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Neuroinflammation: Causes, Assessments and Treatments with Dr Brandon Brock

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Neuroinflammation: Causes, Assessments and Treatments with Dr Brandon Brock

Dr Brandon Brock joined us on a live, interactive video podcast on 14th July 2020 to dive deep into the clinical aspects of neuroinflammation. How to we recognise it, what are the implications and how can we help patients back to an improved state of wellbeing?

Dr Brandon Brock is a world-leading expert in functional neurology and his expertise in this, is fascinating. 

Covered in this episode

[01:28] Welcoming back Dr Brandon Brock
[02:39] Introducing today’s topic: Neuroinflammation
[03:16] Starting at the beginning with a client
[06:49] The problem with sustained inflammation
[09:30] The role of genetics in inflammation
[11:34] Inflammation and neuroautoimmunity
[14:50] Using lab tests and panels to assess genetic predisposition to inflammation
[17:33] Discussing various SNPs and risk of neurological disease
[22:48] How Lyme disease affects the brain
[25:01] Other infections that impact the brain and CNS
[26:38] Treating Epstein-Barr and other viruses
[29:18] Glucosamine and cardiovascular implications
[30:57] Insulin resistance and the brain
[33:18] How intermittent fasting repairs the brain
[35:39] Intermittent fasting protocols
[39:20] Why Alzheimers drugs
[42:06] Meditation and exercises to improve neuroplasticity
[48:58] Can different breathing techniques affect oxygen binding to haemoglobin?
[51:12] What the evidence says about Huperzine
[53:24] Brandon’s approach to treatment
[58:31] The benefits of phosphatidylserine and broccoli sprout extract
[1:01:52] Vestibular neuronitis
[1:05:18] Thanking Brandon and final remarks

Andrew: This is FX Medicine. I'm Andrew Whitfield-Cook, and joining us today is Brandon Brock, Dr Brandon Brock. Doctor, doctor, how many doctors does this man have? But anyway let me read his bio for you. 

He's a clinical practitioner in Dallas, Texas in the fields of orthopaedics, neurology, and integrative medicine. He has doctorates in Family Nursing Practice and Chiropractics, as well as post-doctorate Orthopaedic training from Duke University with additional training in molecular and nutritional medicine. 

He's a diplomate in Functional Neurology and Nutrition, holds board certification in Integrative Medicine and is a Global Research Scholar from Harvard Medical School. And he's currently, currently working on another PhD. 

Dr Brock is on several clinical advisory boards and lectures for several various companies on a multitude of topics. And I warmly welcome my friend, Brandon, back to FX Medicine. Brandon, welcome, how are you?

Brandon: Hey, it's good to be back. Thank you so much for having me. And I miss Australia badly.

Andrew: I miss you, bro. Now, I mean, you and I can chat just for hours, but we need to talk about a topic which is a sad scourge. I mean, we're talking saying it's a sad scourge in the changed landscape of today's COVID-19 virus. But, you know, the scourge of neuroinflammation and the various diseases, which accompany it, are going to be the new key killers for particularly our elderly.

So, I guess to start, you're a clinician. So, when you see a patient walk into your office, what are the key signs, the key clues that you go, "I really need to delve further here"?

Brandon: The fact that they walk in. Our practise has evolved so much. I get it from the beginning, the entry forms that we use, and I studied that before the patient comes in, and you see so many chief complaints. There's really not a way to link it all. Usually not, at least. Not a way to link it into one simple condition.

So, a lot of times they have one thing leading to another, leading to another, and then it kind of all boils together to make one syndrome and then that just explodes into a group of symptoms. And that is a lot of what we see. We have to unravel these mysteries that have been presented to us that have really… they sort of failed the conventional model so to speak, meaning one pill or one procedure or even a multitude, polypharmacy, won't necessarily correct everything.

So, we're stuck having to do a lot of diagnostics and look at it maybe from a different perspective. And sometimes we use traditional and non-traditional models. 

So, I tell you it's really, really cool to be here. I see lots of people popping up and I just want to say hi to everybody that's saying hi.

Andrew: Absolutely and from around the world, so welcome to everybody from Australia and the U.S.

Brandon: I just saw somebody from Texas pop up. I can't believe it.

Andrew: So, with regards to the patients that you see, do you have to very often go back to step one and go, "Okay, let's just do the basic assessments again,” so that you can get a feel for what happens with that person? 

I'm looking at you having a little conversation with Emory Sullivan there.

Brandon: Yeah, the answer to your question is yes. Listen, one of those things that happens very, very commonly is patients walk in, and they put a bag of stuff here and a bag of stuff here, and they've got tears in their eyes and their cheque book is empty and they've spent hundreds of thousands of dollars. 

And that is a culmination of practitioners not communicating with each other which, you know, I'm just as guilty as anybody else. But sometimes we have to just stop and back up.

And I'll give you just a real quick scenario last week. I had a girl that came in that was really suffering tremendously and come to find out she was just really in a terrible relationship, had a terrible amount of stress in her life. Had an enormous amount of adverse childhood events with very little resilience, and this was triggering all kinds of pathological physiology within her body. And nobody had ever stopped to just dig a little deeper and ask her that question. 

And that was really, I think, one of the starting points of her disease. It's really interesting. You know, the literature is showing us now that children with adverse childhood events that lack resilience, up to 60% of those individuals will be hospitalised at least once in their lifetime from an autoimmune disease.

So, we go all the way back to how were you raised, what was going on, you know, what did you experience? And since we've started doing that, we've been using psychological intervention with the appropriate practitioner that works with me, and it's been fantastic.

Andrew: So, with regards to sustained inflammation, which I guess… I mean this follows on from your friend Datis Kharrazian, at the BioCeuticals Symposium. And he spoke about early damage, early neurological damage and then prolonged inflammation or a priming can be set in place, where prolonged inflammation leads to a disease many, many years later.

Brandon: Yes.

Andrew: So, which tissues are most at risk for that early insult, that early trauma? Can it be any tissue? Like, for instance, a football injury or does it tend to have to be a neurological tissue that's damaged.

Brandon: Well, what's really interesting is you can get peripheral inflammation from trauma, or from your guts, or from a fungus, or from a parasite, or from a virus, anything that creates systemic inflammation. And if it ends up creating something like, you know, any of the interleukins, and I don't want to get too much into the immunology but, like, let's say a Th17 or interleukin-17 response and it sort of starts to open that blood-brain barrier. And some of that peripheral information or inflammation gets into the central nervous system and it really just says, "Hey, brain, become inflamed."

So, now you may already have trauma from, say, playing football, or even soccer, or maybe you got into a bar fight. I don't know. It could be any of them. Maybe it's just inflammation from the fact that you have an infection in your central nervous system, too. 

But when you combine the two together, it starts to change the cells that control the environment of inflammation. But I'm making this too complicated. It changes them genetically, and they can't turn each other off but they want to stay on. And so typically with some of these injuries, they stay on for a certain period. They clean things up. They connect everything back together, and then they kind of turn off and they're like, "Okay, cool." 

But the more we have inflammation that is sustained, whether it be in the periphery or the central portion. That's why we like to check the blood-brain barrier. It's so cool because we can see if there's that peripheral gut inflammatory pathology in those LPSs that are really getting into the system, making interleukin-6, coming into the central nervous system, changing microglial cells for over 30 to 45 days, and then the next thing you know you've got sustained problems.

Andrew: So it seems to me like one of the issues of this sustained inflammation is very much like tolerance that we speak of in the gut. And when we need to probably start at the gut, but it seems like tolerance is the key, the switching off of our immune system.

Brandon: Yes, that would be 100%. It's not as simple as what we thought it was. We now are writing genetic panels. And some of these genes that we're running showed that some people don't have the genetic capacity to really switch off microglial cells. And, in fact, some people have the inability to control microglial cells genotypically and phenotypically, and then their interleukin-6 also is out of control so it's much easier to become inflamed. So, what happens is you get to a situation where...man, I tell you. You're going to end up with...

Hold on a second here. Something popped up on my screen.

Andrew: Yeah.

Brandon: I'll just read through it. So, anyway, you get to a situation where, you know, whenever your brain gets inflamed and all these things are happening and you've got these genetic markers. These genetic markers can create a situation where it's not as easy to treat as people think. In other words, it doesn't follow the guidelines per se. 

And so we like to look at new genetic markers, not just apoenzymes, but we look at a few others that are kind of underneath that that will say your microglial cells are going to stay on. Your brain-derived neurotrophic factor that makes it grow is not as good. Your interleukin-6 is going to really turn on and the gene that actually stops that is not there. And so now you're much more prone to that entire story that I just told you about, and that will help us with the dosing in regards to our nutrition, our medication, and sometimes we dose people higher based upon their genetic needs.

Andrew: Okay. I guess what I'm asking though is, when we look at interleukin-6, there's a number of disorders that can have increased inflammatory markers, interleukin-6, CRP, whatever. 

How early should we be checking patients who come in for potential inflammation or neuroinflammation in their later years? Is there any keys? Is there any clues that we can have earlier on in their patient history to go, "Oh, you're really at risk of turning this on," or is that just to do with family history?

Brandon: Well, we've kind of done it this way. We have started looking at people genetically and saying, "You are very prone." 

Andrew: Right.

Brandon: So, we do not want you to become infected. We want to watch for viruses. We want to look for a fungus. We want to look for trauma. And you may not... We've actually identified some people now where we're like, "Hey, you know, you're a bad candidate for trauma. So, please don't go play football because you might be very prone to interleukin-6 just wrecking your life."

And, you know, when you look at this and you look at the way microglial cells can differentiate and change, if they're not regulated both by their internal environment, their genetic environment, and your own internal genome, they can switch on to two different types of cells that are supposed to work together and they end up not working together. 

So, you eat things and then you end up making antibodies within your own brain. And that inflammation that is normally healthy, that cleans things out, can turn into a moment of antigen presentation and now you get neuroautoimmunity and it's a bad deal.

Andrew: And so is this where we're talking about the connection between M1 and M2 macrophages and the M1 and M2 microglia?

Brandon: Yeah. And whenever there is… I mean they're always in interplay and they're always working together. But when you become primed or there's a genetic change and you have sustained components of inflammation, microglial cells have to jump into action. And so M1 is going to do one thing and M2 is going to do something different in a normal state versus an abnormal state.

This is where we end up getting a situation where, especially if Th17 is involved and things are coming in constantly into the central nervous system and making these two things diverge and not do what they're supposed to do, and promoting not just more phagocytosis but more antibody-antigen responses, it's just a matter of which tissue is going to become involved. 

The mature basal ganglia, you might get something like PANS or PANDAS. If it's your cerebellum, you might get something like, some sort of gait disorder or cerebellar disorder where you don't swallow good, you don't talk well, and you're discoordinated in regards to your overall condition. And then there's other things that can affect all kinds of neurotransmitters as well, and receptor types that deal with weakness, fatigability, neuron fatigability, and so forth.

So, there's really cool panels out now that will tell you that if this process has happened, you can see which systems have been tagged and you can work backwards and say “There's inflammation,” and then say, "If there's inflammation, what's causing it?" And you end up finding something like a major fungal infection or a virus.

Andrew: Got you. Can we discuss those panels a little bit? Because Datis Kharrazian alluded to this in a podcast I did with him. So what sort of...?

Brandon: Well, we have... I mean there's different companies, and they're really all good, and there's different types of technology. And in the States, we have something called FDA, which is kind of the gold stamp. And one of the labs that I used has just compiled basically multiple tissues, whether it be brainstem receptors, neurotransmitters, and so forth, even the blood-brain barrier, and even the organisms that are commonly found in the central nervous system like cytomegalovirus, and so forth. They can create a little bit of encephalitis or inflammation in the brain.

We like to run these panels and then I can run a mould panel with it, or I can run that panel and I can run a viral panel with it, or I can run that panel and I can run heavy metals with it. So, you kind of look at the patients.

Andrew: Wow.

Brandon: And I look at their underlying basic labs like their CBC and their comp bio, and stuff like that. And then off of that, and off of their history, if it's central nervous system-wise, I decide which way I want to go. So, like, the other day, I had neurological problems and thyroid. 

And so the cool thing is...well, not cool, but the bad yet interesting thing is that we got this person's thyroid completely under control but we didn't realise, or we do realise now, is that there is a genetic SNP where, even if your thyroid is perfect, it doesn't work well on the brain. 

Andrew: Wow.

Brandon: So, this person still had the neurological symptoms of thyroid, but that gene was homozygously positive. So, it was still a problem neurologically for that person. So we had to start doing other things for that person even though their thyroid was under control, even though their antibodies were dropping, even though we gave them every micronutrient to support everything that was going on, even though we were watching their flares up and down, it still wasn't working in the central nervous system.

Andrew: That would have been frustrating. That's almost chimeric isn't it, two people?

Brandon: Well, it's really interesting because it explains a lot of patients, you know? A lot of patients are like, "Hey, look, everything is going great. I quit losing my hair, my skin is doing good, but I don't have good conversion in my central nervous system of T4 to T3." So then we had to change compounds that we give them and it works out great.

Andrew: Now, I've got a question here. Which SNP? FOX, as in FOXP3, I'm thinking?

Brandon: You know what I'll do? There's about 40 of them, and what I'll do is I'll give you a list of them that you can give to the listeners because underneath apoenzyme E...like, you know, your apoenzymes, like the E3/E3, E4, and so forth. I've got all of the dementia ones. I've got all the diabetes ones. I've got all of the thyroid ones. Even the ones that deal with adiposity. Is your fat going to make you inflamed and is that going to sustain an inflammatory state and go into your brain and cause neurological issues?

Now, real quick, we're seeing this right now with the SARS-CoV-2 situation where you're supposed to have an interferon-gamma response that actually resolves these viral titres. And so what happens is, you become more inflamed if you're genetically prone to have an imbalance between adiponectins and leptins. 

And so when that happens, you can't brush off the viral titres down and they end up making a larger tumour-necrosis-factor-based cytokine storm which goes into the central nervous system. And if it's already primed, you're in very big trouble. The virus can also sneak into the central nervous system, go into your brainstem, affect different areas of your brain to control your breathing. Now you can't breathe because of a central nervous system problem, not just an alveolar problem.

Andrew: Wow. So, hypothalamic dysregulation and… Wow. That's horrific. 

You mentioned something earlier about ApoE and this really interests me and still confuses me. Is it basically like “choose your disease” or are there other factors underlying ApoE which magnify its pathogenicity?

Brandon: Yeah, I'll give you one example. There's ApoC1, which if you have that along with ApoE, it's way worse. And then there's TRIM2, which makes you tremendously greater. So, if your ApoE4/E4 but everything below it is great and your suppressor genes are really good, the E4/E4 is not near as dangerous as a E2/E3 with all the other genetic components that are turned on. 

And the lab that we use will show what is the odds ratio that it will give you, say, dementia and you can add those odds ratios up, and you can start to see a very grim picture or non-grim picture. And it will help us dose the things that we want to use. Like, if you want to use sulforaphane, for instance. We can dose it up. It's not dangerous, per se, to dose it up.

Andrew: Right. And what about other factors outside of ApoE? What are the SNPs do you look at, neurological SNPs?

Brandon: Well, what's really interesting is we're finding out now there's SNPs that are good. So, we've been looking for the ones that are really, really bad. And if they're on, then you have a greater chance. 

But there's some really powerful genetic components that will inhibit negative things. So, we're outlining those as well and evaluating those. And if those guys are turned off, and the bad ones are turned on, and then you have an underlying inflammatory response that is stoking this, there's nothing preventing your tissue from becoming excitotoxic and destroyed, and you losing brain volume. You know what I mean? 

And so once that happens mainly in the frontal areas, you asked this earlier. Which areas are most prone like frontal areas, areas near the blood-brain barrier where it's the thinnest, and then our lateral convexities. This is where your typical Alzheimer patient will get damage, and of course the hippocampus, okay?

Andrew: Yeah.

Brandon: Anyway, and I see over here that genes really can be the final layer to the opinion. And that is true. And I see that a lot of people are kind of happy that we're starting to bring genes into it, because genes are the variable that makes every one of these standardised cookbook routines for treatment invalid. And that includes functional neurology, nutrition, or medication.

So, I have some very unique patients. Just a quick story. I had a guy that came in last week, was getting very rapid dementia. All of his genetic receptors were being oestrogen-sensitive for low oestrogen, even as a man, were very, very, very prevalent in him. He was on hormone replacement and was taking some medication called anastrozole that drops your oestrogen down so your testosterone goes up and your oestrogen goes down, so you feel more like a man. And that medication, as his oestrogen went down, his dementia went up. And we saw that genetically.

We took him off that medication, allowed his oestrogen to go up. He didn't get any gynaecomastia and he started to snap right out of it. We would have never done that ever without seeing a picture of his genetic profile.

Andrew: Right. I'm going to ask a question from Sarah Riley: So, have you found Lyme patients oftentimes have anti-myelin oligodendrocyte glycoproteins or antibodies, or other demyelination and autoantibodies due to the cross-reactivity of Lyme?

Brandon: Yeah. That's an interesting question. The cool thing about Lyme is is we're finding more, and more, and more, and more species of Lyme. And what I'm finding is, a lot of people do Lyme. 

They do Lyme titres and all this stuff. And then they do a CD57 count, which is really sort of a fancy way of looking at some of your natural killer cells, and then we look at 50/30/20. When those get down really, really, really low, we start seeing the blood-brain barrier get really destroyed. We start seeing peripheral and central myelin-based disorders and, in some situations, we have found it as the perpetuator of a PANS or PANDAS reaction. It's not strep. We've seen mycoplasma and we've seen Lyme.

So, I do a dual test for Lyme. I'm kind of paranoid about it. I always want to make sure it's there because the treatment for it is really difficult. But when it's there and they have the arthralgia maybe, very seldomly do they have the bull's-eye rash, very seldomly do they remember the tick bite, and all that kind of stuff. 

But we have found that it cross-reacts with a multitude of tissues; in particular, the plastic coating on the wire per se, whether it be oligodendrytic or whether it be a Schwann cell, and so forth. But it's not just those. We've seen it heavily in the basal ganglia, especially to the D1 pathway if that means anything to anybody. 

And it makes people very, very volatile, out of control. And for those of you that are dealing with PANS or PANDAS patients, these reflexogenic basal ganglionic inflammatory, encephalitic-based mechanisms, they usually go in 20-minute intervals. So, just give them 20 minutes. You're not going to be able to discipline them. They don't understand it. It's a neurologic reflex. Just back off. Give them 20 minutes. They'll usually just resolve.

Andrew: A question from Rebecca: I'm really interested to know what kinds of infections - now, you've already mentioned two - can impact the brain or CNS directly? So, we've mentioned CMV. You've mentioned Lyme. Can I just add a little bit on to that?

Brandon: Sure.

Andrew: Does it always have to be directly affecting neurological tissue or directly crossing the blood-brain barrier, or can it be a peripheral infection and then the signal is sent via the danger-associated molecular patterns?

Brandon: No. Really interesting stuff. So, let's take MERS for instance. MERS will crawl up your neurological pathways into your central nervous system like herpes. And that's why MERS has a 30% case fatality rate. It's devastating. 

Andrew: Right.

Brandon: Cytomegalovirus are any virus that certainly create peripheral inflammation. And if we measure your blood-brain barrier antibodies and they're really terrible and that's getting through, it's just going to go into your central nervous system anyway. 

But we have cytomegalovirus, we have Epstein-Barr that can be convalescent or non-convalescent, and so forth. And then we have HHV-6, HHV-7. And what's really interesting about cytomegalovirus is it neutralises neural progenitor cells. So, you lose brain volume much faster whenever you have a cytomegalovirus and inflammation.

When you get the cytomegalovirus down, you don't have as much volume lost because your neural progenitor cells can actually be produced at a higher rate. And that's really a cool piece of literature that we found recently.

Andrew: Now, there's one from Marty here: how do you treat the chronically elevated EBV titres?

Brandon: I knew somebody was going to ask that. You know, can I namedrop products?

Andrew: If you need to, yeah.

Brandon: Okay. Well, I mean I'll just tell you. Like, one of the things I use is I use Andrographis a lot, especially in this... Listen. So, let me just go to COVID real quick. It's very difficult to use just straight Th1 drivers that don't have also the inhibition or the ability to stop a storm. Some of your Th1 drivers that are very strong like elderberry and Echinacea, they'll drive Th1 to kill the virus or to drop it down but it will perpetuate a storm. Your Andrographis, per se, and your olive leaf and sulforaphane, they'll be very good at being antioxidants. They will also be Th1 drivers, but they'll also reduce the storm. Sulforaphane is a beautiful Nrf2 activator which stops interleukin-6 in its tracks.

So, we could really get back to it but treating Epstein-Barr, I use Biocidin, I use Andrographis. Sometimes if it's really acute… just to let you guys know, if it's IgM, it's acute. I'll use a Th1 driver like Echinacea or elderberry, okay? If it's chronic, so if it's IgG, most people say you just got it.

But if it's IgG and it's four, five, or six times the upper limit of norm, it's probably chronic. So, that's when I'm going to go to my things like sulforaphane, or Andrographis, or olive leaf because they may have an interferon-gamma type response that will lower the titre, but they'll also lower the storm. And then we can give a few other things that will protect the blood-brain barrier. 

So, we use diosmin to treat the blood-brain barrier. This is also called Daflon. It's a prescription drug in some places, but I really think the people that take this will probably not die from heart disease in their lifetime.

Andrew: Right. Wow.

Brandon: It is very, very researched. Now, we've also found that some of the green tea extracts will block receptors on those ACE2 so you don't get the virus. We've also found that trans-resveratrol will block that. We've also found that sulforaphane will block those. And we've also found that glucosamine, that protects your joints, will block those receptors. So, you can actually do some stuff to where you are not going to get infected as easily, in all probability. So, anyway, I hate to get on with that but it's still...

Andrew: No, no. I think that's really interesting.

Brandon: ...interesting information.

Andrew: I think it's really interesting that so many people have gone immune, just immune stimulation, and we really have an inflammatory sort of condition when we're dealing with COVID-19. I love to hear glucosamine come up and poke its head up, because you're now doing a PhD in Cardiology, correct?

Brandon: Correct.

Andrew: So, there was a very interesting… I know this is off-topic but I thought it was neat. There was a UK Biobank study. So this is thousands of people, 40,000, and those people that have used glucosamine for over 4 years had less CVD outcomes.

Brandon: Yeah. Because, look, let me tell you something real quick. Glucosamine and chondroitin sulphate. So, the glycosaminoglycans that are very, very absorbable and the sulfation process, if all that is really good, it will control leptin so you won't get leptin resistance and your adiponectins will get regulated. 

Leptins go straight into the brain and they say, "Okay, look, I'm hungry," but you get leptin resistance. So your leptins go up and your insulin goes up. They both go in the brain, create neuroinflammation, then they get into your central nervous system... or they get into your circulating peripheral nervous system. They go into your joints and make them inflamed and that's why obesity and leptin resistance makes your hands hurt, not just your knees.

So, this is why obesity in some people genetically makes an inflamed brain. In others, it doesn't. But glucosamine and chondroitin is one of those things that stops not just joint… A lot of people are like, "It's just joints." But, no, it's not. It actually treats a load of things. 

And, as I was getting ready for this, just looking at the insulin resistance in the brain is tremendously devastating.

Andrew: Right.

Brandon: Don't get insulin-resistant, please.

Andrew: Well, there's a test here from Michelle...a question here from Michelle: do you test for leptin resistance and what do you test? Do we check alpha-Melanocyte-stimulating hormone? What are we checking?

Brandon: You can just test leptins, adiponectins. You can check...

Andrew: Inulin?

Brandon: We check C-peptide for insulin. And you can run glucose or haemoglobin A1c. And you can put all of this together in a HOMA calculator and look at it, and you can say they're diabetic, they're type 1 diabetic, type 2 diabetic, they have insulin resistance, they have leptin resistance. And so you can see... 

Listen. If you have leptin resistance and insulin resistance, your brain is inflamed. End of story.

Andrew: Yeah.

Brandon: So, I mean you can just sort of count on it and you just pray to God that you don't have some of those other genes because, if you do, your brain is going shrink, shrink, shrink, shrink, disconnection, disconnection, disconnection. And it just depends which gene...whatever gene you have that's going to express because of a decrease in firing, you may get multiple systems atrophy, you may get Alzheimer disease, you may get whatever the case may be.

Andrew: I'm sorry but I'm just laughing. There's a comment here. "Oh, to live in Brandon's brain." Spare a thought for Tara, his wife.

Brandon: Yes. Tara, she should get credit for everything.

Andrew: Now, I've got a question. So, firstly, the question up there is: how do you address insulin resistance… Well, it says address insulin in your patients, but I'm gathering insulin resistance in your patients.

Brandon: I treat it the same way as I do insulin resistance in the periphery.

Andrew: Yes.

Brandon: You know, just with diet, exercise, and really genetically some people are more prone for this than others. It's just one of those things where you got to starve them of the need for insulin. And we have found that fasting is very good for brain. We have found that fasting is very good for autoimmunity. 

I mean, three days of fasting can drop your antibody load down significantly. So, if you're looking at somebody's labs and they're trending towards a flare, we can neutralise that by fasting them for up to 2 or 3 days. I know that sounds kind of cruel but it will drop it down.

Andrew: But intermittent… Sorry, you go.

Brandon: No, no. Go ahead.

Andrew: I was just going to say intermittent fasting can also have structural changes in the brain. 

Brandon: Yes.

Andrew: Is that correct?

Brandon: Yeah, it creates autophagy. It allows basically, if you've ever watched the show "Hoarders," people who keep all the stuff in their house, you know? 

Andrew: Right. Yes.

Brandon: You know, if you're doing something like intermittent fasting, it allows you to eject all of the damaged organelles in a clean house. So, I like to do intermittent fasting after neurological trauma at a certain point because any of the DAMPs that you have, or the debris or the damaged cells, it helps to kind of get those out. And, you know, it makes it a little bit easier for your brain to repair itself and it lowers the debris fields.

Now, remember, when you have trauma and you have debris fields, now that is tissue that can be eaten and tagged as an antigen-antibody response. So, you want to get rid of it. And so fasting might save you from neuroautoimmunity.

Andrew: I want to go back to an earlier question, and it was from Sarah Riley again: have you found anti-VGCC markers to be prevalent in patients with electrosensitivity?

Brandon: With electrosensitivity?

Andrew: Yeah.

Brandon: I don't know. It's a good question. I mean we see them in people with physical activity weakness. We also see that in people that are a little bit apractic and they have slow conduction speeds. But I've never experienced anybody... 

Now, with electrosensitivity, my question would be: are you talking about, like, to 5G networks? Are you talking about to electric shock? Are you talking about to, you know...

Andrew: I'm going to presume that it's electromagnetic frequencies.

Brandon: Yeah, the answer...and, listen, if I don't know, I don't know. And I'll just say I do know patients that say they can feel it and they can sense it. And it's one of those things where I can't explain why, but that's a great question. And what I think Sarah should do is she should research and tell us.

Andrew: What we should do is get Sarah in touch with Nicole Bijlsma and Amie Skilton who can definitely talk to them about that.

Brandon: And I can just tell everybody...every test I've talked about right now especially on the antibodies, I can tell everybody where to get it. I'm almost positive they do it in Australia and the test is probably right around $400 U.S. And it's an amazing test. Really nice.

Andrew: Okay, protocols for intermittent fasting with regards to days on/days off, or hours on/hours off, forgive me. So, 16-8 or 18-6?

Brandon: Yeah, I mean it depends which condition. So, like I said, for autoimmunity, if it's really getting out of control, I'll go 2, 3, or 4 days. If it's blood sugar dysregulation, I'll go anywhere from 17 to 24. I like to go 24 and a lot of times it’ll regulate it. 

For insulin resistance, I'll do it 2 or 3 times a week at 17 hours. And then, you know, a lot of people just do very well with just a well-balanced diet and they go paleolithic or people like plant-based. By the way, genetically we can look at people and say, "This is what you should eat."

Andrew: Right.

Brandon: And so there really is no perfect diet. Some people can't eat oxalates. Some people can't eat histamines. Some people can't go on what's called an autoimmune diet because they're allergic to a common food. And then certainly, when it comes to diabetes and insulin resistance, you have to watch what you're eating.

So, our diets, we don't really have a diet. Every single diet is really catered to what the person needs on the genetic and pathological basis.

Andrew: Got you. With regards to intermittent fasting and changing diets around and things like that, how aware do you have to be of concurrent medications, orthodox and pharmaceutical medications? For instance, if they've got autoimmune thyroid condition and they're on thyroxine. I know. But...

Brandon: No, that's a fair question. I haven't seen it really do much with thyroid medication. Now, what I have seen it mess with, is insulin. And so I would tell everybody out there that, if you have a patient that's on insulin, please be careful, because a lot of times their standard insulin dosages, if they're fasting and their blood sugar starts to drop naturally on their own but they're taking the same level of insulin, they can go into hypoglycaemia very easily and it's something that they've never experienced.

And remember a person that normally has...and I think these units are maybe equivalent but let's say 100 or below is normal for fasting. But a diabetic that's on insulin is not controlled and they're used to 230. If you don't bring them down to 100, it would be like me or you at 40. We would feel like we were going to, you know, pass away. 

So, you always have to be careful. Any time you're doing fasting, people underestimate the power of fasting. And so sometimes you have to fast with a little bit of sugar. Sometimes you have to fast with maybe a medical food that has certain vitamins and nutrients in it.

So, my fasting does not follow any necessarily...not any of the guidelines, but it's close but it's also my experience with it, you know? And you learn that they may say three days is good but, on day number 2, you have a limbic breakdown and they can't make it to day 3. You can see that patient before it happens. 

Andrew: Just with regards to your comment about units. For our Australian listeners, Americans measure glucose in decilitres per 100 mill. Is that right?

Brandon: I believe so, yes.

Andrew: Yeah, whereas we use millimoles per litre. So, there's a difference there, but you can get conversion tables at many different areas. I might ask one of our moderators in the background, one of the elves, to see if they can find the sites that I found for the symposium, for particularly Datis. So, this seems to…  On it, Melissa's on it. I found some great sites where we can look up conversion tables.

So, speaking about drugs and talking about neuroinflammation, talking about, I guess, mainly the Alzheimer's disease. Why has there been no gains in medications, in drug treatment for, like, 40 years. Why are they still hooked up on the end damage rather than the cause?

Brandon: You know, we actually have a gene... There's a genetic test that will show that acetylcholinesterase inhibitors, the common medications, will actually be more harmful than beneficial.

Andrew: Whoa.

Brandon: We run that. And we can also say this that Albion magnesium, magnesium glycinate and malate, we have a version of it that has multiple different types of magnesiums. The drugs like Namenda or Memantine, which are the drugs that block the NMDA receptors, it's just magnesium with a slick patented carrier molecule. 

So, one of the things we do is we get magnesium, we sort of replace that, and then we can get some alpha-GPC and we replace acetylcholine. And then we give some Huperzine and we protect everything from amyloid.

But, to answer your question, the reason why there isn't and there isn't going to be any time soon and the reason why everybody on this live webinar needs to learn about this, is because you're their only hope. That's why I really love doing, like, a series of classes on this because it could be this condition that turns into Alzheimer disease. So, what one pill is going to treat that?

Andrew: Yeah.

Brandon: It's a viral condition that's turning into this. Now, what pill is going to treat that combination? So I could sit here and give you a hundred different loops that perpetuate Alzheimers disease, and multiple of them can overlap, and it's never going to happen until you can genetically change that individual.

And by the way, if they have lost brain volume, it's not about reconnectivity anymore. It's about neural progenitor stem cell growth that has been altered, so that when they regrow, they have to reconnect. 

Andrew: Yeah.

Brandon: So, I mean that's your life. It took your whole life for that to reconnect. So, when you start looking at this, it's not just daunting. It's virtually impossible in the near future. That's why doing things like this, like prevention, health, looking at all the risk factors, stopping inflammation, looking at their genes, being healthy, it's all we have right now. And I really don't have any problems saying that.

Andrew: You just mentioned stuff about things regarding neuroplasticity. So, there's a great… he's actually in marketing in Australia. His name is Todd Sampson. He had a TV show called “Redesign My Brain." And he did this...it was almost like a Houdini thing underwater. 

Like, he got out of a locked straitjacket and he taught himself to go through the steps to do that, hold his breath, to unlock, to calm down. And there was a whole series about “Redesign My Brain.” 

So, have you got any simple exercises or simple interventions that you can teach your patients, that our practitioners can teach their patients, that help patients who have issues or who need to reengage neuroplasticity?

Brandon: Yeah, and one of the… So, there's probably several functional neurologists on here, and they will tell you that the person needs a very good exam, and you need to pinpoint the location, and then activate that area for the greatest efficiency and the greatest good of the patient. And I will not disagree with that at all. 

But there's a lot of people on here that are not. And nobody else is going to practise the world of functional neurology and conventional medicine, so we might as well give some things that help out.

And so one of the things I try to do is I teach a little meditation. And what's really interesting, and I challenge everybody to try this. Try to close your eyes, get in a quiet room and just think about one thing. And the second something else comes in your mind, you stop and see how long it took. If you can get to 10 seconds, you are a master.

Andrew: Right.

Brandon: And so that is very frontal lobe, okay? It works great with, you know, if you have some attention deficit issues. 

And then I'll just do a lot of executive function type things. So, I'll pick out something that I want them to do in their health. Let's say that a guy comes in. He's 45 years old and we could give him 50 supplements, but we're just going to give him one or two. And I will say, "We're going to regiment this and every single day you're going to do these one or two things. And that is building up to the next level which is another thing, and then building up to another thing. And then there's some exercise and now there are some dietary changes." And what you end up building is a pyramid of executive function, and that's frontal lobe.

And so by doing that, you can change a person's life forever, but they won't do it on their own because nobody's challenged them in a way that is structured, organised, and linear. And I have found that to be as effective as almost anything that I've done in some areas where I thought I was super-specific.

Andrew: But that's what we need you for, Brandon.

Brandon: Hey, we could do this specific stuff on top, but you know what? People want organisation and they don't want chaos. And so I think that even if you do enjoy chaos, there is still some linear components to health and the frontal lobe function, and you can make it from the middle-out in regards to exercises or the outside-in in regards to exercises. 

You can organise them in any way you want depending on how well you know the frontal lobes. And you can really make some awesome, powerful frontal lobes where people will get things done, hold the job better, hold relationships better, listen better, inhibit their left brain vocal outburst and their right brain physical outburst. And now they're much more calm.

And so these are beautiful things. And by the way, inflammation can deteriorate the frontal lobes very, very rapidly in regards to synaptic connectivity.

Andrew: One thing that I've just been aware of is, you try and get me to meditate and I worry about meditation. You took me outside on a Friday night looking at a fire. I'm in the zone just staring at a fire.

Brandon: Well, and that's probably your thing. You know what I mean?

Andrew: Okay.

Brandon: I'm a bad meditator. I can tell you right now. So, when I try to do this, for me, my brain is very busy. And so it's something that I've had to...I've really started to work on it quite a bit, because the more I can calm that down, the more I can shift my focus and stay on one thing. Versus try to go to one thing and then I have about 14 other things buzzing around it. And, to me, that becomes very, very unproductive, and I'm not as rapid in regards to finishing projects.

Andrew: I can just imagine Tara walking in with a flame on a phone and going, "Walk this way. Sit."

Brandon: No, she’s more like a whip. You know, you're going to do whatever I need to do, bud.

Andrew: Following on from that, what sort of resources do you give your patients for meditation practice?

Brandon: There's apps on your phone that have… it’s really kind of neat, for the right brain I do a lot of environmental noises. So, sometimes I'll have them listen in their left ear and it's environmental noises. And then it can soothe down like an overactive left brain or an underactive right brain.

There's also some other things that we can do where we do binaural beats where we can put them in the ear and we can find out what frequencies are going to generate the oscillation speeds of certain neurons, and then we can programme that in the background of some music, and they play that. And then the background beat, the binaural beat is something that allows them to oscillate at an equal frequency, and they can relax. It gets a little deeper.

Andrew: Oh, wow.

Brandon: Yeah, that gets a little deeper. And then we use eye-hand coordination and visual stimulation and 3D activation and stuff like that along with that. And it starts to create a brain that will oscillate together, and we call that connection. In other words, it doesn't disconnect any more.

Andrew: Wow, that's really interesting about the music, about having the beats. Like, I'm aware of Pachelbel and other music types where they have that...it's 8 to 14 cycles per second. So it's like, more attuned to alpha waves. It sounds pretty calming and soothing.

Brandon: Yeah, I mean if you're really good at this, and you get a qEEG, and you do a physical examination, and you understand all of these different sort of frequencies and music, you can programme in the background of any song they want and you can almost make it disguisable, yet the brain will pick it up.

Andrew: Right.

Brandon: So you can change a lot of the different waveforms that somebody's having a problem with, and they can listen to it while they're doing biofeedback. And the biofeedback is a hundred times faster. So you do that, and then if you want to, if you can, infuse some nutrients in them that's going to really jumpstart their brain while they take some stuff orally. You can end up getting somebody's brain to perk up very, very quickly.

I mean, I don't know what to tell you, but it works. I mean we've had to figure out ways to get a brain that fatigues very rapidly to not fatigue very rapidly.

Andrew: Right. I just want to cover one last question in this arena if you like from Ian, and that's the impact of sustained nose-breathing while exercising to drive haemoglobin release of oxygen. This fascinates me because of the real differences of advice, if you like, that we get from meditation, the belly-breathing, the deep-breathing, the yogic type breathing, versus things like Buteyko breathing, the shallow...

Brandon: Well, we always know this. The way I've learned this and I may be...Ian, you can correct me if I'm wrong on this. I love watching...I watched it just the other night. I love watching some mixed martial arts stuff, and you can always tell the people who were really trying to pull all their oxygen off their haemoglobin because they start mouth-breathing. 

Andrew: Right.

Brandon: And they don't have that smooth sort of look on their face like they're taking a beta-blocker. They're breathing nice. You can see their nostrils flaring a little bit but, as soon as they start to hunch over or they get into more of a Fowler position and they start mouth-breathing, and their nose is flaring even more, they're struggling to try to mechanically ventilate things through. 

And remember when you mechanically ventilate things through, oxygen is going to lose its affinity at an easier rate from haemoglobin. So, I do think that's a very interesting thing.

I mean, for rehabilitation, we don't see that too much. We see some people come in that have cardiac conditions though, and that's one of the ways that we identify cardiac conditions or even respiratory conditions like COPD. They look like they've been running, and they look like they're trying to pull out every single morsel of oxygen that they could possibly get.

Andrew: Is this the pink puffers and the blue bloaters? Is that what you're talking about?

Brandon: That's right, yeah.

Andrew: The pink puffers.

Brandon: The pink puffers and the emphysema patients. Yep, absolutely. I saw one walking down the street the other day with two tanks strapped to her and two cigarettes, one in each hand walking down the street. I was like, "That is something." I was like, "I don't even know how you do that."

Andrew: That's like a scene from "Judge Dredd" 2000 A.D., you know?

Brandon: I wanted to take a picture, but I would have had a wreck, you know, and then that would have been that.

Andrew: Yeah. A question from Michelle regarding Huperzine. This is a really interesting supplement. It sort of wavers in its evidence. There were some trials that were really disappointing, others that were glowing. Where do we sit with this?

Brandon: Well, there's a couple of things. First of all, we're really wavering about what amyloid is. I mean some people think that amyloid...like, so, you know, you have that beta-secretase that turns into gamma-secretase and it shaves off those oligomers and you should have a monomer.

Andrew: Sure.

Brandon: If it's not appropriate, it turns into an oligomer. It connects together and makes amyloid. And that amyloid is supposed to attach to the cell and then all hell breaks loose.

Well, we're finding that maybe amyloid is protective against infectious disease, okay? So, we don't know. I hate to sound conspiratorial but what I'll tell you is is that there is some evidence that's leading towards that as being prevalent. 

And we're also finding that maybe Huperzine and some of the studies is being pointed at the wrong thing. Maybe it's doing something different. Like, maybe it's dealing with reactive oxygen species and intracellular function, rather than extracellular environment within the brain and amyloid.

We know that a lot of people feel better on it. But maybe it's not doing what we thought it was doing. But some of the literature does show that, if you have amyloid...and also proline-rich glycoproteins are very, very good for the intracellular tangles.

Andrew: Got you.

Brandon: There's actually some pretty good literature on that. So, I mean you can throw some things together and kind of see what's going on. But again you don't want to be that person that gives them a shopping cart full of nutrients.

Andrew: No, that's right. Yeah. I just want to finish off on Buteyko system because Ian made a comment. It's part of the Buteyko system. There's a big difference in breathing frequency. Which part of the AMS is being activated?

So, just along that line, everybody, register for FX Medicine podcasts because I'll be podcasting with Patrick McEwan. I think it's in August, so it'll probably be released September, October-ish. So, yeah, make sure you subscribe to be the first to find out about that one.

Anyway, so treatment stratification, Brandon.

Brandon: Yeah. Well, the first thing in treatment stratification is always, first of all establishing rapport with your patient. I mean find out if you can do anything for this person. If you really don't feel like you can do anything… Well, let me just say it differently. You have to say, "Maybe I can achieve this." And if they want you to achieve this, they're not your patient. But if they're saying, "Look, if I can get this, and you can help me with this, then perfect."

And I think that you need to learn to match with your patient. I think that that's a really big thing. Like, I had an 89-year-old Alzheimer patient that came in and she was in stage 6 Alzheimer disease. I don't treat stage 6 and 7. And I'm like, "What do you want us to do? You know, grow a brain back? We're not there yet." And they're like, "No, no, no, no. All we want you to do is to get her to where she can give us a cue of any type that she needs to use the bathroom." 

Andrew: Right.

Brandon: At first, I was like, "That's crazy," but then I started thinking how important that is for the family. And we achieved that goal, and they were happy.

Andrew: Yeah.

Brandon: Okay, so the first thing is figure out if you're a good practitioner and figure out if, you know, you're going to be able to deliver something that is going to be therapeutically or potentially therapeutically beneficial, okay? 

The second thing is figure out what lab tests you want to do and don't run everything. Become a good enough clinician to say, "I think I need to go over here," okay? That way, you're not wasting thousands and thousands and thousands of dollars because some of that might be treatment money.

But I always like to look for what might be the cause. And so I'll give you an example, just a starting example. I found that I've become an infectious disease doctor. You know, not to my own chagrin. 

But a lot of times there's either a parasite, there's a fungus, there's some sort of infection or infestation or some sort of environmental factor that has gotten into the system that has created a whole load of inappropriate physiological responses. So, a lot of times I have to identify those and then start to reduce those things.

Now, that obviously can lead to a state of inflammation. And in some people just a little, in some people who are genetically prone, a ton. And it might not just be one of them. It might be a food with mould with a virus, and all of those together exceeds what they can genetically tolerate, and now you got to sustain inflammatory response. So now their skin hurts, their joints hurt, and they're starting to get brain fog.

So, I look at this poll over here and there's more people that want to learn about neuroinflammation. Well, one of the very first things that you're going to want to see is: do they have the symptom of brain fog? And for those that have that, they’ll explain it as, "I feel like I'm in a cloud," or “Things that I just can’t... it's not that I can’t,” they have a very difficult time putting it into words.

Okay, so we go from a starting point that we have to control, inflammation that we have to control, and remember...everybody please remember this. I'm going to probably put a lot of people in a very weird position right now. Killing off something can sometimes promote inflammation. 

So you have to look at this and say, "Do I need to draw up inflammation then kill things or do I need to kill things and control inflammation at the same time?" It becomes a very long immunological story.

So, what we found out is we can't separate the immune system from the nervous system. It's just impossible. Okay? So without getting too detailed in that, we control the starter, the in-between thing, which is the fire, the inflammation, and then one is going to get burnt. And in this situation, we're saying the brain. So we have to identify structures that are getting damaged and does that correlate with symptoms.

So sometimes I'll have to lay it all out, and I make each patient a formula. Like cytomegalovirus plus this gene plus high interleukin-6 plus high tumour necrosis factor plus a blood-brain barrier marker that's down plus these symptoms equals Sally Jo. 

And then I'll take all those and then flip them and put down on the top what is the first thing I want to knock off, the second thing, the third thing, and the fourth. And then I work my way down instead of trying to treat everything at once.

The reason why I do that is because, if you give somebody five things and something goes wrong, you have no idea. But if something goes right, you have no idea. That has become the art of my life. The art of my life is making that equation and stacking it to where it's not stacked the wrong way. And so, to me, that is the… Or you could just give them those high-dose steroids. You can call it a day.

Andrew: And leave the infection to run.

Brandon: That's right. Actually make it worse.

Andrew: Marty made an excellent point, "Stop the prolonged use of anti-fun-gals."

Brandon: Boy, you know what? End of lecture right there.

Andrew: We are nearly out of time, but before we go, there's a couple of short questions that I do want to...Well, I say short. You and I talking, I'll tell you. 

Supplements. Which ones have merit? Which ones give you most bang for buck? And indeed, which ones do we really have to be cautious of? Are there any caveats that we need to be aware of with therapy?

One that I'm interested in is phosphatidylserine. Now, for memory and remyelination, things like that, there seems to be some nice evidence and it seems to, after a long lull in research, there seems to be new research picking up, which I find interesting. Having said that, I'm really interested in its other uses like a flag, if you like, or a tag in cancer cells.

Brandon: We were literally going to make a t-shirt that says, "Phosphatidylserine, come eat me."

Andrew: Why?

Brandon: I mean, that's obviously a nerd shirt.

Andrew: Yes.

Brandon: You know, phosphatidylserine will actually help dampen the receptors that say, "Come eat me," like, phagocytically. So we use it in neurodegenerative diseases to slow down the volume loss, okay? That's one of the things that we do. Plus it also can help stabilise phospholipids and bilipid membranes in regards to a healthy cell. In regards to cancer cells, it tends to be different, where it flips up a "come get me" cell.

And so we have to monitor that. If we want to get into cancer, things like VEGF and stuff like that. There's a lot of people now, at least in the States, that are injecting people with exosomes that carry all these cytokines that are supposed to be beautiful. And some of them, like VEGF, can be very good. 

But VEGF can go up in cancer patients and allow blood vasculature to go to the tumour. So you can inject something that can bring more blood flow to your tumour and make it bigger. So this is why we're not ready for some of those things yet.

Andrew: No. So, you mentioned broccoli sprout extract earlier, though.

Brandon: Yeah.

Andrew: Right. Let's talk about that.

Brandon: Yes. It’s one of my favourites. Sulforaphane. We have a version. We call them glucoraphanin. That's a pretty unstable product. We have one product that you can get about 3 pounds of the broccoli sprout extract in one serving. And, if you look through the literature, just about every one of those genes is going to say “sulforaphane is good.” Olive leaf is excellent. We could go on and on and on. With each one of these patients, all the treatment plans look different.

I use a health coach that works for me; that's Tara. She's very, very good at understanding at what I say we need to do and she works with them on their diet. And then I work with them on their nutrition and medication and put together their treatment plan. And we have a psychologist that works with different things. So we have a team put together, and we all work in one cohesive unit. And we found out that we have to, because the family members become afflicted, too, when somebody starts to become, let's say, neurologically declined.

Andrew: Oh, sorry. Now, Bernie's question. Oh, yes. One last question: can we talk about vestibular neuronitis for a tick, please?

Brandon: Yeah, yeah, neuronitis. Okay, so neuronitis is going to obviously create a wicked case of rotational dizziness where… And you've got to remember, with neuronitis, unless you have another disease, it's going to feel like the room is spinning and not yourself. If you feel like you're spinning, it's probably going to be right here in your right parietal lobe, okay? Or parieto-insular vestibular cortex.

But if you have neuronitis, it's usually inflamed and the foramen that it goes through is getting choked off. So you have the vestibulocochlear nerve coming down, and then it splits, and the vestibular nerve comes up, and then it splits. 

And the superior portion of the vestibular nerve usually gets choked off and it allows you to have a pure horizontal, very rapid nystagmus that happens without putting somebody in position like BPPV. 

However, there's no hearing loss because the cochlear part is not involved. Now, if you have something that looks like neuronitis and you lose hearing, it's labyrinthitis.

Andrew: Right.

Brandon: Or, you have an acoustic neuroma, and that creates something called Bruns nystagmus and it switches directions depending on what you're doing.

So, to answer the question, neuronitis is sort of like trigeminal neuralgia, or some sort of idiopathic brachial plexopathy. Nerves have the tendency to crawl down different pathways and it makes them inflamed. So did you get the facial palsy, the trigeminal neuralgia, or did you get the vestibular neuronitis? And I have found it with bacterial and viral infections. Don't forget bacteria. It actually happens.

Andrew: Right. What about when people seem like they're having this vertigo or a neuronitis-type issue, but it may be a PFO? How do you differentiate between that.... You're doing cardiac stuff now. Welcome to this one. A patent foramen ovale in their heart. So, how do you differentiate...

Brandon: I'd do an echocardiogram.

Andrew: Right, okay. Got you.

Brandon: No. I mean, a lot of times you can...if you'll get the mechanical or the electronic Welch Allyn stethoscope, a lot of times you can hear them...

Andrew: Right, okay.

Brandon: ...in the systolic contortion. So, as the atria contracts, you can hear it swish over. And also they're very inefficient, in most of them, because the colour of their skin when they're born will be...it should flap over but if it becomes patent, then by the time you leave the hospital, then it's usually noticed that the child is not the normal colour that it should be.

Andrew: Yeah, good point from Inga: Listen to the heart. A good exam.

Brandon: Yeah, and by the way, those electronic stethoscopes, it actually sounds like it really does when you're learning it on video. I mean, it's beautiful. And you can get them now that runs a single rhythm strip to your computer through Bluetooth. It's amazing, you know?

Andrew: We look forward to you completing your PhD and your research into this, because I think there's going to be some very exciting and practical implications for those people that are interested in cardiology. I am one.

But, Brandon, thank you so much for taking us through just the tip of the iceberg of neuroinflammation today. I know there is so much more to cover. Everybody, please keep your eyes and ears peeled because Brandon and I will...please can we do another podcast on this?

Brandon: We can go every week if you want. I mean this is so deep. I mean we really could pull out just one little specific portion of it and talk about it for an hour or two.

And to those of you that are out there, I want to say thanks for listening to a very broad spectrum that's not specific, but also thank you for getting interested if you are, and learning…

Remember, everything that you learn, whether it be detoxification or whether it be gut function or gut health or thyroid, it all plugs into the brain. It will all have an impact on the brain. So, the more you learn about it, it can just plug right into this topic. So that's why I'm kind of giving the broad view because everything that you know that's specific will plug right into this system.

Andrew: Well, we've already taken a poll and got some ideas for what we should talk about next. But if people have any specific areas of interest, please let us know at info@fxmedicine or on our socials. We'd love to get Brandon involved.

And the whole point of FX Medicine is to improve the skillset and the safety of integrative medicine practitioners worldwide on a non-branded platform. So, please let us know how we can be better for you.

Brandon, thank you so much for joining us and sharing with us your wealth of knowledge. That bookcase is in your head. I can…

Brandon: No. Hey, listen, I just want to say thanks for having me on. You know, this is my favourite. You guys are my favourites, man. I love being...I just love being on here, and I love your crowd and your audience. And I always love going and hanging out with everybody in Australia. It's my favourite thing to do. The plane ride's a little rough but other than that, it's great.

Andrew: Let's be honest. Your friendship and mine revolves around whisky and tequila.

Brandon: Yes. That is true. It does, to an extent, for sure. We've actually sketched things out on napkins at bars. Like, hey, what do you think about this? You know, what do you think about that?

Andrew: Thanks so much for joining us tonight on FX Medicine, Brandon. We'll speak to you soon.

Brandon: Thanks, everybody that joined in. Appreciate it.

Andrew: And this is FX Medicine. I'm Andrew Whitfield-Cook. But who cares? It's Brandon.

Other podcasts with Brandon include


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