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Episode 9 Season 7: Shingles, Dog Context, and The Immune System with Dr. Mohseni

• Jason and Kris Zackowski • Season 7 • Episode 9

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On this week's show we dive into the hidden connections between shingles vaccines and decreased dementia risk, while exploring how humans often misinterpret their pets' emotions based on environmental context rather than actual animal behavior.  Our guest, Dr. Yasmin Mohseni blows us away with the inner workings of the immune system.

Some highlights:

• Shingles vaccine study reveals a 20% reduction in dementia risk, particularly among women
• The protective effect may be linked to how viral infections modify the immune system
• Humans heavily rely on situational context rather than dogs' body language when assessing canine emotions
• A study of 400 college students showed they couldn't distinguish dog emotions without environmental cues
• Dr. Yasmin Mohseni explains why the immune system isn't a simple on/off switch that can be easily "boosted"
• Immunotherapy approaches like CAR T-cell therapy are revolutionizing cancer treatment
• Cancer cells create "fortress-like" defenses that engineered immune cells must overcome
• Understanding your pet's actual body language rather than situational context can improve communication

Dr. Yasmin's links:

Instagram: https://www.instagram.com/doctor.yas_/

Our links! 

Our Website!  www.bunsenbernerbmd.com

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Speaker 1:

Hello science enthusiasts. I'm Jason Zukoski. And I'm Chris Zukoski, we're the pet parents of Bunsen, beaker, bernoulli and Ginger.

Speaker 2:

The science animals on social media.

Speaker 1:

If you love science.

Speaker 2:

And you love pets.

Speaker 1:

You've come to the right spot, so put on your safety glasses and hold on to your tail.

Speaker 1:

This is the Science Podcast. Hello everybody and welcome back to the Science Podcast. We hope you're happy and healthy out there. This is episode nine of season seven. It's a little late coming out today. Chris and I did our best to get it out on Saturday. Normally the podcast comes out on Friday. We had a really exciting and busy week and we ran out of gas. The Bernoulli stuffy launched to the public this week and we had an amazing response. So thank you so much to everybody who supported us by picking up a Bernoulli stuffy in our pre-sale campaign. And then Friday Bernoulli got to play with Chesney, his favoritest dog. Chesney is a service and the dog of the amazing Marla Smith, who does great work for disability advocacy on social media. So we're a little late, but we're here to do it now. All right.

Speaker 1:

In science news we're going to be looking at a protective effect the shingles vaccine may have on folks who got it. And in pet science, are you reading your pet emotions wrong? Chances are. It depends on the context. Our guest and ask an expert is Dr Yasmin Mousseni, also known as Dr Yas. Ask an expert is Dr Yasmin Mousseni, also known as Dr Yas, on social media. She's going to be talking to us about the immune system in an amazing interview. Okay, let's get on with the show, because there's no time like science time. This week in science news, let's talk about disease caused by a virus I think both you and I got when we were young, chris.

Speaker 2:

The chickenpox virus.

Speaker 1:

Yeah, specifically the viral infection that you may get when you're older called shingles if you were infected with chickenpox. Do you remember getting chickenpox? I don't, but there are photos of me and my brother Cam covered in chickenpox bumps.

Speaker 2:

Mm-hmm. Yeah, both my sister and I got chicken pox when we were younger and actually she got some kind of significant scarring because she was very itchy and very scratchy like the cartoon. Itchy and scratchy, but I don't think my case was as extreme as hers, but we both definitely got the chickenpox. Duncan was born in 1997. So I do remember when he was going for his vaccinations, his routine vaccinations they did ask hey, did your child get chickenpox? And I said yes, I believe he did. And they said we have this vaccine, would you be interested in getting the vaccine as well? But then they said we don't necessarily need to vaccinate if he's already had the virus.

Speaker 1:

Oh, did Duncan get chickenpox? I forget.

Speaker 2:

Yeah, he did as a child.

Speaker 1:

Man, that was so long ago. It must not have been very bad.

Speaker 2:

No. And then it makes you question like like did my child get chicken pox? I?

Speaker 1:

totally forgot and you just want to be sure to give them the best chance and keep them the most healthy now we're not going to be talking about chicken pox, we're going to be talking about shingles, and after you recover from chicken pox the virus lies dormant in your nerve tissue and then can reactivate later in life as shingles. So maybe that's something you and I can look forward to as we get a little older. But your dad and stepdad both suffer from shingles flare ups from time to time, and I think Lissa too, your niece.

Speaker 2:

Yeah, but you don't have to wait till you're old. Melissa is 31 and already has had shingles very bad.

Speaker 1:

So it's a really painful rash and a band on one side of the body that you can be covered with it, like it's not like chicken pox, it's a rash, and people who have it they report that it feels like they're on fire, like it's burning, tingling or it's numb before the rash appears, and then the rash itself is really painful and it actually can cause significant nerve pain, vision or hearing loss and then, in really bad cases of shingles, flare-ups, neurological complications. So it's not fun, it's no joke, that's for sure. And then, in really bad cases of shingles flare-ups, neurological complications. So it's not fun.

Speaker 2:

It's no joke, that's for sure, and what we're covering today is a study published on April 2nd in the Nature magazine, and that study investigated if receiving a vaccine with a live virus it's called the live attenuated shingles vaccine and if that lowers the risk of developing dementia. And they use data from a Welsh vaccination program starting in 2013.

Speaker 1:

And that live attenuated version is. It's a weakened version. It's not the live virus. It's a weakened version. It's not the live virus. So it gives you an immune response. I guess it gives them the idea that you're infected with chickenpox or shingles, but you don't actually get it. I think in very rare cases the vaccine can cause. In a live attenuated vaccine it can cause it, but those are extremely rare circumstances. So this study focused on older folks who were born between September 1st 1925 and September 1st 1942. And they used a natural experiment design. It compared people born just before and just after the vaccine cut off, which was 1933. I believe that at that point they'll suggest you don't get the vaccine. So that's why there's that eligibility cut off. This approach minimized bias from health conscious behavior, so people who chose vaccines may also choose other healthy habits.

Speaker 2:

That's right.

Speaker 1:

That can influence your risk of dementia.

Speaker 2:

Comparing individuals born just before and after that date did create a natural experiment similar to a randomized control. It identified a situation where people who get the treatment the shingles vaccine and they were not really different from people that were much less likely to get the vaccine, and so it eliminated that bias.

Speaker 1:

Because you want as little bias as possible in science studies. After they got all the data from the folks before and after this cutoff, diagnoses for dementia dropped at the vaccine eligibility threshold. So those who got the vaccine had a 20% relative reduction and it's not a crazy reduction. It's not like you will not get dementia if you got the shingles vaccine. It was just an interesting conclusion from looking at all the folks who were at risk for it and got to the vaccine.

Speaker 2:

One thing that is more interesting is the protective effect was more prominent in women. They did not see a statistical significant difference observed in the men, and this may be due to gender-based immune system differences in relation to how your body reacts to the vaccine and the immuno response that you get.

Speaker 1:

The study had some ideas, as I mentioned, why that may be. Shingle infections are linked to dimension development and it might modify your immune system in ways not understood that delay or prevent dementia and, as you said, chris, much more prominent in women. Another kind of like thing we should also say is that the study focused on the early vaccines that folks got the live attenuated shingles vaccine. That was one dose using the weakened virus. This vaccine was discontinued in 2020, and it was replaced by another vaccine called the recombinant shingles vaccine. You get two doses and there's no live virus, and a later study from 2024 suggested that this vaccine may be even more effective in reducing dementia risk. So the authors of this study are going to be looking, perhaps, at those folks, but they just need a little bit more time because that's a really new vaccine and I guess they just got to wait for folks to get old enough that they're more at risk to developing dementia.

Speaker 2:

But I don't think that throwing out the evidence from the live attenuated shingles vaccine is something that would be beneficial, because it does show that decline in dementia and it's something that can be studied more.

Speaker 1:

Yeah, for a disease that isn't 100% understood, I think the more we know about it the better. That's science news for this week. This week in pet science we're going to be looking at a study on dog emotions. Do you think you can tell when Bunsen, beaker and Bernoulli are happy, chris?

Speaker 2:

I can tell when they're happy, but this study puts that kind of how can you tell your dog is happy? Into it. Does it with a twist? So for me, because I'm interacting with the dogs and I see what's happening around in their environment, I can see, oh, the Amazon or the delivery persons here and Bunsen's at the door and he's on alert and he's barking. I might attribute that to the fact that, alert, there is a delivery person coming and Bunsen is protective of the house, whereas if I saw that, if he was outside and just barking, maybe I would think it would be a different reaction to something. Yeah, it's the context different reaction to something.

Speaker 1:

Yeah, it's the context that we are heavily influenced by. That's what the study is getting at, though I think when Chesney and Bernoulli were playing, I think they were both pretty happy.

Speaker 2:

Oh, they were so happy, jason, they loved each other. But they are able to pick up on their social cues and chesney did a really great job of putting bernoulli into line. No, I don't want that behavior. And he respected her and he picked up on her cues and he changed or modified his behavior accordingly. I think, as humans though, like you, definitely don't like the being amorous, and that's fair. And as humans, did we read the behavior and then jump into quickly before Chesney had a chance to change it, so being able to read the behavior, but then also, having said that, you don't want the behavior to go too far. So if the dog is in a little bit, giving warning, are we reading the body language appropriately, and if we don't step in soon enough, then it could lead to something far more nefarious or dangerous.

Speaker 2:

So, it's hard to tell. It's hard to tell.

Speaker 1:

It is, and I think that's where we can get to the study crest, because Holly Molinaro, an animal welfare scientist at Arizona State University, thought to test those contexts. She used her dad's dog, oliver, who's an older 14-year-old pointer beagle mix, and Oliver was filmed in a variety of positive and negative scenarios, like being praised, played with, and negative, like being scolded, and in the study it says around a cat. So that would Bernoulli would fit in right there around Ginger. There were 400 college students that were shown edited footage of Oliver on a black background stripped of all of the environmental context. Ah, so just Oliver and unedited footage. After viewing, the participants were asked to assess Oliver's emotional state, which is cool, because can you look at the dog and determine if it's happy or sad without the context of being scolded or being played with?

Speaker 2:

I know, and what they found was in the edited footage participants couldn't distinguish whether Oliver was happy or sad. Only after viewing the unedited footage allowed them, the participants, to accurately identify Oliver's emotions. So this suggests that people heavily rely on context rather than dog behavior alone to assess the emotions of the dog.

Speaker 1:

And here comes the twist. A second group of 513 participants were shown edited clips where positive behavior was shown in a negative context and negative behavior was shown in a positive context, in a negative context. A negative behavior was shown in a positive context. So example Oliver was reacting to a vacuum cleaner, but it was edited to appear like he was reacting to a toy. And what did they find there, chris?

Speaker 2:

What they found was that, no matter what Oliver was actually doing, people based their interpretation solely on the surrounding context. So if the context looked positive, they assumed Oliver was happy. Conversely, if the context looked negative, they assumed the dog was sad.

Speaker 1:

So some of the key takeaways that I think we should think about as dog parents is you probably should be careful generalizing results from a single dog. This is just Oliver, and dogs like Oliver with floppy ears are harder to read compared to dogs with more pointy ears. And Bernoulli and Bunsen have the little eyebrows that move around when they're emoting, which gives their face like a very cartoony like expression when they're happy or scared or sad, whereas Beaker's face can be very muted, like when she's happy, but if she's not happy you don't know what she's thinking because she's just looking.

Speaker 2:

So when she's just existing, her face doesn't necessarily emote. Existing, her face doesn't necessarily emote. And we love it when she's happy because then, like when she's going for a walk, you can tell there's an instant change in her demeanor yeah, we call her blank expression that she has her rbf, which is resting beaker face yeah, that she has her RBF, which is resting beaker face, yeah, which we think is funny.

Speaker 2:

The study emphasizes that humans often misread dog emotions by focusing too much on the external cues rather than the body language, and dog owners are advised to practice focusing more on the dog's physical cues than the environmental factors, and I think that's what we've done a lot watching our dogs in terms of their behavior, especially with Beaker as a COVID puppy. She slinks a bit and she exudes that overconfidence with other dogs but really she's not a confident dog and it's oxymoron or a paradox in her behavior because you think oh, wow, she's's barking, she's like trying to make herself look big because she's obviously very confident, but it's actually the opposite she's puffing up to be I'm big, because I actually feel not confident and one thing that we're doing to mitigate that is definitely taking her to waggles and she's able to play with other dogs and gain that confidence which has been so amazing for her. She's been making friends.

Speaker 1:

The strongest contexts are, as you said, the dog's body language, like their tail position, their ear position and their facial expressions. So you have to remove the context and look at what the dog is doing, not what the environment is doing to the dog, and that's easier said than done. All right, that's Pet Science for this week. Hello everybody, here's some ways you can keep the Science Podcast free. Number one in our show notes sign up to be a member of our Paw Pack Plus community. It's an amazing community of folks who love pets and folks who love science. We have tons of bonus Bunsen and Beaker content there and we have live streams every Sunday with our community. It's tons of fun.

Speaker 1:

Also, think about checking out our merch store. We've got the Bunsen Stuffy, the Beaker stuffy and now the Ginger stuffy. That's right, ginger the science cat has a little replica. It's adorable. It's so soft, with the giant fluffy tail, safety glasses and a lab coat. And number three if you're listening to the podcast on any place that rates podcasts, give us a great rating and tell your family and friends to listen too. Okay, on with the show Back to the interview.

Speaker 1:

It's time for Ask an Expert on the Science Podcast and I'm thrilled to have expert in immune therapy, dr Yasmin Mohseni, with us today. Doc, how are you doing?

Speaker 3:

I'm good, thank you. Thank you for having me on. How are you doing?

Speaker 1:

I'm good. My wife and I are big fans of your Instagram page, so we're really excited to have you on. You do a great job with teaching us all about the immune system and it's just a thrill to have you on our show.

Speaker 3:

Thank you so much. Thank you, I'm a massive fan of your page as well. Your page always makes me smile, and just the dramas between Benulli and Ginger.

Speaker 1:

Oh man, it's drama llama at our house. I tell you that. Where are you in the world, where are you calling into the show from?

Speaker 3:

I'm actually in Los Angeles at the moment. Yeah, I moved here three years ago. It's been just over three years now, but I was in London for all of my life, so I trained there as well. I was briefly outside of London for my undergraduate degree, but, yeah, then the opportunity arose to move to the States and I got to the age where it was like, oh, it really is now or never. So I thought, trade the rain and depressing weather for the sun and the life in LA. Why not? Let's give it a go, and I'm so happy I made that decision.

Speaker 1:

Nice and were you safe from the fires? That's been all of our Canadian news. Were you safe?

Speaker 3:

from the fires. That's been all of our Canadian news. Yes, it was a bit hectic, because for a while we were okay. But then there was this new fire, called the Kenneth Fire, that popped up somewhere out of nowhere and we basically had a two-hour window to just get out, which was very jarring. And so we both went home from work, we packed up the cats, packed up suitcases quick, quick and we just went and stayed with a friend, but luckily that fire got contained really quickly. But yeah, that was definitely an experience. Of course, no power as well. So it's yeah, january was a little bit nuts in LA, but luckily things seem to be somewhat coming back to normal, I think that's good, I'm glad.

Speaker 1:

I'm glad you're okay and like your property and obviously your animals are okay too. Yeah, so I introduced you as a doctor and you're known as Dr Yas on Instagram. Can you chat with us just a little bit about your education background in science?

Speaker 3:

Yes, of course. So I've trained as an immunologist. I got my PhD from King's College London, so initially I trained. My bachelor's degree was in biochemistry. So if we're going to go all the way back in time, I was studying at Warwick University and it was quite funny because when I came to the end of my degree I panicked, thinking as we all do what am I supposed to do with my life, my career? And I thought let me just do a master's degree just to buy myself some time to figure out what I'm meant to do. And my master's degree, I decided, would be in immunology, where I studied at Imperial College London, which is a really fantastic institution, london and I ended up specializing in allergies, which I found was so fascinating. But I realized I just had more questions after my master's degree and I thought I can't enter the job space now. I need to understand a bit more about the immune system.

Speaker 3:

Because I was so captivated during my bachelor's degree where it just seemed like all these cells function in almost somewhat of a society and they all have these different designated roles just to basically keep us alive every day. And it was the humanizing element of the immune cells this guy has this job goes and activates this guy. This guy then goes and follows the call and goes to this area. I just thought this is insane. This is crazy, how this is all cells and I think I don't know. There was this video, which actually I think I'll upload it on my page because it's so fascinating. That really got me captivated. It was just this picture of an immune cell chasing after a piece of bacteria and I thought how is this happening? I have to understand more. So that led me to my master's and then, as I said, I had more questions and I wanted to then go on to do a PhD and I ended up getting the position at King's College London where I was specializing in organ transplant rejection and autoimmunity.

Speaker 3:

It was like developing a type of therapy to hopefully try and stop liver transplant rejection. But that type of therapy to hopefully try and stop liver transplant rejection, but that type of therapy could also be applied to autoimmunity, because essentially it's kind of some I'm gonna say this like it's very nuanced but similar mechanisms in the sense of trying to regulate the immune system, because when you have an organ transplant, your immune system is rightfully doing the correct thing by trying to reject it because it's recognizing it as foreign. It's not you. So you have to be put on immunosuppressants to try and stop that transplant from being rejected, and similarly with autoimmunity that is more your immune system going wrong, though, and your immune system turns on you and starts attacking you. So if you can employ similar mechanisms of just trying to regulate the immune system somehow. So that was what my phd was, and it was very hardcore, very savage, but also very enjoyable.

Speaker 3:

I learned a ton, and I specialized in a type of cell called a t-reg, and the t-regs in the immune system are the main cells that quiet the immune system. They switch it off. Essentially, they control inflammation. So by knowing you have these cells that control inflammation, that stop the immune, basically stop inflammation from happening, quiet the immune system, you can use them essentially in a therapeutic context to hopefully stop organ transplant rejection or autoimmunity.

Speaker 3:

So that was my PhD, and then I went on to a startup, which was founded by my professor and five others, basically using that technology in a liver transplant setting, and I know they've gone on to be quite successful. I think they've got like multiple autoimmune programs now. I think they've just signed a lot of money with AstraZeneca or something to be able to fund the pipeline project, for I think it was IBD or neuro, but pretty amazing stuff. But then I segued over to the US and I came over here three years ago and now I've actually jumped into the cancer space, so still using a type of immunotherapy to hopefully cure solid tumors. So that's my career and where I'm at so far.

Speaker 1:

I appreciate the roundup there. Yeah, I felt like a little bit of a. I felt like I was a bit ignorant because I just learned last week as a grown man that people with organ transplants they have to take those immunosuppressants for probably their whole life. I didn't know that.

Speaker 3:

Yeah, it's one of those strange things, but probably the reasons why you didn't know that is because there's such a focus on finding matched transplant donor, like matching on the blood type, and while we've done a fantastic job in that regard to stop acute rejection from happening, sort of, the antibodies kick off from the get go and then round up the rest of the immune system and just obliterate the organ, the organ transplant, we still have this risk of chronic rejection essentially happening where you can match as close as possible, but ultimately you will have these minor antigens, we say, or like minor, minor, minor, we could say proteins that really are your blueprint, that distinguish you from someone else. And no matter how closely you try and match, your immune system is so highly specialized and evolved to be able to distinguish. I think one of the hallmarks of the immune system is its ability to distinguish you from not you. So that is why, even if you follow all the protocols to match patients accordingly to donors, yes, you will stop that acute rejection from happening, but it's very hard to stop that chronic rejection from happening because ultimately your immune system can tell you from, not you.

Speaker 3:

So, yes, you go on immunosuppressants and the problem tell you from, not you. So, yes, you go on immunosuppressants and the problem, excuse me, with immunosuppressants is that they don't fully halt the immune system. Immunosuppressants have, like, different mechanisms. They might target these cells or these pathways or general bring down, like the sort of function and development of B cells and T cells, which are your adaptive arm of the immune system, but they don't completely wipe them, and for good reason. You need your immune system, don't you, to survive. So that means that your immune cells still have this image of coming round here and there and taking jabs where they can at the transplant.

Speaker 1:

So it's the drive-by just punches it in the face every now and again Exactly, it was like, oh, that's my chance punch.

Speaker 3:

But then that reality is that the half-life of organ transplants. I think it differs, but we know ballpark. We say about maybe 10 to 20 years for liver transplants. I do not know if that's changed since I've left the field five years ago. Liver transplants I do not know if that's changed since I've left the field five years ago, but you will probably, if you are a young recipient, you'll probably need another one in your lifetime, unless if we another transplant in your lifetime, unless if we really optimize the therapies. So that's the big issue. And the other issue is immunosuppressants, especially to this scale for organ transplantation. They're really hardcore on the body right.

Speaker 3:

They usually take a massive jab at your kidneys as well, so they're like nephrotoxic, and also just the fact that, yeah, you're suppressing your immune system, which isn't great, given we're living in a world where everything is trying to kill us. So we need other options, essentially, and that's where my career as an immunologist began.

Speaker 1:

Yeah, there's folks like you working on it, which is amazing.

Speaker 3:

Trying, trying my best. As I say, I've moved out of it now and I've gone into the cancer field, but my passion really is back in regulation. So I do think at some point I will move back into the space of autoimmunity and organ transplant rejection. But we'll see. We'll see how it goes.

Speaker 1:

Yeah, it's all good. You know that was my misconception. Are there other misconceptions about our immune system that you hear or you just like to tell everybody? I'd love to know like, from your perspective, one of the misconceptions that you see about the immune system in general.

Speaker 3:

Yeah, so I think this was. This is an interesting question because I think this was one of the reasons why I decided to start my science communication page on social media Just people needing to realize that the immune system is not a binary on off switch. I think that's the biggest takeaway I want people to try to understand. There is this literature, in the literature nomenclature words such as immune boosting and immune resetting, and that is not completely accurate, unless if we want to talk about in the conventional therapy context where, yes, we do have these mechanisms in place, or like rather hardcore protocols to be able to quote-unquote reset the immune system. But we're talking about really hardcore, like full myeloablation, like intense chemotherapy and then rebuilding with bone marrow transplantation, for example, in like for cancer, patient settings or blood disorders.

Speaker 3:

There's other interesting things in my field where we're using the concept of immune resetting by targeting patients with autoimmune diseases. So we're using a therapy to essentially ablate completely these naughty T cells and B cells that are causing autoimmunity and then, if they're gone, and then obviously over time you rebuild your blood, stem cells kick in and then you rebuild a new immune system. I say new, not just like you just have new cells developing, then yes, in theory you have reset the immune system. But in this long roundabout way I'm trying to say I'm seeing alarming protocols online from the wellness community on with bold claims that, following ABC taking this pill, doing this protocol, doing this sort of cold plunge or even like just walking into Erewhon, do you guys have arrow one? It's this very fancy supermarket or grocery store that's very upmarket from whole foods. It's very la. You always see celebrities in that but arrow one it's called arrow one is e.

Speaker 3:

I'm probably butchering that word in my accent, but e r, e-o-n is like this super fancy supermarket and I walked in. I was like this is ridiculous. How expensive everything is here. It's very elegant, but anyways, point is like this when you go walk through era one, everything is like immune boosting. This drink, that's what's immunity boosting and I just thought this is, I like just chuckle to myself, because it's really not that easy to be able to reset or boost your immune system through a simple pill.

Speaker 3:

I just think the biggest misconception here is, I think, people, I would like people to almost not disrespect the immune system that's been evolving for millions of years. Essentially and I don't mean that disrespect to any influencers that are claiming it's all out of good faith and trying to help people that are desperate with their health but says with the utmost sincerity but even immunologists, we're still grasping the complexities of the immune system. Any sort of central dogma that we believed about the immune system is constantly getting flipped on its head. Now I'm always getting baffled by new findings that we're understanding about the immune system, about just basically, from immune cells shape-shifting into different roles that we didn't classically define them, from having in the body, maybe because of adaptation, in a good way or in a bad way in certain situations. I think a perfect example I can give is my story. At least during my PhD, I developed I say I developed I attempted to develop this prototype proof of concept, as I said, to try and cure organ transplant rejection.

Speaker 3:

So what I did was I developed this type of therapy called a CAR-T reg therapy, which we can talk about in detail later or another time. But what I did, teamed up with my professors, of course, to try and make it super effective, is by making it produce a crap load of anti-inflammatory proteins. Because the idea was, once you inject it into the patient and if you have this therapy that's super anti-inflammatory and target it to this organ transplant, then you're going to create this sort of environment that's very anti-inflammatory. Therefore, hopefully, you should logically stop organ transplant rejection, because if there's an anti-inflammatory effect, then any T cells or B cells that come along and try and take jabs at it are basically dampened. What I found when I created this therapy and put it in my mice was it was extremely toxic for the mice and actually caused the opposite effect.

Speaker 1:

Whoa.

Speaker 3:

Super inflammation, whoa. And then time was up and I had to write my thesis and I was like I couldn't even expand on it further, so it was very disheartening. So that's the thing. It's the fact that we I expected it to have this one effect cause the complete opposite effect, this intense pro-inflammatory response. To any immunologists out there, it was aisle 10, so if they want to go and look that up, they know what IL-10 is, but it's basically a. It's something called a cytokine, but we can just, for lay terms, call it a protein that is just known to be super anti-inflammatory, yet suddenly producing so much of it was causing this opposite effect of mass inflammation.

Speaker 3:

So that's what I'm trying to say is that the immune system is so complex it doesn't follow the rules that we expect it to, and not even on the individual cell level and their individual jobs, but even combined with other systems. I mean, we're now looking at neuro endo immuno axis, for example, like the interface between neuroscience, endocrinology, for example, like the interface between neuroscience, endocrinology, the immune system, I don't know psycho endo immuno. It's just like we have to look at this holistically, and when I say holistically, it's our body as a whole. Our immune system isn't something that's separate from our neuroscience, endocrinology and all the other systems and cells will adapt accordingly neuroscience, endocrinology and all the other systems and cells will adapt accordingly. So that was the biggest misconception, that now I'm switching at least the goal of my page to try to educate people a little bit more on this. It's not so easy to reset or even boost your immune system by at least non-conventional, non-invasive treatments. I hope that makes sense.

Speaker 1:

It's a little more complicated than eating probiotic yogurt and taking a walk in the sunshine.

Speaker 3:

Exactly, but all those things help.

Speaker 1:

They help true.

Speaker 3:

That's the thing. I'm not necessarily an expert in this area, yet I'm trying to grow in knowledge myself in terms of all the basics. But people do neglect the basics, like to support I'm not going to say boost or reset, but to support your immune system, like exercise, stress management, nutrition, staying up to date with vaccinations Like these are the pillars of a well-functioning immune system, and by getting these basics right, you don't need to necessarily be faffing with these other protocols to that you saw online by some influencer to optimize your health. Now, forgetting that last sentence, I mean by getting these basics right, unless if you are someone that is dealing with immune related diseases, then of course, additional interventions may be necessary. Then of course, additional interventions may be necessary. But, yeah, start with the basics and just know that it's not that easy to reset or boost your immune system, but we just need to move to using new language such as supporting your immune system. I would say yeah, that's.

Speaker 1:

I so agree. The pillars are important and you need to support them. But just having one crazy strong pillar does not a house make.

Speaker 3:

No, no, and that is funny.

Speaker 1:

you mentioned the cold plunging things. Those got really popular up here in Canada in the winter because it's cold all the time, so you could just go outside and hop into some water and you have your cold plunge ready for you.

Speaker 3:

I mean I'm not, as I say like I mean I need to maybe fact check myself here in this area. I'm still growing and trying to understand more about all these other ways to optimize my own immune system, because I'm also myself dealing with immune related issues. It always seems ironic that whatever you end up specializing in you yourself end up actually potentially getting riddled with the issue itself. Yeah, which we always I'm open about this on social media about about it as well. But with cold plunges, I'm sure there are other, like a bunch of other benefits that people are exploring at the moment. That's why it's gained a lot of popularity. But in terms of the shock factor, I mean there are other ways to definitely shock your immune system as well, like as well as a cold plunge. So, yeah, it's just fascinating to see the obsession these days with all these potential ways to boost your immunity. So I'm learning myself of what people are interested in trying out.

Speaker 1:

There you go, Though. For anybody listening, all you have to do is go for a swim off the West coast of Vancouver Island. That's your cold plunge. So, you can get your wetsuit on and get some surfing.

Speaker 3:

There you go Cold plunge also are you supposed to get your wetsuit on? I don't know. Are you supposed to just just go for it? Isn't that a proper cold plunge?

Speaker 1:

or are you at risk of serious hypothermia, which I know, just because we vacationed out there and the ocean is chilly, very cold. So it's way more comfortable to go surf, for example, with uh, with your wetsuit on than just in a bathing suit. I'm not sure how long you'd last, yeah.

Speaker 3:

I don't think so. I don't know either. Highly recommend the Californian sun, of course.

Speaker 1:

Hey, can I ask you a question about what you're looking at now with your switch to cancer? Is that something we can talk about just real quick?

Speaker 3:

Absolutely, I could talk about this for ages.

Speaker 3:

Yes, okay, so a little bit about the technology. So immunotherapy has it's basically revolutionized healthcare One type of immunotherapy called immune checkpoint inhibitors that actually won the Nobel prize in 2018. And it's now considered a pillar or a staple for treating cancer essentially. So it's sort of the clue is in the name of immunotherapy. It's finding ways to enhance your immune system to treat various diseases, and that's either helping your immune cells that are already there and giving them something to quote, unquote, turbo, turbocharge them against cancer, or that there is a type of therapy called CAR, t-cell therapy, which so CAR, like C-A-R and T-cell therapy, which I'm in that space, and I was in that space for organ transplantation as well, but an autoimmunity but yes, I've moved in for cancer now where essentially, what you do is you take a cancer patient's T-cells out and you engineer them with, basically, the ability to hunt down the specific cancer that they have.

Speaker 3:

And you grow them to like the millions and millions. Ideally you try and achieve billions of these T-cells that are engineered outside the body, so in a manufacturing facility, and then you re-infuse the patient now with these depending on the dose level hundreds of millions of T cells that are now armed with this ability, like a GPS, to go hunt down that cancer. So that is what I'm doing at the moment. It is really cool, it's really badass. It's been changing the game, especially for blood cancers like leukemias.

Speaker 3:

We know that a lot of patients have been effectively I'm hesitant to say the word cured, but effectively cured or at least in long-term remission because of CAR T cell therapy. So we're realizing weaponizing your immune system really is the future of sort of health and like health interventions. So that's what I'm doing at the moment. I absolutely love it. And cancer is a really complicated one because it fight the cancer cells. It's scary because they fight back and your immune system part of what your immune system's job is basically to go and look for cancer. So right now in your body that's what your immune cells are doing. Your immune cells are going and basically taking like a register, like the class register, just to check that all the cells.

Speaker 3:

I know, that's the image that I have.

Speaker 1:

It's like I love it. That's a great analogy. I'm sorry, continue, I just chuckled because I'm a classroom teacher.

Speaker 3:

Oh, of course. Yeah, so you're effectively an NK cell, a natural killer cell that's walking, floating around, buzzing around, taking the register to make sure that everyone is in check, everyone's behaving well, and then what happens is when they encounter a cell that's stressed out, because stressed out cells, like cancer cells, they become the sort of neat we call it neoplastic like they change. So when they change and become cancerous, they basically can also emit, like these danger signals or do these other things where they pull in receptors and perhaps not knowingly, because cancer cells, especially when they become more advanced, they try and evade the immune system because they know that the I say they know as if, like, we're putting some sort of humanizing thinking element to it, but they quote unquote know that the immune system is trying to hunt them down and kill them essentially. So the immune system then kicks into gear once they've detected that we do have a rogue cancer cell that's arisen. But unfortunately this battle that's ongoing causes your immune cells to become exhausted. So that's the term immune exhaustion or t-cell exhaustion kicks in like they get. They're basically just constantly fighting and they become tired.

Speaker 3:

And the scary thing about solid cancers so basically not like the liquid blood cancers is that they have the capability once they really do advance is to form this sort of fortress to protect themselves like this think of the evil villain with this massive castle with all these like weapons and booby traps in place. So when, when the T cells come, they've got to chew their way through this fortress and once they get inside the castle there's toxic fumes. It's a very hostile environment that basically, they just effectively become dysfunctional. So that's what we're trying to deal with. We're trying to basically find a way to power up your immune cells to be able to deal with cancer, because that's what they normally do anyway, or pre cancerous cells. They usually do a good job of clearing it, even right now, as we speak.

Speaker 3:

And, as I say, one of these methods is something called immune checkpoint inhibitors, where basically one of the ways that cancer cells and even the cells that so cancer cells can manipulate cells like t-regs and those were the cells that I spoke to you about that, yeah, they basically cause immune suppression. They can manipulate t-regs and even other immune suppressor cells to come into the area and basically protect them. It's really scary, it's so crazy how that works. So you know, you have your immune army coming to try and hunt down cancer, but then they encounter their buddies t-rex and m2 macrophages and all these other immune suppressor cells that are basically there to switch them off.

Speaker 1:

So it's like dr evil's fembots he just screwed.

Speaker 3:

They screw up austin powers honestly, basically, like me and my friend, I should give him a shout out, but we haven't done it yet. But we're planning to launch like a, basically like a comic strip on social media of as a comic but like cartoons of all of this happening, because it's just crazy, it's like a war film when you think about it.

Speaker 3:

So one of the ways with immune checkpoint inhibitors is you're basically blocking a couple of the ways that these suppressor cells, or even cancer cells try and switch off the anti-tumor killer cells. So by blocking those, that means that weapon by the cancer cells and immune suppressor cells can no longer work and that helps out our killer cells. The heroes of the story actually do their job. So that's what won the Nobel Prize. But what obviously we're working on where I work at the moment in California, in Los Angeles, is taking sick patients T cells out, as I said, and re-engineering them to be able to go and hunt down the cancer and, yeah, re-infusing them and just basically watching and hoping and waiting to see what happens. So we currently have three phase one clinical trials. One of them is about to start, but the other two we are targeting pancreatic, colorectal, non-small cell lung carcinoma, ovarian cancer and mesothelioma. So those are the main cancers we're targeting at the moment. A majority of our patients that we've dosed are pancreatic cancer patients and I'm not allowed to share yet what's happening, but definitely we'll be releasing press releases at some point soon just to give the update, because that first clinical trial did begin. I believe we've did those.

Speaker 3:

Our first patient in oh, this is embarrassing. When was it? April of 2023? I want to say fairly sure. I want to say 2023. Made a fact check that either April 2023 or April 2020. Yeah, april 2023. Sorry, I can't. I just can't believe it's already been two years since I've been there it's like yesterday since I joined. So, yeah, we have been treating these patients and just, and these patients that come into these trials it sounds scary. A lot of them really are end stage, like they've had maybe not end stage because I don't want. Lot of them really are end stage Like they've had maybe not end stage because I don't want any of them here to get alarmed or something. But it's more, they've had multiple treatment lines that maybe haven't worked or haven't been able to keep them stable. And that's why they enroll into these phase one clinical trials, because we're just trying to give them something else that we think could work, because the other first line or second line haven't necessarily worked for them.

Speaker 1:

That's. It's just fascinating. I literally could listen to you talk about this for like days. This is I've taken down like some notes and I know I read a paper not too long ago about the CAR T cells, that therapy like they're. I'm just you may you'll have to correct me if I'm wrong. One of the advantages is these souped up cells like they stick around in the body so they kind of are bodyguards for a while. Am I on the right track there, or maybe that's a different point.

Speaker 3:

Yeah, this is really cool. So we do have this concern. That's the optimal situation where they stay there, because sometimes we can't detect them in the blood after a while. But maybe there's a lot about this. It because sometimes we can't detect them in the blood after a while, but maybe there's a lot about this. It could be the reason why you're not detecting them in the blood is because they're not actively circulating. It's like when people say, oh, like you don't have immune memory anymore because we can't detect antibodies in the blood, and it's no, it's just the antibody. They're not needed. But the main cells are chilling in the like lymph nodes, for example, or in the spleen.

Speaker 3:

They're just hanging out, they're on vacation, basically, or they're just in the barracks waiting for the call-ups.

Speaker 1:

That's a better one. That's a better analogy. I like that.

Speaker 3:

Exactly. I say barracks. I have no sort of army terminology but I'm trying to learn because I think that the army a lot of immunologists like to refer to the immune system as an army but more of waging war when necessary, but predominantly peacekeepers. Ultimately they're trying to keep balance and peace in your body, because everything outside is wanting to come into the body, because our body is a very nice home. It's like paradise. But essentially so that's the thing with CAR T cells. What we're finding is, yes, that they can still be there and they go and just chill in the lymph nodes and come back out where necessary. And there's really cool studies with certain immunotherapies as well, where they look at something called re-challenging. So when we re-challenge, like mouse models for example, then they're able to definitely clear the cancers, for example, a lot faster. That's like the optimal situation that you'll read in, like these mouse papers, where once they're re-challenged, they're able to just clear cancer so much faster.

Speaker 3:

Because the beauty of the immune system is it has memory. Especially the adaptive immune arm has which are like the T cells and B cells. They have specific and highly specialized type of memory. So that's the aim as well, is that once they've seen it. They can come back out and do their thing. And I know, like with cancer vaccine trials that's with cancer vaccines they're really hoping to like trigger that memory response. But yeah, with CAR T cells you'd want them to always be there and then they come back out where necessary. So did you read? Was this a blood cancer? I'm guessing.

Speaker 1:

I was and all of this is I'm not at your level of expertise at all, but just for the pod, my podcast a year ago or so I related to my students as a video game analogy. It's the immune system has a memory. It's the more times you play Super Mario you can get by the levels faster. And then, because you've souped up these car T-cells, it's like mario's not little mario, he's when mario gets the fire flower and you can throw fireballs. Not only does this immune system have memory, you're now, you're souped up, kind of thing exactly, yeah, that's such a good way of putting.

Speaker 3:

Oh yeah, maybe I'll use, like the super mario kart analogy. I'll cite you, don't worry but, that's such a funny way of thinking about it yeah, you gotta get the kids.

Speaker 1:

You gotta get the kids engaged.

Speaker 3:

Somehow they're sleepy in the morning, I tell you yeah I could definitely imagine and yeah, that's the thing I think you can make science or you can make immunology like how can people not be interested in this?

Speaker 1:

It's so cool.

Speaker 3:

They've evolved over millions and millions. I think I was reading about the first ever phagocyte in life, which is phagocyte means like eating cell. So these are like the macrophages, for example, that just go around and chomp the bad guys and then they have the other, like processing in place to be able to go wake up the rest of the immune army. But how the first phagocyte evolved and we're talking about it's crazy. We're talking about millions and millions, hundreds of millions of even fact check this billion years ago. That part maybe needs to be fact checked. The point I'm trying to say is this is prehistoric at this point and all that's been like. From that first phagocyte we have now developed this extremely intricate, complex immune system that is so powerful that it's it really is a double edged sword, because it's so powerful that it can save our lives, but also it can kill us within minutes, you know, and that's what you have with like cytokine storms that happen, or even anaphylaxis, which is very scary when we're talking about serious allergic reactions. So you do have this equivalent of an intense atomic bomb that could get detonated inside you by your immune cells if things do go wrong. That's I want people to appreciate. I sound like an absolute not, but yeah, flip, I'm a scientist obsessed in my field, but I just want people to appreciate I sound like an absolute nut, but yeah, flip, I'm a scientist obsessed in my field, but I just want people to appreciate right, it's worship the immune system. I want people to really appreciate the complexity and just how it also deserves our respect. And part of my page I'm wanting to segue, when I'm not getting distracted by all the other things going on, is to make people actually marvel and all at this complex immune system that's trying to keep you alive, but also, if slightly out of balance and if it gets so, if it's slightly out of balance, it will do. Its number one priority, I believe, is to get back to balance. That's what.

Speaker 3:

If you ask any immunologist, they have different theories about what the key goal of the immune system is. My key theory is I have two key theories. It's one. It's being keeping non self quote, unquote, so not you out, unless if it's like the good sort of microbes that are inside of you that are helping out and keeping self in check, but also keeping balance, maintaining balance. And if you tip that balance too far to the point of no return. That's when you get things like autoimmunity or at least with situations like allergies and fatal allergic reactions like anaphylaxis, it's you have trigger happy immune cells that just can't distinguish like friend or foe. Essentially this, not this sort of non self that's passing by, it's okay, it's safe, but it overreacts and to the point that, yeah, you can die. So it is. It sounds a bit of a morbid note, but it is extremely complicated and it's extremely fascinating. And whoever whoever says take this pill, take this supplement, it will reset everything and all your problems.

Speaker 1:

And it's hun, it's not that simple, basically we have the old facebook status updates with relationships.

Speaker 3:

It's complicated yeah, oh my gosh, such as everything it's. And I think the people that are trying to preach holistic, that healthcare, maybe the people that are the biggest corporates of actually doing the opposite, which is approaching this with the most reductionist approach, because it really just isn't that easy, guys and I say this because immunology, I think, is one of the most complex fields in biology to understand, and even scientists like me, immunologists like me, we're constantly getting shocked at the new things that are popping up. For example, the dogma for a very long time was that only the adaptive immune system has memory. No, now we're. No, I say now.

Speaker 3:

Maybe people in the field for 10 years have known that now the innate immune system so your first line actually has a type of memory as well. So we're just constantly and we're learning that new cells pop up, like it's just, it's so crazy, it's so fascinating, there's so much that we don't understand and are trying to make sense of. But that's why people like me in the immunotherapy space is having the tools that we have now we are trying to weaponize and to keep up with the fight against things like autoimmunity and cancer. Once we infuse these patients, we learn new challenges. The CAR T-cell realm has tons of challenges, like, of course, the blood cancer's CAR T-cells are working beautifully. However, they have come with their own challenges. We have learned that even if we infuse these CAR T cells to go and destroy leukemia, the leukemic cells fight back.

Speaker 3:

They actually come up with new weapons oh my god, frustrating but that's what's so incredible is like we it's keeping scientists on their toes because it's oh my gosh, this Luke. So one one thing I can talk about one mechanism is like antigen escape and that's if you're reading that CAR T cell paper maybe this came up. But one of the reasons why CAR T cell therapy might fail is because of this concept of antigen escape. So you engineer the CAR T cells to be able to find a specific antigen. That's so for leukemia it will be looking for particular B cell antigen, because leukemia is not T cell leukemia, b cell leukemia. One of the antigens is CD19, for example. That's like a lot of B cells express this particular antigen, CD19.

Speaker 3:

When I say say antigen, just pretend. It's like a little protein arm just sticking out the cell, essentially. But then what happens is we have these cd19 car t cells and it goes and it finds everything that has cd19. So all these b cells absolutely obliterates them. Amazing news patients have complete response, no evidence of cancer in the body, it's all gone. And then suddenly, harrowingly later, two months later, this leukemia pops up again. And you're like how? And it turns out that a fraction of those B cells actually were not CD90, when didn't have CD19, they had another antigen up. So that's the antigen escape. They managed to escape therapy because they actually had another antigen that was being expressed and that the T cell treatment missed them.

Speaker 1:

And there's just so much 99% in the one left, and it grew.

Speaker 3:

It replicates and leukemia is so aggressive. So you know it well, there's like chronic. It's just so much nuance. There's like like the chronic, which is like the slowed burns, but some of the acute leukemias are very fast growing and deadly. It's keeping scientists constantly on their toes. The biggest challenge with blood cancers is this antigen escape fruit. That's just one of the main challenges. But then, as I say, with the solid cancers, which is the field that I'm in, it's how do you deal with the fortress that these solid tumors build? So for some terminology we call it the tumor micro environment. So the tumor micro environment is very much been built up to help sustain the cancer cells and they really do make it a very hostile, toxic environment for the immune cells that will come and try and destroy it. So how do we in the CAR T cell space in solid cancers override that toxic tumor microenvironment? So that's what we're trying to focus on at the moment.

Speaker 1:

Very cool.

Speaker 3:

I could talk about this, for it's so sounds like you need some kamikaze scottish highlanders to take the first charge against that fortress yeah, just screaming at them with their kilts on but then you have that risk of cytokine storms happening oh, so I don't know if you can turn around and come back at you.

Speaker 3:

It's more that they detonate.

Speaker 3:

They're like so amped up that they detonate all that, just that image of like just spraying with machine gun bullets or just throwing every possible grenade or bomb at them that you end up.

Speaker 3:

The cancer cells are usually nestled quite nicely in between healthy tissue. So then you cause this, like you cause this off tox off sorry, off target toxicity where even the healthy tissue get extremely damaged, and then you have that cytokine storm where basically all the other immune cells become amped up and it's this positive feedback effect and eventually it can cause this mass inflammation in the body that can kill patients. We do have things in place now, protocols in place now as an emergency when these patients are getting treatment to be able to deal with cytokine storms. So I do want to if there's anyone that's exploring cardi cell therapy for themselves that are listening, I do want to just say that we now have tools to be able to deal with cytokine storms, but the point is we're trying to find that balance right, like we want to just go and throw absolutely everything in the kitchen sink at these cancer cells, but then no, because you don't end up wanting to harm the patient in effect as well with toxic side effects. It's very complicated side effects.

Speaker 1:

It's very complicated. We end our show ends are in the interview with a couple questions about your pets. We love it when our guests share a story about the pets that they have or pets that they've known in their life. I was wondering if you could do that for us.

Speaker 3:

Absolutely so. I have two cats. I've got two ragdoll mixes. One's a ragdoll Himalayan and the other one is a what we think is a Siamese lynx point. Basically they're brothers and we found them in the shelter. I can't believe cats that flipping gorgeous were abandoned in a shelter. It's just criminal. Actually, I don't want to say that, I don't want to like judge people's situations, but so one of the cats is called shadow facts.

Speaker 1:

I 10 points.

Speaker 3:

If you know the reference shadow facts oh, that's gandalf's horse and lord of the rings, exactly gandalf's oldest friend, basically the inspiration there was. He was like a little shadow, just following me everywhere, but he's so regal and so majestic and we're like it just made sense, majestic to a point. He like a little shadow, just following me everywhere, but he's so regal and so majestic, it just made sense. Majestic to a point, he's a little ragdoll. So he does have, bless him, two brain cells. But and then we have the other. One is called togepi. Do you know the reference? Maybe?

Speaker 1:

oh, I've heard that you'll have to tell me.

Speaker 3:

The name is very familiar, though yeah, so with kids, that's the big clue, togepi, so it's a pokemon it's got an eggshell right and it's the eggshell.

Speaker 1:

It's like an egg.

Speaker 3:

That's all I remember yeah, me and my partner were like pokemon fans when we were kids and we wanted to try and build in like well, we were fans of this anime called dragon ball z Pokemon and Lord of the Rings and Harry Potter. Can we try and name pets after those particular key moments in our lives? So we called him Togepi, because he was this little kitten that kept chirping and we were laughing like he sounds like the Pokemon, togepi, and we're like, oh my God, that's his name, togepi. We have little Togepi in Shadowfax and, yeah, it's so funny because I've always wanted a ragdoll cat, like even before they became popular. I remembered watching homeward bound, which you must have seen homeward bound absolutely and sassy.

Speaker 3:

I was obsessed with sassy as a five, six year old and I know sassy is like a himalayan, but that look, that himalayan, ragdoll, siamese look, I just found adorable. So I always said I was going to get a cat that looked like that and I kept bombarding my partner on Instagram with all these reels. Of course, once you hit Instagram, here's you and your algorithm just turns into that. I think that's actually one of the ways I found you. My algorithm ended up being all these like cute cats and dogs and then my partner was like bless him, famous. Last words was like let's go to PetSmart, let's just humor ourselves. Little did he know that little Togepi and Shadowfax were there and I became obsessed and luckily, actually, the shelter owners told us that. So it's like a shelter, that's a part, it's like a rescue, that's a part of petsmart, yeah, and they said that apparently they had like over 40 applicants, but they picked us.

Speaker 3:

So we're very happy about that so yeah, we have our little boys. They're very cute, they're very naughty, but they're well behaved. I know some cats can be absolute demons, where they just bite, scratch, hiss. I don't even think our cats know how to do that. They're so cute.

Speaker 1:

Yeah, our cat Ginger's a sweetheart too. Yeah, so she's not a hisser or a biter.

Speaker 3:

She seems to really put up with Bernoulli's nonsense. Oh my, she's a saint.

Speaker 1:

Yeah, like when he was a puppy, it was, it was she. We actually spoke to a vet. I'm like what should we do? And the vets? You have to let them figure it out and the cat will eventually fight back. We're like, oh my god, it's not going good for her sometimes, and then eventually she did, and that's how they came to an accord and they're best buds now.

Speaker 3:

Yeah oh, that's amazing. That's so good to hear. When was the last ginger mauling?

Speaker 1:

Months ago, Months. He just, yeah, Lily is obsessed with her, so he'll trap her occasionally, but he just licks her Like he'll just lick her. So she's always soggy, Like you go to pick her up and she's just wet. I'm like, oh gross.

Speaker 3:

Oh, that's so cute.

Speaker 1:

Togepi and shadow facts very cute. Yeah, yeah, do they have offset colors?

Speaker 3:

or does some of them have the black paws that ragdolls might have? So they both have. They both look like typical shadow facts. Looks like a typical ragdoll himalayan mix, which is very fluffy and has a black face, black paws oh, cute tail but togepi is siamese lynx point, so he has that lynx point on his face.

Speaker 3:

He's very beautiful, looks like a siberian, but yeah, because they got dumped at the shelter together. But they're from different litters so we think that they have one parent in common and the other one might be, yeah, like a different or maybe two, but yeah, they're different letters. So toga b is a little bit younger. They're very young. Their shadow fax is two and a half and toga b is turning two in 20 days.

Speaker 1:

Yeah, very cute. Do you post your cat pic pictures on your instagram occasionally I'm I apologize if I've missed them no, I haven't.

Speaker 3:

I usually put them on my stories, but you know what? I think I might start doing that because I think it would be fun to put them on my stories. But you know what?

Speaker 1:

I think I might start doing that because, I think it would be fun to include them on my grid as well we'll take my wife and I'll take a look at your stories to see if we can get an eyeball on them. But yeah, so much, I appreciate you sharing your stories about your cats. That's adorable thank you, yeah, they're very cute uh, so we're at the end of the chat. Thank you, so so much for being our guest today. Doc, I mentioned you're on Instagram. What's your handle there for people to find you?

Speaker 3:

Yes, so it's doctor, but as in D-O-C-T-O-R dot, y-a-s underscore, so doctoryas underscore. That's where you can find me on Instagram.

Speaker 1:

Perfect, we'll make sure there's a link to you in the show notes Anywhere else on social media or a website you'd like to point people to not yet.

Speaker 3:

There's things cooking up at the moment, but yeah, for now, I'm, for now I'm just on instagram. So, yeah, that would be great. Thank you so much decent.

Speaker 1:

I so appreciate you giving up your time. Thanks so much for chatting with us. As I said, I have about 17 follow-up questions about the immune system, but I want to respect your time and thanks again for being a guest today.

Speaker 3:

Of course. Thank you so much. This was so fun.

Speaker 1:

That's it for this week's show. Thanks for everybody coming back week after week to listen to us. A special thanks to our guest, dr Yas, and a big shout out to our top tier patrons on the Podpack Plus plus. If you want to support us or hear your name at the end of the show, check out the link in our show notes. Okay, chris, who are the top dogs?

Speaker 2:

amelia fettig, re oda carol panel, jennifer challan, linea janet karen cronister, vicky otero, christy walker, sarah bram, wendy diane mason and luke helen chin elizabeth. Thank you. Debbie Anderson, sandy Breimer, mary Rader, bianca Hyde, andrew Lin, brenda Clark, brianne Haas, peggy McKeel, polly Burge, kathy Zerker, susan Wagner and Liz Button.

Speaker 1:

For science, empathy and cuteness.