Welcome to the next big idea. An incredible journey of innovation, passion and game changing ideas. Let's see what this team brings to the table. Can you imagine a situation where your hand keeps shaking and you can't eat food? Well Parkinson's patients go through this each and every day with each and every meal. Two years ago I was at a family function and I saw my uncle Arjun who has Parkinson's. It was very hard for him to eat. Using the spoon, all of the food was spilling out and I felt deeply dissatisfied with this. I empathized with this and I wanted to come up with some solution for this. So about myself, I'm Arav Anil who is studying in 12th grade from Bangalore. So I've been into robotics since the past 8 years and I really want to create a solution for this. So this is the team. Me and my team Vidya Sagar and my team Vidya Sagar are the founders of this company called Robo Electro Steam Studio with our mentor Ashwini. So what is the problem with Parkinson's? Parkinson's patients have tremors. So their hand keeps shaking like this all the time. So while eating with the spoon, all the food falls off and it's really hard for them to eat. So they have to depend on another person to feed them. So due to this, they feel dependent. They feel that I'm relying on somebody else. That person should feed me. So they feel that I'm burdening another person. So because of this, they feel socially embarrassed. They can't eat properly in social gatherings. They spill all the food and no person would like to sit with them. So this is the main problem which we want to target. So the solution which we have come up with is a smart self stabilizing spoon, which even if there are tremors, the front part of the spoon is always parallel to the ground. So even if there are tremors, the food won't spill out of the spoon. So we are currently in the process of validation and we have tied up with RV College of Physiotherapy who's helping us to validate this product by testing on several patients, including Parkinson's and other stroke patients who have tremors. So this product includes mechanical design, electronics and software. So it's a combination of all the three and electronics. So in the future, we'll also implement machine learning and IoT so that the accelerometer and magnetometer data can be logged and it can be shared to a cloud so that the doctors can get more information about the Parkinson's patient and his tremors. And we'll implement machine learning so that the PID algorithm, which is implemented inside, which will control both the motors, can automatically adapt to the patient's tremors. So in Parkinson's, there are three types, low level, medium and high. So this is the frequency levels. So in the low tremors, it is around 2 hertz to 4 hertz, the frequency of the tremors. And high, it ranges from 8 to 12 hertz. So currently we are targeting only in the low to mid level tremors, which is from 2 to 7 hertz. So according, if we add machine learning, it will automatically adapt to the frequency of the tremors and adjust the PID values. So before starting off this project, we talked to some experts and doctors and also some Parkinson's patients. We got a lot of feedback and testimonials, which made us more aware about what was Parkinson's, what problems they faced. And after we finished the product, we gave it to a few Parkinson's patients who gave us more feedback. So coming to the value proposition, this tool is a lot different from the competitors because it's non-intrusive. There are some solutions which have electrodes. So it is intrusive and it is not a reliable method. So our tool is a corrective impediment device. So it's non-intrusive. You can just hold it and you can start eating. And we tested out the accelerometer values and it comes, we got to know that the spoon shakes 70% less than the hand. So if they're directly eating with a spoon without the smart spoon, more than 70% of the food spills off. And we got because of this and the data which we are logging into the cloud, the doctors will get a more detailed information about how the tremors are increasing or decreasing in the patient and cost effective. This is one of our main unique selling points because there are two other competitors who are based in the US and both of their prices are very high. Ours is almost half the price of that. So we want to target, especially the Indian market because Indians we are, we want an economical product, a cost effective product. We can't spend thousands, I mean tens of thousands of rupees for one solution. So we are mainly targeting the Indian market. So if a Parkinson patient uses this, what benefits will he have? So first thing, he'll be independent. He need not depend on another helper to feed him. He can eat his food independently and reduce social embarrassment. He can worry less about spilling and focus more on enjoying the meal. Can you move on to your product? Yeah, I'll show you a demo also. Now I'll show you a demo of this. So all of these components, they're all 3D printed and we are using a microcontroller which takes the values and accordingly adjust the spoon also. So the first five seconds, it will calibrate the sensors. So even if there are tremors, the spoon is always parallel to the ground. So this is the roll compensation and this is the pitch compensation. Yeah, so coming to the market and traction, our time is around 8.8 million people because all over the world, the Parkinson's disease, the number of patients who are Parkinson's is around 8.8 million and our SAM, which is 800,000, we want to acquire around 800,000 customers by the end of two, three years and currently our SAM is 110,000, which is our target for the next one and a half years. So this is a photo of us testing with a real Parkinson's patient. We got a few feedbacks from them and we made the prototype better so that we can handle the customers better and that certificate is a certificate from Arie College of Physiotherapy whom we have tied up with and they will be helping us to validate this product with many other patients and publish a paper in the medical journal. After this, we are planning to file a patent also. So competitive analysis, we have two main competitors in this field who are based in the US, which is Lyftware and GynoSpoon. Both of these are at a cost of around $200, which is not at all suitable for the Indian market. So what is better in our product? Main thing is the cost. So currently this will cost around 5,500 rupees to manufacture and we will be selling at 8,500 rupees. So our net profit would be around 3,000 rupees, which is around 35%. So this is less than half the price of our competitors, which is our main USB. And coming to the revenue streams, we have primary revenue stream and secondary. Coming to the primary, which would be B2B sales directly to hospitals and physiotherapy clinics. So we can sell in mass to the hospitals and physiotherapy clinics, who can then intern sell it to the Parkinson's patients and get more data about the tremors. Our secondary revenue stream would be acquiring tremor data. So using the accelerometer and magnetometer values, it can log the data and give more insights about the disease. So coming to the technology, first we designed all the components in CAD design using SolidWorks. And we 3D printed all the components added the electronics and made multiple prototypes. So initially we designed all the components in CAD. And then we 3D printed all of these. So all the white color components you see here, they're all 3D printed for the prototyping. We have this is the main sensor called as the IMU, which is the inertial measurement unit. It consists of accelerometer, magnetometer and gyroscopic sensors, which will measure the tremors, acceleration and angle values. It will send it to the Ordino Nano microcontroller. This runs a PID controller, which is proportional integral and derivative. It uses this values and it controls the motor drivers, which will in turn control the two motors. This is for the roll and this is for the pitch. So I just want to know the durability of the product. Because people will be washing the spoons, all those things. Your product contains batteries, the sensors, the motor parts, the like the boats here, sensors, all those things. So I just want to know how long does it sustain? And if suppose there is any water leakage in the product, the water engine enters the like the boats. So what will be the scenario in that case? Yeah, so this was one of our initial prototypes. And as you can see here, everything is exposed. All the motors, all the gears, they're all exposed. And we got some feedback from the Parkinson's patients and we made it more covered like this. So currently, this is not waterproof. And in the future, we would want to add a silicone covering, which will make it waterproof. And now we are using 3D printing, but in the future, we'll use silicone and injection molding, which will make it watertight. I think that the radius of the spoon is as much more bigger because Parkinson's people like they don't have a stand, they don't have a capability to catch the bigger product or the weight product. So how do you think this product will meet the requirements of the Parkinson's patient? So as you might know, Parkinson's patients, it's very hard for them to hold a spoon. Main reason because is our spoon is very sleek. It's very small. We can easily grip it, but Parkinson's patients due to their motor inability, it's very hard for them to hold. When we surveyed lots of professionals, they told that the ideal diameter is around 35 mm. Currently, 35 mm diameter, which is around this much. This is the optimum size. I mean, you have a competition, right? Yeah. In US. So what's the weight of the product? So liftware weighs around 150 grams and gyno spoon weighs around 450 grams. So there's a huge variation in the market. But when we talk to the experts and the real Parkinson's patients, and we came, we actually tried out with a few different spoons, one which has a higher weight, one which has a very low weight, one which has a normal weight. And they told that if it's very light, their hand will shake more because lesser inertia and it will increase the tremors. But if it's very heavy, then their hand will get tired after a few minutes. So by that, we came up to the conclusion that the optimum weight is around 250 to 300 grams. So what innovative things do you have in your product? The unique selling point or the innovative point of us is the cost effectiveness. No, no, no, that is cost. So what is the niche point over there? Yeah. So these two products only stabilize the spoon, nothing else. Its sole purpose is to just keep the spoon steady. That's it. So what are future plans is adding IoT so that the tremor details, the accelerometer data can be logged and we send to the doctors. So if you without the spoon, there'll be some amount of tremors and with the spoon and the stabilization that tremors would reduce. This data can be used by the doctor to further analyze the patient's recovery if it's increasing or decreasing or if it's just staying the same. Using this, this data is invaluable. We can use this to give to doctors or we can use this data to give to other companies who are researching about Parkinson's. See, what is your plan of action down the lane for next five years? Yeah, our short term plan for the next one, one and a half years is to mainly focus on B2B to hospitals and physiotherapy clinics so that we can address a large scale in a less time. So we plan to sell around 3000 to 4000 products in the next one and a half years. After that, using getting investments and using their help, we can expand more and possibly even expand to B2C direct to customers. Yeah, are we are planning to scale the product? Like who will do manufacture a product? You know, if you are going for a very low scale, we're helping you to manufacture a product. Okay, so currently we are using all 3D printed parts and in low scales for mass manufacturing, we'll switch to injection molding, which can produce a lot more parts in less time. And we'll also make PCBs and reduce the size. And we'll also tie up with a manufacturer to better to better manufacture this product. See, I'm okay with all your innovations, all those things, but the you have to see the size of this phone, you have to go the we have to research the the entire diameter, the entire radius of this phone so that you could be getting a more information based on that. So research with a lot more park is impatient with more a lot more autism patients, like I just want the spoon size to be like based on the feedback. Please consider the spoon size based on your feedbacks. Yes, in the final product, we will reduce it to the optimum 30 mm diameter with your innovation. It's completely an awesome product. Please go with that. Okay. And one more thing, I just want to add one more thing, we presented this in a few competitions also in a robotics competition called as World Robot Olympiad. This is an international competition, where we presented this in Germany in last November, where we won the first place and represented India. That's nice. Thank you. Thank you. Thanks a lot. And now it's time for judges opinion about the pitch. You folks are rock stars. Keep it up.


Welcome to a new edition of rational art. I'm joined at the table today by Amanda Maldonado. Did I get that right? You did. Thank you. Amanda, welcome to the table. Welcome to the Captain's lounge. Thank you so much for having me. I'm super excited to be here. It's wonderful to have you here because I love talking to our local artists. Awesome. And we have got some really good talent in this town. Yes, we do. And looking at your stuff, you've got to be bubbling up to the top. Thank you. So let's start off with the basics. What actually got you into art? So I've always been into art since I was a kid and went to art school or art school, but I studied art in college and became a graphic designer as a way to make art professionally and still have some sort of creative career. But it wasn't until about six years after college that I felt good making art again just because it was a bit of a painful experience.  I'm successful now. I am successful because I've made it as a graphic designer in art career. I achieved my goal. Just a matter of interest, can you explain the differentiation between a graphics designer and a fine artist? Yeah. What is the difference? Okay. So fine art is really broad. It can be really whatever medium and creativity you want to choose, but it's more for you or commissions. Graph design is a little bit more narrow and it's more commercial based. So you're doing stuff for businesses, for nonprofits, you're trying to like help get the message out and communicate design. So really one is doing what someone else wants, like in advertising, and the other of course is doing what you want. Yes. Although you can still get paid as an artist doing commissions. Absolutely. Absolutely. But yes. Okay. That's great to know that differentiation because really they're one of the same except who the audience is. Yeah. Very similar. It's a nice way to have creative expression and feel like you're in a creative field and not stuck in a job that doesn't suit you if you're wanting to do something creative still with your career. Do you miss doing the graphic art stuff or are you really happy and embedded doing what you want to do? I love this. I also do some freelance graphic design for downtown Longmont and then I might be doing some for the city soon too. I like that my previous job was art director for Simply Organic. So it was graphic design but also kind of leading the charge on what that looked like. And I didn't care about spices. That was the company and I was really falling in love with Longmont at the time. So I was making these sort of products and just felt more drawn to being in Longmont and spending more of my energy on it. And so now that I get to do some of that communication work for the city it allows me to highlight the things that make me feel good and feel welcome here as profession getting paid while still separating myself a little bit from that and doing some of the sketchbook art that's like this is something that's just me, what I want to do. Right. Does any of your work end up in the local galleries? Yeah, I've got stuff at Firehouse Art Center and the map here is at Walnut Gallery as well. We're going to talk about that in a few minutes. Yes. So and then I have some of my prints at Miko Coffee Shop on, right by Cheba Hut on Long's Peak. And then Mountain Fountain and Hygiene, the Boulder Bookworm, Java Stop. Excellent. What mediums do you like to work in but I think you cover pretty well everything don't you? Medium-wise? No I mostly do watercolor and pen and ink. Oh okay. Yeah and I don't know if I can show these now. Absolutely please. So this is my watercolor set. I keep this in my purse at all times and it allows me to do these sketchbooks and do work on the go. And then I also use my fountain pen a lot which is pretty awesome. I love this guy. It makes me extremely happy. It does and what I like about having this is it gives me the chance to pursue whatever is in the moment and engage with it a little bit more deeply or experience it or if it's a place that I really love I can celebrate that by making something that recognizes that space. Right.  Is that basically what happens? Yes and no sometimes it stems from like stress or anxiety where I'm feeling like a little awkward and this just calms me down. It's kind of like a soothing moment but other times I'm just with friends and it feels really good and I'm just like all right we're going a lot of it we go on art dates. Oh okay. So we're doing an art date tonight with some friends at a house. Oh nice.  It's a fun way of doing it. Yeah and some of it's just like I'm feeling creative but I don't feel like making something special. I just want to like get that energy out like with practice and so it might be the salt shaker on a table or just working it into when I have time instead of you know if you're really busy especially if you're a mom I'm not a mom yet but I'm going to be soon or not pregnant yet but it's nice to just work it into what you're already doing so if you're waiting for your food at a restaurant you can work it in anytime you might normally pull out your phone right it's a great time to pull out your sketchbook instead and then just yeah and then just draw it some fun to get there like wow that's cool. My artistic talent when it comes to anything like that is about that much I can't I can't draw to save my life put me behind a camera I'm fine. I teach glasses but when it when it I've got a funny feeling my daughter and my wife forget very upset if they knew I was going to you to learn how to do this. I get it. They're both fine artists. This is great let's let's talk a little bit here individually let's talk about this one first the Callahan house that's up on Hova okay now this is something that you did out there what what's the backstory? This was another friend date a friend of mine asked me if I wanted to go to Callahan house to have coffee and she was going to write in her novel and I was gonna just bring my sketchbook and relax and kind of get out some of the stress that I've been feeling in preparation for holiday markets at the time okay and luckily there are a lot of flowers still blooming at Callahan house it was like in October perfect and because Callahan house is like a public building and like a public park you can just hang out at the garden on their wrap-around porch and just have a nice little friend date so actually I'd like to put a little plug in here if if you have not looked around the Callahan house gardens it's well worth it they've got a nice little car park there it is all built up there now but find somewhere to park have a look around it's a great place to visit if you've got to spare 10 15 20 minutes and totally free and totally free and java stop coffee shop is just around the corner I'm free is good and their java stop coffee is pretty darn good as well yeah so I knew I was gonna be doing a class the following year this year right on Callahan house flowers garden tea party paint and sip and I was like well I'm just gonna start practicing painting flowers and it's a very relaxing fun way to just get some energy out too so right that was in preparation this is the graphic let's spin the page okay so this piece here is a study for a commission that I'm doing for martini's bistro they wanted me to take a nice historical painting of of a there's a snapshot of the historical building that's going to be unveiling on March or April 19th okay gonna have like a wine tasting and stuff I'm most I'm halfway done with it now so it's really fun excellent thank you it it just stands out thank you it just stands out it's beautiful I also did this one because it was I did this at this time because she wanted a fall theme and I was like all the leaves are about to fall tomorrow because it's gonna snow and it was like so pretty it's just nice sitting out on a warm fall day I also like the one over here about the coffee with the council yeah that's fun it's something that they do here in long months every month they have coffee with the council and you're able to go along meet some council members sit down ask your questions it's one of the nice things that does happen here in longmont we're going to talk about a fun one now this to me is amazing um this is going to be quite a challenge because hidden in this drawing and this is the smallest version of it hidden in this drawing are 39 pumpkins 33 cats 15 dogs and six ghosts talk about this and talk about the real size okay so um I made this map um in october of 2020 it took me nine months wow um I don't know if you ever heard of incotober before yes so for anyone who doesn't know incotober is a month long of prompts every day you do a different prompt and you try to draw an ink um some people are branching out from me and it's just a good excuse to try and make art every day and um my uh my own prompt that I made for myself was to do a building every day from downtown longmont and in order to fit um the minute details of bricks on buildings I had to choose a very small section of long months so it's late um just the 300 block of downtown and a little bit of kimbark and um and kaufman and um it took me nine months to finish I finished it in june of 2021 oh wow this is six by eight you should have stretched it to a year like that you could have started ink month and finished oh goodness and then you could say buddy I need to have a month yeah I was so excited to finally launch it and share it with people though and because that summer in 2021 we um things are starting to open back up and I could go to restaurants again and share it with friends and doors I um was very excited about having that um launch because then in the fall we were all wearing masks again right um but another part of why this being done during covid was significant is um the feeling of community and connection and the celebration of long when it was really when I fell in love with longmont I really wanted to quit my job as a graphic designer and just be be able to devote more of myself and my time to the community right I noticed it's the speak easy mm-hmm my favorite bar top favorite bar down here in longmont yes so you know we often have our staff meetings down there um you want to come you want to come down and and paint one of our staff meetings that would be that would be delightful would that be fun yes and if we sit in the back it's nice and quiet and won't get disturbed and for some reason I'm picturing that um that uh image of dogs playing poker on a poker table oh yes I love that picture I feel like we can stage it and do something similar yeah why not you've got three dogs here so you know that's wonderful thank you now let's talk a little bit more about this this comes in other different sizes mm-hmm that people are able to purchase yes so talk a little bit about that yeah so um that size is six by eight and it is double-sided there's a postcard on the back that is really neat thank you what a great idea and then in here they've got fun facts here in here this tiny type is another fun fact about the city that's wonderful thank you um and then the 18 by 24 size you can get at walnut gallery um on my website um firehouse art center or java stop coffee shop um and that one is 150 for the big print for the big print yeah I bet that I bet that keeps people guessing yeah yeah it's fun I am like you just need a magnifying glass it's a prize in the amount of detail you can see at six by eight you can still if you're looking really hard many many eons ago we're going back decades now the company I work for I used to be in computer aided design and um the company used to sell um flatbed photo plotters because we used to have to uh the way that you produce a printed circuit board is you design it you digitize it in and then you photo plot it at one to one scale so you can then go and make the printed circuit board anyway the the plotter had arrived I'm in Switzerland at the time uh Metler instruments and uh they wanted a test to make sure this thing maintained accuracy across the whole bed and it's something the company had never thought of so I made the amazing maze nice and I designed 10 templates and I covered a piece of uh I covered it all I don't know it had to have been about 30 inches by about 20 inches and we're talking about gaps that was so small and there is only one way through it is this hand drawn no this I managed to copy and paste so I I made it so I could copy and paste and rotate and everything would match that sounds like a lot of fun oh it was it really got wonderful in a great way it was it was so fun to do but of course I'd also made a uh solutions because there's only one way through it and I do know of one person that did actually do it wow because I gave it to a few of my friends and they made coffee tables out of them because it was so interesting yeah I want to talk about this one okay because this one is just wonderful let's take the clips off all right let's put this down here tell us a little bit about this so um this was done at um Old Oak Coffee House in Niwa and um I had just gotten my new fountain pen ink which is now waterproof and I was excited to finally test it out and I wanted to really just draw the whole scene of the room I started thinking I'd just do like one side panel and then um just kind of like in my in my head trying to like crop it and be like what would this look like as a panoramic um and then uh I just love drawing people and different scenarios because like oh there's a guy reading a book there's a guy reading a newspaper these are like moments that we can all relate to and be kind of excited about like it's nice seeing it's like oh man that sounds so nice having a cup of coffee right now or having a date with a friend and getting a chance to catch up I really need that connection and I like highlighting that in here there's so many little moments that you can relate to and just kind of feel that sense of like longing right and and it was also just a lot of fun it took me about three hours and it was while I was on a date with some friends um we're all making our own art projects right so have you ever been down to speak easy I have twice okay yeah because I think that because of your absolute attention to find detail if you just did a picture of the back wall bar it would be stunning I've done a few bars um but not not in a fine amount of detail because uh I'm out of energy there's so many tiny pieces and labels that's right but I'd love to do that that be a fun project and remember something like that I can always take photographs but I do love painting in person I know I understand there's something about it that just feels more tangible and like really meets that need of like connection right being a part of a space yes so um yeah most of my art and why they're in sketchbooks how often do you get interrupted do people come across and say what are you doing can I have a look not that often really yeah it's it's not too bad most of the time um I'm trying to draw someone and trying to to make sure they don't notice because you're staying people can feel and they're staring you're staring at their face like their profile and sometimes they tend to keep turning their head just away and I'm like well like the corner of your eye and not a none of your nose is not interesting that looks weird that's true so I have to pretend that I'm not looking at them and then quickly get like a get the bit you split second the moment their head goes back um but sometimes afterwards I'll show them because I don't want them to think that I'm a creepy stalker and I'm like I was just drawing you here it is that's nice and then we got this one which I think is is just gorgeous talk a little bit about that thank you so um this is a friend of mine we were playing um a fake campaign and I'll know if you've ever heard about fate but it's like D&D but it's like a mini campaign with slightly different rules oh okay so it's meant to be done in one sitting or like a handful of sittings compared to like something and stretch on for years um and uh we were just all world playing and being silly and I um was getting a little tipsy and awkward and I was like I'm just gonna draw her because I need to like chill out right now um but it was just really fun like oh cool I like I'm like inspired by this moment I love it yeah I just think it's a beautiful beautiful drawing thank you see even even though it's two colors the face is flat you can see the expression yeah that is very very difficult to do thank you along the lines of the art we talked about this let's talk about the coffee mug okay where did this come from so um this is a coffee mug that I hand painted um uh it's originally from a thrift store and then I bring it home and I get these enamel markers that uh are dishwasher safe so you just draw on it you let it dry for four hours and then you um put it in the oven to seal it after doing the map people really liked all the different um buildings and stuff and I didn't have the energy to do another map to include more stuff well you didn't have a spare eight months no I didn't so um I wanted to uh kind of take a shortcut and do like little sections so in this mug you have the Longmont Museum um you have Kanimoto Park um and then you have the Sugar Bee Factory so it's kind of a way to bring in some of the places that are on the outskirts of Longmont that didn't have time to draw a whole big city map understand and and make hand painted art that I can share with um with the community yeah I mean I have seen uh those maps that they do as cities where they use a very strange perspective and buildings three times taller than they're meant to be but that is is spot on scale wise thank you which is takes them doing yeah it's definitely not true accuracy but it's meant to fool the eye into thinking it is and that's one of the really fun things about being an artist is you can you can make reality not reality and it's and still get away with it and um and also just one of the fun challenges when you get to that point where you're like oh maybe I could try this right and that play is so so awesome that's good Roosevelt Park yes one of the most beautiful little parks we have in town yeah talk about Roosevelt Park for a little bit okay so this piece here I made during a um a class that I was teaching nature journaling and um it's just kind of a easy entry into getting into watercolor and ink and um the same experience of drawing from from what you see right and um the the piece that I've made here is you have um Manilda the um the giraffe statue um this is the one of the pillars it's the entrance to the park where it has the name we've got Long's Peak and Meeker and nowhere in the park is this a scene and that's again that's that fun play on reality versus fantasy but it's something that you can take and pull together to highlight the best parts of the park so you've got that giant cottonwood outside of the um memorial building um you've got the statue you have the rose garden that um cool uh like house shape frame where all the roses grow on it and it's just a it took something kind of dead and wintery and pulled out all the beautiful browns and greens gave it life purple yeah and it doesn't feel winter it feel but and it still feels vibrant right so I mean that almost looks springy yeah which is kind of nice yeah before we wrap this up why don't you talk a little bit okay about these awesome so this piece here is um one that I made at the Longwood Artist Guild meeting um it was a talk being given by um someone from a gallery just talking about like how to get your artwork in galleries one of the easiest ways to draw people is when someone else is talking so they're um drawings that I may wear two people are sitting on a couch when they're talking if someone's looking at me and talking to me like one on one it's much harder because they get uncomfortable or they're they'll start moving their mouth while I'm but I can catch people while they're listening right and um so that was a really fun way to get that in and um the guy in the middle Bernie um he came right up to me at the end of the meeting he was like let me see what you drew I saw you looking at me so I'm starting to build a bit of a reputation around around the artist community where they see me doing that they're like let me see it afterwards and I I love that um I love being caught out afterwards and I'm being like yeah that would show it to you so that's nice yeah and last but not least about this okay so this piece here I really enjoyed it was the first time that I um made a piece where I started with a subject matter which is the bench and the guy on the bench and then I was like what if I try to connect from behind him to the light post to the tree to the bouncy house to the people in the crowd because normally it would have been too much of a challenge for me to want to try and this time it's where I started really investing in my sketchbook and I was like but what if right and it was so exciting when just seeing that come to life from something you don't think you can do to while I've really created a depth in like this much space um where you only have like an inch of height but it looks like it's going off like a hundred feet into the distance and that's just kind of thrilling that's nice but this is uh from the june concert series oh okay um downtown on fourth and kim bark um that downtown lawnmower was putting on in june excellent I know that you would like to talk about this and I think it's important you're also a teacher yes talk about that okay so um my creative business is queen studio and um it's queen studio meant to kind of encompass more than just the arts and the other assets that I work on um and I I love trying to help people give themselves permission to be creative I meet a lot of people who are just like this sadness and deep sense of longing when they say my art and they're like I just wish I could do that and I'm just like I'm here if you need it like I want to help you heal from those experiences and that pain of like every time you make art you feel like crap about it and it doesn't it's not a rewarding experience so my goal as a teacher isn't how to make you better as an artist because I have my own healing process that I had to do and I like trying to help facilitate and give those words of affirmation that people need to hear to get past that point of pain and so not making it be better but helping them find ways to do it more often so that they can become more prolific and then be more comfortable creative rewarding positive reinforcement and then because of that when they start having fun they'll start seeing themselves get better naturally you just need to keep doing it right so and but I don't want to be like a chore oh I just have to practice I want practice to be like oh these oh what about this these experimentations you know the thing is when you're studying music you have to play the same chords over and over and over and over and over and over and over and over again okay and I could never ever ever do that when it comes to art like this the subject is wide open exactly the problem I have is whenever I try and do art like this it looks like it was done by a one-year-old with a crayon I am absolutely useless useless put me behind a camera I'm great yeah but this it's way over my head and I it's it's part nurturing environment and part simple lessons and tools right so you know I don't expect you to be able to take amazing photos on your phone you know it's it's trying to give them a few tools so and and I did a class last night and that aha moment three of the women were like oh I get it I really want to I want to keep experimenting with us I can't wait to take it home I can't wait to show someone else and I can't wait to keep playing with watercolor and that that's the moment that I look for is giving you just enough enough tools so that you feel excited about experimenting you know just just enough and then you'll start pushing it you'll start trying how do I get past here and as a teacher when you hear that that's got to be yes we did it yes it's such a great feeling I'm like oh yay I'm succeeding as a teacher so Amanda thank you so so much for coming in it's been an absolute pleasure talking to you do you have any final words um obviously not yeah be awesome and love art I'm Nigel Aves your host this is rational art coming to you from the captain's lounge studios thank you goodbye


Hello everyone and welcome to another episode of Resiliency Radio with Dr. Jill. Today you're in for a real treat for multiple reasons. One is in this post-pandemic error. We have more complex chronic illness than ever before and more sequelae of this virus called COVID and today we're going to dive deep with one of the world's leading experts. If you listen to us on iTunes, Spotify, YouTube, please stop and leave a review and there's many more episodes that you can find there. But today without further ado, I wanted to introduce my guest, Dr. Bruce Patterson. Dr. Bruce Patterson, medical doctor, received his undergraduate degree in training in molecular biology from the University of Michigan in Ann Arbor. He then received his MD at Northwestern University, Feinberg School of Medicine followed by a residency in pathology. During the early stages of the AIDS epidemic, Dr. Patterson began investigating cellular reservoirs of HIV using molecular and in situ cell-based technology patented in his laboratory and used today around the world. He would determined that enough HIV virus was present in infected individuals to account for the massive destruction of the immune system. This paradigm altering the work, I'm sorry, this paradigm altering work was published in Science in 1993 and featured in the Scientific America, Rolling Stone and on the Discovery Channel. Dr. Patterson has authored over 150 manuscripts and book chapters focusing on single cell biology and diagnostics. He was formerly associate professor of pathology and infectious disease and director of virology at Stanford University. He currently serves as CEO and founder of Incell DX Incorporated, a growth stage company that has translated his research discoveries into state-of-the-art single cell diagnostics and cancer, immuno-oncology and infectious diseases, especially our topic of today, COVID. Welcome, Dr. Patterson, that is quite a history and I'm so glad to have you here today. Thank you, Dr. Jill. It's a pleasure to be here. Yeah, so I always like to start, and I mentioned this before we get on, is you have quite the journey and it's interesting because you at Northwestern, I was at Loyola, so we're both in Chicago for some time during residency and training, but this journey through all that you've been through, tell us, first of all, how did you get into medicine and then what was your path into all the scientific discoveries that you made through the years with HIV? I mean, really a family affair. My grandfather and my aunt are both PhD scientists and my aunt was a classical virologist from the 60s and 70s. So back in the days where we didn't have all this great molecular biology and he had to grow the viruses on chick embryos, that was her thing. And then I think I was about 17 or 18 and I went to her lab and she showed me an electron microscope with magnified virus 100,000 times and I was sold.  And what's interesting is back then they called it the Norwalk agent and it's actually the Norovirus, which is our cruise ship virus, which lands a few cruise ships in port unexpectedly. So that was the start of it and then of course molecular biology was in its infancy and I just have been riding that molecular wave as it infiltrated medicine all that time. And the interesting thing was the AIDS epidemic really pushed the envelope on molecular medicine and molecular diagnostics and those techniques, much like COVID, as we'll talk about, has really pushed the envelope on new wave immunology techniques and discoveries. What I love that because it's really been such a lifelong and you can tell because it really takes, I always say that curiosity is a mark of genius, but you clearly had that way back at 14 or the first time you looked at the microscope and it really takes that, especially in a new era of medicine with these complex and crazy viruses like COVID. You have to be curious and you have to think outside the box to get the answers that you've been coming up with. So then obviously I read a little bit in your bio about your work, but you made some massive discoveries with HIV. Do you want to tell us a little bit about that because I think it's fascinating. Well, when I first started in HIV, there was this two different things. There was patients dying of these horrible immune deficiency syndromes, Kaposi sarcoma, lymphomas, etc. And then of course there was this virus, but putting together it's the virus causing AIDS was the big question when I first started. And there was even very prominent scientists saying, well, you know what, HIV virus doesn't cause AIDS. So my training in molecular biology and pathology really was instrumental in saying, well, maybe we're just not finding it. Maybe we're missing it. And I think that was the big thing that I was working on at the time was, hey, maybe we can't find it. I'm going to try and do molecular biology in these single cells of the bodies, body instead of fluids, etc. And try and find where the virus is hiding. And we were able to do that. And again, able to quantify that, which allowed a lot of early work in antiretrovirals, including I was just talking the other day about my involvement when they're developing the protease inhibitors and figuring out that it really took people at CD4 counts of single digits, seven or 10, and a few months of therapy, and they're back up in 100. So it's one of those moments that you never forget. You look back and say, wow, that really changed the course of everything as HIV infected individuals are living healthy, long lives now and still have it. But you've been really effective at treating it with drug therapy. Amazing that you have that background. And then again, now we're in this new era, well, we really need to think outside the box because what is your, what's the big overview? COVID is such a different thing than we've encountered before. So do you want to frame it for, I told you before we have a lot of physicians and people interested, but I know a lot of patients, clients give us a framework for this virus. And why is it so different from things that we've experienced in the past? You know, it was interesting, you know, it's different, but it's not in some ways. And, you know, I was in China in January of 2020, actually doing, we had developed a new immune profiling test, over 150 different biomarkers, both cell-based and plasma-based, for looking at CAR T therapy and cancer. And we're in China talking to a company over there, and I was in Shanghai. Someone said, well, there's this, I was supposed to go to Wuhan, you know, the next day to visit another lab, another customer of Insultia X's. And it was canceled because of this, there was this virus and everyone was talking about it. I saw one of the really, really early papers of this virus and some of the lab results.  As we later learned, you know, the cytokine storm, but, you know, it was in immunology, you know, we have all these different arms of the immune system, adaptive immune system, humoral cellular immunity and hypersensitivity, et cetera. But this was clearly an innate immune response, which is basically what our body has when it hasn't seen an infectious agent before, you know, and it was heavily macrophage burdened, meaning macrophages were playing a very significant role. And that was one of my major areas of research in HIV. So you had this massive immune activation of macrophages production at Interleukin 6 and TNF Alpha, which, you know, really were part of the initial pathogenesis and QCOVID and elements of that still exist in long COVID as well.  But and then the other thing in our first study in acute COVID found that, you know, the CD8 T cells were just as low as the CD4 T cells were in HIV. So acute COVID patients with the Alpha variant were supremely immunosuppressed. And that is the nugget that people aren't considering as we're dealing with the post-acute speli of COVID is that people are are immunosuppressed to varying degrees with acute COVID. What does that do? Well, it reactivates chronic herpes family viruses, EBV, CMV, HHV6, herpes simplex, etc. It also, in patients who have either undiagnosed or poorly treated Lyme, the bugs start to replicate again. And so, you know, and so what happens is all this is going on.  And that's all well and good as when we first described it in long COVID. And but the fact of the matter is all of those chronic inflammatory diseases have the same primary symptoms. So symptom-based diagnosis of long COVID is highly, highly non-specific. It could be long COVID, it could be long Lyme, as we call it, it can be MEcfs, it could be fibromyalgia, it could be long VAX. So all of those have the same primary symptoms. So the necessity for a diagnostic was critical. And the fact is we have it and nobody is saying we have a diagnostic for long COVID. It's absolutely absurd. We published it two and a half years ago this signature for long COVID and we developed a long hauler index and it's still highly, highly sensitive, highly specific for long COVID. And now our latest paper, we can differentiate long COVID from Lyme, MEcfs, long VAX and fibromyalgia. And you know what? It is the most critical tool that we have. I need to be long-winded, but- No, this is so relevant. So I would get excited because you're right. I mean, I deal with this complex chronic disease, so CFS, ME, Lyme, long COVID. And for me, when I heard you really speak about in depth about the cytokine patterns, which we'll talk about, and your lab tests and how to differentiate. And I've been using your lab tests for a while, but the more data that you guys bring out and the more patterns that you're showing us, it is a game changer for those of us dealing in this chronic world because we can say, this is much more likely to be your Lyme Borrelia reactivated or it's more likely to be a true long COVID panel and it's treated differently. Absolutely. And another important aspect is negative predictive value. As physicians and scientists, everyone loves to talk about sensitivity and specificity. And as I used to teach residents both in Northwestern and Stanford, I always said that sensitivity and specificity work after the fact statistics. Like you do a study, you look back and say, well, what was the sensitivity and specificity? But as a physician, you get a lab report. You're looking at a number and a test result. What is going through your mind saying, what are the chances of that actually being positive? Or what are the chances of that actually being negative? What your mind is doing is actually positive predictive value and negative predictive value. And having a negative predictive value for long COVID of 98 percent really says we can say who doesn't have long COVID. And you know what? In the days of all this inflammation and the major symptom being fatigue, it's almost important to say who doesn't have long COVID as it is to say who does have long COVID. Because as you say, the treatment is subtly different. We had this other discovery which showed that all four of those chronic inflammatory conditions have vascular inflammation at their heart. But there's also subtle differences and subtle changes in this drug combination that we just submitted to the FDA for our clinical trial. Hey everybody, I just stopped by to let you know that my new book, Unexpected, Finding Resilience through Functional Medicine, Science and Faith is now available for order wherever you purchase books. In this book, I share my own journey of overcoming life-threatening illness and the tools and tips and tricks and hope and resilience I found along the way. This book includes practical advice for things like cancer and Crohn's disease and other autoimmune conditions, infections like Lyme or Epstein Bar and mold and biotox and related illness. What I really hope is that as you read this book, you find transformational wisdom for health and healing. If you want to get your own copy, stop by readunexpected.com. There you can also collect your free bonuses. So grab your copy today and begin your own transformational journey through Functional Medicine in Finding Resilience. Yeah, so gosh, there's so much I want to cover here. First of all, just for those listening, what you're talking about is innate immune system, which I've been dealing with for decades with mold and Lyme and complex chronic illness. And most of our patients have had some things like that or know someone who has many of our physicians who listen treat these conditions. So a lot of our listeners are going to be aware of that. But just to frame it, this is this arm of the immune system. Like you said, it's kind of the first activator or first responder that maybe doesn't have antibodies already made or those kinds of things. And it's typically cytokine driven, which is why we saw with just regular COVID, it so much of the disease and the mortality was related to this. It's literally like the activation of our own systems and our own systems are killing us because they're in the cycle of activation that cytokines, right? Right.  Right. And my colleague Joe Balanti always talks about, you know, damaging immunity. And the reality is, yes, some of these inflammatory products that are indeed trying to help clear a virus or clear a bacterium or otherwise are damaging, our tissue damaging. IL-6, TNF-Alpha are two great examples. And in our February paper, we showed that TNF-Alpha is the major driver of fatigue. So, you know, if you if anyone remembers, I mean, acute COVID was just the fatigue and the respiratory symptoms were just the major findings. But, you know, when you looked at the pathology more closely, it was blood vessel inflammation. Because what was happening is these activated monocytes, macrophages, non-classical monocytes, where we later found the S1 protein months after infection, they bind to blood vessels through the fractal kind, fractal kind receptor.   The other thing is Moravarok, the CCR5 antagonist, is elegant in the immune system because it does two things. Number one, it restricts the migration of inflammatory cells all over your body, including through your blood-brain barrier. But what it also does is it repolarizes monocytes, macrophages away from that pro-inflammatory phenotype where it's making interleukin-6 and TNF-Alpha. So, this drug combination we use is absolutely exquisite in terms of targeting the pathways that are underlying the symptoms in long COVID, long Lyme, ME-CFS. And that's driven by the fact that the blood vessels are inflamed and dilated, well, dilated blood vessels do, headaches, migraines, brain fog, tend to this. Post-exertional fatigue, right? All that, yeah. Cotton cold and sensitive. Yes. I can't tell you how many times I'm telling this, and I've seen a patient literally come on telemed with a blanket over their shoulders because they're so cold. And so temperature regulation is just completely thrown off, and that's my window into their blood vessels before I even look at their lab report. Oh, that makes so much sense. Because of your research, I've been talking to patients that really COVID is like a disease of endothelium, which is what you're saying, right? At the core, this macrophage activation. And let's talk just briefly, because one of the things you're testing in your panels as well is the retaining of the spike protein in these atypical macrophages, right? And that's part of the problem is they become activated, and then they go. Do you want to talk just a little bit about what happens in the macrophages with that spike protein?  They were home, but by no stretch of the imagination, was their immune system the same. It was abnormal, but it was abnormal in a very different way than in acute COVID. And that's where we used machine learning and AI to say, okay, how is it different? Why? And that's where we found this signature for long COVID. And the long hauler index is interleukin-2 plus interferon gamma divided by CCL4. Well, if you look at literature from the early 2000s, atherosclerosis, with unclassical monocytes bind to blood vessels and basically migrate into the blood vessels, what's liberated is type 1 cytokines, interleukin-2, interferon gamma, which just happens to be the numerator of our long hauler index, which was found by machine learning and AI 20-some years later. Wow. Unbelievable. And then you also mentioned, I've heard you speak multiple times about this triad of the vascular inflammation with the SCD40L, the CCL5 rantes, and then the VEGF that's at the 3. Can you tell me about those and what the pattern you've seen with that triad? Well, that was very helpful because obviously the first protein of the thrombotic pathway on blood vessels is SCD40L, CCL5, and VEGF. So that's the instigator. That's like, you know, the macrophages have activated endothelium if that is elevated. And is that, you see the timeline as well, see that up first, and then the rest of them follow over time?  And it was an unbelievable telemed session a couple of days ago that after eight weeks of therapy, she was 95% back to normal after having suffered for three years. And so these stories are just almost daily during our telemed of patients getting better. And the reason is we're treating the underlying cause and we're not. So anyway, these macrophages bind to blood vessels. Well, let me just be clear for those listening, because a lot of people think the virus is still around. The virus is long gone, correct? This is not about the virus retaining its fragments and then this activation of immune system. Is that right? Yeah, okay. And it's an RNA virus. You don't expect it to be around for a long time. It doesn't have the latency machinery that the chronic herpes family viruses have. And so and we were the only ones who've done whole genome sequencing of the entire SARS-CoV-2 genome. We did that in the non classical monocytes when we published that two years ago. And then we looked into tissues of long COVID patients before all this reinfections going on. And we found fragments just like we found in, you know, in monocytes macrophages. And those fragments represented less than 5% of the genome. And my point is, you know what, you can't build a building with 5% of the bricks. So in all the techniques that they're using to say, oh, there's, you know, viral persistence tissue, which I believe. We published it, you know, there was a viral, there's persistence of fragments of RNA and persistence of protein S1 in the non classical monocytes. But at the end of the day, they're all using techniques like droplet digital PCR, very short fragments, insight to hybridization, short fragments. You know, they're not doing whole genome sequencing when they're, and it's a big stretch and I keep saying this over and over again. We can talk about persistence. I love talking about persistence, but it's persistence of fragments or as Jez many years said, viral debris, I love that. But the fact is, there's a huge difference between persistence and replication competence. Yes. And it makes sense to me, like even on a microbiome level, we know the fragments like LPS cause a massive immune response, right? So we can have fragments of viral particles that cause immune response, which is very different from the virus continue to replicate.  And the reason is there just isn't any viral replication, except the caveat is, and we published this in 2021 that we found viral replication out to 87 days in one long COVID patient who had very low CD8 counts. So yeah, three months, you know, which is the cutoff for long COVID. So I'll always admit, you know, if you're at three months or four months of long COVID, yeah, there could be viral replication. But when you're talking six years or months, three years, you're not going to see it. I'm still waiting for that paper that says whole genome sequencing reveals alpha variant RNA in long COVID patient three years after infection. I haven't seen it. And it's not common. Well, that makes sense. Because where do you again, I've been doing 20 years of the chronic fatigue, fibromyalgia, the long Lyme, all those things before COVID. And we've been seeing these immune dysfunction activations. And the same question has been in the Lyme community. Yes, we know these spirochetes persist. But is it truly that infection, or is it the immune response that's creating inflammation? I agree. I think more and more we're determining it's actually this long immune response that is dysfunctional and weakened immune system that's more likely to be part of the culprit than just purely the infection. Absolutely. And I brought that question to the Lyme community. There's articles showing the peptidoglycan cell wall peptidoglycan and in arthritic joints from patient Lyme arthritis, I'm like, those are just setups for phagocytosis by monocyte macrophage lineage cells and persistent presentation to the immune system. And that would be another mechanism for post treatment Lyme disease, chronic Lyme disease, whatever you want to call it, where your refractory antibiotics, that's where we come into plagues. We found the blood vessel inflammation in chronic Lyme. And you kind of alluded to, but I want to be really clear for those listening. So first of all, you can actually determine through the long haul index, the height, like the likelihood and what's the percentages of like sensitivity and specificity of how accurate that test is. And this is the long haul panel, the cytokine 14 panel through your lab. Healthly about that and the specific cytokines and patterns. So, you know, so like I said, machine learning and AI brought our 158 panel down to 14. We're now using that on all of our machine learning for various different immune conditions. And now we're getting a little bit into some of the autoimmune diseases like chogrens and others. But what it basically shows, when I look at a panel, I look at several things. Number one, I look for that SCD 40L, CCL 5, VEGF pattern of vascular inflammation. And undoubtedly I'm going to, I'm going to find it. And there's different severities. And maybe they just have SCD 40L, like you said, at the beginning. Or, you know, maybe there's a little bit of lingering VEGF. That's the first thing I look for. The second thing I look for is the long haul index. And so, you know, if it's in normal range or as it elevated and how elevated is really important based on our new algorithms. So when I start searching for Lyme patterns, my three bullet points are elevated interleukinate plus elevated interferon gamma. Elevated interleukin 13 plus elevated interferon gamma. Or a long hauler index greater than six. Wow. Okay, that makes sense. 0.6. It's probably long COVID. If it's really high, I'm sending it off for Lyme testing. So I'm having this aha listening to you because I've been treating Bartonella, Obesia, Borrelia, forever. And what I know about Bartonella in particular is I'll use VEGF as a marker of activity. And I haven't because I haven't had access to your panel for that long been regularly using the other vascular markers and some of the new stuff you just mentioned. But it makes sense because Bartonella in particular is a vasculitis like it causes more vasculitis than any others. And again, I only knew about the VEGF, but this is making so much sense because what I was starting to see was my own little tiny one marker indicator of vasculitis, right? Which is what you're seeing in different ways with COVID. But you're able to now with machine learning and looking at these cytokine panels to put out this, we have the symptoms buckets. It's the same for Lyme and long COVID and chronic fatigue. And you're basically saying now we can actually look at cytokine patterns and say which is which. Exactly. And the latest in this is coming out in a new paper, which I should be sending off to a preprint server after the holidays. But we have a new Lyme index much like the Long Haller index. And the Lyme index, interestingly, in the numerator is TNF-alpha. Well, TNF-alpha, which we published in February in our outcome study with treating long COVID patients, TNF-alpha interleukin2 are the major drivers of fatigue. So now you can start to correlate which cytokines are actually representation, representation of those symptom clusters, right? Like migraines, this versus fatigue versus the brain fog. Fascinating. And you come up for a second, but did you say IL2 and TNF-alpha are the two that are more correlated with fatigue? Yeah, it's in our February paper in Frontiers and Medicine. But the most, you know, that was a 20 patient study, Moravrock and statins and long COVID. We did five different symptom scores, fatigue, dysautonomia, neurocardiac, and shortness of breath or dyspnea. And, you know, and then we looked at our entire panel and looked at those biomarkers and how they would respond to six to 12 weeks of Moravrock and statins. What we didn't, we expected, you know, the fatigue score to go down and maybe even dysautonomia because we've seen correction of those symptoms. All five symptom scores went down with statistical significance. But most importantly, as we didn't stop there, we told our bio statisticians to then correlate what symptoms correlated with reductions in what biomarkers. So we closed that loop of infection, inflammation, symptoms, treatment, infection, inflammation, symptoms, treatment. And that that circle, you know, I have not seen closed for any other marker in any of these chronic diseases where you say, oh, there's, you know, all this, especially early on in long COVID. Oh, there's this autoantibody and that autoantibody. And my first question was, okay, what symptoms does it cause? Yeah. Right. Right. And if you bring that autoantibody down with IVIG, for instance, does it, does the symptoms get better? No one closed that circle. And it was really important for us to close that circle between biomarker, symptom, and treatment of the, with a very targeted approach with our two drugs at the actual proteins that are causing the symptoms, not the symptoms. So, you know, for instance, here's a great example. This new paper that comes out, serotonin, and we did this clinical study, long COVID patients are responding to Prozac because it elevates serotonin. You know what, you know what the most important thing that lower serotonin levels are? Chronic inflammation. And you know what, cytokines lower serotonin levels, interleukin 1 beta, and TNF alpha. Yes. And we've seen in IL-6 too, all the studies on depression, IL-6, right? I don't know that that correlates with serotonin, but depression, absolutely in the studies that correlate with IL-6. Glad you mentioned them because from a mental health aspect, you know, in our 40,000 plus patients, I mean, the amount of anxiety and depression is, is incredible. And you know, their physician will throw them on this and that, this, this drug, that drug, at the end of the day, when you resolve the inflammation, it goes away. Yeah, I've been known to say, I think all depression anxiety is none, is, is, is organic in nature in the sense that there's some other cause of it. Now, I shouldn't say all because there's always exceptions and genetics and stuff, right? But I feel like more and more and more toxic load, infectious burden, cytokine, immune inflammation is really at the root, I would say 80% of my clinical mood disorders and, you know, any sort of psychiatric diagnosis frequently, if we get to that root cause, it's a game changer. It's amazing because we're starting to see, you know, I just read a paper the other day about dysautonomia and Lyme, you know, it's like all of a sudden, long COVID, we opened this Pandora's box for these chronic inflammatory conditions. And you know what, there was differences that allowed us to model that. But you know, there's also a lot of similarities. And you can see anxiety and depression in, in chronic Lyme, you see, and so all of this stuff is starting to come together under this rubric of, you know, an altered immune system and chronic inflammation. And here's another example, Pan's Pandas, you know, I probably have somewhere around 50 Pan's Pandas patients. And you know what the classic was, let's immunosuppress them and then give them IVIG. Well, you know what, the problem is, it's post-infectious. And you don't know if the infection is cleared. So, you know what, they always say Pan's Pandas is from strep and recurrent strep. Well, you know what, I have a handful of Pan's Pandas patients that all have a chronic herpes family virus that when it reactivates, it ticks, the symptoms, everything gets worse. When you press the chronic herpes family viruses, it gets better. But the other thing we found in Pan's Pandas and the reason why I think there was, it was hit or miss for IVIG treatment was that there's a chronic inflammatory component that nobody had ever identified before. And so just taking away auto antibodies wasn't doing it. And it wasn't doing it because there's also pretty significant chronic inflammation. But when you treat the chronic inflammation, for instance, with Morabroc and statins, and then you do IVIG at the same time, these kids are really responding. So, I love that because I think even we talk about IVIG, I have a lot of patients that are on that. They do well, but here's the deal. We think it's just that immune system, but the truth is it actually has a very potent anti-inflammatory mechanism as well. Same with the statin. It's kind of an equivalent. We're thinking about this cholesterol issue. That's really the side note, right? It's really this anti-inflammatory. And maybe you could talk briefly, because you alluded to this, but statins, your mechanism of action is much more directed to the endothelium. What is it that it blocks exactly? You mentioned it earlier with the statins. The protein called fractal kinase. It's made by themselves. And believe it or not, these pro-inflammatory, non-classical monocytes have a fractal kinase up there. And so, to keep them from binding to the blood vessels and causing inflammation, let's down-regulate statin, down-regulate fractal kinase. Well, statins down-regulate fractal kinase. And we don't use cholesterol lowering doses of statin. Yeah, you're using like 10 or 20, like quite low doses, right? I miss that. I'm like, no, we're not giving you massive doses of statins for the rest of your life. It's six to 12 weeks with a quarter of the dose that you would give for cholesterol lowering. And it's just an exquisite anti-vascular inflammation agent. So, great combination. We're making it into a single pill. Perfect. More avarok. And like I said, our RCT will... Which kind did you choose for the trials? We chose a tour of a statin. And the reason was when I was treating kids with long COVID, they responded so well. I mean, I would say kids, you always say six to 12 weeks. People with more neuro symptoms, maybe even longer than 12 weeks. But kids, I mean, some is as little as four weeks, and they're better. They're completely better. And four to eight weeks is about the standard for kids, because they probably don't have a lot of other comorbidities. But I was using a tour of a statin because there's studies published on the safety of a tour of statin in kids. They're getting better faster. So then I started to use a tour of a statin in adults. And with the SCD-40L be the main marker of that fractal kinin activation? Is there any correlation with one of your cytokines with knowing that the... I wish we had fractal kinin. Right. That's what I'm wondering. Like, how do we know for sure, even though we know the... Like we can understand the mechanism and see that. Is it that triad that you mentioned before? Okay. So the SCD-40L, the VEGF, and the RANTE, the CCL-5. Okay. Got it. And in that way, you know if someone has high on those, it's very likely they have the fractal kinin, the atypical macrophages. And again, this, I suppose, it could be another mechanism besides long COVID, but that mechanism is absolutely involved in most long COVID, right? Absolutely. And also involved in chronic Lyme and ME-CFS and maybe many others. You've had some significant success with Sjogren's syndrome. Yes, I've been seeing that too. So let me take the jump here because I'm in this functional world and seeing the diagnoses and obviously POTS dysautonomia is at an all-time high for all of these underlying reasons. Is that because of the vascular inflammation? Is that usually the link to that? Yep. When happens, when blood vessels are inflamed as they dilate. Okay. When they dilate, your blood pressure goes down. When your blood pressure goes down, your heart rate goes up.  And then the other thing is these inflammatory cells, you know, I've seen infiltrates of the inflammatory cells around, you know, the vagus nerve. Yes. And we're going after these vagal nerve stimulators, which is a nice idea, but I'm like, that's not going to fix the root cause, right? I mean, and that's a thing, you know, there's so much out there on these different, what works, but most of them are just, are very transient.  And I'm not really a big, big, big supporter of that, because really the anticoilins aren't, aren't work. And we tried Plavix a year or two ago with all of our protocols. And, you know, it just wasn't adding anything. And, and, you know, microclots are, are difficult to, you know, to look at when I see, I've seen pictures of microclots. And as a pathologist, I said, those look like epithelial mesenchymal transition cells for EMTs. I'm leaving tell under microscope, huh? Don't give me a microscope. Yeah, these EMTs are formed when there's tissue damage, of course, is an acute COVID. And then that makes so much sense, because really at the core, this is our immune systems damaging endothelium. And that's this whole cascade. And so how do we go? And the only reason the clots happen is because it's repair. It's our mechanism, right, trying to repair the damage to the endothelium. So that makes, so it's actually doing what it's supposed to do. But of course, and then. Absolutely. And so, and then these epithelial cells fuse with macrophages and cause an EMT. And you know what they express? CCL 5 and CCR 5. And so then they migrate to areas of inflammation. So macrophages actually expressing VEGF, or is that just a signal to get more blood flow? It would actually, do you know where express VEGF. And that's why we talk about the tumor microenvironment and tumors. Yes. And the inflammatory infiltrates that come into the tumor microenvironment.  And you know what directly decreases VEGF is Maravarok. So all of this is just exquisite. And I think as I was sitting there in a hotel room in China, I was really thinking about the cancer literature and our work in cancer and and CCR 5. I mean, I initially started with some of the early trials of Maravarok and Vikravirac and others in the early 2000s for HIV. But then obviously, you know, we started talking about this more exquisite role in the immune system, basically as the quarterback, right? It's telling immune cells where to go, when to go. And it can be both good and it can be bad. So it's our job to exploit the good aspects of it. And the bottom line is it's not immunosuppressive. Yeah. Everyone's throwing on people on steroids, you know, yet again, another long COVID paper in nature with high cortisol. Well, you know what? Or no, low cortisol. I'm like, because everybody's on steroids. Yes. Yes. First, steroids and LDN is like, you know, the first like, it's like a reflex. Here's your LV, here's your steroids, you know. And we're not really going to the root. Now, is there anything, obviously in my world, I loved if I could use curcumin or lumbrachinase or any of these things. Is there anything that you've seen that has any effect even remotely close to the medications that you've been seeing success with that's on the realm of natural agents? You know, it's a good question. I mean, his patients come in with lists of those agents. And I mean, my first question is how's that going? And then my, but you know what, all kidding aside, I mean, we've looked at some of these agents with our panel. I mean, we actually, we have a non subjective means to test anything and everything for its anti inflammatory activity that would contribute to, you know, improvement in the pathology. So, you know, it's really hard to say. I typically tell patients, you know, don't stop, don't stop. I don't, you know, I, it's neither here nor there. But I mean, obviously the only one I talk about is turmeric, because turmeric, for some reason, increases blood levels of morale rock. So. Oh, interesting. So that's kind of just a nice synergistic effect with that makes wonderful sense. One other question that I know people are thinking, because we talk about mass activation, and that's obviously connected. Is this because we get cytokine activation, mast cells are part of our immune system, and they're becoming activated and prostaglandins and histamine are part of this. Can you correlate, like, how does that fit in at all? If, if anything, with the whole idea of mass activation? Having been in long COVID for so long, and some of the early theories, you know, mast cell activation was one of them. People took various agents, and you know what, they really weren't that effective, H1H block and that, you know, and you know what, to me, if there was really a lot of mast cell activation, I'd see elevated interleukin 13 everybody. Yeah. So, so. And you did say just with a lot of, with long Lyme, that was one of the patterns with, it was IFN gamma and interleukin. Yeah. Yeah. Okay. So maybe in that particular subset, there's more mast cells versus not. Fascinating. Well, what is the future?  This is just game changer for those of us out in the field actually practicing medicine. What do you see as the future? What things are going to be coming out? What's next? So we've had so much good news, especially in this last, last quarter of the year. Number one, we're seeing really broad reimbursement. And that makes us extremely happy because now, you know, it's not just a long COVID test. Originally, we were coding it as long COVID. The fact is, now we have the new algorithms to detect chronic Lyme and have suggestions of ME-CFS that presented this meeting about a month ago that there may be five different immunotypes based on cytokine profiles that we discovered for ME-CFS. There may be five flavors at a minimum immunologically. I mean, we all know that it is very heterogeneous. We don't really know what the underlying cause is, but we're starting to map that out on an immune profile level so that we can use targeted therapy and ME-CFS that is independent of bacteria or whatever that could be causing it. That's exciting because I think sometimes a toxic load, infectious burden, which I'm dealing with on this level, it's so hard to determine exactly what, but if we can go straight to the immune system and say, this is what's happening and then we know what to target, it almost, it does matter, but it almost doesn't matter what the original cause was, right?  So coming out at the end of year, reimbursement for the test, which is very, very exciting. The fact that we now have these patterns, which separate and define long COVID, Lyme, ME-CFS, even fibromyalgia, is all very exciting so that we can really treat them because they are treated differently. And then most importantly, great work by my team at InsultDX and in getting our trial design for Maravrock and Statens in long COVID, all that written up, all of that, all the additional information, all of it's been submitted to the FDA and we're really excited that 2024 we'll get our trial underway and get this hopefully at some point get an approval. The good news is they're already approved drugs so it's a different pathway where we're really looking at efficacy as a major focus. So it's going to be exciting year, but it's all been springboarded by the use of this diagnostic in chronic inflammation. And it's really resulted in great, great patient outcomes and that's the thing that gets me. I mean, I've gotten letters and calls and everything, but the most, I mean, this one girl is 12 years old, wrote me a letter on colored paper with colored pencils. Thank you, Dr. Patterson, for making me better. And you know what?  All that work that for me started in the late 80s in viruses was all worth it. I love that and that's just such a great way to end here because like truly that's why you and I do what we do is like to see the patients faces that, you know, see a change in their health and that's the reason I get up every day and I know for you too. And it's a long road sometimes, but I just want to say I've been in this role the long time in my little tiny window of functional medicine as an MD, but I see the value and that to me, this is not only this conversation, this podcast and all the work that you do is profound. Like this is a game changer. And if you're listening, you just listen to history being made and it's going to continue for you if you stay tuned to the studies that Bruce Patterson's work and group is putting out. So I just want to say on behalf of all physicians out there like me, thank you truly because this is the kind of game changer. These are kind of those pivotal moments like when the cell danger response came out and we understood that and some of these things are always game changer. So thank you. Thank you. Thank you for your work. Where can people find your work, your information, the lab, give us some websites and places and resources that they can find you and we'll list these. If you're listening or you're driving, we'll list them everywhere this podcast is shown. So www.covidlonghaulerswithins.com is the best place to get a hold of us, me. It's been a, it's a functional website, we're about to launch a physician's link so they can order the test directly for their patients and it's been, that's where all our information, all our publications, talks, etc. all reside there. And of course, if you search on YouTube with my name in long COVID, you'll find, I'll be just about everything we've ever talked about. Thank you. As always, here we are. We're recording around the holidays so thank you as always. Once again, here you are taking time right close to the holidays to share this great information, truly from the bottom of my heart. Thank you for your work. Thank you for your intelligence and your genius and curiosity and I hope I can continue to support the work that you're doing.


Ambassador Hill, thank you very much for coming to the Australian National University today for the John G lecture. I wanted to start by asking you about the role of weapons of mass destruction. Despite the challenges in the Middle East, conflict in Eastern Europe, even problems and tension in Asia, we still don't seem to hear the word nuclear very much. Do weapons of mass destruction matter these days? Well I think they sure do and I think we've got a couple of issues that are very serious and you know one of the problems is they are so important and yet some of these issues that we're dealing with today, whether it's ISIS or Ukraine, are so urgent and often the urgent crowd out the important. But sooner or later I think these weapons of mass destruction, these programs that are being pursued vigorously frankly by the North Koreans and sadly by the Iranians as well, will have to grab the world's attention. So I think it's a good time to be talking about that but also be talking about how some of these issues are embedded in broader problems. You mentioned North Korea and we've seen them pushing steadily towards a nuclear capacity. We've seen chemical weapons used in Syria. Do you think these reflect a bit of a turn back on the global preventions and prohibitions against nuclear weapons? I think it is fair to say that the global governance with respect to WMD is really being challenged. It's being challenged definitely by the North Koreans who simply don't acknowledge it. In fact they too have chemical weapons stocks. It's been challenged by the by the Syrians but it's also being challenged by the Iranians. And I think all represent serious challenges and if those challenges are not met especially with respect to Iran you could see further spread of these weapons such that I think the global governance of them really begins to fall apart. One of the fears a lot of people have is terrorist groups getting weapons of mass destruction. Do you see that as an issue when looking at a threat such as ISIS? You know when you look at something like ISIS it is quite clear that they would do anything they feel they can get away with. Certainly that was the case of Al Qaeda. They killed 3,000 people in New York. They would have been happier for 30,000, 300,000, 30 million. So you do you are dealing with organizations that really have no scruples and therefore the potential that they could get a hold of weapons of mass destruction and have a capacity you know whether they get it from the internet or somewhere else I think is quite worrisome. Finally the John G Memorial Lecture is honoring a Australian diplomat who is heavily involved in the Australia group in chemical setting up the chemical weapons convention. What is there a role for middle-power countries to be involved in non-proliferation discussion? I think there's a very important role for middle-power countries. First of all many of them most of them do not have nuclear weapons themselves and they have a very important interest in making sure that others don't get a hold of them and also that the nuclear weapons states fulfill their own obligations to begin building down. So I think it's a very important role. It's also a role that I think is filled very credibly by middle-power countries. I mean they are not looking to keep their nuclear weapons and have others do away with theirs. They want to keep it a safer world so I think it's a very important role and I think Australia in particular has had an important role looking at issues of materials and purchases that are consistent with nuclear weapons proposals. These nuclear weapons programs these types of things and I think the legacy of John G is an extremely positive one not only to his family to himself and to Australia but also to the world. Well thank you very much. Thank you.


We are at our quads and coffee event. This is our open house event where people come out, drink some coffee, and of course fly some quads. Today we're trying out all of our indoor flyers. We've got skylights, we've got the Vision 40, we've got the Bobito, we've got all sorts of fun things. People are flying around inside and having a great time. For the first time here, we've got more drones built up. One spot that I think we've ever had before. It's so cool to be able to pick up everything, touch it, feel it. Look at the skylight. How clean is this thing? I love it.  Really incredible experience. It's a city attract. I'm 13 and I ride dirt bikes and fly quads. I'm from Orlando, Florida, Arboret. I want to do freestyle and cinnabar. You can see everything. I can see the future. Mike from Gemfan and Gemfan actually sponsored this event. We're helping us put it together. We really appreciate it. And on top of everything else, we've got a goodie bag for everyone that's coming through and posting stuff in Gemfan. What do you want if you come to Quads and Coffee? Okay, so here you'll find more props and more props and don't forget the stickers. Everyone wants the stickers. You just go for the stickers. Of course, more skits, Roto Riot stickers, and this is a limited edition Roto Riot Rampage Moonlight Prop. These are LED props. This is one of the coolest things we ever did with Gemfan. Limited edition. You get these props to actually light up. So if you fly in civil twilight, you can actually see your glowing props. They're amazing. Of course, the larnyard. Got to have some necklaces in there. If you guys didn't make it to this Quads and Coffee, you better make it to the next one. The band don't only make the best props, but they make the best branching and the waffles out there. These waffles, we're bussing, bussing. Thank you, Gemfan. Ultra times 10 bussing. Thank you. Yeah, man. We're going to see if we can get in there and burn up a few packs. So you did this? Yeah. We sure you want to claim this. I'm asking you right now in this spot, are you sure you want to claim this soldering spot? That's an amazing job. Look at this. Look at that. 16 years old. That was amazing. Shred it too hard. Shred it too hard as a prototype, Drew. Oh, no. No one else even got a chance to fly it. No one. No. I was just testing it out. I got a little too aggressive. That's me. Whoopsie. It's available by Rotorite. Some of those. Oh, are we out on that? Justin found these injection molded ducts that fit really well. We just flew it around. Fly is great, but I'm not happy with it after one crash. I mean, it was a hard one. Something a little bit better for this, but this is definitely a prototype. The concept is super cool. Super cool. Ducted dribble, it's definitely coming, but we're going to make it more durable than that. Hello. This is Gabriel. How long have you been flying on the sim? For like, this will be like 15, 20 hours. 20 hours on the sim, but you've never seen it, like, never held a drone before. I've never been on a sim. I've never been on a sim. I've never been on a sim. I've never been on a sim. You've never seen it, like, never held a drone before? I've never, like, actually piloted a drone. I've put the goggles on yet. So today's going to be your first day? Yes. Excited? Oh, yes. Are you nervous? Yes, very nervous. It's not your drone. If you crash it, we have to fix it. You don't have to fix it. That's awesome. We're going to do videos. It'll be fun. Yeah, thanks. Let's see if I don't break any of the walls. You're in the trial over there. Did you crash anything bad yet? I crashed everything so far. Oh, good. Perfect. That's what you should do. There we go. All right. He's in the channel. He's got the Star Wars French Run. All right. Hard left here. Hard left here. Boom. Boom, baby. Hit the cap. Hit the flow. You're in the flow. You're in the flow. Yes. Yes. Right in the wall. Stayed in the flow. That was great. That is awesome, man. All right. We're here at Bubby Land. And Bubby Land is a little kind of mock office that I created for people to fly the Bubbito, which is my little nano drone. We're here at Quaddon Coffee. And we're going to be letting a bunch of people fly it today. I planned out all of the obstacles very strategically. Look at this. We've got a little dive right here for all of the gear. You can do matty flips. You can do backward slides. It's a really small gap, but the Bubbito is a really small drone. And my goal is to hit every gap to make sure it was possible so. I have a lot of these little shelves with a lot of holes for people to fly through. You can matty put this as we did all soon earlier. Power loop the table and the gauntlet of the day. There's a dive behind here. Right there. So that's the gauntlet for people. So far, only me and Mike Durand from Gemfan have been able to get it. Little things like this. Gate entry. It's a small gap, but you can hit it. It's like I wanted to make the most awesome little freestyle pitch for Bubbito. I'm Ian. We're here with the Road to Ride guys. We're about to fly one of these little Bubbitos. It's just probably the tiniest FPV drone I've ever seen. Yeah. I just started flying FPV like two months ago. So we're definitely going to crash a few times. Let's go. I do a bunch of stuff with Bobby Sutherland for the Wakescape League. We did some other stuff with Space Mob guys this year. So that was a lot of fun. Check it out on YouTube. Just search for the Wakescape League. Oh, nice.  This little guy is crazy. I film a lot of wakeboarding, so I'm like following people. I'm pretty good at following people. But FPV is totally different. I just got into it like two months ago. It's a totally different game. Like Acromode is not anything like you would ever fly in a DJI drone except I guess maybe the DJI FPV drone. After flying DJI stuff for like seven years, it feels like I'm just starting over again because I feel like a beginner again. It's been a lot of fun and it's going to be another journey. Everything together too. It was amazing. Peace. Thank you.


Item number SCP-169 Object Class Keter Special Containment Procedures Because of its size, SCP-169 cannot and almost certainly will never be contained. No structure on Earth is large enough or strong enough to contain SCP-169. The location of SCP-169 is not precisely known, but imaging satellites and analysis of eccentricities in the Earth's orbit suggest SCP-169 located in the Southern Atlantic Ocean, possibly stretching around the tip of South America. The Addendum 0-20 Any satellite footage of a shift in the land masses produced by SCP-169 is to be excised and destroyed by embedded agents. Description SCP-169 is surmised to be a marine arthropod of enormous size, known as the Loliathan, by generations of sailors in oral history. Presumed at first to be a myth, SCP-169 was detected on ██-19 by Mobile Task Force Gamma-6 during an investigation of paranormal activity around the ██-archipelago, coordinates ██-South ██-West. During Gamma-6's investigation, Dr. ██-6-0912 discovered the archipelago to have moved at least three kilometers from its original location. Though initially Dr. ██ believed this motion to be due to unusually quick continental drift, a reconnaissance mission performed by the USS ██████ revealed the archipelago to be the protrusions of rock-like plates covering an enormous organic mass. The Foundation would brought in immediately to begin threat management. Dr. ██████ and Dr. ██████ Gamma-6-0421 estimate SCP-169's body length to be between 2,000 and 8,000 kilometers. The creature is thought to have existed since the Pre-Cambrian Era. No other specimens have been sighted. Almost nothing is known about SCP-169's habits, such as its reproductive capabilities, if any, food source, and nesting area, if any. Results regarding SCP-169's pending approval. The archipelago, known as the ██████ Islands, have historically been uninhabited, though claimed by ████-17 upon hand over to the Foundation. Presence was evacuated on the pretense of rising sea levels. Though the archipelago had remained above sea level for several millennia, any change of death by SCP-169 could result in the disappearance of the entire archipelago. SCP-169 moves slowly, less than 1 kilometer per week, but seems only to be adrift. Its method of propulsion is unknown. Regular seismic tremors seem to indicate breathing about every three months, causing minor shifts in the island's terrain, suggesting that the creature is probably dormant. Submission suppression. The USS ████ was scuttled with all hands immediately after the discovery of SCP-169 with the permission of the American government. The public is forbidden from entering the archipelago created by SCP-169 due to the conveniently large number of resident endangered bird species. As indicated above, satellite footage is to be doctored in order to suppress knowledge of SCP-169's movement. NASA is currently cooperating with the Foundation in keeping the existence of SCP-169 quiet, and is currently permitting the Foundation use of their satellites for photographic use. Addendum 0-20 In 1990, the US National Oceanic and Atmospheric Administration, an American scientific agency unaffiliated with and unaware of the existence of the Foundation, detected an ultra-low-frequency underwater sound emanating from around ████ degrees south ████ degrees west, approximately ████ kilometers from the southwestern coast of South America. Despite the best efforts of embedded agent ████ IA-1522, news of the sound leaked to the media receiving significant media coverage. Foundation analysis concluded that a massive underwater organism was the source of the noise, and SCP-169 would hypothesize to be its source, as its head is well within the possible locations of the rest of SCP-169. The sound confirmed Gamma-6-0-421's hypothesis that SCP-169 is gargantuan in size. Future efforts by scientific or civilian teams to determine the source of the noise must be stopped by any means necessary.