Plasma Exchange is Healing Neurological Diseases? With Dr. Syed Asad | TPE Blueprint #16

What if your brain isn't just aging, but what if it's actually under attack? And what can you do to stop or even reverse that decline before symptoms ever show up? Today I'm joined by Dr. Syed Asad, a board certified neurologist and brain health pioneer who's blending cutting edge detection with regenerative tools like plasma exchange to rewrite the future of cognitive decline.

Doctor Said Assad, it's awesome to have you here and you know, brain, brain health, brain talk. I mean, just everything brain. I think that's a big topic right now, you know, across the board, I'm sure in, you know, in the, in the medical community, but also just on the streets, you know, with everyone. And yeah, that's what I want to talk about is kind of your perspective and with your work. I want you to give us just a little, brief little background on what you've done as of yet, but also just where things are at now, but where we're going with brain health and what's even possible.

Sure.

And how plasma exchange and all that, because you've been doing it, which is really cool.

Yeah, yeah, for sure. So I will start with.

You mentioned the brain is in the limelight. Maybe this is a neurologist's bias, but I think the brain should have always been in the limelight because the brain is the highest organ. Right. It's center command. It basically controls everything.

As far as.

The field of neurology, which is what I've been practicing for the last 20 years.

It started out with.

People being able to make diagnoses but not being able to do a whole lot. The joke used to be diagnose idos. And you know, and unfortunately there's still conditions like that, from Lou Gehrig's disease to Alzheimer's disease, et cetera, where beyond a certain point, there really isn't a whole lot you can do.

The cool thing is that over the last few decades, there's been more and more interventions. And I think that's what pulled me into the regenerative medicine side, where I was definitely interested in treating my patients who came in with symptoms of Parkinson's or symptoms of dementia. But I was always fascinated with the idea of how about if we prevent this from happening in the first place, how about if we figure out that someone is headed in that direction and do certain things where we can avoid this, or once it starts, what can we do to prevent it from getting worse? And I'm not just talking about symptomatic treatment, I'm talking about Actual disease, disease modifying treatment.

Can you break down the difference between symptoms? I think that's fairly obvious. But the disease modification, the second part there. Yeah, I'd love to.

Yeah, yeah. So I'll give you an example. So for. With Alzheimer's disease, it's a complex pathophysiology, but in short, you've got these two bad proteins, you've got hyperphosphorylated tau, and you've got beta amyloid that basically clumps together and forms amyloid plaques. The amyloids outside the cell, the tau is inside the cell. And these two, along with inflammation and other things, damage the neurons or kill the neurons. And that's basically the decline that you see in people who have Alzheimer's disease. So symptomatic treatment would be something like donepezole, which is a medicine that increases acetylcholine in the brain, which is nice. If you give the brain more acetylcholine, it functions a little bit better. But you're essentially rearranging the deck chairs on the Titanic. The Titanic, unfortunately, is going down. And so disease modifying treatments would be a way to figure out that once those amyloid plaques start forming or once the neurofibrillary tangles with the tau start forming, what can we do to make sure that process doesn't persist or maybe even figure out when a person is heading in that direction to avert it all together? And that's where a disease modifying treatment would come in.

Interesting. Okay. And yeah, we already seeded that. You've been using plasma exchange for a while, you said for what, 20 years, right? Thereabouts. So, yeah, we'll seed that for just a little bit. I want to go a little, kind of set the scene a little bit more. But that's already intriguing is how it's been used and how you're now doing it. I'm curious on the detection side, like, I guess, what's the approach? Are there new improvements now? And I guess what are the tools? How's it done?

And are you specifically talking about dementia?

I guess with any kind of neurological disease, where would you start? And maybe some. What are some of these symptoms where you're finding people? What's the first step? When you see someone, you're like, okay, sure, yeah.

So broad categories with neurology are.

There'S.

The central nervous system, which is the brain and the spinal cord, and there's the peripheral nervous system, which is the nerves that come out of the spinal cord and basically connect with muscles at the neuromuscular junctions. And spread from there in broad strokes. You've got diseases of the central nervous system like dementia, like stroke, like epilepsy, like multiple sclerosis, and then you've got diseases of the peripheral nervous system like neuropathy and myasthenia gravis. So when you're approaching a patient with neurological conditions, you first localize where the disease is, then you come up with a differential diagnosis of possibilities. Then you test your diagnosis. If it's a central nervous system disease, you might want to do an mri, you might want to do a spinal tap, you want. You might want to do blood work. If you. If it's a disease of the peripheral nervous system, you might want to do an EMG nerve conduction study. So there's different testing modalities. As time has gone on, the technology has gotten better and better. And so we just hopefully are doing a better job of nailing down the diagnosis. And in the case of neurodegenerative diseases, if we make the diagnosis ahead of time. So, for example, let's say someone who would normally start having memory problems, let's say in their mid-60s, and they would go to their primary doctor, then they would go to a neurologist, then they would get, you know, testing, cognitive testing, scans, etc, and they would get a diagnosis. Let's say Someone has an APOE genetic test of E4. E4 that puts them at high risk for dementia. Let's say they're only in their early 50s right now, and with that genetic profile, they get blood work that shows that they're also already spilling amyloid and tau proteins from their brain into their bloodstream. And then you do an amyloid PET scan that shows amyloid deposition has already started in their brain. They're cognitively completely normal, but they're showing signs of early dementia. Well, that would be the time to strike. And if you can remove either the factors that trigger the amyloid entire pathology in their brains, or have a mechanism to remove those bad proteins or stop their accumulation by the time they reach their mid-60s or beyond, you might actually change the direction of where they're heading.

Interesting. Okay. So, yeah, I've definitely heard of that gene. So basically having a genetic profile. And you said that's. Would that be a blood test primarily where you.

Yes, the E4, E4, that. That would be on a blood test.

Blood test. Okay.

And. And now, I mean, the amyloid and tau are CR markers as well. When I was in training, we would do spinal taps to look for amyloid and tau. And. And that's Fine. I mean, that's, That's a good way to do it as well, but, yeah, a lot of people don't want to be poked in their backs. And so a blood.

Little bit more aggressive.

Yeah, A little more invasive. So blood works easy.

I got you. Okay. Well, that's. That's interesting. So detection. Yeah, Lots of ways to go about it. It makes sense depending on what's going on.

Are you seeing trends? Like, are there different trends now in the world we're in? Like, are. Are these types of diseases popping up earlier or in different ways? Are there different maybe more often cases that you're seeing than before?

Yes, if you look at the epidemiological data, there are more and more cases now. Some of that could be related to the fact that we're living longer. So for dementia, for example, you know, the longer you live, the higher the probability that you'll end up with dementia. Some of it may just be better diagnostics where back in the day, maybe people. People didn't even realize that, you know, they had these issues going on.

True.

Especially in mild cases.

But there is definitely an increase in prevalence of these conditions, and that is probably related to many of the risk factors. So there's, you know, in this day and age, people are more sedentary than our ancestors were. That's just because we live in a comfortable world and, you know, don't need to work as hard as our ancestors did. There's, you know, foods that we're eating or lifestyles that are promoting more what we call vascular risk factors, which can be a risk factor for neurodegenerative diseases. There's pollutants and toxins. There's processed foods. There's. There's more inflammation.

Yeah.

And also, just in terms of one of the things I always talk to my patients about is sleep. Sleep is foundational. We are designed to spend a third of our life sleeping. That's eight hours out of every 24 should be dedicated to sleep. And again, that's not by accident, that's by design. Because sleep is not just restorative to the brain, it repairs the brain. And nowadays, you know, I. I love coffee, too, and I enjoy watching TV and, you know, video games, whatnot. But if we overdo it, if we do those things to the detriment of our sleep, if we don't make sleep a priority, then we pay the price. And that also increases the risk of at least neurodegenerative diseases.

I want to tap in on the sleep part because, honestly, like, I know I I think it's just a lot. I, I like to say I think I'm kind of normal in this, that like, I know I don't get enough sleep, but I think it's because of the activity. It might be the phase of my life with kids too young kids around. But I don't want to give excuses here. I want like, what's your protocol to sleep? Like, just lay it on me the most.

Yeah, no, I'm so it's interesting. When I was in training and this is again not a very long time ago, just over 20 years.

We used to be told during the residency training that sleep is overrated. In other words, in healthcare we were told, you know what, you guys, you know, if you're on call for 36 hours, that's okay, don't, you don't need to sleep, just, just do your work. And I think that was noble in terms of like, you know, trying to take care of patients at, at night when. But the problem is.

If you continue that for too long, if you really deprive your brain of sleep and especially components of sleep like deep sleep and REM sleep, there's certain things the brain does during those phases that are lost when you're not getting those phases of sleep. So it's not just the quality, it's also the quantity. It's not just the quantity, it's also the quality.

Sure.

So you were asking what's a good number? So we have this ultradian rhythm, this 90 minute rhythm during the day and at night. So for example, when you're sleeping, your brain goes through stage one, two, three rapid eye movement in 90 minutes. And if you get about five 90 minute cycles, that's pretty healthy. So that's seven and a half hours. And if you wake up and you were just dreaming and you finished that dream and then you woke up, that means you just finished that, that 90 minute cycle. And, and, and generally you'll feel good if someone wakes you up out of like REM sleep. You're not going to like it groggy and everything. Yeah, you're going to have that sleep latency. And, and so for most people that's, that's a good amount. But what I also tell people nowadays in, in the age of Apple watches and Oura rings and whatnot, I tell people, and I do this myself and I actually show them my, my sleep data and I tell them, I'm not showing off, I'm just telling you that you can do this as well, is monitor to make sure that the combination of your deep sleep and REM sleep should be about 40% of your total sleep time and that's a healthy amount.

That's super helpful, thank you. Absolutely. One with an apple watch that I'm always looking at the metric. I don't necessarily now I know, I mean, that's great. Is there a timing that you like to shoot for for going to bed, waking up? Is there a window?

Yeah. So I use both the apple watch and the oura ring. And the oura ring actually tells you your chronotype. So once you've worn it for three months or more, it'll figure out your chronotype. So your chronotype is the ideal go to sleep time and wake up time for your brain. And it actually varies from person to person and it's good to know what yours is. And this goes back to the time where we probably lived in groups or tribes and the saber tooth cat could attack at night and so someone had to keep night watch. Right. So within the same family, people will have different chronotypes. So I always knew that I was someone who went to sleep early and woke up early. And sure enough, my wearable told me that I'm supposed to go to sleep at 9 or 9:30 and wake up at 5, which is what I do anyway.

It's natural. Yeah, yeah.

But it determines that not just based on your habits, but based on your heart rate and based on your temperature and based on a whole host of other parameters and it figures out what your ideal is. And so I think I encourage everybody to figure that out. My daughter, who's 22 and she's doing her master's degree right now, she figured out that her chronotype is go to sleep at 1am, get up at 9am and so I told her she's learning video game design. So I was like, cool, that's a cool field where you can choose your hours, hopefully. So just choose, you know, a job where you can basically stick to your chronotype so you don't have to compromise how your brain is wired.

I've seen that for me and it's a little later at night and I'm like, yeah, I can't be right. You know, I've always heard earlier, but.

Yeah, no, so it's not one, one size doesn't fit all. And I think in society we've kind of been again trained that you should get up early and you should go to sleep early. And that's not true for everybody. You have to figure out what your chronotype is and hopefully design your lifestyle according to how your brain is wired.

That's right. I mean, kids though are that wild card where you're just like, oh, gosh. But the season. So.

Yeah, yeah, yeah, no, I've definitely been there. Mine are 22 and 19, so it gets easier.

Thank God.

So.

Well, and you mentioned inflammation as well because of course, inflammation is the root of what basically all disease. Right, agreed. Yeah. So talk to me like, how do you think about inflammation then? I'm also thinking of, you know, obviously we want to reduce inflammation. There is a healthy component to it. But how does that relate to what you're seeing in neurological diseases?

I'm going to answer that question, but I'm going to talk about something else first. So I did a certification in acupuncture like 15 years ago and I was always fascinated by it, but I thought I was just going to learn another medical modality. But it's a 3,000 year old art and the philosophy behind it was fascinating to me. So I practice a little bit of acupuncture on my patients, mainly just neurological indications. But in acupuncture they talk about.

Balancing the forces, right? So there's yin and there's yang and you want balance. Now in medicine we call that homeostasis. And everything needs to be in homeostasis. Everything needs to be in balance. Right. And so for example, we have the autonomic nervous system. There's sympathetic and there's parasympathetic rest and digest, fight and flight. Right. And if you are too hyper adrenergic and too hypovagal, that's, that's a problem. You want to, you want to bring balance to the force. And so your question was about inflammation. And like you said correctly, you want to have inflammation so that when you get injured, inflammation is what repairs the, the injury. But you don't want that to turn into chronic inflammation, which like you said, and I agree, is the root of almost every malady that we have out there, and especially in the brain that that tends up being ends up being a huge, huge problem in a lot of conditions that we see.

Hello, my name is Kerry Stewart and I did the brain protocol for the MD lifespan. I was struggling to recall names of couples and so I shared this with the doctor. That's when he introduced me and said, I think you're ready and let me explain to you a TPE because this is going to help your memory, your focus, your clarity, and I truly believe you'll be a wonderful candidate for this. I have had Five tea PPE protocols. And each time I have improved. And it's not until this last one that I honestly, I am feeling so back on top of my game. Like my brain fog is gone. I am focused more, I have more clarity. This was life changing for me and I feel so much better for it.

Do you feel like there's a better grasp these days with things like plasma exchange to, I guess, to attack the bad, the chronic inflammation?

Yeah. So, interestingly, we were talking earlier on about the fact that in neurology we've used plasma exchange for a long period of time. And interestingly, the indications are mainly for inflammatory and specifically autoimmune conditions. So in myasthenia gravis, for example, people develop antibodies that start attacking their neuromuscular junctions. So where the nerve ends, there's a synapse, and then it connects to the muscle, and at the nerve ending, the nerve releases. When the action potential gets to the nerve ending, it releases acetylcholine. The acetylcholine crosses the synapse, attaches to the acetylcholine receptors and activates the muscle. Well, in myasthenia, you have antibodies that attack those receptors and damage the receptors. So the, the nerve is not able to activate the muscle, and it tends to have a predilection for certain parts of the body. So people start noticing their lids are drooping, their eyes are not working together, so they become, they have double vision, they can't swallow, they can't talk, their arms and legs are weak, they can't go upstairs. So. And in severe cases, it affects the muscles of breathing. So if they can't breathe, they end up in an emergency room with a tube down their throat. So it can be a pretty severe and debilitating condition. So with myasthenia gravis, for a long time we've used plasma exchange where we'll take their blood out, remove the plasma that has those bad antibodies and put normal saline, albumin and put it back into the system. And in that way, we clean their blood of these bad antibodies or auto antibodies that are attacking their.

Their, their receptors. And, and again, that's. That's true for other autoimmune conditions as well. I was, I was mentioning cidp, which is short for chronic inflammatory demyelinating polyneuropathy. That's a little bit of a mouthful.

Yeah, I'll look it up later.

But in that condition, you have antibodies to the myelin on the neurons, and it rips the myelin off the neurons, by the way. The acute version of that is also known as Guillain Barre syndrome or acute inflammatory demyelinating polyneuropathy. And so in those conditions, you can do the same thing. You can use plasma exchange to remove those bad antibodies. But the cool thing is that when you're doing plasma exchange, if you can also remove other inflammatory proteins or peptides, if you can remove toxins, if you can remove microplastics, if you can remove, you know, mold, then you're really getting way more benefit than what we previously thought.

Yeah, yeah, it's. I mean, I. There's an episode, maybe a few, back where I went through my old toxin test. It was actually Dr. Savage. I heard mine. Oh, did you? Yeah. You know all about me then. I don't need. Yeah, got a lot of mold in me. About to get the TBE very soon, though. At least the first of four, so.

Oh, really? Okay, so I'm.

I'm in the process. Well, I'm getting my test tomorrow, so we'll see.

Oh, very cool. Well, there you go. You learn a lot. Have you ever had one before? Toxin test? No. No.

I mean, because, you know, it's one of those things I've. I've always practiced traditional medicine, and again, I still practice traditional medicine, but I started getting interested in regenerative medicine, I want to say, maybe four or five years ago, so it's pretty recent, and started going to the meetings and it was an eye opener. Because a lot of things that we just don't think about.

As the potential triggers for a lot of conditions that we see. I feel like we're not really paying a lot of attention to those things. And then we're just treating the disease once it already happens.

So what, since that shift, I mean. Yeah, it hasn't been too long, four or five years or so. What has. It's almost like what has surprised you? And then maybe as a second bit, what are you doing differently now with that new info in your practice?

The evidence is staggering. I think that's the part that surprises me. It also surprises me that.

Unlike people like Dr. Savage and Dr. Lee, more people are not waking up to this. And I'm talking about healthcare professionals. And maybe because we're just kind of so hyper focused on what we're doing that we're not looking outside the box and just doing things the way we've always done them.

You're in your bubble in a way.

You're in your bubble. Yeah. I'll give you an example. Okay, so Parkinson's disease, right. Alzheimer's is the number one neurodegenerative disease, and Parkinson's is number two. So that's pretty important as well.

Mitochondria are the cells in all, are the batteries in all of our cells, right? Whether they be neurons, muscle cells, any cell in the body, energy is produced by mitochondria. So mitochondria is what, what drives that cellular activity. And what happens in Parkinson's is that pesticides will affect the mitochondria, the mitochondria which power the vacuoles that eat up the bad proteins. So now the vacuoles are not getting powered up. And so alpha synuclein, which is one of the proteins that causes Parkinson's, is piling up inside the neuron and damaging the neuron. And particularly there's neurons in what's called the striata nigra tract that is sensitive to this particular issue. And so when the striata nigra cells start degenerating.

And stop producing dopamine that goes into a part of the brain called the basal ganglia, people start presenting with loss of facial expression, tremors, shuffling, gait, right. So when the patient walks into my office and they've got a masked face and they have rest tremors and they're, you know, shuffling, and I'm like, oh, you have Parkinson's. And I can, I can do a scan, I can do a dad scan to confirm it, or I can make a clinical diagnosis. And then how do I treat them? I give them different forms of dopamine because dopamine, the neuron that's not producing dopamine.

Is causing these issues. So when I give them a dopamine type drug, either a dopamine agonist or carbidopa levodopa, I can improve their quality of life. Am I going to stop doing that for my Parkinson's patients? Absolutely not. If it's improving their quality of life, I still want to do that. But how about rewind, like maybe 10, 15, 20 years from the onset of this condition? And if they are heading in that direction, are we able to power up the mitochondria and maybe improve the vacuole, you know, the vacuole function, the vacuum cleaner function, and prevent that pathology from happening in the first place. And those are some of the things that got me into utilizing hyperbaric oxygen and molecular hydrogen and near infrared light therapy. And because a lot of them are modalities that decrease reactive oxygen species, decrease inflammation, improve mitochondrial function, and, you know, those are things that people can do while they're healthy. But if they have a predisposition, genetic predisposition, for example, to these conditions.

They can hopefully.

Avert it or at least mitigate it.

Do you see regeneration happening on that level as well? Like when, when going through some of these treatments?

Yeah. So, you know, most of when we talk about neuroregeneration, a lot of what we're talking about is brain plasticity.

So for example, if someone has a stroke, a part of their brain is damaged. Unfortunately, that part's not coming back. So we do things for secondary stroke prevention. So ways to prevent another stroke from occurring, but also retraining the parts of the brain that are not damaged to compensate for the parts that are damaged.

Oh, that's interesting. Yeah.

So we do the same thing in brain injury medicine as well, and that's helpful. When I was in training, we were taught that once you lose neurons, they never come back. They're gone forever. They're super specialized. That has since been proven wrong. Okay, so now we know that you can actually grow new neurons in parts of your brain like the hippocampus, which is the memory part of the brain. And one of the ways to do that is to. There's a substance in our bodies called bdnf, Brain derived neurotropic factor. And one of the best ways to get BDNF is regular cardiovascular exercise. So, you know, so there's, so to your question about regeneration, there's also some evidence for neuroregeneration with modalities like clinical hyperbaric oxygen therapy. So again.

You know, there's not going to be one treatment that's going to work for everybody. It's, you're probably going to have to try to attack it from all sides. And that's always been my, you know, modus operandi. Like for my patients, I've always started with, listen, lifestyle is important. So diet and exercise, sleep, stress reduction, managing triggers. You know, let's, let's start there. Let's, let's lay that as the foundation. And then, you know, if there are supplements, if there's medications, if they help. Absolutely. If there's, you know, therapies that help, let's, let's bring that on. If there's interventions, procedures that help, let's, let's bring that on. And that's why I'm excited about plasma exchange, because that's one more modality. Do I think it's the end all, be all? No. But do I think that it's a really, really, you know, exciting treatment modality that potentially can be initiated early on, and even, even, you know, as, as the disease progresses to mitigate the symptoms and potentially be disease modifying. Yeah, I'm excited to, to see how it goes.

Yeah, yeah, it's early and I'm sure there's more applications to come in the future as well. And, and then paired up with a protocol that you're probably already doing, maybe adjust it or put it in a different part of it, you know, of the process.

I know you're going through the process. I'm excited to go through the process partly because I do want to see what kind of toxins I have. I want to see if the treatment removes those toxins, but I want to walk through that process because when I send my patients into this, I, I would like to know what they're going to be going through.

Yeah. Once I do it, I'll just put it on the record. I will talk about it. Yeah, like I've already already put the toxins out there. Might as well talk about everything else. I really don't care. But I want to help others and yeah, it's such a exciting time, I guess.

Just to wrap up like. Well, I'm just. My takeaway. I'll just say this is like we can all, we all have the ability to do things like move more sleep more higher quality. You know, it's almost like do the things that you have the ability to do that. Yeah, you have that control. Not saying we can all do that perfectly, but at least you're in that control more or less, right?

That part of it, yes. And, and it's funny. So I used to get patients and I, you know, we, we do some screeners. One of them is called a PHQ9 to see if they have depression or vegetative signs of depression. And I tell them, listen, you're, you're really depressed. I, I need to put you on an antidepressant. And they're like, doc, I've heard all kinds of bad things about antidepressants side effects. And yeah, I'm like, okay, well why don't you use my favorite antidepressant? They're like, what's that? I'd say, hit the gym six in the morning. And so while I was basically, I was sincere in my recommendations, but what my patients taught me over the years is some of my really depressed patients, they were like, doc, I don't even have the motivation to get up and brush my teeth in the morning. Okay. How do you expect me to hit the gym at 6 in the morning? And I'm like, yeah, that's easy for me to say because I don't have that problem. But for a lot of people, they're stuck on square one because they're just very, very depressed. And people think of depression as psychiatric and psychological. I think of it very much as a neurological issue. In fact, I think of psychiatry and neurology as basically an arbitrary separation of a continuum. Right. Because the amygdala is part of the brain. The frontal cortex, prefrontal cortex is part of the brain. The limbic system is part of the brain. So as far as I'm concerned, those are all brain conditions. And now we know that in severe chronic depression there's inflammation, right. In ptsd, there's inflammation. Right. So it's not just like we tell people, oh, it's in your head, get over it. It's not, it's not that easy. So I guess point of saying that is if, if those people can be helped with removing.

The inflammation that is at the heart of these conditions, then we can get them moving. Now I always tell people if I treat them like with my brain injury patients and they get better, I, I don't need for them to be on the symptomatic medicines forever. We can taper off the medicines, they're just a means to an end. But if those medicines are going to get them going cognitively, mood wise, you know, better sleep, better control of headaches or other pain issues, then let's do that. Once we get them better, start putting more lifestyle stuff in there and, and you know, reducing the medications because that's. The medicines are not the goal.

Yeah, I think that's actually a great way to in, you know, wrap, wrap up our chat just because it's, you said it in a perfect way. It's a, it's a great balance of everything. You know, it's because I know there's a lot of fear, you know, with, with folks starting medication, some people less of a fear. But yeah, it's a continuum. It's all connected. Yeah, yeah.

And understandably so. I'm, I, I tell patients I'm, I'm very conservative when it comes to medications because I do realize that there's effects, but there's also a list of side effects. And, but we always try to make sure that there's. The risk benefit ratio favors utilizing a medicine. And again, I, I also draw the distinction between disease modifying drugs and symptomatic drugs. I'm not against symptomatic, but if, you know, like if someone has high blood pressure and untreated hypertension is the number one modifiable risk factor for a stroke. I really want them to get their blood pressure under control. Now, whether they do it with diet or exercise or medicine or all of the above doesn't matter. Those numbers need to be perfect. But if it's a pain issue and it's mild and they can tolerate it and they can manage the pain with physical therapy and exercise. Absolutely, why not?

I love it. I mean just to wrap this up, where's. Do you have any place where you would love folks to go explore a little bit more about you, what you're doing, things you're putting out into the world?

Yeah, absolutely. They could go to our website. It's universalneurocare.com and so it has some of the, you know, it has all of our colleagues and it has all the modalities that we have and.

Some of the things that we're moving into. So.

Yeah, very cool. Yeah, I'll put that in the show notes as well. That'll all be linked up. Dr. Syed Asad, this has been great. I mean, I'm gonna go sleep. I gotta go. How about naps? Actually I'm gonna wrap it on that. Like yes, no naps.

Okay. So if you look at the circadian rhythm, it basically, you know, all your hormones and blood pressure parameters and everything else goes up, then it goes down a little bit and there's a smaller rise and then it goes down. So it's like we call that the diurnal rhythm.

Yeah.

And. And so in a lot of cultures, in a lot of human cultures, an afternoon nap would be part of their routine. Right. Like the siesta.

Yeah.

And so that's fine if you know again, depending on what kind of work you do, like I wouldn't be able to do it at work. But, but I know Google has. Google the company. Don't they have like those pods that's. They do.

I've been there before. I've seen. Oh yeah, there you go. Yeah. And I love siesta. I've been to Spain too and I'm like, man, I love the siesta concept. Why don't we have it here in the States? Right, right.

So yeah, So I think if someone can do that. There are some recommendations though. So if you complete a 90 minute cycle during your mid afternoon nap, that takes away your brain's appetite for sleep at night. So if you have that tendency where you take a 90 minute nap but then can't sleep at night, it's better if you are taking a nap to limit it to 20 minutes because then that doesn't mess up your appetite for sleep at night. So as that makes sense, we recommend like, even setting an alarm and making sure you get up in 20 minutes.

Awesome. Okay, cool. We're leaving it there. That was just like an open loop in my mind. I had to close it, so. All right. Dr. Assad, appreciate your time so much. This has been great.

This was fun.

All right, thank you, thank you.