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332: Resiliency Radio with Dr. Jill: Infections & the Brain: Inflammation Drivers - Nikki Schultek

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Nikki Schultek, the Executive Director of the Alzheimer's Pathobion Initiative (ALZPI), shares her journey from being misdiagnosed with multiple sclerosis to recovering from Lyme disease and co-infections under the care of Dr. Charles W. Stratton. Her experience revealed that many autoimmune conditions are actually driven by persistent intracellular infections rather than primary autoimmunity, a concept central to her work as a "collaboration architect" who bridges gaps between researchers, clinicians, and patients. Pathogens such as *Chlamydia pneumoniae* and *Mycoplasma pneumoniae* can infiltrate cells, steal mitochondrial energy, and prevent programmed cell death, creating "zombie" immune cells that trigger neuroinflammation through heat shock proteins. This process mimics the plaques and tangles seen in Alzheimer's disease, representing the body's failed antimicrobial response to these ubiquitous infections often missed by standard IgG titer tests that only indicate past exposure. Schultek introduces the concept of the "pathobiome," describing it as a pathological ecosystem where pathogens, toxins, and immune dysfunction interact within the body's terrain, disproportionately affecting women. Through the ALZPI global consortium, researchers utilize unbiased sequencing technologies to map pathogen loads and immune responses in infection-associated brain diseases, including Alzheimer's, Parkinson's, ALS, epilepsy, and PANS/PANDAS. Her work highlights that infections like the Epstein-Barr virus are causally linked to conditions such as multiple sclerosis, urging the scientific community to integrate clinical observations with data to accelerate effective therapies for these complex chronic illnesses. By focusing on direct detection tests for chronic respiratory infections linked to asthma and long COVID, the initiative aims to shift medical understanding away from treating symptoms alone toward addressing the underlying infectious drivers. Dr. Jill concludes the discussion by encouraging clinicians to explore Nikki Schultek's research and visit her website to understand how this consortium is advancing medical discoveries and transforming clinical practice. She urges patients to educate themselves, ask informed questions, and seek out providers capable of assisting with complex chronic infections, particularly those manifesting as neurodegenerative diseases. The host emphasizes that Resiliency Radio seeks to highlight field researchers who drive foundational change without seeking personal glory, inviting listeners to engage by commenting, sharing the episode with interested individuals or their doctors, and tuning in next week for a new installment of the show.
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Hey everybody, welcome to Resiliency Radio. Your go-to podcast for the most cutting-edge insights in integrative and functional medicine. I'm your host, Dr. Jill, and with each episode we dive into the healing heart of functional medicine. I bring you innovators, medical experts, and today a researcher that you may have not heard about but who is doing great work with collaborations on infections and chronic illness, especially as to do with the brain. If you or a loved one has been diagnosed with dementia or you're concerned about your brain health, uh look no further. You are going to love this episode with Nikki and all of her collaborations. Um she talks about herself as a collaborative architect, bringing people together to do the research to give us as clinicians foundation. So stay tuned, you're going to love this interview. Before we jump into the interview, I want to remind you that you can find products and services for your brain health, for your gut health, and all things in between at drjillhealth.com. Some of my favorite brain products are the BDNF Essentials and the CogniCare. Um I also love the Brain Mag, which is part of our pink drink, uh Dr. Jill's pink drink, the thing I drink every single morning. Check those out at drjillhealth.com. And if you haven't yet seen the documentary, you can check that out at doctorpatientmovie.com. It's now also streaming if you have Amazon Prime, which who doesn't nowadays, you can catch that Dr. Patient Movie there um with your subscription to Amazon Prime. And finally, if you are looking for a functional medicine provider for complex uh complex chronic illness or mystery symptoms, you can uh call our clinic. We are accepting new patients. Our number is 303-993-7910, or you can uh email info@flatironfunctionalmedicine.com. Okay, let me introduce Nikki, who is executive director director of the Alzheimer's Pathobion Initiative, ALZPL. Um she's also principal founder of Intercellular Research Group and founding director of the PathoBiome Research Center at the Philadelphia College of Osteopathic Medicine. She earned a BS in Business Administration and began her career with Pfizer and Genentech. Following her own recovery from Lyme disease, which you'll hear about in this episode, Nikki dedicated her work to advancing research into infection-associated chronic illness, including Alzheimer's disease, PANS and PANDAS, and asthma. Um, you're going to love this interview. Um, let's jump right in with Nikki and join the show. Nikki, I am so excited to have you on Resiliency Radio. We talked just briefly before we started this interview and what I love about you is you're bringing this whole other area. I deal with a lot of medical doctors and experts on the brain and Alzheimer's, but we're all in this field seeing these clinical manifestations and um, trying to make sense of it with the current research. You're out here making a difference in the world of research, giving us data, and actually validating what we're observing in clinical science, which is the brain is so much more complex than we thought. Plaques are not the whole answer, and there's a whole brain microbiome that's affecting our brain health and many other things that you'll talk about today. I couldn't be more excited to have you on to talk about your research and I get especially excited to talk to researchers because again, I'm in my clinic doing patients one-on-one, but you're out here paving the way for what we see in clinical practice. And one of the things you talked about that I love to start with is how you're really this hub of bringing together people who might not otherwise talk to one another. How did you get into this field? Give us a little bit of your journey. >> First of all, thank you, Dr. Jill, for having me. I'm thrilled to be here. Um, I absolutely love your energy and I love the way that you just anchored the start of our conversation. So, you're seeing patients, right? You're you are a practitioner, clinician, boots on the ground dealing with the type of patients that our team, our global consortium is studying, right? But in fact, how I got here is I'm a patient. So, I was extraordinarily sick and um was misdiagnosed for about a year. I ended up finding out that I had multiple chronic infections including one that people commonly know as Lyme disease. Um a bacterial infection transmitted by tick bites and other means um that I contracted along with co-infections. I also uh ended up learning in this crazy journey of a year of horrible one after the next autoimmune diagnoses that I also had a chronic respiratory tract infection uh that I had never heard of called Chlamydia pneumoniae and that's really that one bacterial infection is sort of how I arrived on the scene and decided to start bridging silos and it all began uh of course figuring out that I was sick with these infections, right? Finding a doctor that could accurately test and diagnosed me, treated me um using antimicrobial therapies in a manner which frankly at the time initially made me very uncomfortable. Uh the idea of aggressive antimicrobial therapy. I had a background uh working for Pfizer and Genentech and at one time I worked in an anti-infective space calling on microbiology labs in hospitals. So, I a lot of people hear the word resistance, right? Which antimicrobial drugs not working any longer because the germs figure out a way around it because they've been exposed to it. So, I had these concerns, yet I was being faced with life-threatening symptoms. And my kids were three and five, right? I'm a mom. I was completely incapacitated. One of the things in my diagnosis that uh was disturbing, the differential diagnosis, was they feared I had multiple sclerosis based on my symptoms. >> Yes. >> Now, I do not have MS. I didn't have lesions on the MRI, but the neurologist at the time in Connecticut said, "This doesn't mean you won't get it. I see patients like you all the time where you smolder and you have these symptoms and the symptomatology leads to lesions." And so, I left just like absolutely terrified, anxious. And I had developed cognitive symptoms, too. Now, I was in my early 30s. So, what I decided once I got on treatment by an infectious disease specialist and medical microbiologist at Vanderbilt named Charles W. Stratton, who specialized in this chronic bacterial infection of the lung called Chlamydia pneumoniae, not the sexually transmitted Chlamydia, but a cousin >> Yep. >> of that germ that you get when someone coughs and you inhale it, you know, he had looked at that germ from the vantage point of, "No, not just an acute infection, but chronicity." So, the idea that it could take up residence and now you have in an area of the body, whether it's the lung or the bladder or the brain, >> Mhm. >> that it could be creating inflammation. And we all know inflammation is bad, right? Most diseases go back to inflammation that are chronic. So, I got treated by Dr. Stratton. And it was funny, as soon as I started to feel better, I said to him, um he asked me to call him Chuck. I was reluctant at first. I'm like, "Okay, fine, if I must." He's like, "Please call me Chuck. Um don't call me Dr. Stratton." So, I was like, "Okay, Chuck." He said, um you know, I I right, what I basically said was, "What are we going to do about this? You know, like this is major. Like I had had multiple devastating conditions, including this severe and refractory asthma, go into remission with antimicrobial drugs." And it turned my perception of autoimmunity on its head. And I said to him, "Don't you just want to scream from the mountaintops with all these publications you have and other people? Autoimmunity is is under, you know, under poorly understood, poorly characterized. We have chronic infections, right? Not a hit and run, it's a continual hit. It's an accident over and over. So, he said, "Yes, but he said, "Take it easy. You're not all the way better yet. This treatment is going to be a long road." So, he he you know, encouraged was encouraged by the fact that I wanted to help. And as soon as I was well enough, I decided I needed to just start contacting these people studying infection and chronic disease and introduce them to each other cuz they reference each other in their papers. You know, they'll write a scientific paper. And so, I said to Chuck, "Have you ever had a meeting with Dr. David Hahn who studies asthma in the same bacteria?" "No, we never sat down for a meeting." "What about John Carter in Florida?" "No, we haven't." Um you know, it's like, "Yeah, I did meet Dr. Brian Balin once who studies the role of that bacteria in Alzheimer's." So, we started getting together the main cast of characters studying that one bacteria and chronic disease. And from there, I start, of course, becoming tangential in the reading. And I myself knew that I had been diagnosed with Borrelia burgdorferi which can also cause some of the same disorders that Chlamydia was linked to. Yes. >> Yes. Yes. >> You know, including bladder pain. I had a diagnosis of interstitial cystitis that was brutal, but it went into remission. I remain in remission. I don't have it anymore. So, that's how this all sort of began. And the idea to be a collaboration architect, to bring scientists together and physician scientists that have patients, and people in the lab, and data scientists, and all different types of domains. People studying fungus, bacteria, viruses, parasites, animals, you know, veterinarians. We work with Dr. Ed Breitschwerdt at NC State. The idea behind it was that everything is so siloed, and the body is not. It's an ecosystem, right? And we are very much the brain, especially, has been thought of as this sort of like off-limits area, right? And this blood brain barrier is this impervious shield. Nothing can get through it. It's not really the case. And the brain is interacting with the gut. >> Mhm. >> And the brain is also subject to insult from infections. >> Yes. >> And not just things that create a cytokine storm and hurt the brain from the outside, but things that can actually, like a Trojan horse, inside the very cells that are made to protect us, our immune cells, it can enter some of these pathogens and then go right through like they're just crossing the George Washington Bridge into Manhattan. So, um So, the idea of bringing these different people together was really like, okay, no one's listening. >> Mhm. >> You know, decades, you know, there have been so many different research teams publishing papers. Let's just take the example of Alzheimer's and infection. Since literally the 1980s. And even actually before then, Dr. Alzheimer himself, you know, the gentleman from which the disease is named, published a paper in the very same year as another scientist named Oscar Fischer, 1907. Most people don't realize that this could have very easily been called Fischer's disease because their results were neck and neck in publication. They both were living in a time when syphilis, sexually transmitted infection, in the same family as Lyme disease. These are spirochetes, literally you know, like a corkscrew. Um everyone knew that if you got syphilis and it advanced to tertiary syphilis or severe infection, it could get in the brain and cause a dementia. >> Mhm. >> Well, it was really interesting because Dr. Oscar Fischer, and even Alzheimer himself, acknowledged the possibility that there was an infectious component when they went ahead and saw the brain of someone that died with the disease and saw plaques. >> Yes. >> These tangles, they said, "These almost resemble bacterial colonies." And isn't it's very ironic because today, on my team, you know, we have this Alzheimer's Pathobion Initiative Consortium, a global, multi-disciplinary team, purposely as diverse as it can be, with backgrounds even patients, you know, like myself, people that have lived experience and also expertise in these fields. What some of our teammates have discovered is that the bad guys, the plaques, the amyloid plaques, or, you know, the kindling of a and then the tau tangles, these these tangles in the brain, uh you know, that have been referred to as flames, like kindling and flames, right? These one-two punch uh in the people that we lost to this devastating neurodegenerative disease, may actually be antimicrobial responses that are your body's way of fighting something that hasn't been appreciated. And the research demonstrating that has now been repeated. >> Hey guys, just a quick interruption of this episode to remind you, if you have not yet got my book Unexpected, I dive into the healing journey that I went through with cancer and Crohn's disease, complex chronic illness, mold-related illness, Lyme disease, and more. Um be sure and check it out at unexpected.com. You can get it anywhere books are sold. It's right behind me here on the shelf. Um if you want a signed copy, hop on over to drjillhealth.com and order it there. Just put in the memo who you want it signed to, and I will personally sign and send you a copy of the book Unexpected. Okay, let's get back to our show. Now, Niki, it's so great because a Promutter and any colleague of mine that are really in the weeds like you are, we know those are just bearers of what's happening underneath and we know that any drug that targets that is not even effective because we're dealing with these underlying inflammatory issues like infection and toxin. It makes so much sense and again, we have a lot of providers here that listen to they're going to love this episode with what you've already said because so often in my complex chronic patients that many of them neurodegenerative cancer autoimmune are the top three things we see. Infection is always in toxin are these these things that that play into the immune system and create these autoimmune responses and inflammatory responses. And I love that you started your journey with chlamydia pneumonia. I check every single patient I suspect with infection for mycoplasma and chlamydia pneumonia because these co-infections, they're actually more common than Borrelia burgdorferi and they are insidious. They've been associated with chronic fatigue, autoimmune and all those things. You can keep going but I wanted to just interrupt and kind of validate what you're saying from a clinical perspective. Uh, because every day in my practice I'm seeing that and when I see that chlamydia pneumonia, I know we have to be treating it. >> Yeah, uh, I really so appreciate that because like you said Dr. Jill, it's so prevalent. So by the time people reach middle age, like 50 to 80 years old, the prevalence, like if you do population wide studies of blood indicates that it's similar to herpes viruses which are ubiquitous meaning everybody nearly everyone has them upwards 80% and then as old the older you get um, you know, one of my colleagues cracked a joke and said, "Yeah, you get old and we each are becoming a germ bucket year over year." So it's kind of funny [laughter] but I'm like and I certainly feel that way with my own experience with mycoplasma pneumoniae. >> Yep. >> Like lifelong asthma that was way out of control and you know, these um it's so key to look for these infections but yet it's it's not something that the average practitioner even thinks about. Um, they're not testing for titers to chlamydia and mycoplasma. We really need um, better direct detection tests for C. pneumoniae. Um, and then, you know, the the thing that that's wild about that bacteria as an example is just how it really lines up with Alzheimer's specifically in terms of its behavior. So, to kind of geek out on that bug it goes inside the building blocks of the body, which are the cells, regardless of essentially any cell type can be vulnerable to this particular pathogen. It preferentially infects um, the lining of your veins and vessels and arteries like endothelial cells. Yes. And it uh, absolutely loves immune cells like monocytes. And and it once it's in there, it like you know, steals energy. It's like it plugs its little plug into your mitochondria, your powerhouse of your cell, and takes the very fuel that we rely on for survival, cell division, and for your immune cells themselves to work properly. And then it does something else nasty. Once your cells are supposed to die so that new ones can take over and they can divide and we have a fresh set of cells, it delays that programmed death because now it's sort of like I cracked the joke like that show The Walking Dead with the zombies. >> Yep. >> You now have like a zombie immune cell that should have died 72 hours ago, but it's got a passenger aboard that wasn't welcome in the first place that's taking energy. And a lot of the things we see with Alzheimer's are mitochondrial dysfunction, >> Yes. >> depletion. Well, you have a mitochondrial parasite, right? And other organisms can do this. You have uh, dyshomeostasis with certain metals, you know, like the findings of like aluminum for example, calcium. This pathogen can do that. Dyshomeostasis of iron, it does that. And then you start saying, "Hmm, you know, uh neuroinflammation." So, Chlamydia releases um something called a heat shock protein number 60. And when it does that, it's really bad because we have that in our cells in our brain. And we begin to release our own Well, it's like a matching campaign in a bad way. Instead of like fundraising, it's like a nasty toxic soup. And so, when people talk about these things, these infections, that their job is to become chronic because they can't live outside a human cell, it literally can't survive without us. You know, the idea that the pathogen has been cleared when we know that it's as persistent as it is, and the assumption that it's gone from a short course of, let's say, a Z-Pak is really a fool's errand. And so, um you know, it's it's been something that our team one of the pathogens, and it's not the only one that we're focused on because there's definitely a pathobiome. And >> lot of research too just to validate your point on ME/CFS with these intracellular pathogens as a primary. So, and just to clarify, a lot of people out there, a lot of docs, a lot of patients know about Lyme disease. That's very real, very prevalent. But I often see these co-infections being just as big of a deal, kind of like the case where you presented your own journey. And if they're missed, I mean, literally docs should be checking. Let's just talk briefly about if you know any of the research around Right now, we do titers, and the best that we have are some PCR. There are some other specialty labs. But the the general Quest, LabCorp, whatever we have IgG and IgM. And typically, if it's an older infection, you're not going to see that IgM. Although, sometimes you see that reactivate and pop up. Um but if I see both of those really high levels and a whole infectious burden, I start to suspect is there any more research on better ways of diagnosing versus just seeing those high IgG titers? Is that the >> Yeah, so it just depends on the pathogen, right? So, in the tick-borne illness space, you have some fabulous labs, I'm sure that you use. You know, you >> I'm talking just mycoplasma chlamydia because the tick-borne, yeah, we've got that PCR, we've got Yeah. >> [laughter] >> No, and we've we've had um honestly, Dr. Jill, like I've had numerous meetings with different um you know, diagnostic companies highlighting the importance and um you know, chlamydia and mycoplasma would make a phenomenal respiratory panel for chronicity because they've both been strongly associated with asthma. And asthma is now second to long COVID, the most common pediatric autoimmune diagnosis and thus, I think if we caught kiddos early in life before their lungs remodel and get filled with mucus and end up with lung damage like what I have um from years of untreated asthma and mucus and inflammation and infection, then you know, we would have if we had a better direct detection test, we we don't have something like that. Now, there are hospitals if someone has pneumonia, so this is important. As you know, you can get a a bad pneumonia which requires hospitalization from a And if you are fortunate enough, you know, in the sense to be in the hospital, they can do direct detection. Like they can look for those organisms, okay? And so, that would really be the only context in which a patient would access it is if it's going to be like your average laboratory testing with Quest and LabCorp, it's going to be chlamydia and mycoplasma immunoglobulin G and immunoglobulin M. And a lot of times if providers like so, let's say I'm talking to a patient that has concerns and I say, well, that's kind of suspicious for these certain infections and then they go to their primary care doctor and ask for the test. The test comes back with extraordinarily high levels of immunoglobulin G for mycoplasma. That practitioner is likely to say this is a historical infection. You fought this infection at one time. It does not indicate active infection or chronic infection and people that study those organisms might disagree. >> I would agree with you 100% cuz I'm checking these and I obviously well first thing is in my clinical experience anyone with Borrelia I bet 90 to 95% of them have these co-infections one or both of them so it's super common. But I think many practitioners are focused on the Lyme and Bartonella and Babesia and they're forgetting that these also are huge players like in your case. And if I'm seeing that there's this piece that's not because really right now we are a little limited with the science. So if I see these really high like four times normal titers I suspect and the clinical you know symptomology and the responding to either intracellular antimicrobials or sometimes natural agents. All that together puts a clinical picture even though all I really have is a really high IGG, right? >> Yeah. >> And you're not and you're not doing something wild or heretical. You mean it's it's patient-centered care, right? Because if we go back to a time before we were so sophisticated I'm going to put that word in quotes and we had all of these fancy tests to rely upon. Practitioners did have to use in some way shape or form a little bit more leaning on that clinical picture. You know, hearing that patient's story listening to the etiology of like the onset of it. For example, with asthma a lot of patients will say, "You know, doc my asthma began I got a respiratory infection. I got like a cold. I got a nasty bronchitis and I never got better. Now I have wheezing and and you wouldn't believe how many people's asthma starts that way." So we you know, myself and my coworker Dr. David Hahn, who's an absolute pioneer in the infectious asthma space, you know, we publish on that and we we call it an easily identifiable syndrome, infectious asthma syndrome, where if the patient story lines up with this, and those patients, many of them, most of them will respond to azithromycin therapy, um, longer term, you know, um, in in the dosing regimen that Dr. Hahn and others have used in their studies is like anywhere from 250 mg, uh, Monday, Wednesday, Friday to 500 mg Monday, Wednesday, Friday, three times a week cuz the drug builds up in your system and remains steady. Um, but it just if infections are are treated early, it's so important. And then in the future, obviously we know that broad-spectrum antimicrobial drugs have impact, too, that may not be positive on constituents of the gut microbiome and otherwise. You know, may leave people vulnerable to certain fungal infections like Candida. So, we do need better solutions. And that's part of like what we do in our team is with basic research, right? Showing how do these infections work together to lead to a disease? Well, we can figure out how to intercept. And, uh, in the future, targeted therapies will be amazing. And I really believe we'll get there or therapies that are, uh, supporting the immune system. You know, there are different angles and ways of going about this that we don't have yet. And, uh, unless somebody really underscores this problem, um, you know, we we won't have those solutions. >> I love that you mentioned that cuz I've always talked about with like Borrelia, I believe I would just go out on the street and test 10,000 people for Borrelia burgdorferi. I might find 20 to 30% of them walking around with Lyme, a true infection, and yet they're not super symptomatic. They may not know they have it, maybe they feel really good. Um, and what I've observed is it's not a combination of just the infection that they've been exposed to, a tick bite when they were 12, but it's that plus a weakened immune system and like these sentinel cells that aren't, you know, doing their job that have inflammaging or um, or immune um, you know, resilience, all of this thing. But what happens is just like you said, you have this antibiotic or antimicrobial therapy, absolutely core, but at the same time, sometimes IVIG, sometimes beta glucan, sometimes astragalus these other things that are actually supporting that natural function of T cells and B cells to help you. I find that's kind of the perfect combo of of really getting someone off the antibiotics and onto a optimal life, you know, without that infection weighing them down. >> Absolutely. And um, you know, and again, to bring it back to like, you know, vulnerable point of vulnerability for me, I've been playing whack-a-mole with this thing for 10 years. And I've had um, you know, it's been such an incredible journey of not only learning, you know, and becoming uh, a member of the scientific community and you know, going from being a patient to studying for like a decade and diving in and, you know, now writing grants and papers and and getting research project projects funded for teams all over the place. But also going through this journey, aging with these infections. And how, you know, for example, perimenopause and and has affected, you know, some of the things that never were addressed properly. So, for example, Dr. Jilly, you've probably heard this before, I initially, when I got sick, I had this air hunger and I kept describing it to the asthma allergy doctor and I was like, this isn't like asthma, this is different. This is new. I've had asthma forever, this is not, you know, quacking like a duck, barking like a dog, this is something else. And I had rib pain. And uh, then I had this this bout of dizziness that was disturbing and I was like, oh my gosh, am I having a stroke?" And I had all these other symptoms. Well, fast forward to now, I'm a part of an IRB study at North Carolina State University, and with newer detection methods, blood that I gave in 2021 revealed that I have Babesia microti. >> I knew it. I was going to say Babesia. >> [laughter] >> So, yeah, and you know, and then so I never like, you know, to my community of chronic illness patients that and people that might be listening that you know, relate to a story like mine in some ways, you know, as a patient, is that I'm still learning and the science is catching up and you know, I started working with an I LADS doctor in December, or I'm sorry, last August, in December initiated treatment for Babesiosis very slowly because when you're treating for this red blood cell parasite, you can actually lose too many red blood cells, right? Because like the Chlamydia organism, this is living inside a red blood cell. Yuck. I don't want anyone hanging out there. Thank you very much. So, I had some of these symptoms that Dr. Jill, because I think of perimenopause and the reduction in estrogen and the changes my body is going through, plus a term I want to throw out there that we think is really important and you alluded to it, but immunosenescence, which is my immune system's getting older. >> Right. >> Everybody does, by the day. So, you know, my husband and I joke, you know, he's healthy as a horse, doesn't take, you know, participate in any of my vitamins that I'm suggesting, no pills, runs these races, uh has likely been in contact with just as many tick bites as I was in Connecticut, and may have Borrelia on board. We haven't tested him. Some people tolerate infections, and we know this already, right? So, it's just like, you know, there are certain individuals who got COVID, I guess the most modern example or poignant one now is people that got COVID, barely got a sniffle, got better, moved on with their life, no problem, fine. >> Yeah. >> Some people got COVID and are debilitated still. They're in bed. They're in a dark room with a new diagnosis of ME/CFS or, you know, some horrible chronic disease. And, you know, many of the practitioners have noted that these people have co-infections. And so, with COVID, it appears that there's uh a level of immune suppression. >> Yes. >> And, you know, when you bring the immune system down just that much, and let's say you were somebody tolerating your Bartonella, your Babesia, your, you know, Chlamydia, you were coexisting with it at one point in time. And that's why we're called the Pathobiome Initiative, by the way. >> I >> So, love that, Niki. And I want to speak to if you don't know Amy Proal, she's got a research um I'll leave um uh >> Allie Bio. >> Yes, yes. I was like, I bet you you either know each other or should know each other. I've interviewed her on the podcast, but what I loved is she was bringing um validity to what we were again just like you are to overseeing the clinical practice. And one of the things we saw post-COVID was I call kind of call it the triad. Um we would have decreased in uh cortisol and adrenal dysfunction. So, often a fatigue specifically associated with the thyroid axis, like hormonal axis. But, T cells, kind of like this inflammaging, would retain spike protein, and these macrophages would hang around. They should be dead and and dysfunctional, but they're just hanging around like those zombies and dysfunctional. So, this T cell ability to fight the innate immune system, these infections keep them down, was really impaired post-COVID. And then, B cells would get overactivated, start the autoimmune chain. So, it was real common. And then, Amy brought to um to the forefront with her research that typically, there was this reactivation of Epstein-Barr or Bartonella or Babesia or Borrelia, all the big Bs, right? The triad that we see so often. And so often, when I'm seeing this long COVID, I'm like, "Okay, do you have retained dysfunctional macrophages where your T cells aren't working? Do you have reactivation of Bartonella, do you have And when we find that or even these atypicals like Mycoplasma Chlamydia, those are some of you. And so very frequently, I'd guess 80% of these long COVID patients are this combination of exactly what we're talking about. Someone who was functioning over here and then dropped below the way radar and then it started hit doing the whack-a-mole that you described of infections popping up and their immune system has just been kind of trashed. And so then we try to figure out, okay, do we need to treat those infections or restore immunity or both? But it's so relevant. >> And yeah, I'm super familiar with their work. I think what Polybionics you're doing is phenomenal. We're thrilled to have them out in the ether with us. You know, we have very synergistic work and you know, it's just it's like an incredible time. Honestly, like I in 10 years have never had more genuine hope that we are sitting on the verge of a tipping point of things changing. But you know, the the pathobiome concept that we talk about, people will be like, well, what's the pathobiome? And it's a great question because it's a relatively new word. Hasn't been around forever. >> describe that and talk cuz we talked about biofilm stuff. We've talked about all this stuff that is so fascinating, but let's kind of focus the last, you know, 10 minutes or so. This I want to know what is the Alzheimer's pathobiome initiative and then also help us link this to the brain cuz I know a lot of people are wondering could I get Alzheimer's? Could I get dementia? Is there an infection involved? I'll let you go with it. >> Yeah, so this Alzheimer's pathobiome initiative global consortium, it's multidisciplinary and we actually don't just study Alzheimer's disease. So Alzheimer's is a very it it's it's a catch-all for a lot of different things, right? It's a description of a form of dementia. So the dementia is the umbrella underneath it. Alzheimer's is the most common form, but then there are others that people have heard of like frontotemporal dementia, vascular dementia. Um then there is Parkinson's disease that has some overlap. Um like in the brains of patients with Alzheimer's, you may also find some of the Parkinson's disease uh bad guy pathology, alpha-synuclein, which may also be a response to infections, by the way. Um and then you have other brain diseases that have similarities, and we study those, too. So, we look at We're studying PANS/PANDAS, which are the pediatric autoimmune neuropsychiatric disorders associated with infections. Um PANDAS refers to specifically strep infection, whereas PANS refers to kind of like dementia's the umbrella. PANS refers to that this can be from long COVID, can be Lyme, it can be mycoplasma, chlamydia, cytomegalovirus, a whole lot of other things can trigger these um symptoms in kids. But we also are looking at uh ALS. We're studying epilepsy. So, our team is looking at infection-associated brain diseases. And studying them in a uh holistic and integrated fashion, sharing specimens among different labs, studying the same cases, the same people that we lost to one disease, uh being looked at using multiple different sophisticated technologies, and we're looking for a few things. We're looking for uh infections. And we're doing so in using very specific approaches, also unbiased approaches that look for everything that's there, um using technologies like uh something called sequencing that will map out DNA, uh which is the genetic material from pathogens or germs. And then we also are looking at the immune response. >> Mhm. >> We are also in women, because many of these diseases target women disproportionately, 2/3 of Alzheimer's and 2/3 of multiple sclerosis. Two infection associated brain diseases that target women. We are looking at what happens in the context of hormonal shifts. What happens to the immune system? What happens to pathogen load to the pathobiome, which the word pathobiome just to step back for a second is really key. We chose that very intentionally even though we knew people might not know what it means yet. Because okay, the microbiome is a word a lot of people have heard of, right? And when I hear that word, I think like Kumbaya. Like it's all the the gut bacteria are happy. I have a healthy microbiome. The word microbiome I feel like has like a positive connotation for me. I don't know if that's true for you, too. Um and pathobiome has the word pathological woven into it, meaning troublesome. >> Yes. >> And it doesn't just refer to the germs. So yes, I can I call it, you know, organized crime. You get to a certain point where the immune system is malfunctioning either due to an infection or due to some other element of aging, hormonal shifts, exposure to mycotoxins, you name it. Any of the insults that can We call that the exposome, the things that you're exposed to in your life. Um chemicals at work, you name it. Something brings you down and now all of a sudden you have disproportionate numbers of bad guys in the community. You have uh like a mafia or a mob type situation. And we even know that certain of these bad pathogens collaborate with each other >> just like my team collaborates. >> Yeah. >> And we don't want that. Um so the pathobiome takes into account not only the community, but the terrain. And it it refers to also the health of the immune system. So our team feels um you know, and we're not the only thing that we should be looking at. Like the stuff that we're interested in I I mean that's this is what we are studying, the role of infection and the immune response to infection in the diseases that target the brain that are neurodegenerative, neuropsychiatric, and otherwise, but we also think that other ideas should be welcomed at the table because let's take Alzheimer's for example. Billions and billions of dollars have gone into developing therapeutics and we still don't have something that is truly effective, affordable, safe, uh accessible to most patients. So, we just essentially feel that we know enough already that infections have been strongly linked with a variety of neurodegenerative diseases and the linkage between MS and Epstein-Barr virus is so powerful >> Yeah. >> that it's you know, now when you read the literature on it, the word causation is used. >> Yes. >> You know, people used to say often association, right? It's It means it's in the ballpark, it may not be causing it, but now the the research is just so compelling that Epstein-Barr gets involved, you know, this huge military database study revealed that essentially if you did not get Epstein-Barr, you didn't get MS. And that's wild. So, it's >> You know, we have to start using common sense, right? Where you know, like a lot of what you probably do every day with your patients, which is you look at the person, you listen to their story, you're leveraging quite a bit of common sense and experience, right? On top of data that you get from lab tests. And we feel that we should be doing this as a scientific community also. >> Wow, this is such a great It's just so exciting to me because here you are bringing people together and this multi-collaborative group, um what do you call it? Architectural collaboration? You have some really cool words in there, but it's just >> call it collaboration architecture because >> [laughter] >> I couldn't think of a way to describe what I do, um you know, um and and I was hoping that it could become a thing, you know, that other people that are adept at, you know, reading broadly and enjoy tangential learning and science and then can also socialize with a lot of different people and build bridges, you know, and and form alliances that that people could do this. And there are other people that like myself, you know, patients with lived experience that leverage business skills or other acumen that they have and and get involved. So, thank you for saying that, I mean, it's >> Yeah, it's so exciting because it's what's needed for even clinicians. We need to start really collaborating because there's so much that we're seeing and as we share stories and share what's working and talk to So, to me it's a super exciting cuz on this level you're bringing the information down trickling down to us in the clinic, you know, seeing the patients and and giving validation to some of the things because truly the average research back in my medical school days, you know, say something was started to be seen as a pattern, it'd take 20 or 30 years for that to get into clinical practice. We can't wait that long. So, you're really accelerating the pace with your work. If you want to find out more about you, the the lab, the work, the all the different things, what is the best place where they could come and maybe even donate money to the to the cause? I mean, by all means I would love to see that happen. >> Yeah, so we have So, my research center at the Philadelphia College of Osteopathic Medicine, a medical school, is called the Pathobiology Research Center and it's www.pcom.edu back back splash PBRC. So, like Pathobiology >> in the links, guys. If you're driving or whatever, or you all include that, but yes, [laughter] I will. >> Um, so the university center, you know, uh, PCOM is my collaboration hub and it is a nonprofit, so donations can be made. Um, there's like a giving page for PCOM. Inquiries can be sent directly to me and then I can send people, you know, along to a place where they could donate. We also uh have a website for the consortium, so that's alzpi.org. So, it's alz like Alzheimer's, p like pathobiome, i like initiative.org. And there, there's a whole collection of education podcasts, symposia, publications from our team, and um really that website is definitely geared toward clinicians and researchers and and life sciences professionals. Um but I do get a ton of emails from patients all the time cuz I've shared my story so widely, and I'm always happy to provide resources. I'm not a practicing clinician, I'm not a doctor, um but I do frequently recommend that people that suspect they have infection-associated chronic illness find a doctor like you, Dr. Jill. Um you know, that I often offer people the ILADS, the International Lyme Associated Diseases Society, or for pediatric cases, uh the MAPS. >> Yeah. >> And um you know, which both have provider searches. And then, of course, there are, you know, the Dr. Bredesens and uh Dean Ornish, uh Dr. Per- Perlmutter. I feel like I always mispronounce that, and I feel so badly. >> Yeah. >> It's a tongue twister for me, but I'm so grateful. Thank you so much for for hosting this and for having conversations, you know, that are that are really getting people thinking. >> You are so welcome, Nikki, and thank you for taking your uh difficult journey, but also taking it and transforming and really this ability for you to be a connector and bring all these people together is really extraordinary. Like I I am just amazed, and again, like I said, you are doing something that we in the clinic can't do. So, keep up the great work. I am so happy to support you. I hope you guys listening out there have enjoyed this and will also go to those websites. If you're a doc, go to the research, uh do some reading, educate yourself. Um and Nikki, good luck with the rest of the journey because I think this work is super impactful and super important. >> Thank you, Dr. Jill. I appreciate it. Thanks for all you do. >> Hey guys, as you can tell, I get super excited when we talk to another um type of provider. This in this case, Nikki takes her personal story and has started the consortium for all of this great research and work that helps pave the way for new discoveries and ability for us as clinicians to actually change the way we practice medicine. So, I hope you will go out if you're a clinician, read her research. Um the website she gave there will be in the links below. Um if you are a patient, I hope you'll educate yourself and ask the right questions to your doctor and make sure you find someone to really help you. And hopefully, you'll find every week on Resiliency Radio, we are bringing you great, incredible interviews with these kinds of people that are doing the work out there on the field, um not looking for glory, but just uh really changing the way we view medicine and giving us that foundation of research in order to take things to the next level. Um hope you enjoyed this interview as much as I did. If you do, please leave a comment, share with someone who you might um think would be interested. Or if it's your doctor, why don't you share this episode with your doctor so that we can educate the providers out there to start to be looking for these complex chronic infections, especially in the realm of neurodegenerative diseases. Anyway, guys, I'll see you again next week for a new episode of Resiliency Radio. And until then, be well.