going to his daily routine.

He works at a golf course so he can golf for free because he retired and everything. He's not going to exercise. He is not really going change his diet, but in the last two years, he's used GLPs and he has radically transformed not only his physique, then also too when you look at a lot of the markers on a blood panel, what he is done. Can you talk about what the GLP's are doing to our hearts in a good way? Yeah. Let's start with the vascular system. So GLp1s, and this is based off of randomized clinical controlled study.

The GL p1 in select trial, in patients that were non-diabetic had a reduction in cardiovascular events. So, we're talking about independent of weight loss and independent glucose control, they saw a production in all-cause mortality reduction and cardiovascular event. What they found when they break it down into mechanisms is that GLP-1s reduce inflammation in that vascular lining. That endothelium is vital to our overall vascular health, and it's considered one of the largest organs we have.

Not the large, but it is up there, because it takes a lot of surface area. It's anti-inflammatory, it produces anti inflammatory compounds, one the most powerful of which is nitric oxide. And GLP-1s reduce the amount of adhesion molecules, meaning the molecules that allow, that grab onto LDLs and internalize them into the wall. It reduces chemicals that are inflammatory. And even, you know, there's data that shows that it can maybe relax the arterial system and lower blood pressure a tiny bit.

A lot of, really fundamental changes that happen in the vascular lining that completely independent of what it's doing from a glucose standpoint. So imagine if you add that to a person, you know, just those anti-inflammatory effects and then they also have a glucose problem, and they're also overweight and extra fat releases its own library of inflammatory cytokines or hormones.

We're reducing it multiple different areas, multiple, different pillars of insult to the artery. So really, really helpful from a vascular standpoint. And there's even experimental studies that show that using GLP-1s with maximum goal-directed therapy can potentially help in reversing plaque, some of that soft plaque. So it's part of the foundational care that I have with almost all of my cardiac patients that are worried about atherosclerosis.

Then when we look at the actual heart muscle, it does some really foundational metabolic changes to the heart and muscle. The heart-muscle is unique in that it shifts from different fuel sources depending on output. It's the only organ that does that. because it can either function at a really slow idle where it just pumps, you know, 50, 60 beats per minute and in a good case scenario, or it's got to go up to 150 and it has got use a different fuel source. So when you use GLP-1s, it optimizes what it needs to burn when it is rested and then changes and shifts what is going to be used optimally when is goes up.

When glucose is gonna be use versus when fats are gonna used. And that's good for performance, it's for general health, but when you have somebody that has heart failure or an enlarged heart, that metabolic spectrum or that balance is off. And so something like a GLP-1 helps to re-establish a proper balance. Yeah. Let's talk about BPC 157 and, you know, Thames and Beta 4, TB 500. Most people, and rightfully so, are like, Hey, I tore my shoulder.

I hurt my knee. And I'm going to use these there, which they do really well. But I think a lot of people don't realize the breadth of healing that they're inducing in the body. Can you talk about, specifically for the cardiovascular system, what mechanistically they're doing and why there might be a use case beyond just, you know, I hurt my shoulder and my knee, What they could actually do to heal some of the things in the vascular system in body? Yeah, the BPC and thymus and beta-4 work really well together in in vascular system.

They're different areas, but they synergistically have a great effect. BPC can stimulate, I don't know, more than a hundred types of genes and it does it quickly. So it stimulates epigenetic change fast. But what it primarily, and the biggest effect is on improving nitric oxide. We're back to that again. It helps to improve how the genes that transcribe nitrous oxide, the enzyme, the ENOS enzyme that makes it helps to improve how your body's utilizing the

nitric oxide that's existing and how you can make it more efficiently. So in all different tiers of that vital gas, that chemical, you know, the BPC helps with that. What it also does is, and nitric oxide helps the endothelium, the Endothelin is vital for outgrowth of new arteries. And it helps to regulate it, not in a fashion that the body can't control. So you don't get this uncontrolled growth of blood vessels, which is sometimes some of the concerns I see online with PPC.

It doesn't do that. It's a modulator. So what also happens is BPC can stimulate something called VEGF, which is another growth factor that helps make the artery arterial branches and further angiogenesis, further arterio growth. But again, it's modulating effect. and they're short acting. So you get a pulse and this is how the body works best. It works in a cyclical manner and it takes a pulse of something, gets a stimulus, checks and sees if this stimulus should be followed or not and then can

either inhibit it or can encourage it. BPC helps the vascular lining. You add in TB4 which has Effects on fibrosis, effects on collagen deposition, just like BPC does. Actually, it's the actin skeleton, which is that cytoskeleton. And then it is an anti-inflammatory. So when you look at how that affects the vascular system, the combination of improving nitric oxide and then being anti-inflammatory from another standpoint

where it inhibits some cytokines and other inflammatory markers, it makes a really good effect to reduce the overall inflammatory burden on the endothelium and keep the things like LDL particles from grabbing on and causing plaque. So great for healing, great from maintaining overall health, and great form managing inflammation. Yeah. Speaking of growth factors, everyone loves the growth hormone peptides or GHRHs and GHRPs.

What are your thoughts on those? Maybe specifically, I think everyone that has tried them probably more or less thinks that they're a good thing, but what are you thoughts around those around heart health? And I have a lot of people that ask me, is this something that I've to worry about? The growth of my heart, like is going to make my hear grow or is it actually the opposite to like, are they improving metabolic health is actually going beneficial for our heart long term. So the, what we want to do is we wanna separate the information that's out there about synthetic growth hormone with the that on secretagogues and,

uh, you know, growth, hormone, releasing hormone growth or releasing peptide, two very different animals and how they stimulate the system. Synthetic growth has a long lifespan to it, has long half-life. So once it's injected, it is constantly stimulating the system steadily and our bodies can't regulate it. Can't inhibit it so we get this steady growth stimulation that just can, that doesn't stop and then if we are doing long cycles of it this is where we can uncontrolled growth. We get that six pack behind, you know, a large abdomen And then this is where we start to see acromegaly and that's where see large hearts.

That's what we see hypertension because it causes fibrosis, it cause uncontrolled cellular growth. When we look at secretagogues, we'll look growth hormone releasing hormones, growth hormones releasing peptides, they have a really short half life to them, you know, on the order of 20 minutes. So when that's injected, it's only going to stimulate your system for that period of time. And then once that is done, our body gets to take stock and and use our inhibitory mechanisms or our promoting mechanisms as it sees fit.

So our body can regulate it. If you're only doing one shot a day, 20 minutes of stimulation to an optimal testosterone peak, that's not going to cause any untoward growth. It doesn't cause an aggressive growth of abdominal contents, of bones, you know, the heart muscle. And in fact, it improves metabolic health because It's, you know, our system works best with a push-pull. So you can get a Push and you could even use these multiple times a day because on average you're still going to be off of that stimulation more than you

are going be on it. That half-life makes a big difference. And then the ability to adjust the doses. Synthetic growth hormone, You can do that too. But again, the stimulation is constant and it was often used at high doses these growth hormone secretagogues, very different animal, don't cause any of those problems from a cardiac standpoint. What I will say is that they do need to be cycled because the constant stimulation can sometimes make the receptors adapt and less sensitive to them.

So two months on, one month off is often what I do to maintain freshness and also to give the system a little bit of a break because if it's constantly used, there can be some increase in cortisol and receptor desensitization. So I just cycle those. Yeah. Probably one of the more common questions I get, and this is relates to BPC and TB or TB4 and also the growth hormone peptides. As a doctor, you'll hear these platitudes of like, oh, well, that causes angiogenesis or increase in VEGF.

That's going to cause cancer. Or it feeds growth hormones, which can feed cancer as a Doctor. How do you think about that? And if you had a patient that's coming in, it's like hey, I really want to do these, but I'm worried about cancer, maybe I don't have cancer at all. There's nothing to indicate that I do. how would you speak to someone that might be concerned about So there's two situations, if you have no history of cancer, then we can do some screening tests to see if there is any risk. I usually like to do an IGF-1 prior to starting just to what their baseline is.

And if it's really elevated, that's cause to look for cancer. If it is normal or low, we know that they are going to respond well to these. For the most part, if you don't have a history of cancer and your IGF-1 is good, then we can start without a problem. I can just reassure them that talk to them about the lifespan, talk them the half-life, and the fact that these don�t indiscriminately stimulate this because, well, number one, they're doing it for such a short period of time.

All these peptides are really sensitive and have short lifespan to And then they're more like modulators. These are messenger systems that our body uses anyway. BPC, we make. GHRHs, We make, GHRP, that's also known as ghrelin, make all of those hormones. Same thing with TB4 and Bpc. I mean, all these are natural compounds that we made. We're just reintroducing them. Synthetic growth hormone is not a natural compound.

So it's very difficult for our body to regulate it. And that's why it just has that long lifespan and that effect. That's kind of the dialogue. If it is somebody that has had a history of cancer, it depends on what cancer. Is it active? Is in remission? How long has it been in Just because they've had a history doesn't exclude them from being able to use these. The real question is whether it's active or not. And this is where it gets a little bit gray, because when you look at the studies of, say, tessameralin, Tessamaralin is a GHRH.

with the original studies that looked at it in HIV patients with aggressive Kaposi's car sarcoma, they actually saw regression of the Kaposis sarcooma when they were on tessameralin therapy. So, and what we know is that when you stimulate growth hormone, there are many, many different isoform metabolites. One of those is an IGF binding protein that will actually be anti-tumorogenic. So you're making actually anti-tumorogenic compounds by giving a secreticog.

And that's experimentally proved. There are some studies that are showing that it is safe to use that, but it's still a gray zone. You've got to be careful. If there's medical legal aspects to it and other physicians that may speak out against that and that becomes a problem for the prescribing physician. But the data seems to support being able to use it. Yeah, I think it's one of those things too. It's very easy to talk in theory.

In a lot of the peptide world right now, it is in-theory because we don't have the quote-unquote human studies, even though we have lots of anecdotal data of people using peptides in a very healthy manner to improve their health and stuff. It's kind of dangerous when we start to extrapolate one way or the other, you know, theoretically of like, oh, this, like in theory does this. Therefore, it's going to cause these issues. So I think it is just one thing to keep in mind. But like you said, there's also as much data out there to suggest, not in fact that it doesn't, but then in the opposite, that is actually helping. Especially when you look at cancer and the metabolic nature of cancer, and not all cancer is, we improve metabolic health.

A lot of times that's gonna bode well for us. Yeah, I think there's a lot more options to improve metabolic health than using, say, secretagogues, you know, in that situation. Yeah. I, think we just have to be, we have, to, be prudent and just kind of look at what's the best way, the, best options for the patient, as well as what has not been used that we can still lean on that doesn't really introduce any risk. Yeah. Last thing on peptides.

Mitochondrial peptide are huge right now and for good reason. A lot of people gravitate to the mitochondrial peptides because they're like, hey, I don't have any energy and I seem to be doing everything else right and still don t have energy, which they can absolutely work well for that. Specifically around the heart again, how do you see mitochondria peptidies playing into heart health and are there any favorites that you have that would say might be better than the other for heart specifically? Yeah, I like SS31 as a mitochondrial peptide.

It functions by improving cardiolipin. Cardiolippin is that structural protein that keeps the inner mitochondria membrane nice and folded. And that's important because the folding helps to keep all of the the molecules or the little mini structures that make ATP and make NAD keeps them together. Because if it separates, that distance between them, if flattens out, the mitochondria then don't function well and that can be what happens in a person

that's got chronic fatigue. So, SS31 helps to re-establish that and make the mitochondria much more efficient. So that's usually one that I look at. I don't start it necessarily right away. What I do is I want to get the right precursors in there because when I'm establishing mitochondrial health, I wanna make sure membrane health is good because the Mitochondria sits in the membrane. So I'm going to feed them the right formula, formulation of omega-6s, omega 3s.

Maybe get them on some urolithin A, some supplements to help improve the mitochondrial structure, and then hit them with an SS-31. And the dose usually ends up being higher than what we think, probably an order of 20 milligrams a day. So it's high. Because of that, it makes it expensive. That helps to reestablish the mitochondria. And then when they do, like when the exercise or when want to do their activities, they'll have the ability to it on their own.

and then I'll layer into the others. Humidin is really important too, helps with autophagy, it helps the vascular system. Again, back to the endothelium. helps maintain a healthy endothelium and maintain reduction in inflammation because the endofelion itself regulates that and if it's healthy then that's going to do it. And then the last one I'll add in there once I know that their system can make energy well if I want to push it, that is when I do MOTC.

So MotC is the sort of like, it is not the first go to because if i put that in a person that has got a system that can't really produce it It's not really doing any good and it may actually tip them into a place where they're feeling worse. Yeah. I've seen a lot of people lately, again, just because peptides are so big. They hear Matzi does all these amazing things, which it does, but they'll go right to it. And then in three or four weeks, they are actually feeling a whole lot worse and I don't know if this is the right way to say it, it's almost like redlining their system to where it is pushing and pushing.

There is nothing there. to push and they're kind of stuck in the driveway, so to speak. So I've always, I'm always more in a camp of human and SS 31 first to kind clean up and make sure everything's there. And also too, most people feel really good after taking those. In my experience, whether someone's more healthy or even if they are more inflamed, they feel good and then come in with Mozi when the environment's right. But I just, it seems like as more people are being exposed to Moci, but I think it's about context of understanding where it is at because I see a lot of people actually having the opposite intended outcome of why they started in the first place.

Yeah, that's a great observation and it's great analogy because that really what's happening. You've got a system or you think about it as a car that you can put Really, I mean, you could redline it and it'll just pump out a lot of smoke and make a really hot engine. The engine will just get really high and eventually it will break down as opposed to fixing the engine, making it more efficient. And you don't have to red line it as much to get the same amount of output.

Yeah. Last topic for today, I want to talk about SGLT-2 inhibitors. So I got turned on to these probably about a couple of years ago and just started reading more and then started using ones myself. And the longer I've been on them, and again, just tracking your typical blood work things, but I just keep seeming to get healthier and healthier with no downsides. Obviously, they come from the diabetic world, much like the GLP-1s do.

But I think when I talk to a lot of people, there's a lotta hesitation around those because they think of like diabetic medications. It's like, oh, I don't wanna be on a diabetic medication for life, or I wanna use a diabetics medication because I want to be like hooked on the drug or whatever. But can you talk about conceptually SGLT-2s and maybe what they're doing from a longevity standpoint, especially for someone that might not be diabetic. Maybe they need to lose five pounds or whenever, but I there is probably some misconceptions around how they would be used in the context of longevity.

Yeah, yeah. So SGLT2 inhibitors, sodium glucose transport inhibitor. I forgot what the L is. But it blocks a certain transporter of sodium and glucose. Kidneys are interesting. It filters everything through, pushes everything into the urine, and then it reabsorbs a lot of the stuff that we need back. So the sodium and the glucose get reabsorbed back as it goes through the kidney.

This medication, SGLT2 inhibitors, prevents that re-absorb so you pee out more glucose and more sodium. It sounds like it's simple and it would have a minimal effect, but what it does is it triggers a whole cascade of things that have profound effects on our system. What it do is, it kind of tricks our body into thinking it is fasting when it really isn't. And so it stimulates the AMP kinase system, that's the system that improves our metabolic efficiency.

That's what we do when we're fasting. It improves our ability to burn fats, you know, it's our rest and recovery system as opposed to mTOR, which is our building and pushing system. So this stimulates that and by doing that, employs all of our metabolic pathways that improve our cellular efficiency. When it does that in And the SGLT2 receptors are not just in the kidneys. That's where it's found most concentrated, but those receptors were also found in a heart, in vascular system, and the brain.

It's in pancreas. I think there's some of the muscle. There are a few isolated places, In those tissues, we see improved efficiency, improved metabolic health. So it's also found in the gut too, which is interesting. And that's why it can recalibrate the microbiome, improve gut health, you know, short chain fatty acids which are important for gut, improving that metabolism.

It's got a multi-system effect that is perfectly in line with what we're trying to do with longevity. It's a systems approach that good longevity care means you're improving all of the systems or many systems at once to help the overall organism function better. So SGLT2 inhibitors meet all that. They do all these things in multiple different tissues. Yeah. I think it's interesting too, is maybe this is a prediction, maybe a little bold.

They'll probably make Metformin obsolete, assuming that people can affordably get them because MetFormin is so cheap. The SGLT2s are a bit more expensive. But I if you look at the cost benefit, if said you could have an S GLT or two or MetFormin, I would take S glt2 all day because of the benefits you have. And you don't have any of drawbacks of Met Formin that a lot of people have, so. That's right. Yeah, I did a lecture a few years ago and that was part of it. That was a gist of, it was about Metformin being old news and SGLT2 inhibitors should be the one that you use now.

So I agree. Well, wrapping up, the thing I appreciate about you is you practice what you preach. Not only are you living this in your professional world, but you also live it in personal life. Can you just give people kind of high level what do you do from a principal standpoint, Diet lifestyle, and you don't have to go too into the weeds, diet lifestyle and then supplementation peptides that you do on a daily basis. Yeah, I try and keep my sleep schedule regulated as consistent as possible.

So sleep usually by 1030, wake up around 5, 530. I'll do something for my mental health in the beginning, which is usually some sort of either hobby reading or other activity that's non clinically related. And then by six o'clock, six thirty, I'm in, the gym, and it can be any number of things about six days a week. And then after that, my meals, usually I'm a Mediterranean, high protein, and high fat meal.

That generally works for me. I don't really count macros, but I'll try and get in as much as it keeps me full. It's probably, I probably need more protein. One of my deficiencies, one of the habitual sort of issues that I've got to work on. From a supplement standpoint, I take a daily dose of baby aspirin, Cialis at low dose for my vascular health, Telmasartan at a low-dose, because I'm not hypertensive, and low dos, meaning not enough to impact my blood pressure, but it has really good longevity effects,

stimulating pathways a similar way. When I have an SGLT2 inhibitor, i may take it, Uh, it's usually trisepatide and I have, um, testosterone as part of my replacement therapy, uh, other supplements, vitamin D, magnesium, urelithin, a, if I'm going to do a fast, I'll take spermadine for, for a week prior to my fast. Um, you know, fast that much except just a little bit of intermittent fasting because I want to maintain my caloric intake.

Uh, but it's more about performance, uh, goals for me. And so I'm more. Taking in the adequate amount of calories than inhibiting them. So I don't utilize fasting as much. Um, and my, the, of the peptides I use, I mean, i'll use a test of Maryland, if a Maryland regularly. cycle those that works really well. I prefer Tessamerelin for vascular health and Epimereline is a good add-on to that. Um, I will cycle in, uh, SS 31 and epitalon quarterly.

because they help with overall metabolic health and the epithelium for my sleep cycles. BPCNTB4 I'll use for many of my regular injuries. I'm never really without it for more than a few months, so it just ends up being cycled in to help treat injuries Awesome. Well, I think that's a very good summary of kind of the pillars that we all need. And then kind based on what you just said right there from your own personal health, very similar in a lot of things I do.

I always tell people, there's hundreds of peptides out there, you can go down the rabbit hole. But after those core things, the rest are kind just gravy and we're just kind playing with stuff that is nice to have here or there. Those are really good. Yeah, well, I'm sure there's much, much more that we could talk about, and hopefully we will in the future. But thank you, Dr. Avid, for coming on today. Just in closing, what's the best place for people to find you online? And then if they want to work with you how can they reach out to you? Yeah, I'm online. I have an Instagram page.

It's Dr. Underscore Abed Hussein. On YouTube, you can find my link there. That's also just Dr Abid Husain. And you could find me at Boulder Longevity Institute. Available to taking patients if you're interested. Awesome. And we'll have the links down in the description for everyone to check that out and make sure you go support him and support the guests that come on the show and so graciously donate their time to help spread this information and help make your lives better. So that's it for this one. Hopefully we can have Dr.

Abed back very soon because there's a lot more topics that I would love to talk for three, four more hours about that we talked about today. Show him your support. Yeah, exactly. I show him you're support and we will see you guys in