Episode #226: Microglial Activation in Chronic Illness with Dr. Jonathan Streit, DC, CPN, IFMCP

Why You Should Listen

In this episode, you will learn about the role of microglial activation in complex, chronic illness.

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About My Guest

My guest for this episode is Dr. Jonathan Streit.  Jonathan Streit, DC, CPN, IFMCP is a Functional and European Biological Medicine practitioner.  He has dedicated his professional life to helping patients with complex chronic illnesses.  His passion for this type of work grew from walking with his wife through her own battle with Epstein Barr and Lyme disease.  Since then, Dr. Streit has focused his career on applying and advancing these approaches to address the deeper roots surrounding chronic illness.  He’s the co-founder of the Institute for Restorative Health, where he and his team use their BioRestorative Method™ a comprehensive approach that blends European Biological Medicine, Functional Medicine, neurology, nutrition, and terrain-based healing principles.  Dr. Streit has trained with internationally recognized leaders in healthcare, completed postdoctoral work through the American Institute of Postural Neurology, and teaches pathology and functional medicine for the University of Integrative Health doctoral program.  With nearly two decades of clinical experience, he has supported patients across a wide range of chronic health challenges.  To bring these insights to the many still struggling without answers, he wrote "Silent Spark: An Unseen Force Fueling Chronic Illness and How to Heal", a book that sheds light on the often-overlooked deepest roots keeping people sick.

Key Takeaways

• What are microglia and their role in chronic illness?
• What are the M1 and M2 states of the microglia?
• What symptoms or conditions may be associated with chronically activated microglia?
• What cytokines and interleukins do microglia produce?
• Is there any testing available to explore microglial activation?
• What are the most common triggers of the microglia?
• Can the microglia remain activated long after the threat is gone?
• What are the primary roles of the microglia?
• What conditions are associated with under-pruning or over-pruning?
• Does microglial activation overlap with Mast Cell Activation Syndrome?
• Does the limbic system play a role in microglial activation?
• How has COVID further complicated the microglial conversation?
• What is the role of the microglia in neurodegenerative conditions?
• Does the external environment play a role in triggering the microglia?
• What is the gut-brain-microglial axis?
• How do hormones impact the microglia?
• Can EMR/EMFs be a trigger for the microglia?
• What is the role of chronic stress in microglial activation?
• Do the microglia play a role in pain syndromes or seizures?
• What treatment options are available to support the microglia?

Connect With My Guest

InsituteForRestorativeHealth.com

Related Resources

Book - Silent Spark: An Unseen Force Fueling Chronic Illness and How to Heal

Interview Date

December 11, 2025

Transcript

Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast.  They are not a full replacement for the discussion.  Timestamps are provided to facilitate finding portions of the conversation.  Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed.  Please Contact Me with any corrections.  

[INTRODUCTION]

[0:00:01] ANNOUNCER: Welcome to BetterHealthGuy Blogcasts, empowering your better health. And now, here's Scott, your BetterHealthGuy.

The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.

[0:00:35] SCOTT: Hello, everyone, and welcome to episode 226 of the BetterHealthGuy Blogcasts series. Today's guest is Dr. Jonathan Streit, and the topic of the show is Microglial Activation in Chronic Illness.

Dr. Jonathan Streit is a functional and European biological medicine practitioner. He's dedicated his professional life to helping patients with complex chronic illnesses. His passion for this type of work grew from walking with his wife through her own battle with Epstein-Barr and Lyme disease. Since then, Dr. Streit has focused his career on applying and advancing these approaches to address the deeper roots surrounding chronic illness.

He's the co-founder of the Institute for Restorative Health, where he and his team use the BioRestorative Method, a comprehensive approach that blends European biological medicine, functional medicine, neurology, nutrition, and terrain-based healing principles. Dr. Streit has trained with internationally recognized leaders in healthcare, completed postdoctoral work through the American Institute of Postural Neurology, and teaches pathology and functional medicine for the University of Integrative Health doctoral program.

With nearly two decades of clinical experience, he's supported patients across a wide range of chronic health challenges. To bring these insights to the many still struggling without answers, he wrote Silent Spark: An Unseen Force Fueling Chronic Illness and How to Heal, a book that sheds light on the often-overlooked deepest roots keeping people sick.

And now, my interview with Dr. Jonathan Streit.

[INTERVIEW]

[0:02:14] SCOTT: Today, we're going to learn about the role of the microglia in both health and illness. This is a topic that we haven't really covered on the podcast in any great detail. And so I'm honored today to have Dr. Jonathan Streit here to talk with us about microglial activation and his new book, Silent Spark: An Unseen Force Fueling Chronic Illness and How to Heal. So let's get this microglial podcast activated. No pun intended. Thanks for being here, Dr. Streit.

[0:02:44] DR. STREIT: Absolutely. Thank you for having me. I appreciate it.

[0:02:47] SCOTT: First, talk a little bit about your personal story. How did chronic illness, how did microglial activation enter your own life and fuel the passion that you have for both the work you do with complex chronic illness patients, but also really serving as the spark for writing your new book?

[0:03:05] DR. STREIT: I think that anyone that is in chronic illness, you kind of are essentially called to do it, called to work it, right? And so, if you didn't get through it yourself, you helped someone that you love, right? For me, my wife was kind of the pivotal point for me. And as I'm working with her, trying to figure things out, I'm also working in chronic illness. I've been doing it for 20 years now, almost.

And when you see patients that you work with get better and then you see some that you do something very similar that have very similar stories, very similar symptoms, and they not get as well, that keeps me up at night. That type of thing, it doesn't make sense to me. And so in an effort to try and make sense out of that, I'm sitting down, "Lord, tell me – give me something to understand here on what can I do for these patients that are seemingly not getting as far as I'd like them to get."

And so, time passes and moves on, and I get introduced to a book called The Angels and the Assassin, and it is a book about research in microglia. And it is a little bit more pointed towards the neurodegenerative things, like Alzheimer's or dementia. And I started reading it because my mother-in-law suffers from frontaltemporal dementia. And so, I'm reading that, trying to figure some stuff out, and then it clicks.

This chronic illness, Lyme, Epstein-Barr, mold illness, you name it, is activating these little immune cells in the brain, and they're turned on, creating a cascade of inflammation back downstream. And that's where I started thinking this could very well be kind of another area that we can really focus on in the chronic illness spectrum, because nobody's really talking about it. There are some people, of course, in the research world, that type of thing. But we're kind of dancing around something that is extreme. It's the elephant in the room that no one's actually talking about, I think.

And so, when I started researching, and I started reading journals, and I started reading other books about it, I had about 100 pages of notes. And I realized – because I'm not a writer, Scott. I'm not a writer. I feel bad for the editor because they had to do a lot of work. I'm a talker but not a writer. I'm like, "I need to write this book." Because this is all the information right here, but it's a dense topic. I mean, it is a very dense topic. It is hard. And so, one of my goals is to take these hard-to-know topics and bring them out in a fairly easy-to-read, easy-to-understand way of doing things.

I started with my wife, and it just went from there, to my mother-in-law, to my patients. And I think it's going to help physicians and patients all over trying to look at chronic illness through a little bit different lens.

[0:06:23] SCOTT: Yeah, I think the only podcasts where we've touched on this before were traumatic brain injury and also the PANS/PANDAS realm. And they were just kind of not really the entire focus. So, I'm excited to learn more from you. I think this is a critical topic.

Let's set the stage for the discussion. What are microglia? You've said they're both involved in neuroinflammation and neuro protection, that they're both a silent spark of inflammation and a regenerative force. Are they considered part of the immune system? Are they white blood cells? Are they macrophages? And at a high level, what's their role in supporting health? And then, where in the body do we find microglia?

[0:07:06] DR. STREIT: Alright. Microglia are the central nervous systems resident immune cell, and they align more with macrophages than anything else. They are even a little bit specialized in that case, because macrophages are usually built within the bone marrow, and they proliferate there, and then they go out into the peripheral aspects of the body. Whereas microglia actually migrated there in utero from the yolk sac, and they set up shop in the central nervous system, and that's where they stay. And so, they don't leave the central nervous system. I think that's important to understand in the world of microglia. They're spine – spinal cord, and then they're in the brain.

They are densely impacting the limbic system and our memory centers, which we'll get into later, I'm sure. And yet when a microglia becomes activated, meaning there's some type of toxicant there's trauma, there's a chronic infection, they actually change their morphology. They become less docile and less delivering nutrients to the brain, and they become more what we call phagocytic. Or they start to envelop these areas in the body. Think of it like a gardener, right? If you are a Japanese gardener in a dynasty long ago, the samurai or the ninja, right? They got their tools taken away for their martial arts, and they then used rakes, and they used their tools in the garden to sweep everything up, but yet they're actually silent assassins, right?

When we look at microglia through the lens of that Angel and the Assassin like the book was writing about, they can deliver really good nutrients to the brain. But when they get activated, they deliver, kind of like in other words, a death blow to neural networks in the brain. I mean, that book was pretty pivotal for me in trying to understand microglia.

[0:09:23] SCOTT: Let's talk a little bit about the M1, M2 states of the microglia. What are they? And then is there kind of a corollary with microglia and inflammation in general, where maybe short-term activation of the microglia could be beneficial, but that more chronic, never-ending chronic microglial activation is really the concern? And maybe to summarize it, are they friend or foe, bodyguard or villain, Jekyll or Hyde?                                                                                        

[0:09:53] DR. STREIT: Yeah, I'm really happy that you asked that particular question because they are a little bit of all of that. When I look at microglia, it's kind of like a chronic illness. I think a lot of people resonate with this analogy, and it's kind of like a family member. And sometimes our family members are there, and they're supporting us, and they're helping us. And sometimes they're caustic. And yet we can't get away from them because they're family. And so we look at microglia in the same way.

Scientists use M1 and M2 as an explanation for regular macrophages and how they work. An M1 state is an inflammatory state, and an M2 state is a natural, more normal anti-inflammatory state, if you will. M1 is actually a kind of a moniker for macrophages and their peripheral state inside the body, versus microglia. They just kind of use the same terminology here. M1 is an activated microglia. M2 is the natural form that's delivering good nutrients to the body.

[0:11:04] SCOTT: Is it fair then to say that the M1 state is more attack, more driving of neuroinflammation? Where M2 is more healing, more cleanup, or janitorial service, more resting state, more neuroprotective?

[0:11:22] DR. STREIT: Absolutely. M1 is going to be your activated state. I’ll use the analogy. I didn't write this in the book, but I use it in my office a lot. Microglia are like these monkeys that live in this giant, beautiful tree in the Amazon, and they're going from neural branch to neural branch, selectively picking the ripe fruit, selectively pruning the dead leaves. And then they're dropping that down to the soil below, and it becomes fertilizer. Right? That's the M2 state, where everything is natural moving.

Now, if we have a toxicant or an infection that's slithering up the trunk of that tree, they start going absolutely crazy, and they start swinging from branch to branch, picking fruit. It doesn't matter if it's ripe or not. They break branches. They create chaos. And that's that M1 state. And so, I really look at that and say, "Okay, how do we calm these monkeys or these microglia down?" And that's what this book is about is how to take something that's active and chronically active and reduce it. Because you're right, Scott, it is important to have acute M1 activation because it saves our brain. It does support us. But the problem is chronic, long-term activation of microglia. It becomes a detriment to our body.

[0:12:51] SCOTT: I thought you were going to say the M1 state was the monkey poop. But anyway, that analogy didn't quite go there.

[0:12:58] DR. STREIT: The monkey poop, that's the fertilizer, man. That's a parasympathetic activity there.

[0:13:05] SCOTT: What symptoms or conditions lead you to think about activation of the microglia as a significant contributor in a patient in front of you? How they present? What drives you to more deeply exploring the microglial contribution to their condition?

[0:13:24] DR. STREIT: Well, I think it's important, because we developed the BioRestorative Method. And that's a six-node understanding of the body. It's kind of like a filter at which we look at everyone through. We look at the autonomic nervous system, we look at the gut microbiome, the terrain, we look at neuroplastic retraining, epigenetic nutrition, we also look at heart-brain coherence. And it naturally fits in that neuroplastic retraining side of things.

And so, we don't necessarily just say we're going to look at microglia, and that's all we're going to do. It's a bigger part of all that we are trying to do here. And so, I think that's important. Because you come in and you have a chronic illness, we know – scientifically, we know that microglia are activated. And they're probably chronically activated depending on how long you've had that illness.

Now, we want to limit that. And that's what this book is about is slowing that microglial activation. But if someone came in my room and they had cognitive decline or they had PANS, or PANDAS, or some form of autism, things like that, those are all classic states of microglia activation, chronically activated microglia.

[0:14:40] SCOTT: How long does a microglial cell survive in the body? And what are the pros and cons of their survival duration? Do they, over time, become more primed, or more reactive, or more trigger-happy when that next insult arrives? Wondering if you can talk to us a little about the concept of microglial priming or microglial sensitization.

[0:15:07] DR. STREIT: Yeah. When microglia become sensitized, basically they become hyperaware, right? We've had a longstanding chronic infection, maybe head trauma, Lyme, Epstein-Barr, mold illness, any of these types of things are going to create an environment that is rich in microglial activation.

And just like anything, if I rub my arm right now, it doesn't hurt. But if I keep doing it for 3 hours, I'm going to have a rash on my skin. It's no different than that. They become sensitive. They become hyperaware of their surroundings. And I think it's important to know that we are a combination of everything that has ever happened to us, right? Our tissues hold our thoughts and our traumas. Our ACEs, adverse childhood experiences, are a factor that play into that.

And so when we have lifestyle factors that are traumatic, our microglia inside our brain become extremely hyper-aware of our surroundings, and then they will start to secrete those inflammatory cytokines more and more and more, which becomes the problem that we're talking about.

[0:16:25] SCOTT: The advantage of the computer over the human is the CTRL+ALT+DELETE reboot function.

[0:16:31] DR. STREIT: Oh, my goodness. Yeah. Wouldn't that be nice to have just – yeah, I'm not going to take on that thought or memory anymore. Yeah. CTRL+A. And now, CTRL+DELETE.

[0:16:42] SCOTT: Neuroinflammation can be the result of this microglia releasing cytokines, releasing interleukins. They can also release anti-inflammatory molecules depending on that M1 or M2 healing state. What are some of the key cytokines, or interleukins, or mediators that they produce that are either pro or anti-inflammatory? Are they also releasing growth factors that support repair or neurogenesis?

And then building on that, we talk a lot in the Shoemaker's CIRS, mold realm about TGF-beta 1, which we use as a way to explore chronic inflammation triggered by something, commonly mold or Lyme. When it's elevated, there is often an attempt to reduce it, sometimes using tools like Losartan. I'm wondering how you see TGF-beta 1. Is it harmful? Is it beneficial? Are you working to specifically reduce it? Or is it elevated for a reason?

[0:17:46] DR. STREIT: When we look at an M1 state, that's your activated microglial state. They're going to start secreting things like tumor necrosis factor alpha. They're going to do interleukin 6, IL beta 1. They're going to release all these complement factors as well. Not to mention reactive oxygen species, or ROS, iNOS, all of these types of things that are inflammatory to the system, even COX-2. That's going to increase our pain signals and all of these types of things.

If we're in an M2 state, which is that repair anti-inflammatory state, it's going to be more things like interleukin 10 or TGF-beta 1. And that's kind of where you're talking about a little bit is that TGF-beta 1. Because centrally, inside the brain, microglia will secrete TGF-beta 1, which is anti-inflammatory, in the brain. But yet in the body, when you look at it through the lens of mold illness, TGF-beta 1 is often times a problem because it shows us chronic inflammation peripherally. That one is a really hard one. And I wish I were a cell biologist and I could probably tell you a little bit more about TGF-beta 1 and its incredibly complicated history.

But using something like an angiotensin receptor binder like Losartan, we can do that in some ways naturally because our flavonoids are in essentially ARBs. Things like I've mentioned in the book, apigenin, or fisetin. Those are both fairly potent flavonoids, bioflavonoids that we can utilize. We can also use things like quercetin. I'm a fan of honokiol. I write about that a little bit in the book.

And so, we look at those types of things, and they can act peripherally as an anti-inflammatory agent against that. I don't have the luxury of being able to use – luxury and the detriment really of pharmaceuticals. That's not my world. But I think what we have to do is when you're in this natural world, as you know, Scott, is you have to really start thinking outside the box. And you have to get into the biochemistry a lot more because you want to have the same effect for your patient as maybe a drug does have, but yet you don't want any of the side effects of that drug. I think that's where we're at.

Now to answer your questions on the growth factors. An M2, or an anti-inflammatory microglial state, it does release brain-derived neurotrophic factor, glial-derived neurotrophic factor, or even a nerve growth factor. We're going back to that monkey analogy. That's that ripe fruit that's falling to the ground. Or secretions, fertilizing the soil underneath. And so that's your true state of an M2 is really getting that back into that brain-derived neurotrophic factor, which is so healthy for the brain.

[0:20:49] SCOTT: How do we test for whether or not microglia are detrimentally activated? Obviously there's signs, and symptoms, and conditions. But are there some labs that you use that kind of support that diagnosis? Maybe some cytokine or interleukin panels, organic acids potentially? Any imaging? Or is this largely a clinical diagnosis?

[0:21:12] DR. STREIT: I would say that you can go down the path of using something a CytoDx, which gives you a lot of the interleukins, the tumor necrosis factor. You can do specialized testing like TGF-beta 1, or you could do these types of things that you can find like the Shoemaker protocol type things. You can look at MSH or VIP. You can look at all of these lab markers.

And I think often times, if my patients tell you about me, I don't get hung up on diagnosis very much. Because I feel that in the natural sense of things, a diagnosis is really just kind of a branding that you put on someone, and then you are treated with a classic set of pharmaceuticals for that particular diagnosis.

Now, I know a lot of chronically ill people, they're like, "I just need to know the diagnosis. I need to know what this is." Well, if you didn't know, but yet you still got benefit, isn't that a benefit? Because I can tell you right now, for some people, not everyone, but for some people, especially in my experience, when we found out that my wife had Lyme years and years and years ago, we were excited. We finally have a diagnosis.

But then comes the realization that mainstream medicine isn't really that good at that diagnosis. And so now you're like, "Now I've become this diagnosis." And I refuse to go down the road of calling anyone a Limey, or a spoony, or whatever the monikers are these days, because I do not agree with labeling yourself with that."

In the treatment room, I can do those things. I can look at that. But that's an increased cost for our patients. And I'm going to treat it the same way whether I know it's there or not. But my scientific side is interested. And I have ran the CytoDx panel. One in particular patient, a third of the markers were elevated after 3 months of doing this type of dietary process and the supplementary things. They're all gone except for RANTES was high, and they had an autoimmunity anyway. And so, I was pretty excited about that. That really got me excited about the supplementation and the dietary aspects of microglia.

[0:23:30] SCOTT: I totally agree with what you were saying. You label it, you internalize it, you own it. And then in some cases, you never get rid of it, right? It's become who you are. And so, I've rejected that as well. And I think it's a slippery slope particularly in the genetic SNP arena, where you then internalize brokenness or unfixable. And maybe that is actually the epigenetic influencer of gene expression, much more than that SNP –

[0:24:02] DR. STREIT: Than the SNP itself is, yeah.

[0:24:04] SCOTT: 100%. For people listening, the CytoDx test is from Diagnostic Solutions Laboratories, the same people that do the GI MAP, if I'm not mistaken.

What do you see as the common triggers for activation of the microglia? You mentioned infections, you mentioned toxicants. But let's talk a little about the microglial triggers. We'll dig into some of them later. But which infections, or toxicants, or toxins, in your opinion, lead to the most significant activation of the microglia? And are there key triggers that you also then screen for in assessing a patient when you're thinking about those activators of microglia?

[0:24:48] DR. STREIT: It takes me kind of back to looking at through the rolodex of patients that I've had over the years. There seems to be a very common thread when you're talking about Lyme, or you're talking about Epstein-Barr virus, or any of these things. There is usually a trauma, whether it's a physical trauma, like I hit my head, or I crashed my bicycle. Or I had an emotional trauma, I had a family member pass away, or something like that. That then, all of a sudden, seemingly out of nowhere, I have all of these symptoms known as Lyme, or Epstein-Barr, or whatever it is. And that always struck me as this straw that broke the camel's back type of thing.

But really thinking about it now through the lens of microglia and their ability to become sensitized, when you have Lyme in your body or you have Epstein-Barr, our body can often times just deal with it. I would say I have no scientific basis of saying this, but it's just through the years, I would say the majority of people are going to have antibodies to Lyme. I know, there's studies. 95% of the world has antibodies to Epstein-Barr. We know that these things exist in our system at any moment.

What was the straw that broke the camel's back? Or in this case, what sensitized the microglia? And it's often times a head trauma, or it's some type of emotional trauma that just rocks your world. And I would say that's the number one trigger for microglial expression is head trauma or intense emotional trauma.

But there has to be an underlying infection, like a stealth infection that's just kind of laying there to take advantage of that inflammatory cascade. Then you end up getting this problem child of a chronic infection that's creating this microglial expression. And then people like you interview all the time that work for these people to try and remove the infection, or subdue it, or get someone into remission, you can have the infection under control but yet still have all the symptoms.

And that's why I wrote this book, because that presentation frustrated me as a chronic illness physician because Lyme is not a problem. Epstein-Barr, your numbers are better. You're not testing for it the way we test, but yet you're still feeling like junk. Well, then I found out that microglia can stay locked in and hyper-aware. And they will secrete these interleukins, and these TNF alphas, and all of these inflammatory cytokines that pass the blood-brain barrier that then communicate with the body's immunoinflammatory state. And then, all of a sudden, you feel sick, but yet the infection's gone, but yet you have all the same manifestations. And I think that's why I wrote the book.

[0:28:00] SCOTT: You say in the book that microglia can be like soldiers who remain on high alert and cannot disengage even after the war. Does that mean that the original trigger, the infection, the toxicant, the toxin for chronic microglial activation, could completely have left the scene of the crime? It's entirely gone? Which, in many cases, is probably not reality. But let's assume it's entirely gone. And that the microglia themselves are now the core issue rather than a symptom or manifestation of an earlier trigger. And if that's the case, where you think the triggers are largely mitigated and yet the microglia are still activated, does that then shift your treatment focus?

[0:28:49] DR. STREIT: I think what we want to make sure is we say if microglia become hyper aware. That's what I'm saying. We want microglia. We need to have them, right? And we want them acutely to help the brain as well. But it's that chronic phase that we want to limit. And what I have found just in the research is that they can stay on hyper-aware long after something is no longer affecting us.

Now, I would agree with you. We're never going to see Epstein-Barr leave. The virus is going to be in our body. We're going to have antibodies to it. It's going to be latent somewhere in the nervous system. I think the same thing is probably true for Lyme. We can live a normal, healthy life, but it's there like any other bacteria in the body.

And so, if it's there, the microglia are seeing it because we still have antibodies floating around. And so, they still get activated in a way that continues to secrete cytokines that increase that inflammatory process. And so that's the goal. It's a co-treatment, right? Someone comes here to our office, and they're here for Lyme, or they're here for some mystery illness. It's a part of our process. It's not just you're only here for this situation. No, we're going to look at the entire body as a whole.

[0:30:17] SCOTT: You've said that microglia are bodyguards, essentially the brain’s maintenance crew. They have many roles that you outline in the book, including immune defense or surveillance, clearing away of debris, supporting neurons, pruning synapses, repairing damage, monitoring and communicating with other surrounding cells, and modulating brain activity.

Let's talk a little about what the microglia do when they encounter an infection, or a toxin, or some cellular debris. How do they respond to that? How do they remove that trigger, or danger, or insult? Do they hand it off to some other cell? What is that process?

[0:31:01] DR. STREIT: All right. We have two versions of microglia. The M2, which is the anti-inflammatory. It's what we call ramified. It has these nice, long, spindly arms like that monkey, where it uses its arms, its legs, and its tail to climb around the tree. And so, they're very thin, skinny, and they can go from branch to branch very easily. That's that ramified, non-threatening microglia.

Then, all of a sudden, if they find something, or they're triggered by a cytokine, or they're triggered by a hormone, or they're triggered by something, or trauma, they actually become amoeboid-like. Those arms get really, really swollen and thick, and they start grabbing a hold of things and ingesting it. And that's where that phagocytosis comes in. It actually breaks down whatever it's finding inside of itself, and then it's actually releasing more cytokines to recruit more cells to the area to clean up that area.

Now the problem with that is, is chronically-activated amoeboid-like phagocytic microglia. That's a mouthful right there. What you're going to find is that they start accidentally breaking good neural synapses. They start degrading appropriate synapses, and that's what leads to brain fog, cognitive decline. Further down the road from there, we get the Alzheimer's, and the dementia, and all of those types of things.

And now, I don't want to scare people. I think it's important just. Because you've had Lyme for years, doesn't mean that you're going to go out and have Alzheimer's. I'm not saying that. But what I am saying is, is that in every Alzheimer's case, they're finding activated microglia, and in dense populations. And I think that's important to see.

[0:32:58] SCOTT: You say that chronic microglial activation is like an engine that, when left unchecked and unmaintained, leads to cumulative wear and tear. Can we think of addressing microglial activation kind of like the bucket analogy, where there's many contributors or triggers that overflow the bucket and eventually then lead to symptoms? And the goal then is to create enough margin in the bucket so that it's not overflowing, so that our symptoms are no longer present. Or do we need to find and mitigate every possible trigger that an individual patient might have to stop that chronic microglial activation?

And then building on that, how far down the treatment path of someone with complex chronic illness, many contributors or triggers, do you have to go before the microglia eventually kind of stabilize, shift back to that more health-supporting M2 scenario? How readily do they shift back and forth? And are all microglia in the same M1 or M2 state at the same time? Or can we have microglia in different parts of the brain and spinal cord that are behaving in different ways?

[0:34:13] DR. STREIT: The way I understand it is, when we have microglial activation, it's not just one cell gets turned off and then it convinces every other microglia to become active. I don't find that in the literature at all. I like your bucket analogy. I think that's important. And I don't think that we need to focus on every single trigger. Because the body doesn't look at triggers in that way.

Yes. Okay. We have mold sufferers. We have Lyme suffers. We have Epstein-Barr sufferers. We have CIRS, and CRPS, and all of these named categories. But what is the underlying factor of every single one of them? Cytokine release and inflammatory signals. And so, if we can reduce cytokine signals, we can reduce microglial expression and activation. It's less finding all the triggers and more calming the terrain.

[0:35:16] SCOTT: Let's talk a little bit about their role in pruning synapses. What does that mean? What does it mean in terms of our memory, negative thought patterns, normal brain development, neuroplasticity, adaptability? How do the microglia determine what to prune? And can they both prune too little and too much? Can they essentially lose their discernment similar to molecular mimicry, with an infection driving autoimmunity? And with that loss of discernment, prune synapses that are beneficial or important. And can that over pruning itself then lead to complex chronic disease states or conditions where that aggressive over pruning is actually leading to other problems?

[0:36:12] DR. STREIT: I kind of look at an analogy kind of like if you open up your refrigerator, right? And if you have kids, there's stuff all over inside there that you're like, "What? When did you make that? And how old is that?" Right? And so, at least in our refrigerator, this is the way it is.

In a classic state, when you open that up, you're starting to prune in an M2 state, right? We're pruning. We're taking out the diseased foods. We're taking out the smelly foods. We're organizing everything. And this is how the brain consolidates memory. It's how it helps new neural connections. We look at this as like, "Okay, let's remove the things that need to be removed." And it's different chemicals that are at play that the microglia say, "Okay, that needs to be pruned away." Or that particular branch is no longer being used, it releases a particular chemical. The microglia in an M2 state go over there and selectively prune that off. No different than looking in the fridge and pulling out what needs to be pulled out.

Now you're left with a well-organized refrigerator that you can see, and you can remember where everything is. And that's that memory consolidation as well. And so, we can look through the refrigerator, and we kind of have a picture of it in our mind because that's where the milk goes, that's where the tea goes, that's where this goes. You kind of have an idea.

In an under pruned state, you have the junk that's left in there. If you have an over-pruned state, you have no food, right? And so, you don't have the brain-derived neurotrophic factor. You don't have the glial-derived neurotrophic factor, and your neurosynapses aren't as healthy as they need to be. Then they start secreting cytokines or debris, and then that activates even more microglia. That's where that cascade in Alzheimer's or dementia starts to creep up, and then they lose memory, these types of things. I use analogy a lot, Scott, in what I do because I think it – I don't know. It resonates with my own brain more as well, versus the science as well. I hope that's okay.

[0:38:33] SCOTT: Yeah, it's great. As I read the book, I felt there was a lot of overlap between microglial activation and mast cell activation. And in fact, one of my colleagues, Brendan Vermeire, calls it microglial activation syndrome. How are microglia and mast cells similar or different? How are the triggers overlapping or not? And then is the treatment approach conceptually the same in that we are trying to calm the mass cells or microglia, while at the same time addressing the triggers to bring longer-term resolution of that activation state? How much, in your mind, conceptually, does microglial activation and mast cell activation overlap? And can mast cell activation itself be a trigger for microglial activation?

[0:39:31] DR. STREIT: Yes. Yes. And partially. I love that question. It's because there is absolutely correlation between mast cell activation and microglial activation. Absolutely. And there's a lot of crossover. And you'll see in our mast cells, we're going to look at – I look at it more like those are – I know that they're in the brain, but we're going to look at them peripherally, versus microglia centrally. And they're secreting all the same or a lot of the same cytokines as microglia are.

The question, though, is treatment-wise. There's even things that I've written in the book, like oleamide or honokiol that actually support both MCAS and microglial activation. And so, there is some crossover there, but they aren't exactly the same. They do have different factors that they promote. I'm not necessarily like your friend. I'm not an expert in MCAS. But I do understand that there is a giant correlation between the two. And I think working on microglial activation. Because what I found is that when you lower that, I do believe that it starts to lower that MCAS susceptibility as well. And I don't know which one is greater. And I think they both deserve a lot of attention.

[0:40:55] SCOTT: Dr. Neil Nathan, one of my key mentors, and Beth O'Hara, over the years have brought to our attention the connection to the limbic system, to the vagus nerve, the nervous system, tying that into mast cells, and kind of created this triad of healing being working on the limbic system, the vagus nerve, and the mast cell activation. We know the number of mast cells is higher in the limbic system. You alluded to the microglial portion of the limbic system as well.

And so, when we're thinking about the limbic system, the vagus nerve, is there a connection there that's key in microglial activation? When we think about the limbic system, is there a connection to the microglia? And is there a need for us to feel safer in our bodies, in our world? And that feeling of safety from the limbic system perspective, from the vagus nerve perspective, is that having a direct impact on how activated the microglia might be?

[0:42:07] DR. STREIT: Yeah. Microglia are extremely active in the limbic system. And in fact, honestly, anyone that's going through limbic retraining, whether it be Annie Hopper’s, or Gupta, or Caroline Leaf, any of those particular limbic retraining systems, honestly, this book, I think, would be a good one for them to read. Because neural networks that are set up in a chronic state, they're kind of caustic, right? Our mental state can increase the amount of inflammatory signals being released. Our stressed state will do that.

And so, you're right. Fear and safety are very important in the body. But we also know limbically that the limbic system, as our threat assessment and avoidance mechanism, it will keep you in the bed under the covers every day for the rest of your life because that's the safest place to be. And that's not living. All right? We have to stretch in order to grow, right?

We have to get up in the morning. We have to go outside of our room. We have to eventually walk outside. We have to walk in the grass for those people that have Lyme. And for a lot of them, that's really hard to do. And obviously, you have micro exposures along the way that support this is a safe practice, this is okay, all of these types of things. And lowering that stressed state will reduce microglial activation.

But it's important to know that when we look at those new neural networks, that's a neurogenesis that's happening. That's new nerve growth and new synapses when we start to rewire the limbic system. And microglia play an essential role in that process. They're BDNF, GDNF type state. They're releasing these growth factors that are supporting that appropriate state.

If you have microglial activation going on, it's going to be a lot harder for you to utilize your limbic training practices because you don't have the growth factors there in abundance that you really want. And correct me if I'm wrong, Scott. I haven't seen any limbic retraining program speak about or talk about nutritional understanding with regards to microglial activation.

[0:44:41] SCOTT: I don't think so either. But what I just heard you say was implementing some of these strategies to calm the microglia could be very synergistic with implementing one of those limbic retraining programs.

[0:44:53] DR. STREIT: Absolutely. Absolutely.

[0:44:55] SCOTT: When we think about Lyme, co-infections like Bartonella, Babesia, have you seen any one specific vector-borne infection that is more commonly a significant driver of microglia activation? And do you find that they can ultimately get to the point that they don't need ongoing antimicrobial interventions to keep those microglia in their more anti-inflammatory M2 state? Or do you find that some people need longer term or even lifelong support for those triggers of microglia activation?

[0:45:33] DR. STREIT: What I have found is it comes down to two or three different things that I've really noticed over time. Mold toxins are an issue. And I think they're a big issue because your body doesn't get rid of them. And I love Neil Nathan's work. And essentially, lack of better terms, chelating mycotoxins out of the body, I think that's very important. Looking through his work to figure out how to appropriately nutritionally remove these mycotoxins, because they're constantly creating a problem in the body. Yep, Toxic. It's a great book. Great book.

The other aspect, I didn't really write about much in the book. It's actually Mycoplasma. I found that that is creating a large issue for the body. Now, interestingly, what I found in here is that it is a lung issue, but yet it's more of like – the way I kind of explain it to my patients, when I find it on them, is it's almost like lung-associated biofilms. And it's preventing the exhalation of toxins.

And I talked to everyone about you have four routes of detox in the body. Respiration, perspiration, defecation, urination. And women, if they're childbearing, they have menstruation. They have a fifth detox route, which is incredible for their bodies. But the number one route, the 70% of all detox is through the lungs. And so, if we have this Mycoplasma that is preventing our lungs from detoxing appropriately, it's building up inside the body.

This is what I found, even a little bit before COVID, but it really came to light post-COVID, because we have what I called the tidal edema. It basically upwelled everything that the body had tried to figure out, and it just came to the surface. And then once COVID was gone, you're left with the massive amount of debris and trash that now the body has to create a response to get rid of. And Mycoplasma is one of those things that just popped up. And I think that's a bigger factor than most people are thinking it is. And Lyme and Epstein-Barr are kind of tied, to be honest with you.

[0:48:02] SCOTT: I totally agree. I definitely see Mycoplasma a lot, and probably isn't something that's discussed much I think initially from the work of Dr. Garth Nicolson is where we started to learn about it. Did a podcast on that many years ago. But I agree, it's an important one.

The world changed in March of 2020 with the COVID pandemic. Wondering how COVID's been another layer in microglial activation. Do you find that it's more persistence of the virus? Do you find that it's more spike protein as a toxin? And have your patients that have had microglial issues related to COVID been more from the wild-type exposure or those that had the COVID vaccines? Are there specific tools that you're finding helpful in mitigating either SARS-CoV-2, or the spike protein thinking kind of in the realm of spike protein binding strategies?

[0:48:59] DR. STREIT: Yeah. I've come across Augmented NAC. I've come across different other binders, if you will, or neutralizers of spike protein. I don't use Augmented NAC in the clinic yet. I still have questions about how they're augmenting it. I believe it. I read the research, but I just haven't used it in the clinic yet.

I would say across the board, the person that didn't get the vaccine, they're better than those that did have to get it or chose to get it. And it has to do with that spike protein machinery that just is now a part of their body. And that's one of the strategies I use for that, Dr. Ardis talks about it at length, is nutritional nicotine. And I'm a huge fan of that. In fact, it supported my ability to get a little focused and finally finish one of the five books that I'm in the middle of writing right now.

I look at that and I think, "Okay, it did help with that." It's non-addictive, anti-inflammatory, neurosupportive. Microglia respond to it really well. And it puts them into that M2 phase. I think it's a winning combination. Some augmented NAC nicotine, and then other strategies like Andrographis, or Quintessence, things like that.

[0:50:28] SCOTT: Yeah. The nicotine conversation is definitely interesting. Dr. Jill Crista has talked about it in mast cell activation, in POTS dysautonomia, in Ehlers-Danlos syndrome. I definitely think there's a lot of ways that that could be helpful for people.

We see many complex chronic conditions these days such as autism, PANS/PANDAS, MS, Parkinson's, ALS, Alzheimer's, Schizophrenia, even depression and anxiety. You say in the book that chronic microglial activation contributes to neurodegenerative diseases by promoting persistent inflammation and excessive synaptic pruning, leading to cognitive decline and the continuation of complex chronic illness. How do the microglia both potentially create or drive, or potentially help to bring resolution to these more significant crossing into neurodegenerative disease conditions?

You've said that protection can turn to fire. So, how much of a role does chronic excessive microglial activation play in these complex chronic illnesses? Does the location of where in the CNS, in the spinal cord, in the brain the microglia are activated have some role in which condition may manifest? And how much of a role do we think microglia activation play in complicating conditions like Lyme, mold, and even CFS/ME.

[0:52:01] DR. STREIT: When we look at – when I was reading all of the literature that I was reading, a lot of it had to do with neurodegenerative diseases. And when we look at Alzheimer's, or we look at, more specifically, dementia, or frontal temporal dementia, I would have to say there is a driving factor with M1 microglial activation in those particular issues. Same thing in autism.

I don't know enough about ALS to say that I'm assuming that microglia have a role in that, but that's more of a lateral sclerosis. I don't know if they're as affected in that. But when you look at all of these, something to think about is also our omega-6 to omega-3 ratios. We know in someone that has a high omega-6 to omega-3 ratio in their body, their microglia are a little bit more primed than another person.

I forgot to mention that's another way that we can kind of look at the inflammatory state shows microglial activation. Not necessarily that it's a sign of microglial activation. It's about the inflammatory state. Each of these, there's been research. For instance, schizophrenia, 70 to 1 omega-6 to omega-3 ratio. And if we can start working with anti-inflammatories lowering microglial activation, the question is, is can we start to reverse some of these neurodegenerative diseases? And I think we can.

Science isn't there yet, but they are studying. They're studying things like 40 hertz. In the book Angels and the Assassin, it talks about they created Alzheimer's mice. And in those mice, they used a fiber optic cable into the center of their brain and flashed light at 40 hertz. And they had plaque removal of about 90% in a short amount of time. There was plaque removal.

Now, what removed the plaques? The light shining in the area switched the M1 to an M2 state. The M2 state then cleaned up its mess. And I think that's incredible. And that's what really excites me. Now, I wish it was sooner than later because of my own mother-in-law having FTD. I think in the next 10 or 15 years, we're going to have frequency-based correction of neurodegenerative diseases, and at least in that realm of things.

And I do believe, we look at Parkinson's, it's substantia nigra. We look at depression is in different centers of the body. Anxiety is in different centers of the body, the frontal cortex. I do think that wherever our microglia are centered and active probably has a role in what it is that you're suffering from.

[0:55:01] SCOTT: One of the cool things, my full body red light panel has the option to pulse at 40 hertz, which is an additional benefit of doing full body red light, right?

[0:55:12] DR. STREIT: Yeah.

[0:55:13] SCOTT: What role do microglia play in autoimmunity? Are the microglia a contributor to autoimmunity? Have they themselves lost discernment and potentially are then attacking healthy cells in an attempt to protect us that really has gone awry, creating localized autoimmunity in the central nervous system? Or is it more indirect in that they're producing cytokines, interleukins, reactive oxygen species, which are then driving or contributing to more systemic autoimmunity? What is the role of microglia in conditions like rheumatoid arthritis, lupus, Hashimoto's, Graves, and other autoimmune conditions?

[0:55:56] DR. STREIT: Looking back with what I've looked at through patient labs and stuff. Vibrant America has a neuro – an autoimmune neuropan…

[0:56:09] SCOTT: Neural Zoomer.

[0:56:10] DR. STREIT: Yeah, the Neural Zoomer. And looking at that, this is where I found anti-alpha-synuclein. I found other autoimmune categories that scare the heck out of it because their central nervous system autoimmunities. That's Parkinson's at age of 30, these are not good things to want to see.

And so, understanding, seeing those tags of saying, "Hey, there's an autoimmune issue built in the CNS." Redoing those tests years later find that there's nothing there. That is to me a confirmatory situation that what we're doing is working for lowering microglial activation, and how microglia activation are affecting central nervous system autoimmunities.

Now, there are aspects of Lupus, of Hashimoto's, because there's a lot of cytokine issues with that. When I see that, and they activate our microglia in our brain – and remember, if our autoimmune panel, just an ANA, we can change ANAs. I've seen it many times. You go from 1 to 360 for Lupus, a speckled pattern, or whatever. And it's now 1 to 90, or 1 to 80, or that type of thing. And that's exciting to me because we're reducing some of those.

Now, I'd rather someone feel better and still have autoimmune than not have autoimmune but feel bad. You know what I mean? I don't ever suggest people go out and get a Lyme test once they start feeling better to confirm they don't have Lyme again. That doesn't make sense to me. Because the antibodies are going to be there. Why psych yourself out and just say, "Oh, it's still here." That's just a limbic issue. Then, all of a sudden, we are feeling all the feels that we did when we had Lyme in the first place.

[0:58:16] SCOTT: Let's talk about the external environment as a contributor to microglial activation. We could think about mold, we could think about mycotoxins. Even in the book, you mentioned air pollution. Is exploring mold in the environment something you commonly have your patients do? And then extending that toxicant conversation further, heavy metals, pesticides, chemicals, plastics, and other toxicants that could impact the state of our microglia, how much of a role does detoxification and drainage play in mitigating chronically-activated microglia?

[0:58:55] DR. STREIT: Yeah, I would always say that terrain is king. If we can clean the terrain, we can do about anything, right? Our bodies are designed to heal themselves. And the terrain is a problem in most of us because of how many toxicants are in our environment or in our mind. We have some toxic thoughts going on that we need to capture and remove. And we have some toxic people in our life that we need to, if we can, remove our self from. And then we have a toxic environment.

When we look at the terrain, we want to build drainage networks. We want to have the French drain of all French drains draining our marshy backyard, right? That terrain. And so that to me is pinnacle when it comes to working with any person irregardless of a microglial activation or not. Because what we find is that if everything is at that level, if we can get to that level where we have a clean terrain, everything seems to just work better.

Removing pesticides, absolutely. Removing mold, absolutely. I talk about mold because it is a big problem. But also, it's in our environment every day. And in fact, if you've ever heard of homeopathic constitutions in the body, where we have Aspergillic, or Mucor, or Penicyllic constitutions, these are our communication networks. And so, we technically need these non-Candida yeast in the body anyway.

There are aspects to our environment that are good for our internal environment. But mycotoxins are a problem, yet they're not every problem known to man. It gets really hard, especially when you're in mold toxin support groups, or Lyme. It gets to be like, "This is my moldy home. What's yours look like?" And it almost becomes a competition of who's got the moldier environment, which is wild to think about.

But yes, if you're going home and you're in a moldy environment, it's going to be really hard to heal. But it's no different than if you go home to a toxic environment from either family, or perfume, or Air Wick fresheners in your house. It's an environmental challenge that needs to either be removed or mitigated somehow.

[1:01:30] SCOTT: I live in Colorado and do a lot of hiking. I'm amazed how many people feel the need to put on perfume to go hiking in the outdoors.

[1:01:39] DR. STREIT: You can smell it from 5 miles away. I mean, maybe that's what detracts bears. I don't know. But yeah. No. I used to live in Colorado Springs. We'd be up in the mountains. I mean, I mountain bike four days a week, and it always amazes me. I'm like, "Why am I smelling vanilla fields right now? This doesn't make any sense."

[1:02:00] SCOTT: I just did the Manitou incline a couple months ago, which was just a tremendous experience.

[1:02:06] DR. STREIT: Yeah.

[1:02:06] SCOTT: You say in the book that microglia can create reactive oxygen species. That's free radicals. Many people with chronic illnesses are dealing with an oxidative stress burden. How much of the body burden of oxidative stress do you think is correlated to the microglia? And then are there specific interventions that you might implement to reduce reactive oxygen species to support better redux balance? And is that reactive oxygen species intended to be the response to an infection, where reducing it potentially is slowing the response to a trigger? And when we're thinking about free radicals, I'm wondering if you've explored the implementation of hydrogen water or hydrogen gas inhalation for that oxidative burden.

[1:02:59] DR. STREIT: I would look at microglia as more like the gasoline in a spray bottle, versus the overall arching cause of ROS. You have a burning field, and the firemen come out and they put that field out, but it's smoldering. But if we don't turn off the microglial activation, it kind of sprinkles a little bit of gasoline on the fire. And that's that spark, right? That's that silent spark that then everything starts up again. And so, I would say that microglia are more on the persistence of the problem and not the cause of the problem.

When we look at mitigating factors with ROS, we use hydrogen. I use hydrogen at home. We inhale hydrogen. We do it an hour a day in my home. We do it for 30 minutes, mixed with a specialized lymphatic system that we have here. We do that at the same time with that. Hydrogen is a very important factor in the detox of the body. Really breaking down those reactive oxygen species, the hydroxy-free radicals to be more specific.

When we look at other factors, I mean, we could look at methylene blue. I look at methylene blue with kind of my eyes wide shut kind of, because it's still a synthetic dye. And I'm still having a hard time in my – even though there's probably 1,200 studies on the effectiveness of methylene blue, I have a hard time with it. But it does reduce ROS at the mitochondria. And I think that's extremely important and extremely impactful.

And I do know that it supports taking M1 phaged microglia and morphing them into that ramified M2 phase. And so, it calms that monkey in the tree down. And so, I look at these types of things and it excites me for what's coming through the advent of technology through 40 hertz vibratory sight lasers. I think that we will eventually have the ability almost like the – what is it called? The laser knife for cancer? Brain cancer? I'm thinking something like that where they can resonate at 40 hertz at the level of the substantia nigra, or the Alzheimer's, or dementia. And we can start really affecting the microglia from an external to internal point using technology. But we're not there yet that I know of.

[1:05:40] SCOTT: The methylene blue conversation, I was going to ask about that a little later, but that's interesting that you are exploring that for calming potentially the microglia. I think it also is helping some people with Bartonella, which could be a trigger for microglia as well. You talk in the book about another dye called Brilliant Blue G as well that people can learn more about when they take a look at the book.

Let's talk a little bit about the gut. How do you know when a patient has a gut-brain microglial axis-driven condition? Does gut inflammation from foods, from microbial dysbiosis, intestinal permeability, does that impact microglia in the CNS? Does microglia activation itself have any impact on motility, intestinal barrier function, even on microbial diversity potentially? And then talk to us a little bit about lipopolysaccharides, endotoxins. Are those activators or triggers of microglia?

[1:06:45] DR. STREIT: When we look at the gut, I always discuss the importance of gut microbiome with our patients. It's a part of one of our six nodes of the BioRestorative Method. When we look at that, I draw a picture out, and I talk about the cells of the lining of the gut, and how they eat short-chain fatty acids, and primarily butyric acid or propionic acid. Butyric acid is one I use a lot of in my clinic. And that butyric acid goes in, and it actually gives nutrients to the lining of the gut.

And I talk about the lining of the gut. Because if you have leaky gut, you have an inflamed gut. If you have an inflamed gut, you have cytokines that are released in the body. If you have an inflamed gut, you're more likely going to have bacteria, and the like that are supporting the creation of more glutamate than other neurotransmitters. That leads to anxiety, which obviously is a brain-associated situation.

We have glutamate that's being released, and that actually communicates with the brain, and that increases activation of microglia as well. There is a direct link between the gut and the brain. And we want to utilize acetylcholine as a, in a way, reducer of microglial activation. But glutamate itself is going to be a problem. And that kind of leads me into a little bit as a side note with calcium channel activation.

We have these voltage-gated ion channels in the body, and calcium is one of them. And that's where EMF and electromagnetic radiation effects. It opens up those calcium channels. And those calcium channels depolarize, and it secretes the neurons and whatnot. Start to create or secrete glutamate. Then glutamate breaks down, and it becomes – in an offshoot, a byproduct of the glutamate breakdown is ammonia. And so now we have an ammonia accumulation in the brain in different areas causing inflammation, which then depolarizes more glutamate. So, we have a problem. And that's every time we stick our cell phone to our ear, we're getting calcium channel ions to release locally. And so that's where EMFs and those types of things play into microglial and gut-associated changes and challenges.

[1:09:22] SCOTT: When you see that someone has – and now we can do some testing. Vibrant has some options. When you see someone has high glutamate, how do you approach reducing that glutamate excitotoxicity?

[1:09:34] DR. STREIT: Whenever I work with leaky gut, I don't go right to glutamine powder to support someone's leaky gut. And the reason why is anything that's left over in the glutamine becomes some type of glutamate that then can stir the pot, especially in those with anxiety, or depression, or microglial activation, which is pretty much anyone that has a chronic illness.

I look at utilizing – I don't use GABA either that much, just as a kind of a side note. Because whenever I look at GABA, I think, "Okay, the body should make this on its own." If I raise GABA to a certain point, it will actually reflexively raise glutamate as well, as it's teeter-tottering its homeostatic nature. If my glutamate is high, you've kind of broken through that homeostasis of glutamate, and GABA is low.

If I give you GABA, this side might not be broken. If I gave you 500 milligrams of GABA, that could actually raise our glutamate as well. So, I want to make sure I don't do that. So, I give a gamma amino, which is L-Theanine. It's a glutamate scavenger. It does pretty well at lowering dietary glutamate, as well as endogenous creation of glutamate. And then I give butyric acid.

Now, people might put those two together, gamma, amino, butyric acid. That's GABA. But it's not in its one connected form. It's brick and mortar. The body can use the butyric acid to support the lining of the gut to heal and seal the gut. And then it's going to use L-Theanine as a way to reduce glutamate, that is going to heal and help the inflammatory environment of the brain and the gut. And then whatever's left over becomes GABA. And the body uses it the way it's supposed to.

LPS, or lipopolysaccharides, are basically microbial bits that are extremely inflammatory. And if you want to activate microglia in a lab, you pour some LPS on it. It'll instantly do it. LPS causes Alzheimer's. That's how they're creating, in a way, Alzheimer's mice, is they're injecting them with LPS, high-dose LPS. And that's creating Alzheimer's.

We look at LPS as an extremely toxic brain-associated neuroinflammatory agent. And so, if we have LPS in our environment, that's very toxic to our bodies. I do think that somewhere along the way, maybe that will be a target for intervention is how do we melt LPS? How do we get rid of LPS kind of like microplastics? How do we get rid of microplastics? That will be an invention, probably in the next 10 years, as well, which is exciting to know that we can fix maybe a lot of problems that humankind created with microplastics.

[1:12:45] SCOTT: You've said that chronic microglial activation influences systemic inflammation, metabolic dysfunction, and cardiovascular health by perpetuating immune and hormonal imbalances. I want to focus just for a second more on the endocrine hormonal side of things. How does microglial activation vary by gender? How is it impacted by hormones? When we're thinking about mast cells, we often think of estrogen as a potential trigger, progesterone as a potential stabilizer. When we're thinking about microglia, is estrogen increasing inflammation in pain? Is it protective or anti-inflammatory? How do hormones impact microglia? And is there a place for bioidentical hormone replacement therapy, or BHRT, in supporting the microglia?

[1:13:34] DR. STREIT: I'll kind of like go right off the bat here in the gender differences of microglia. It comes down to receptors of corticoids, glucocorticoids on the receptor of microglia. Women's and men's microglia have the same amount of receptors, but women hold on to the glucocorticoids longer. Your stress levels, as your cortisol rises, women can't clear that as quickly as men clear it. That's just the nature of it.

And so, we look at that. And so, the longer that's there, the more likely we're going to have an inflamed M1 state in microglia. Because high stress, high cortisol will convert the M2 to an M1, right? And so, we want to make sure that we reduce overall cortisol exposure in a safe and effective way. But that is the difference between men and women.

And I don't know. I write in the book where I think it has to do with why, in my office, 70% of my patients are female, if not more than that. And is it that cortisol? You can't break that cortisol down fast enough? And so, then it activates that inflammatory cascade in the body and in the brain. I don't know. But that's my theory behind it.

When we look at estrogen's role – now, when researching this, it really did change the way I kind of approach estrogen. Because back in my earlier years, I was extremely anti-soy, anti-flax, anti-estrogen in any way, because all it does is just cause problems and chaos. And then it was explained to me a little bit differently. And then I learned that estrogen is anti-inflammatory when it binds to microglia.

I'm thinking, "Okay, well, if microglia, when they bind to estrogen, increases your anti-inflammatory state. Is this one of the reasons why, when women go through the change of life, that inflammation starts to creep up, cardiovascular issues start to creep up? All of these new set of symptoms start to creep up. Is it purely microglial? No, absolutely not. There's so many receptors of estrogen throughout the entire body. But is it a something to think about?

And that's where BHRT comes in with utilizing whether it's topical, estriol, or a bioidentical estriol. I'm not opposed to those things. I'm not opposed to using – progesterone reduces an M1 to an M2 state. It's pretty much always anti-inflammatory. And so, I'm a big fan of progesterone. In fact, I'm like I said, I'm a chiropractor, so I don't have the ability to prescribe. But if there are three things I could prescribe, it would be progesterone, LDN, and Nature-Throid, that type of thing. Because I feel that those are all really good avenues for supporting the body's hormonal system without creating a problem.

[1:16:48] SCOTT: One of the other things that is a great resource in the book is Dr. Streit has outlined the SPARK diet for optimizing microglial function. Looking at things like olive oil, omega-3s, healthy nuts, and polyphenols. SPARK stands for simple stabilizing foods, polyphenols, anti-inflammatory fats, restorative minerals and micronutrients, and ketone-supporting strategies. Great resource in the book for people that want to learn more about that.

You talked about EMRs and EMFs being a potential impact on our microglia as well. Wondering if there are any top strategies that you've found for reducing or mitigating the impact of EMR and EMF on our biological systems.

[1:17:36] DR. STREIT: Yeah. We utilize things like Safe Space in our office. We use QiFi, which it emits a mass amount of scalar wave that kind of mitigate intrusive EMFs. I personally will use Aires Tech, their pendants. I like those for me. Actually, Scott, I talk maybe a tiny bit about this in the book. I don't remember now. But I actually created an additive that goes into a – I work with a company called Quantum Vital Technologies in British Columbia. And we create all-natural skincare. And I use this additive into the skincare, and it's been showing a reduction of EMF exposure in skincare.

Anything you can do to distance yourself, because it really comes down to the power is how close you are, the field strength, right? And so, we need to just stay away from holding our cellphone. I'll talk a lot about the finger rule. Hold your cell phone right here. Because nobody likes to be the guy that's on speaker phone in the middle of – yeah. You're that guy?

I get it. There's some rules like that. Throwing on EMF-reducing strategies on your cellphone, on your electronics. I've got those stickers on all of my devices as well. Anything you can do to mitigate, I think, is appropriate. Yep, you've got it all. I've got my Aires Tech on. I've got my safe space on my laptop and all of that.

[1:19:12] SCOTT: The only thing I will say for people listening is reduction of exposure is still the cake, and all of these harmonizers and other things are the icing on the cake. I know Dr. Klinghardt has an E Shield cream. Maybe similar to what you're talking about as well. That's interesting. And I'll have to learn more and put that in the show notes as well.

Wondering if with people with chronic microglial activation, do you see the mental-emotional triggers being significant? You mentioned ACEs, or adverse childhood experiences, or events. And are you then finding tools like EMDR or other mental-emotional trauma strategies helpful?

[1:19:56] DR. STREIT: When we look at EMDR, if we can desensitize the fear, or the phobia, or the addiction, that's all prefrontal cortex, that's all limbic system, right? It's amygdala, it's all of that. If we can kind of modulate the activity in those areas into a less stressed state, we're going to reduce microglial activation every time.

I'm a fan of EMDR. You had mentioned just a little bit ago Mark Wolynn's book. I've worked with Mark, and it was profound for me. And so, it really supported something that I needed support on, which then obviously lowers my stress level on certain factors. And so I'm a big fan of EMDR. You can use the Pulsetto, the vagus nerve stimulator. You can use a CES device. We use that one in the clinic. There's also Apollo Neuro, which I utilize. I like a lot of these tools to just really support that vagus nerve.

And you have to be a little bit careful on the vagus nerve. According to Porges, there's two routes. You got the polyvagal theory. You got the dorsal and the ventral. Social connection trumps all devices. You can have all the devices in the world, but if you don't have social connection, they're going to be limited on their ability, I believe.

[1:21:22] SCOTT: Let's talk a little bit about chronic pain. Conditions like CRPS, which you mentioned, or complex regional pain syndrome can be debilitating. The couple of clients that I've had that have dealt with that, it's just a really, really tough thing to deal with. We also know fibromyalgia, which was one of my earlier diagnoses many years ago. How does chronic pain tie in with central sensitization with microglial activation? And in patients with chronic pain, are you then focused both on the microglial activation, as well as finding tools simultaneously to help them symptomatically with their pain?

[1:22:01] DR. STREIT: Absolutely. When we look at central sensitization, to explain to people, that's when an area – for instance, if my elbow hurts, and it chronically hurts, then is the pain in my brain, or is it in my elbow? A lot of people are like, "Well, it's in my elbow." Like, "Well, maybe the original injury was in the elbow, but you're feeling it in your brain, right?" And so, if my elbow hurts, it's firing a very specific area in the brain.

Central sensitization is, when that hurts for a long time, it starts to spread. It goes up to the shoulder, now it's in the wrist. Right? In the map of the brain, it's called a homunculus. It's kind of a weird artist rendition of different sensory aspects of the body, but it starts to expand into other areas. And so, when we look at microglial activation, that is a problem because it does increase central sensitization. And then microglia gets sensitized as well, and then they start acting inappropriate. And so, I believe that we can reduce central sensitization. And I believe that we can actually help the sensitized microglial cell become less and less sensitive as well. And that's this entire book is associated with, with reducing its activation's hyper alertness.

[1:23:26] SCOTT: Let's talk a little bit about the blood-brain barrier, and how the breakdown of the blood-brain barrier may then allow some triggers into the brain, into the nervous system that further activate microglia. Are you using any of the S100B-type testing to see how the blood-brain barrier is functioning? And are there specific things then that you might implement that are more supportive of healing or optimizing the blood-brain barrier?

[1:23:57] DR. STREIT: I don't necessarily test that particular. I mean, I'm not working on TBI or a lot of stroke pat – I mean, some of my patients have had strokes in the past. But I'm not working on a new stroke-type patient. I will look at things like CRP. I'll look at homocysteine. I'll look at fibrinogen. We can look at TGF-beta 1. We could look at our CytoDx panel, that type of thing. And so, we know that this inflammatory state is a problem.

And the way I look at the blood-brain barrier is we can add things that support the barriers of our cells, the barriers of our body. I talk a little bit about plasmalogens, ProdromeGlia, those types of things. I look at egg lecithin versus oil lecithin a modifier for barriers, cell walls, that type of thing. Because I like animal-based lecithins, because I feel like it makes more sense for the body to kind of more of a synergistic effect, versus using plant-based oil lecithins.

But I'm a fan of ProdromeGlia. I don't recommend it to a lot of patients because, honestly, it's kind of cost-prohibitive, unfortunately. But I do talk a lot about high-dose fish oil, in a 2:1 EPA to DHA ratio. 3 to 4 grams a day if their gallbladders can take it. I think that's important, because that's going to build the blood-brain barrier better than about anything.

[1:25:35] SCOTT: I've historically thought about seizures as potentially being related to Bartonella or to parasites. But I want to talk a little about the connection between chronic activation of the microglia and seizures. Is there a connection there? And then are there specific things that you would think about in terms of interventions to try to minimize those people that are dealing with seizure disorders?

[1:26:02] DR. STREIT: Yeah. When we have seizure disorder, that's going to activate microglia. And then once that microglia become chronically activated, it's going to create a sensitization for that person to have recurrent seizures. Because, once again, microglia are that little fire that keep the coals burning. It's not necessarily the fact that the seizure cause is caused by microglial activation. But yet, we know that the M2 state is going to be supportive of someone that has seizure disorder. We want to still lower that M1 activated state to an M2 to support someone with seizure disorder.

[1:26:46] SCOTT: It's a little bit of the chicken or the egg lecithin.

[1:26:50] DR. STREIT: Yeah, I like that. Yes, it is a little like that.

[1:26:52] SCOTT: I want to talk just very briefly about nitric oxide. There are many potential benefits of nitric oxide, particularly on the eNOS, or endothelial NOS side, where there are some potential concerns is on the inducible or iNOS side. You've said in the book that iNOS is the emergency flamethrower that's meant to kill invaders, but can burn up healthy tissues. You say that microglia can activate iNOS as well.

One of the advantages, as I understand it, of supporting the nitrate, nitrite, nitric oxide pathway is that we don't have that same potential for iNOS issues like we might have with arginine or citrulline. Wondering if you still think there is a place for supporting nitric oxide. Or if because of the potential iNOS issue in microglial activation, if you would stay away entirely from things that are taken exogenously to support nitric oxide in the body.

[1:27:55] DR. STREIT: We want to utilize that pathway. I mean, it's a pathway that's designed for us. But like you said, we want to do it in a very specific manner. And this is why I don't really use L-arginine. I don't use a lot of citrulline, because it goes down the pathway of that iNOS pathway. We can do beets, we can do green leafy vegetables because the gut microbiome is actually what breaks it down. And that improves your nitric oxide production. I'm going to look at it through that lens versus any other lens. I'm not going to give you nitric oxide boosters because of that.

Now, I do like things like Ipamorelin, or kava, or honokiol in moderation, in the right settings, because those allow us to convert away iNOS, which is kind of an interesting caveat of those particular peptide and nutritional products.

[1:28:52] SCOTT: Peptides have become a very interesting area in the last several years. They can really help with inflammation, modulating the immune system, supporting the brain. Are there any specific peptides that can shift microglia back to that health-supporting M2 state? And what's been your experience with tools like larazotide, BPC, Sermorelin, Ipamorelin, Semax, TA-1, Cerebrolysin when we're talking about microglial activation? And then any conversation these days about peptides? I would be remiss to not ask about your thoughts about GLP-1, semaglutide, or tirzepatide in terms of their role in supporting microglia.

[1:29:36] DR. STREIT: Yeah, peptides are a fascinating category of things. And I really started studying them. Now, I can't inject anybody. Part of my licensure, I'm not allowed to do that. But that doesn't mean I can't research the heck out of it and try doing these things on myself, or my loved ones, or anyone that's willing to try. Right?

What I looked through the research, what reduces microglial activation are two particular ones, BPC-157 and Cerebrolysin. Those both actually confirmed science that they reduce microglial activation. When we look at theoretically strong indication, but not necessarily peer-reviewed, so says the papers, are thymosin alpha 1 and Semax. Those both are able to reduce microglial activation pushing towards an M2 configuration.

Now, I believe that Sermorelin, as well as Ipamorelin, can do the same thing because of their introduction of growth hormone and how that's going to increase your BDNF. It's going to increase your GDNF, all of those types of things. But I don't have the scientific literature that will prove that.

When I wrote this book, and I have over a hundred cited references, it was important to me to speak in a way that medical doctors, us natural health and wellness, that we don't necessarily need a double-blind placebo-controlled trial to know something works. But I wanted that for them.

But larazotide, that's an interesting one, because larazotide – I've only found a couple areas that you can find this. But it's a pill you can take, and it actually is supporting the body's ability to reduce zonulin intrusion into the barriers. If we have zonulin in our gut barrier or in our blood-brain barrier, if we can remove that or reduce zonulin's impact, we can seal these particular barriers up. And I think that's really important to really look at these peptides, because I do think that they're the wave of the future.

[1:31:48] SCOTT: Any brief thoughts on semaglutide or tirzepatide in the microglial realm?

[1:31:53] DR. STREIT: Yes and no. Tirzepatide in micro doses have been shown to be pretty effective for the body. But quite honestly, with all of the issues that we're seeing with semaglutide and these other GLP-1 particular drugs, I'm reticent to commit to utilizing those quite yet. But I believe the safety profile of everything else that we're looking at here is pretty stout. And so, I'm not worried about those.

[1:32:28] SCOTT: When we think about immune modulation, if the trigger of the microglial activation was an infection, maybe even an environmental toxicant, can we reduce the microglial activation by modulating the immune response by balancing T-helper cells? Also creating more tolerance and discernment within the immune system. If we think about low-dose naltrexone, or low-dose immunotherapy from Ty Vincent's work, maybe even desensitization tools like NAET from Dr. Devi Nambudripad, do those fit into the conversation? If we modulate the immune system's interaction with these potential triggers, can that calm the microglial activation?

[1:33:13] DR. STREIT: It absolutely does. And that's why one of the reasons why I would love to be able to prescribe LDN is for that reason, because it is an immune modulator. I'm absolute fan of Andrographis. And Andrographis, as the herb, I think is an unsung hero in a lot of clinics that they don't realize like, "Oh, that had Andrographis in it." That's really what's working the best, right?

And so Andrographis to me is an immune adaptogenic herb. And when I say that, it's because it is antiviral, it is antibacterial, it's all of these things. But it's also in the realm of Lyme or Epstein-Barr, our bodies have become hyperimmune to – we don't get sick anymore, but we are affected by everything. The immunoinflammatory cytokines are just through the roof. Andrographis reduces those. And if it reduces those, it's good for the brain.

[1:34:15] SCOTT: King of the bitters, Andrographis.

[1:34:17] DR. STREIT: Yeah, king of the bitters. I love this stuff.

[1:34:19] SCOTT: You talk about sleep as being microglial medicine. Things like magnesium, glycine, theanine, skullcap, honokiol, oleamide, and valerian can help the microglia by supporting restorative sleep. Wondering if you can tell us just a little bit about oleamide. I've not heard of that before. How that ties into the endocannabinoid system? Do you also find that things like CBD or CBN can be helpful for microglia? And then adding to that, where does melatonin for NLRP3 modulation, inflammation modulation fit into the microglia discussion?

[1:34:55] DR. STREIT: Oleamide is a fatty substance that builds up in our nervous system when we are not asleep. It builds up as we are not sleeping. And what ends up happening is if we can build that up to a certain point, then the brain starts to say, "Oh, I need to break that down," and it stops breaking down anandamide. Anandamide, that's what actually binds to your cannabinoid receptors, which then allows for rest, relaxation, acetylcholine release, and you just kind of feel this calm effect.

Oleamide is a cheat code in the biochemistry. If we take oleamide, we upregulate the amount of that that's in the system. Then the body will say, "I shouldn't be breaking down this anandamide anymore. I need to be breaking down this oleamide." And then that leaves our CBN receptors and CBD receptors, CB-1 and 2 to be exact, open for recepting. And then we end up having that calm effect from that. That's how oleamide works.

When we look at melatonin, melatonin fixes leaky mitochondria, right? When mitochondria break down, it releases chemicals that upregulates our microglial activation. I like to use melatonin during the day. Now, that might sound really strange to a lot of people, but melatonin is night-activated for most people. Now, if you're a person that lives in a closed room, you're probably going to get sleepy if you take melatonin during the day. But I like it during the day because it's not going to mess with your endogenous supply at night. So, I like it in the day. It drains the brain. It increases the glymphatic flow, which supports getting rid of all the toxins in the brain.

[1:36:48] SCOTT: As Dr. Klinghardt would say, melatonin plus dark equals sleep. Melatonin plus light, not going to lead to sleep for most people.

[1:36:56] DR. STREIT: Correct.

[1:36:59] SCOTT: How often do you find oxygen fluctuations in people dealing with maybe sleep apnea acting as the trigger for microglial activation? Could a CPAP potentially be a powerful tool in calming microglia?

[1:37:14] DR. STREIT: All hypoxia increases inflammasomes. All hypoxia does, whether it's mouth breathing, or tongue falling back to the back of your throat, so you need a CPAP. Or you have biofilms in your lung that are not allowing for that expression of O2 to CO2, and likewise. Hypoxia increases inflammasome. Inflammasomes increase microglial activation. Anytime that we can introduce oxygen into the system in a controlled, appropriate manner, it's going to support microglial cells.

Now, HBOT is kind of an interesting category. Because, hyperbaric oxygen, we want that. I think that's great. But if you're not adding antioxidants to that, a ton of antioxidants, you can actually cause a little bit more oxidative stress in the body, which then increases inflammasomes as well. You have to be a little bit careful with some of these oxygen therapies.

[1:38:11] SCOTT: Maybe drinking some hydrogen water before we get into the HBOT.

[1:38:15] DR. STREIT: Yeah. Yeah. I like that. I like that.

[1:38:18] SCOTT: So, I'm just going to mention a number of interventions that you highlight in the book. People can get more detail there. I then have a couple of follow-up questions, but you talk about so many amazing things in the microglia realm. PEA. We've talked about low-dose naltrexone, many of the fats, EPA, DHA, resolvins, and protectins. You talk about maritime pine, plant stem cells, turmeric, curcumin, resveratrol, kava, Honokiol, theanine, sulforaphane. No lack of tools here. Vitamin D, vitamin B, magnesium, specifically threonate or taurate, apigenin, MCP, or modified citrus pectin, kudzu, ashwagandha, Andrographis, we touched on, luteolin, choline, fisetin, ketones, NMN as a precursor to NAD, butyrate, nicotine as well, so many others. Check out the book for that.

But I wanted to talk specifically about a couple of those items in more detail.

Of that lengthy list of potential interventions, are there a few top tools that you most commonly reach for? If I had to pick, I'd probably go with luteolin, low-dose naltrexone, maybe sulforaphane just because it has a lot of other applications. I do like PEA, Honokiol, and butyrate. In fact, I take all three of those every day. What rises to the top of your clinical toolbox for microglial activation?

[1:39:49] DR. STREIT: Honokiol, butyrate, nicotine, PEA, those are all on the top of the list. I'm also a fan of apigenin, and little less fisetin. Those are hard to get past the blood-brain barrier. But peripherally, they are a good flavonoid to use to lower inflammatory indexes in the body. But butyrate, for sure, and Honokiol are some of the best that I found. And fish oil. I mean, there's so many. To look at all of the research on all of those and figure out what my favorites are, those would probably be my tops.

[1:40:23] SCOTT: And LDN, which you highlighted a couple of times as well.

[1:40:25] DR. STREIT: Yeah, but I can't prescribe that. It can't be one of my top favorites, but it is in there.

[1:40:31] SCOTT: Interestingly, a lot of the things in your list for microglial support also support mast cells. So, it's kind of nice to have a lot of those that are twofers essentially. Wondering if you've explored fucoidan at all, which also has beyond many, many other benefits appears to be beneficial for the microglia.

[1:40:52] DR. STREIT: I have not. No, this is new to me. Send me some information on that.

[1:40:57] SCOTT: You mentioned choline in the book. You talk about alpha GPC. Wondering what your thoughts are around phosphatidylcholine. Does that have a role in supporting microglia? And have you seen specifically people doing more IV phosphatidylcholine protocols having less activation of their microglia?

[1:41:16] DR. STREIT: Phosphatidylcholine, it's kind of a tricky one with regards to microglial activation, because it can actually technically create a pro-inflammatory process. But it also does it on the anti-inflammatory. I don't do a lot with phosphatidylcholine for that reason. Now, if I've worked on someone for a while, and they have post-concussive syndrome, and I have them on other therapeutic interventions that lower microglial activation, I'm going to use phosphatidylcholine because it is good for the brain in those cases. But I would rather use something more plasmalogen-based to really support that in that way. For me, anyway, that's going to be either ProdromeNeuro, or Glia, or your high-dose fish oils and egg lecithin.

[1:42:04] SCOTT: I definitely am a huge fan of ProdromeGlia. That's my favorite of his products.

Fisetin is a senolytic. Apigenin is a senomorphic. How does cellular senescence enter the microglial discussion? Can supporting autophagy potentially remove any of those long-lived microglia that are overly primed or activated? What's the difference between a primed microglia and a senescent microglia? Or could it be that generalized cellular senescence in the body itself is triggering microglia?

[1:42:41] DR. STREIT: When we look at senolytics, that's going to support the breakdown of weakened cells. And xenomorphic is going to reduce the inflammatory cytokines generated by dying cells. Right? The thing is, irregardless of our age, the aging cell, whether it's a microglial or anything else, you're going to secrete a cascade of inflammatory signals. And it says, "Hey, remove me. Remove me." Right?

The more senescent a cell is, the more chaos it's going to deliver as it's dying, as it's being phagocytized, and all of that. I believe this is where kind of like keto flu or methyl flu come in is because we have these nutrients that support our ability to break down senescent cells. And then as they're breaking them down, they're screaming, and crying, and kicking on the way out. Right? We end up getting a response for that.

Now, interestingly, in the world of microglia, senescent microglia, like you said, are those old guard that have been around for quite a while. The sentinel on the wall for years and years and years. I don't know if – because I have a little bit of conflicting information in some of the science. Some science would say that they can actually renew themselves from a senescent state, which is pretty cool. And others say that as they as die like any other cell, other microglia come in, break them down, utilize their parts and pieces, and move on. I'm a little hesitant in saying one way or another what a senescent cell can do. But a primed cell is basically priming the pump. It's ready for action. Senescent cell is that Chevy that you have a neutral and you're at 4500 RPM not going anywhere. It's just spitting out smoke and oil.

[1:44:45] SCOTT: With many of the supplements and herbs that we've talked about, wondering if there's any combination products that you commonly reach for. In the mast cell world, there's lots of mast-cell-focused products now that combine several of the top materials, herbs, supplements, and things like that. Are there any combination supplements aimed at microglia?

[1:45:07] DR. STREIT: Not specifically at microglia. That's something that I was thinking about actually creating. But the one that – because I use Honokiol specific. I use apigenin specifically. I use fish oil specifically. But I just came across Troscriptions, their sleep, Rest Ease, or something like that. And it's got Honokiol, agarin, CBN, CBD. And I'm like, "All right, this sleep aid is going to actually be a supportive agent for microglia, for sure."

[1:45:40] SCOTT: Yeah, I think that's Dr. Ted and Dr. Scott that are behind that company. I know they have a number of good things.

[1:45:45] DR. STREIT: Yeah, that's a good one. And so that one's been kind of in my repertoire of talking to people about going out and getting that.

[1:45:54] SCOTT: So, as we get down to our last two or three questions here and wind things up, and I know this is not in your scope, but you do cover it some in the book. Are there any tools in the pharmaceutical realm that you think could work better than some natural tools? When are steroids or biologics potentially helpful in this realm knowing that they also might lead to less immune containment of chronic infections? You talk about tools like Humira, hydroxychloroquine, doxycycline, minocycline, and others. And I wonder if when someone has chronic Lyme, and they're taking maybe more minocycline specifically, and have a beneficial effect, is that because they reduce their infectious burden, or is that because they have calmed the microglia? And then adding on that, where does ivermectin potentially fit into the microglial conversation?

[1:46:45] DR. STREIT: With the biologics and the pharmaceuticals, none of them right now have an ability to not create a lot of other chaotic problems in the body. They're still trying to figure those things out. Hydroxychloroquine, it has a pretty darn good long track safety record. Minocycline, other than it being low-dose minocycline, I think is more appropriate for a microglial or its anti-inflammatory effects. Those types of things I do believe will support microglia.

When I look at the advancements in technology, I get excited about microglia transplant therapy, which is something that's being researched. How do we introduce fresh, new microglia into a disease east state? Can we remove ones? Those types of things. I think that's interesting. But I would personally stay away from a lot of the biologics-type situations and look at more of the minocycline.

For instance, my wife, when she got bitten as a 9-year-old and started getting issues, didn't really know that it was Lyme. But she went on antibiotics for her acne at the age of 13. And she had no problems until she came off the antibiotics at 23. I do believe that it wasn't necessarily killing the bacteria off, but it was supported her inflammatory pathways to the point it just was under the radar.

[1:48:20] SCOTT: Any role for ivermectin in this conversation?

[1:48:25] DR. STREIT: Yeah. I mean, ivermectin, it's a reducer of about any immune inflammatory cytokine. I believe ivermectin has a place, and that it does support your immune inflammatory cytokines. I can't give it, prescribe it, or anything like that. But I think there is a place for it.

[1:48:42] SCOTT: Last question before our wrap-up question. Are there any tools that we did not discuss in the physics realm that have application here? What about light therapy, sound therapy, PEMF, frequency-specific microcurrent? And then building on that, I know we talked about 40 hertz as being helpful in this realm. 40 hertz in the book you say causes neurons to release VIP, or vasoactive intestinal polypeptide, which signals the cleaning system to get to work. In the Dr. Shoemaker realm, VIP is used as a nasal spray. So, wondering if you've used VIP nasal spray in patients with microglial activation.

[1:49:24] DR. STREIT: I haven't used the nasal spray yet. It is something that I think isn't inappropriate for most of our patients anyway. But we'll use red light therapy. You can actually get out and get a Vielight. I'll have some people go out and get Vielights, where they put the red diode up their nose. And there's a Vielight Neuro that syncs it at 40 Hz now. They’re even on top of the 40 Hz side of things.

Sound therapy at 40 Hz. And it's not just going and playing 40 Hz on the internet. That's not what we're talking about here. But you can do binaural-appropriate, binaural beats type thing. I'm always leery about telling people just to go on YouTube and find that because I don't know what is in the background of those tones. I have a harder time telling people like, "Hey, go do that, or go do this."

But we use a table here called the Satori, and it vibrates at the same time the music is playing. And it's at the same vibration that the music is playing. And so, we can get a really good set on the brain, the theta or gamma wave. Microglial is the gamma wave that we can really utilize with that particular bed.

[1:50:38] SCOTT: Do you guys have a Toys R Us sign hanging outside your clinic door?

[1:50:42] DR. STREIT: It feels like that sometimes. We got all these therapies. Just our patients are able to use them every day. So, it's kind of an exciting thing to see.

[1:50:51] SCOTT: My last question is the same for every guest, and that is what are some of the key things you do on a daily basis in support of your own health.

[1:50:58] DR. STREIT: I do hydrogen therapy every day. I think it's important for oxidative stress. I periodically will use methylene blue myself. I use nicotine every other day. 7 and a half milligram. That's my own pattern. I follow more of like that Mediterranean-style diet. I'm not completely against carbohydrates. I'm gluten-free. I'm limited dairy, unless it's raw, organic, from an A2 cow that lives next door, then I know how they're being raised.

I focus on my electrical terrain. So, I ground. I make sure that I'm doing any type of grounding technique, whether it's taking my shoes off, putting my feet on the ground, or a grounding mat.

Get movement every day, and detox the brain, support the brain. Those are the things I do every day.

[1:51:52] SCOTT: Good stuff. Such an amazing and important conversation. And I encourage listeners to get the book Silent Spark: An Unseen Force Fueling Chronic Illness and How to Heal. So grateful for your generosity of time, your knowledge for activating our brains, activating our minds, and hopefully not activating our microglia. Thanks for being here, Dr. Streit.

[1:52:16] DR. STREIT: Thank you for having me. I appreciate you.

[1:52:18] SCOTT: To learn more about today's guest, visit InstituteForRestorativeHealth.com. That's InstituteForRestorativeHealth.com. InstituteForRestorativeHealth.com

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Disclaimer

The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.