In this episode, host James Maskell sits down with Nikki Schultek, founding director of the Pathobiome Research Center at the Philadelphia College of Osteopathic Medicine and founder of the Alzheimer’s Pathobiome Initiative, a global research consortium.
Schultek’s path into this work began with her own illness 11 years ago – a multi-system chronic condition driven by a tick bite and co-infections including Chlamydia pneumoniae, which went misdiagnosed by 12 specialists for a year before Dr. Charles Stratton at Vanderbilt identified and treated the underlying infections, restoring her to roughly 95% of her former health. That experience, and the fear of not watching her young children grow up, led her to found Intracell Research Group and later become what she calls a “collaboration architect” – connecting siloed researchers across immunology, microbiology, neuropathology, and epidemiology who study different pathogens (herpesviruses, Chlamydia, Borrelia, Bartonella, fungi, syphilis) but rarely collaborate with one another.
The conversation covers the evidence linking infection to Alzheimer’s disease: animal studies showing pathogens like C. pneumoniae can induce amyloid-like plaques in wild-type mice; the historical near-miss in which Alzheimer’s disease could have been named after Dr. Oscar Fischer, who described bacterial-colony-like structures in tangles and plaques during the pre-antibiotic syphilis era; and emerging research suggesting amyloid and tau may act as innate immune “firefighters” responding to infection rather than purely destructive proteins. Schultek highlights her consortium’s 2023 landmark paper in Alzheimer’s & Dementia, which catalogued 86 case reports of infectious dementias reversed through targeted antimicrobial treatment.
Maskell and Schultek also discuss the heterogeneity of individual cases – from periodontal pathogens like Porphyromonas gingivalis to tick-borne co-infections – and the need for precision, patient-specific approaches that account for genetics, exposome, and hormonal factors. The episode closes with a discussion of what’s needed to move the field forward: greater federal and philanthropic funding, better multi-pathogen and host-biomarker testing, industry investment in targeted (rather than broad-spectrum) antimicrobial therapies, and expanded insurance coverage – particularly for PANS/PANDAS families currently priced out of diagnostic testing.
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About the Guest:
Nikki Schultek is the founding director of the Pathobiome Research Center at the Philadelphia College of Osteopathic Medicine and founder of the Alzheimer’s Pathobiome Initiative, a global research consortium studying the role of infectious agents in neurodegenerative, neurological, and neuropsychiatric disease. A former patient whose own multi-system chronic illness was driven by tick-borne and intracellular infections, she now works as a “collaboration architect,” bringing together researchers across immunology, microbiology, epidemiology, and neuropathology to advance infection-associated chronic illness research. She is co-lead author of the 2023 landmark paper on the Alzheimer’s Pathobiome Initiative published in Alzheimer’s & Dementia.
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About the Host:
James Maskell is a healthcare entrepreneur and founder of The Evolution of Medicine. For over 20 years, he has worked to scale functional medicine through community-driven models, group visits, and practitioner infrastructure. His work focuses on moving medicine upstream – toward prevention, lifestyle intervention, and systems-based care.
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Transcript:
Diverse infections are being found in brain specimens from people that we lost to these devastating conditions like Alzheimer’s. If you can make animals sick using the same infectious agents, and you can get pathology, which has been, by the way, branded as being all bad, and that’s another matter we can discuss in a moment, that these things are credible pieces of evidence.
And if we say– If we think the number of lives lost every year to Alzheimer’s disease in the States alone, but then globally, it’s staggering. You know, Alzheimer’s being the most common form of dementia, and we essentially don’t have anything really to do for the majority of people. People will continue along the progression.
The new drugs are not particularly safe, accessible, or affordable, uh, or effective. So it really does lend itself to needing a bigger movement and a bigger push. Hello, and welcome to the podcast. This week, we are talking about the pathobiome. We are gonna be talking about it with Nikki Schulte. She is the executive director of the Alzheimer’s Pathobiome Initiative.
She’s also the founding director of the Pathobiome Research Center. We’re gonna get into the pathobiome. We’re gonna talk about what it is, how it affects people’s brains, and how clinicians like you could be on the front lines of helping take this movement forward. I think it’s gonna be particularly interesting to you if you have gone to many environmental medicine conferences, you’ve learned about Lyme, mold, and, uh, all the different types of infections, and particularly how they can deal with brain diseases and lead to brain diseases.
This is gonna be a very validating session. Enjoy. A warm welcome to the Evolution of Medicine podcast for the first time, Nikki Schulte. Welcome. Thank you so much, James. I appreciate being here. Nikki, I’m really excited to have you on here because it’s a confluence of so many things that we’ve spoken about on the Evolution of Medicine over the years.
But let’s just start off. You are the founding director of the Pathobiome Research Center, and maybe we could just start as to what the pathobiome is and how it reflects, uh, you know, the, uh, the work that you do. Absolutely. So people often know the word microbiome because it’s really entered common vernacular, right?
And when I hear the word microbiome, I think of, you know, a friendly community in balance, and, uh, especially when we think about the gut microbiome, people have come to realize that this is an important concept, right? So fueling the good or even neutral things that are living in your gut rather than fueling things that could be inflammatory, right?
Certain bacteria, for example. The pathobiome is a newer word, and I love it, especially given my own life experience, and it refers to not just the microbes or the microbiome, but it refers also to how the body’s responding to them. So you can have, for example Certain bacteria, viruses, fungi in your body at a given point in time, and they’re not hurting you.
You have a, uh, relationship with them in which they’re just either neutral or, you know, they’re not harming you, they’re not creating an inflammatory state or a disease process. But then you have the ones that either because they, they become more prevalent, certain groups of organisms that have behaviors that are very pro-inflammatory, or due to aging itself, you know, immunosenescence or the aging of the immune system, you get a disproportionate share of the bad guys.
And sometimes I even refer to this can become a situation of organized crime, where they’re working together and you get a disease state. You know, and for example, uh, there’s a evidence for a brain pathobiome in Alzheimer’s disease, in multiple sclerosis, in the pediatric disorders PANDAS and PANS. So really across the human lifespan, this has kind of been neglected, the concept of a pathobiome as a very plausible disease driver or part of the puzzle.
Yeah. No, I’m really excited to, to go there. You know, I think in the functional medicine community, you’ve had a lot of people with the intellectual curiosity to follow this thread, right? The earliest people that I ever met who were talking about PANDAS or were talking about Lyme disease or otherwise, you know, were people in those community.
But it’s, it sounds like you really have a, a focus on research, finding truth, and understanding what’s happening at a very deep level. Absolutely. After being sick myself and realizing how siloed my own care was, the approach to my own case, which involved multi-system complex chronic illness driven by infections like Lyme and co-infections with even human-to-human pathogens, things that people, you know, the average clinician gets no training on essentially in medical school, uh, or practitioner, I should say, things like Chlamydia pneumoniae, which is a respiratory bacteria that is incredibly prevalent in the human population.
50 to 80% of people have been exposed and infected by middle age, and yet most people don’t realize it can become chronic because it lives inside your cells in the very building blocks and can drive chronic inflammation. It’s not an infection that wants to harm you or kill you. It just wants to steal from your mitochondria, your very energy source.
And so, you know, yes, we’re interested in the research because what I experienced as a patient is literally informing everything that we are doing as a team, and it’s a global consortium that we have formed called the Alzheimer’s Pathobiome Initiative. My research hub for me is at the Philadelphia College of Osteopathic Medicine in my Pathobiome Research Center that I founded there.
And the importance of it is this, it’s that- We decided that these problems are very complex, and they involve multiple systems of the body. Even just to understand the brain, we have to go beyond the brain, take a systems level approach, the body as an ecosystem, and understand how the exposome, which is everything that you come in contact with across the human life, coupled with your genetics and a variety of other factors, whether you’re a man or woman, uh, whether you’re an adult or a child, and how those lead into the development of devastating neurodegenerative, neuropsychiatric, n- neurological diseases.
Because we really don’t have good solutions right now for patients with diagnoses like the things that I was being worked up for when I was ill 11 years ago. You, you call yourself a collaboration architect, and, um, I just wonder if you could give us the sort of the space in which you’re collaborating and some of the, who some of the key collaborators are in your work.
Sure. Absolutely. So I work with an incredible group of people, some of them for a decade or more. Um, some of them are more recent to our collaborative. I literally just got started, James. I had been a stay-at-home mom when I got sick. I had previously worked for Genentech and Pfizer in the industry. Really appreciated that experience from understanding the business side of healthcare.
Also had the privilege to work in a lot of hospitals, which gave me a really interesting view of somewhat of this lack of integration and the silos that existed in healthcare. You know, our team, uh, came together first very grassroots. So I decided after being extremely ill for a year, finding a doctor that studied infection-associated chronic illness and was an infectious disease specialist, Dr.
Charles W. Stratton at Vanderbilt, who became my physician and diagnosed and treated me for these chronic infections, placed me into remission. You know, I like to say about 95% of what I was before this all happened to me. And I said, “How can I help?” You know, this is a crazy big problem. Like, I, I start– It hit me like, wow, if all of these different autoimmune processes in different parts of my body were being driven by an infectious process and my immune system’s response to it, what else and who else was being impacted by this at any given moment?
My kids were three and five. I feared that I would not get to watch them grow up. I was literally making those plans, taking notes, writing things down that I would wanna pass on to them, because in my differential was multiple sclerosis, because I had neurodegenerative and neurological and neuropsychiatric symptoms that were devastating.
And for me, finding out that a tick bite was a tipping point, right, that could lead otherwise extremely healthy young 30-year-old who was running half marathons to be this sick, that I had 12 specialists that were so focused on their one system of the body that I got misdiagnosed repeatedly for a year until I met this polymath who understood this interaction, Dr.
Stratton. We ended up conversing and becoming closer. He started as my doctor. He became my friend, then he became a collaborator when I started Intracell Research Group, Intracell owing to the fact that a lot of the organisms we study are inside the human cell. And then we really zeroed in on the brain.
At first, it was just a collection of scientists I started introducing to one another very informally that studied this bacteria Chlamydia pneumoniae. And then we really started to grow because of, of course, in my own case, I realized it’s not about a single pathogen. We have to get immunology involved.
We have to think about microbiologists. We have to think about people studying fungi, parasites, bacteria, people that are experts in population health, epidemiology, veterinary medicine even, because of the One Health and the integration of, you know, different species interacting. So today, what it has become, and indeed I call it collaboration architecture, is what I felt is my best contribution to being part of the solution to a problem that is really big, and it’s to put some incredibly powerful tools of science and some of the brightest minds that never might meet one another, because they work in different areas, to get them together.
And that has been the thing that I’m most proud of, you know, work-wise, is getting these incredible collaborators together. So we work with people like Dr. Or Shemesh, who learned how to do expansion microscopy at the MIT, that now has two labs, one in Pittsburgh and Hebrew University. This allows us to see things in brain tissue that normally would only be able to be visualized with the world’s most expensive microscopes, but now we can do it at a much more cost-effective rate and more accurately.
We have, you know, Dr. George Perry, who founded the Journal of Alzheimer’s Disease. We have Dr. Brian Balin, who is the pioneer of chlamydia infection and Alzheimer’s disease here in the United States. We’ve worked with Dr. Ruth Itzhaki in, in the UK, who first is the, is the individual that really brought to light the issues of herpes viruses that cause the cold sore getting involved in Alzheimer’s.
Uh, Dr. Brent Harris, who’s an incredible neuropathologist helping us with understanding the nuances of specimens that we end up utilizing for our research. And the whole purpose of our research project is this: How do we use this incredible team and take the knowledge that we can amass, leveraging technologies that have yet to be brought together and aggregated, and also data sharing, to advance this chronic illness concept of the pathobiome and into a place where it is receiving enhanced federal funding?
Philanthro- philanthropic funding is also already kind of onto this. Like, I think that there are a variety of individuals who have lived experience with these chronic infections or identify as Lyme patients that have started various advocacies that have done an amazing job funding research. But what we really need, James, is like a, a bigger picture federal investment in this concept, and, uh, I think that probably resonates with you, too, as my guest, based on your experience.
Yeah, it definitely does. And on behalf of the clinicians who will listen or watch this, because I know for them, you know, they feel that Because some of the leaders in this, in this world, uh, you know, me- let’s say someone like a Dr. Richard Horowitz in the Lyme world, you know- Mm-hmm … speaks at integrated and functional medicine conferences, and many doctors in this space, like, take on this information, and some have even treated- Yeah
these kind of cases. You know, they feel like the rest of the world isn’t listening or isn’t paying attention. But what you’ve just shared is that there is a, a, a large and, and it sounds like growing group of people who are paying attention to this world, even though, you know, the average, uh, doctor down the street w- might still poo-poo a PANDAS diagnosis, for example, right?
Today’s podcast is brought to you by a number of different organizations that can all help take this movement forward. First and foremost, I wanna mention the Integrated Medicine for Mental Health Conference. In this podcast, you’re gonna hear about Dr. Richard Horowitz and the way that he’s, uh, working with this group, and he’s gonna be doing an extended session at IMMH this year.
You’ve got Dr. Dale Bredesen, you’ve got Kat Toups, you’ve got a number of people speaking on things like PANDAS and other areas of integrated mental health. So check out immh.org, and if you’re interested in conferences, I highly recommend this. It’s four days. There’s tons of CMEs. Get in there. And also our mission partners, because if you look at this disease type specifically, what will it take to build an army of practitioners that can contribute enough data to move the needle?
One, you gotta have a system that can track the data. That’s what TrueNeura is. Join the mastermind. Come and join the software. Be part of a community that is moving the needle in this space. Second, Freedom Practice Coaching. How do you build episodes of care, and how do you actually learn to sell episodes of care so that you can actually have patients in the system and you, and they buy all the testing so that you can actually contribute towards changing the field?
Three, Fullscript, right? How do you actually order the tests from Fullscript labs? How do you order the supplements? How do you organize and orchestrate all of the care in the background? Fullscript is that. Go to goevomed.com/fullscript, get an account, get set up your own chronic disease or your own pathobiome journey, all possible within Fullscript.
And then finally, BigBoost Marketing, the team over there. How do you actually bring these kind of patients into your practice? This is why they’re the mission partners, because all of them are here to help you achieve the mission that we are gonna talk about with Nikki today. Enjoy. Yeah. We– There has been, I would say, you know, having been in this for a decade now at this point- I- in the last three years, there has been this tremendous uptick in momentum.
You know, the federal government here in the US, HHS, announced back in December a Lyme disease initiative, um, more specifically invisible illness. There have been, you know, just tremendous advances in terms of, I think, patient awareness around these issues growing. And really what we can learn from medical history, um, particularly with HIV, is that patient advocacy and, you know, being loud as, as people that suffer from complex chronic illness will go a long way.
But some of the challenges I think that we’re looking to address with our consortium approach, they help handle what I think is a really big problem why we haven’t seen movement in this field faster, is that the different research groups that work on these problems— So let’s say you’re someone studying human herpesvirus 6 and its relationship to asthma or its relationship to a neurodegenerative state.
You’re not necessarily collaborating with the other virologists working on different pathogens like cytomegalovirus or human herpesvirus, you know, one of the other human herpesviruses or HSV or a bacterial group such as people studying Borrelia burgdorferi or Bartonella henselae tick-borne infections, and they’re not necessarily working with the people studying fungal infections.
And all these groups are out there, and they’re linking these infectious processes with very credible data to these diseases, right? Like X bacteria or fungi can drive this biological process and symptomatology in an animal model, and also we find it in the specimens from people that died with the disease in areas that were sick of brain, for example.
But It doesn’t advance because it seems that it’s small if you look at it, and it’s dispersed in this way. But when those groups really come together, the Lyme people, the viral, the fungal, the parasitic infections, with people actually studying the diseases that have curiosity about the exposome, it becomes a really large group, and it’s a large group of patients potentially impacted.
Yeah. Trouble is, they’re just classified. They get a label for their disease. They may be told, “You have rheumatoid arthritis. You have mild cognitive impairment. You have MS.” And really what they may have going on is an infectious immune medi- mediated syndrome being complicated by other things, even molds and mycotoxins, like we were discussing before, you know, other exposures such as heavy metals.
So things that, uh, are modifiable have to be emphasized, and we felt that mechanistic research, basic research, has to be happening at the same time as clinical research, and population research has to happen. But, you know, I think the change is coming, and I’m incredibly optimistic. Yeah. I share that optimism, and part of the reason I share that is that for the last year and a half, I’ve been engaged in a weekly mastermind for doctors who are interested in reversing cognitive decline and, and Alzheimer’s.
Awesome. And in that methodology, you know, the, the way those practitioners have come together, you know, we, there is, there is testing for mycotoxins, for Lyme, and for these other co-infections because it is so prevalent. I would say that, you know, doctors who are interested in treating chronic systemic illness, when they come into this group and look particularly at Alzheimer’s and cognitive decline pathology, even though, you know, some of the patients that we look at and some of the cases we look at would be, you know, mental illness or, or others, because there are psychiatrists and, and so forth in there as well, but they are all continuously shocked at the prevalence of these, you know, of the pathobiome in these patients, looking under the hood.
And so I’d love to, to like jump into the weeds a little bit for you, because I know that- Yeah … some of those people listen to this podcast. And, you know, as someone who’s on the cutting edge of bringing those fields together and looking at it specifically in the realm of Alzheimer’s pathology, what can you tell us, you know, to get ahead of what we might find clinically to help understand, you know, what’s really going on in the brains of, uh, patients with Alzheimer’s?
Let’s start with the, the, the pathogens that, that you see and, and the sort of patterns of pathogens that you see, and even like the progression of illness, because I know that, you know, an, an untreated and autoimmune disease might turn into Alzheimer’s, you know, over time- Yeah … because ultimately the root cause hasn’t been dealt with.
Yeah, so I think what, what is becoming abundantly clear from work within our consortium and then outside our consortium is that it’s very heterogeneous. So every single patient, I think, is an N of 1. The, the- The preponderance of different organisms that can be found in the diseased regions of someone with Alzheimer’s is pretty incredible.
So lots of viruses have been identified, various bacteria, including spirochetes, both spirochetes from the mouth as well as the old spirochete that nobody really thinks about too much, but we should be, um, syphilis Uh, Treponema pallidum. You know, it, it’s a, it’s a really interesting thing, James. If we go back in history, recently I made a video about this and then spoke about it at the Am- American Society for Microbiology, the, uh, the discoverer, you know, the Alzheimer himself and Dr.
Oscar Fischer were neck and neck publishing within the same year. So very easily we could’ve been calling Alzheimer’s disease Fischer’s disease. Fischer actually had a bit more of a robust set of work, and in Fischer’s writings, early writings, uh, he mentioned that the tangles and plaques looked like they contained bacterial colonies.
And at that point in time, syphilis was raging. This was before penicillin was discovered, and then it wasn’t really until the 1940s that penicillin became widely available. And the thing is, we have totally forgotten, it would seem, that with regard to dementias, there are plausible infectious and dementia pathways that we know about.
So, for example, tertiary syphilis results in dementia, right? And the neuropathological findings, according to Dr. Judith McCloskey, who has five board certifications, including neuropathology, she’s one of the most published individuals in the Lyme space with regard to dementia, that a dementia brain and a neuroborreliosis brain or a neurosyphilis brain neuropathologically are nearly indistinguishable.
And so what we know, though, is also that other groups and our group are finding other things. You know, so, so fungi can be found in brains. Uh, you know, then animal models are very informative, so if you take some of the things that have been found, like Chlamydia pneumoniae, and give it intranasally to mice, they develop amyloid-like plaques, and these are not transgenic or genetically modified mice.
These are wild-type mice. Multiple groups have shown that, including Dr. Balin and Dr. Chacko and her team in Australia. Then you have the herpesviruses that can induce a inflammatory state, phenomenal work by Dr. Dana Cairns at Tufts, you know, highly recommended, that essentially human, uh, you know, reactivations, uh, as demonstrated by an animal model of herpes may not even ne- necessarily involve a cold sore or a sore showing up, but that these reactivations due to stress events, when, when someone’s put under stress, whether it’s another illness or mental stress or physical stress, that this thing can reactivate, and essentially it’s like a traumatic brain injury that occurs.
And if you think about these things cumulatively over the course of a lifetime, these things can be compounding on one another, and that’s where polymicrobial issues are very likely. And so understanding each individual patient, you know, each individual case and what’s happening. For example, one person might have terrible periodontal disease and Porphyromonas gingivalis, which can cause perio disease, could be the primary driver of their cognitive decline.
But that same person might also have had a tick bite and contracted Borrelia burgdorferi and Bartonella henselae and Babesia microti. So understanding the landscape of the pathogens, but also inflammatory markers in that patient Considering genetics, considering nutrition, considering exposures in the home, such as mold and mycotoxins, hormones, uh, where do they stand hormonally?
Things, other things other than pathogens have to be evaluated too. And so we very much stand in advocacy for a precise approach, which I think is something that, that you obviously believe in also. Yeah, absolutely. I think we’re obviously on the clinical side, right? And, and seeing, uh, now a, a methodology that reflects looking at all of those kind of markers.
You know, Dr. Burke’s key thing is, is, you know, time is brain, right? In that you have to understand what is driving the pathology as rapidly as possible because you’re losing two MOCA score points, you know, a year in your 20s, and it goes to four MOCA score points, you know, below that. So there’s a curve by which people are dropping off.
And so if you don’t have a clear understanding right from the first moment of what’s driving the pathology, then you can, you know, s- you, you can sort of swim upstream for a while and do some lifestyle stuff, but ultimately you’re being sort of dragged under by the anchors of these, you know, these, uh, infectious agents or toxic agents or otherwise.
And, uh, yeah, it’s very, uh, for the individual. And one of the things that’s been really exciting for me is You know, having seen how long it’s taken for doctors to get to being able to reverse some of these chronic illnesses, so like SARS and autoimmune disease and, and, and some of these brain diseases, you know, this has been a long journey ’cause you’re not taught this in medical school, right?
So you have to go in, and you have to go to a bunch of conferences, and you have to implement, and you have to get it wrong a bit, and you have to try and, you know, f-find out what’s going on, go to another conference, have a conversation in the hall. And one of the things that I’ve seen in the last year and a half is just that a, a patient case with all of the data laid out and then someone talking through, someone who knows how to do this, talking through, like, how they weighted all of that information and what it led to do and in what order, has led to the confidence of clinicians really speeding up.
And that to me has been a huge unlock because I, I think like you, sit at this and say, “If this is true, what are we gonna do about it?” Right? Yeah. Uh, and, uh, so that’s been w- you know, really incredible to see. And so I, I share some of the optimism in the fact that this is being seen and that ultimately all of that data is crunching into a place where we can say, “Okay, when a new patient comes in, and they have this sort of certain phenotype, this combination of, you know, of a pathobiome, for instance, you know, this kind of treatment protocol worked in this way previously,” and learning from those, you know, those kind of cases.
So I, I’m, I’m confident on our end that a lot of insight is happening and acceleration is happening. But I, I would love to know from your perspective, like, what, what would be the most helpful to your work? You mentioned a, a federal, you know, federal support. But, like, for the clinicians who listen to this, who are sort of working on the, the front lines, some of which, some of whom are tracking their outcomes, what is the most useful for your work to, to move forward in a powerful way?
You know, if, if clinicians are listening, so I’ll say this. In 2023, we published our landmark paper for our Alzheimer’s Pathobiome Initiative in the Alzheimer’s — Alzheimer’s & Dementia, the journal of the Alzheimer’s Association. And it was a massive effort of me bringing together and co-lead authoring this essential research plan to identify infectious agents, identify the key questions that need to be resolved and answered using the tools of science, and then to also…
It was a call for collaboration, and so basically we put our ideas out to the world. It was a little unconventional, and invited people in, you know, to our midst to say, “Hey, how are we going to tackle this? Join us.” And it did result in a great deal of that. But one of the things that keeps me up at night within our own paper is 86 cases of infectious dementias.
Now, these were all different types of infections that were identified, and in most cases, the reason that the case report got published was that the clinician treated the patient for the infection using precise treatment, right? So if you had Cryptococcus neoformans, a fungus, you got an antifungal. Uh, the majority of the cases were identified using cerebrospinal fluid.
If you had, for example, Lyme disease, Borrelia burgdorferi was found, you were given intravenous penicillin, was given quite a few times. And then the reason they published the case was that they, the patient experienced a reversal. And some of the cases, the patients had a– One example was an Alzheimer’s case for nearly a, nearly a decade and a half to two decades that experienced a drastic improvement in memory scores following treatment.
So these beg the question, you know, if diverse infections are being found in brain specimens from people that we lost to these devastating conditions like Alzheimer’s, if you can make animals sick using the same infectious agents, and you can get pathology, which has been, by the way, branded as being all bad, and, uh, that’s another matter we can discuss in a moment.
You know, that, that these things are credible pieces of evidence. And if we say– We think– Just to think about the number of lives lost every year to Alzheimer’s disease in the States alone, but then globally, it’s staggering. You know, Alzheimer’s being the most common form of dementia, and we essentially don’t have anything really to do for the majority of people.
Like, people will, will literally, you know, uh, continue along the progression. The new drugs are not particularly safe, accessible, or affordable, uh, or effective, most importantly. So it really does lend itself to needing a bigger movement and a bigger push. So you’re asking regarding, you know, what is needed?
I think that Because the United States government is the biggest funder of medical research in the entire world as a single entity, it’d be phenomenal to see, and I think we are seeing some greater support for this federally, you know, entire pools of funding at different institutes within the NIH, for example, or even beyond NIH, to look at multi-system complex chronic illness from this lens of the pathobiome, and that the mechanisms to fund the research become a bit more innovative and open and multidisciplinary, you know, so that teams that are doing things that are tr- potentially transformative can work together.
And, uh, we, we really love the team science mechanisms that the government has created. But truly, you know, the, the way to support the effort forward is to stimulate multiple different spaces at once. So we really need mechanistic research, so basic research, population studies, like the work that our colleague Graciela Muniz-Torrera is doing, looking at large human data sets as well as, uh, longitudinal cohorts to get information about the prevalence of various infections, the use of hormones, and how that impacts disease trajectory ultimately.
We also need pilot studies because we have drugs to potentially intercept and help people today, so there’s no reason to wait for the perfect solution. And we’re working to develop a testing approach that would hopefully integrate looking for multiple microbes that could be problematic, and then also host markers too, the markers in the person that could tell someone, for example, the way that we get mammograms or colonoscopies or various other screenings, we may be able to start looking at this in a, at a point in the not-so-distant future and tell someone, coupled with clinical baselines, which, which most of us don’t have, right?
We are– Most of us are not given a baseline of our cognition when we’re at our finest. We end up getting cognitive testing much later on, and very intelligent people, those people can often be missed because they, they may perform at a level, you know, they may have subjective memory complaints, but those people are challenging.
So yeah, I think we really need, um, really a tremendous amount of federal support and philanthropic support too to stimulate multiple different angles of this. Well, well, well, let’s go there where you said we should go, which is an understanding of the Alzheimer’s pathology, you know, as, as maybe a protective mechanism rather than a pathological mechanism.
Is that something that is aligned with what you’re seeing? Yes, and we have members of our group, our consortium are really the innovators that have documented these, these qualities. So when we talk about amyloid and tau, you know, you have, uh, some have referred to it as, you know, kindling and fire, but it’s more akin according to the research that’s been published demonstrating these things are innate immune defenses, that these might be the firefighters showing up in response to an insult or something that is aggravating them.
And not the only, doesn’t have to be the only thing, but one of the things that can induce these things is infection. And that’s been demonstrated by Dr. Will Eimer at Harvard and, and Mass General Hospital, as well as Dr. Or Shemesh that I spoke about previously. They’re in the same consortium, but worked independently, uh, and both published within the same year on induction of tau hyperphosphorylation of tau, tau tangles in, uh, in response to infection.
And so if these things are a response to infection, and then, uh, Dr. Eimer and other colleagues, uh, Dr. Sosha, Rudy Tanzi, they’ve demonstrated that A beta has antimicrobial properties. So if the pathology itself is there- I think evolutionary biology is so important to keep in mind. Why is it showing up? You know, does, is the human body this incredible machine, right?
Uh, what an incredible brain too that human beings possess. It’s a c- supercomputer. Would it do something at such a large scale if it weren’t serving some sort of purpose? And can that become problematic? Sure. There’s always the double-edged sword of immunology, right? The, that fine line between autoimmunity and an immune system that is handling something the way it should be.
So I think it’s really important, not just in Alzheimer’s disease pathologies, but when we think about, uh, disease related pathologies and other neurodegenerative conditions and other conditions throughout the body, that we ins- understand what are the induction pathways. Because largely the treatment space has gone to developing biologic drugs to suppress pathways, and when we suppress some of those pathways, we don’t get people better, not, not many at least.
So, so many people suffer with autoimmune conditions, as you know, and I get to be one of the people that is mostly well today from things that typically don’t get reversed. I had a diagnosis of interstitial cystitis, which is a incredibly painful bladder pain disorder. You know, that responded robustly to antibiotics.
So the question remains, you know, just because you have an absence of proof isn’t proof of absence. And the example of clean urine from people with interstitial cystitis is a great one. Routine urine screenings look for obvious pathogens, but they’re not able to detect pathogens that are intracellular or less, uh, you know, more stealthy, is the word I’m looking for, or things that could be in the lining of the bladder itself that would require a biopsy to reveal.
So the whole idea of, I think, where medicine has to go, is digging deeper and being more precise. Yeah. Precision is the future. I totally agree with that. And you know, one of the things that I’m just feeling right now is that I’m feeling, you know, maybe a big out breath from my community listening to this because, you know, I think pr- doctors and practitioners in our community that have taken on these kind of cases and have, you know, gone to lectures where these kind of, uh, ideas have been spoken about, have been sort of made fun of, I think, in the last decade or two for, you know, pathogens.
I mean, it just literally came out of your mouth. You’re talking about, like, these stealthy, stealthy things. And so it’s wonderful to actually hear that this is being taken seriously, and that there is research coming in from around the world to back this up. Because I’ve always felt that one of the, the focuses on the functional forum was to be a collaboration architect, was to introduce practitioners to each other, but really take- what was happening at these conferences from being sort of hokey and hippy to being, you know, future forward-facing, and to say that this is, you know, where medicine has to go because ultimately, you know, if you’ve experienced something like you’ve experienced, or I think the most obvious would be something like PANDAS, where you have a rapid onset, you know, mental illness in a child where there’s no history, and then if you treat it right, you…
Nothing else works, right? You can do all the drugs, and then suddenly you bring it back to treating the infection, and then the child not only gets better, but ultimately has, like- An extremely high quality of life for maybe another 70 years. You know, from an economics point of view, from a human point of view, from a first do no harm point of view, that is such an elegant solution that once you’ve seen it, you can’t look away.
Yeah. So I think any of the people in our community, once they’ve experienced that kind of elegance of solution, you know, are hooked by either working on cases of, you know, a- adult brain disorders or, uh, geriatric brain disorders or pediatrics. And, you know, I would love for many more in our community to get involved and to track their outcomes in the right way so that we can contribute in some ways to, you know, to the work that you’re doing and also to the, the, the greater, the greater mission of just removing this unnecessary suffering from society.
So many things you said there that I want to respond to. So first of all, we are working in pandas and PANS, our team. The brain pathobiome is our wheelhouse, and we are super aware of the devastation that these conditions have, um, you know, firsthand. You know, we have many people experiencing these, these terrible things, and kids can also go from a, you know, sort of more of a slow progression, a slow burn as some parents call it, where it’s sort of a relapsing and remitting course where they may only have some behavioral difficulties and handwriting problems, and they think it’s a disciplinary issue at school.
And there just is, like you said, there are solutions to these problems if that child gets properly identified and treated. Uh, but, you know, it really does require something that we’re passionate about, which is the bidirectionality of the communication between clinicians on the, on the front lines that are willing to treat, to come back to research groups like ours and say, “This is what we found clinically.
How does this match up in your mechanistic models, in your population studies, in your, uh, animal work?” And then back again from the research lab to the clinicians indicating, you know– And, and this is the point of a consortium that includes clinicians, right? So we were, we had the privilege of Dr. Horowitz coming to our weekly call.
Our team, global team convenes once a week for 30 minutes for years. And, uh, he presented his incredible case of, you know, reversal of patient, a patient with p-tau and amyloid beta plasma biomarkers indicative, and cognitive issues indicative of an AD diagnosis Alzheimer’s, that was able to be treated effectively, leveraging his approach to handling, you know, all of the things that we’ve discussed, including infectious agents.
And, you know, this, this is something that is beneficial for so many different categories. It saves lives. It saves money. It’s, it dramatically reduces human suffering. But the challenge I think that- You’re describing where, you know, the eye rolls, right? You talk about a stealth pathogen, somebody rolls their eyes.
I think hit them with 10 studies or 20 or 100 or 1,000, because that’s where it comes to citing the evidence and having the evidence that you need, and that’s where we come in. You know, there’s a very robust body of literature. When you just say stealth pathogens, I mean, the way that these organisms operate is really particularly things that live inside our cells.
They’re using us to survive, right? We are their Earth. We’re their ecosystem. And so the consequences of those things, they’re not going to be the things that make you f- uh, sick very quickly. It would be more of a simmering pot over many decades. And because they don’t really want their ecosystem to die, they want the host alive so they can continue stealing from our mitochondria and utilizing our resources and sequestering things so that they can remain alive.
And even you’re, I’m sure, very aware of this, but there’s a linkage, of course, between microbial infection and atherosclerosis, heart disease, uh, you know, which had been previously first demonstrated with oral microbiome. You know, people with dental issues having this relationship to heart disease, healthy mouth, healthy heart.
Well, really, we also know healthy mouth, healthy brain. But in some cases, some patients, their microbiome, or it’s, it’s a pathobiome, even if they take great care of their mouth, they’re still developing recession of gum tissue and so forth. So it’s understanding disease risk too in certain individuals, you know, that may have…
You know, like when I fell ill, I was already doing everything right. I was eating healthy, running, exercising, not abusing my body. And I tried a ton of natural strategies to mitigate inflammation during the year when I was misdiagnosed. I ended up having to lean on traditional antimicrobial drugs. And I think that there are gonna be cases like that, of course, like mine, you know, where you have a advanced case.
But I do also feel that a lot of people can benefit just from lifestyle changes alone, you know, and preventative strategies. Yeah, exactly. Well, a final question. If you wanna go and do an episode of Air that does all of this testing, it’s expensive, right? I’d love to just get your thoughts on the democratization of this science to the rest of the population and the pathway towards that, because ultimately, we want this to be a standard of care, not something that’s only, you know, accessible to people who can afford the testing.
Yeah, this is one of the greatest challenges. You know, I’ve made my whole story of what happened to me and the work we’re doing public, and people will reach out and say, you know, “What do I do? Where do I go?” And frequently, you know, I will make recommendations and give people resources. You know, for example, the International Lyme and Associated Diseases Society provider search, which has been now added to the HHS Invisible Illness website.
I sit on the board for their ILADS Education Foundation, and I’m so thrilled to be able to support this organization. But I know there are other root cause practitioners in the world, you know, looking at upstream drivers. I think it’s going to be a really big challenge, as you said, you know, democratizing, you know, making these things available to more patients.
I think one of the keys is going to be companies developing solutions around these problems. You know, so, so things that– People think about profitability as a bad thing, but I studied business and appreciate economics. The economics of the infection-associated chronic illness story are kind of missing.
With proper economic stimulus, also federal funding follows. And so I think I would love to see more companies, and they’re out there, developing better testing for infections, companion biomarkers, the things like Molecular Bio- Biosciences has with their brain autoimmune panel that can be used to help diagnose kids with PANS, PANDAS, and autoimmune encephalitis.
You have then the need for companies to develop innovative solutions for infectious agents, you know, targeted therapies, right? Where you’re not knocking out, you know, everything but the kitchen sink in your gut with antibiotics, but you have something perhaps more tailored to specific organisms. So I think once those things start happening, you’ll start to see the tip of, you know the pressure and tipping point of things becoming covered, right?
So insurance coverage, I think, is a huge issue. I know it is in the PANS, PANDAS community, where the testing itself may be inaccessible to parents to even unveil the problem in the first place. Well, look, I think there’s a lot of work for us to do together. Thank you so much for spending the time with us here today.
I know you’re very busy and got so many things, you know, that you’re balancing, and I, I really do look forward to continuing the conversation, particularly with these group of practitioners that I’ve got to know, you know, quite well over the y- last year and a half that are learning every week on how to reverse cognitive decline using a precision medicine approach.
I really think it’s the future, and, uh, it sounds like that’s lining up with what you’re seeing. Thank you for being on the front line and bringing everyone together, and, uh, look forward to updates from my community to yours and your community back to ours, and ultimately that we can be part of, you know, something tremendous in understanding the root cause drivers of all these brain diseases in our lifetime.
I’m your host, James Maskell. This is the Evolution of Medicine podcast. We’ve been here with Nikki Schulte from the Alzheimer’s Pathobiome team and many others. We’ll put all the details of her work in the show notes, so you can see, you know, what, what all the different areas that she, uh, she’s working in.
Thanks so much for tuning in, and we’ll see you next time. Thanks for having me, James, and thanks to everyone listening. So we are here asking practitioners about their practitioner journeys, and the reason why is because Journeys is a new product from Fullscript. Journeys allows you to set up your own lab offerings as the top of the funnel.
Give the patients what they want. They wanna know about themselves, and it’s the easiest way to bring them into your practice. We have all types of practices from across the country that are building their own unique lab panels for their own unique practices, selling them to their community, and acting as a great funnel into their practice.
This is a massive innovation. I think this will accelerate the evolution of medicine. You can go to goevomed.com/journeys to find out more. Set up your own journeys in half an hour and transform the health of your community. Go get ’em. So that was the podcast. What an epic session. Thank you so much for tuning in to The Evolution of Medicine podcast.
We will be back again next week, and thanks so much for tuning in, and we’ll see you next time
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