Everyone’s Brain Needs Primary Prevention

James Maskell:
I’m going to go so far as to say that 2026 is going to be the year of the brain, and you’re seeing for the first time, cognitive decline being reversed very soon, improving the neurobiology of our patients is the work in hand, and ultimately, primary prevention means a disease or condition that is averted.

Hello and welcome to the evolution of medicine podcast. This is season two, episode four, and today we are going to be talking about the push for primary prevention. If you like the podcast and you’d like to see more of it, we’d love to hear from you. You can watch us on YouTube. You can get it anywhere that you get podcasts and audio, and we’d love to connect with you on social media. Please leave a comment, please like, please subscribe, and please pass this on to another clinician who needs to hear it.

So I mentioned we’re going to be speaking about primary prevention, and today’s segment comes from not necessarily the news, but an article that I read that I thought would be music to the ears of our community. And this article is written by Dr Eric Topol. Many of you may know him as a leading voice in conventional medicine. He wrote the book The creative destruction of medicine. He also wrote the book super ages, and has been a leading light in conventional care, talking about, sort of the cross section of technology and the future of medicine. And he wrote a recent blog that caught my eye, and it was called, it’s Time for Primary Prevention in Medicine.

I’m just going to share with you a couple of things from the article that I liked, but first and foremost, let’s look at the image that he has used for the description, and essentially, if you’re listening to this at home, it’s a pyramid. At the base of the pyramid, you have primary, prevent diseases from occurring. Then next up you have secondary, detect disease and decrease severity of all diseases. Then we have tertiary, decrease decrease complications, ie morbidity, mortality and disability. And then at the top quaternary, avoid unnecessary medical interventions.

So this is his showcasing of where primary prevention fits into the into the system of medicine. And ultimately, primary prevention means a disease or condition that is averted. The term was coined and introduced by Lavell and Clark in the 1940s and now 75 years later, we’ve yet to achieve any substantive primary prevention with a three with a notable exception of infectious diseases on the three major age related diseases that he focused on in his book super ages, cardiovascular, cancer and neurodegenerative we have not prevented the latter two.

So he goes on to talk about how this is such a big deal. Instead, our healthcare is now centered on treating these diseases, which has limited success for many cancers and even less. Thus far, no disease modifying impact for neurodegenerative diseases like Alzheimer’s and Parkinson’s. No less, there’s a profound economic benefit of primary prevention for reducing the cost of such treatments, such as tailored oncology drugs or support of people with dementia in long term care facilities. I hope this brief review will convince you that primary prevention is a great and largely unfulfilled need, and that in the light of recent advances, should be given the highest priority.

The key problem is that we haven’t had the ability to do it until now. So going through the rest of the article, what you’ll see he starts talking about large language models. He talks about personal health agents, which, by the way, has health coaching as a center part of it. And he talks about epigenetic organ age clocks. He talks about continuous protein monitoring that was new to me. And essentially he’s he’s essentially showcasing that this, this one graphic that in 2025 for primary prevention, we have vaccinations, lipid panels and promoting healthy behaviors. But in the future, we’ll have all of these other things, like organ clocks, the epigenetic clock, biomarkers like P, tau, 217 and inflammation and this kind of information.

He says, we’re at the dawn of primary prevention. Not only are there many new layers of data, organ clocks, biomarkers, genomics, biosensors, but we have multimodal AI and agentic AI to analyze the data. He talks about some of that, and ultimately, this is, this is what I thought was interesting. So now let’s talk about why I think this is interesting. So first is that pyramid should be quite familiar, especially if you followed my work, because the thesis at the end of the community cure was about, how do we reorganize medicine, and I look towards the naturopathic therapeutic order, which looks very similar. In fact, it’s also a pyramid.

And what do we have at the bottom of that pyramid? What could we learn about preventing and reversing chronic disease from the naturopathic therapeutic order? So the lowest level is dealing with the determinants of health. So establish the foundation for optimal health. Then we have stimulate the healing power of nature. So stimulate the self healing mechanisms, and then.

Third is support and restore weakened systems. Now Topol does talk a little bit about lifestyle, but he doesn’t talk about these three areas. And these are three areas that practitioners in our community and people are looking at that already facilitates primary prevention. If we look at a damaged organ systems, which is the third, which is support and restore weakened systems. That’s clinical nutrition. That is nutrition. That is what is possible. That’s what a lot of functional medicine practitioners are doing. That’s what this world is. So there’s some highlights from there.

Ultimately, in my book, I talked about the fact that this bottom layer could be done with groups, because ultimately, if you want to work on the social determinants of health, you have to work on loneliness. And so I think this is really interesting, because the answers are already within us. And I would challenge Dr Topol to say, if he thinks that no progress has been made in the primary prevention of neurodegenerative diseases, he’s just going to the wrong conferences, because the conferences that I go to, there’s plenty, plenty of action in those areas.

Look back at the Journal of Alzheimer’s 2022 the use of precision medicine to prevent and reverse cognitive decline. You’re seeing for the first time, cognitive decline being reversed. Very soon, you will see the results of the event, Thea study, which will show you know similar, similar things. Although I can’t comment on the details of it, yeah, because it’s not out, but I have seen some of the details at some recent conferences. So it is true that we have made progress. It’s just that progress is not being seen at the conferences that he’s going to. It’s the conferences that we’re going to.

I would love to give a shout out to the PLMI thought leaders consortium that I was at a few weeks ago, led by Dr Jeffrey Bland, incredible lineup of speakers. So there was Dr Bland, Dr Hyman, Dr Robert Lustig gave a talk about reactive oxygen species and neurodegenerative disease you had. Dr Perlmutter, younger and older, giving a great talk. And ultimately, you know, all of the speakers really touching on the brain and neurodegenerative disease as a key area where, you know, there is, there is success.

One of the things that I just want to share, one of the key questions that was asked during one of the panels was, in the time of great division, what should we be doing? And essentially, Austin Perlmutter shared something that really spoke to me, which is that improving the neurobiology of our patients is the work in hand, because ultimately it’s doing that work that allows people to think clearly, allows people to be with each other, allows people to connect, and that is the number one thing, why I feel compelled about this, and why I’m proud to work with a network of practitioners who are improving the neurobiology of their patients, whether that’s the goal or Not.

So this is something that I think is interesting. It’s in the news, but good to know that Eric Topol thinks we’re moving towards an age of primary prevention, and I’m all for it, and I know that the answers are going to come from this community. Now, something that came up at PLMI was interesting was Dr bland acknowledged the fact of the recent Nobel Prize in Medicine, which was the discovery of regulatory T cells, or T reg cells. And it’s interesting that that discovery was made in 2002 2003 and it’s 2223 years later here, now that the Nobel Prize is awarded, what it brought back to me is the realization that it may be years down the road by which medicine actually realizes or acknowledges that all of the information that’s being shared at the current functional medicine, precision medicine conferences like PLMI is the medicine the future is going to take some time, but we’ve got to start delivering it now.

And so I want to give a shout out to the next PLMI conference that’s coming up April 17 and 18th. I’ve been going to this conference for a number of years. I think it’s incredible, because you don’t have the bounds of CME education, and so, you know, the practitioners are very clear about what they’re doing in clinical practice, and this year’s lineup is ridiculous. So you’ve got Dr Bland, kicking it off. You’ve got Dr Perlmutter, you’ve got Dale Bredesen, you’ve got Phyllis Z, Patrick Hanaway, Elroy Vojdani, you’ve got Tom Williams, you’ve got Austin Perlmutter, Ashley Koch, Peter Staats, who is one of the inventors of the technology for optimizing vagal tone. And then Peter Kozlowski is batting cleanup there. It’s a great lineup.

I’ve been to this conference a number of times before. Always high quality, if you can be in Chicago the 17th and 18th of April next year, I highly recommend it. Let’s talk about one other area that is big in the news right now, and that is the future cost of healthcare. And I’ve got this article from the AP. It says, what Americans think about rising healthcare costs. According to a new poll, most adults are worried about health care becoming more expensive, according to this new poll, as they make decisions about next year’s health coverage, and a government shutdown keeps future health care costs in limbo for millions, six in 10 Americans are extremely or very concerned about their health care costs going into next year, a worry that extends across.

Age groups and includes people with and without health insurance. Many Americans have health care anxieties too. A poll found that four in 10 Americans are extremely or very concerned about not being able to pay for health care and the medications they need, not being able to access health care when they need it, or losing or not having insurance. But here’s a graph that I want to share. The economic and health care issues are top of mind. So the economy is top then health care, then crime, immigration, gun policy. It’s slightly different depending on, you know, depending on the different groups there.

But obviously a lot of this has to do with the shutdown. A lot of this has to do with some of the, some of the reports that are coming out about how much health insurance is going to increase next year. Ultimately, I want to come back to something that I’ve been talking about for a long time. About for a long time, which is that the best thing that you can do if you’re concerned about your healthcare costs is to be healthy. Because ultimately, most of the healthcare costs, if healthcare costs are 90% chronic illness, you can massively reduce your chances of getting a chronic illness by participating in primary prevention.

I think these things go so hand in hand, and you, as the practitioner, can be a custodian of that in your community by getting out into the community talking about these changes, talk about primary prevention, talk about what it’s going to take to get healthy, and showcase some of the work that you’ve done in your community with some of your patients. So this is hot for patients right now, and I hope that you can jump in and be a blessing in your community. So this is what’s happening in the industry right now, is there’s a lot of conversation about brain.

I’m going to go so far as to say that 2026, is going to be the year of the brain. Why do I say that? Because we have Dr Bredesen’s preprint coming out in December, possibly being published in April of next year, we already see that this conference is focused on it. There’s a lot of talk about the brain, because unlike any other condition, there are no drugs and there is no competition for the work that is being done in our community. And that’s why I’ve been hot on this topic for a long time. So each week, we have different supporters, we have different mission partners.

Last week I mentioned the work of BigBoost Marketing. BigBoost is if you want to launch a brain health program in 2026 for the year of the brain, BigBoost is going to be your partner to bring patients into your practice who are looking for these kind of services. So you can see the details on the screen. If you go to goevomed.com/bigboostguide, you can get their free download, and you can see how Uli is helping clinics like yours bring in new patients for a bain program.

Our second mission partner that I want to talk about, we’re actually going to go into a little bit more detail today, because this is true neuro, and true neuro is our mission partner, because they are making it much easier for clinics to run this kind of brain program. I’ve been working with Dr Burke for the last year and a half to really understand, you know, how to make it easier for clinicians to do this protocol, because in theory, it’s complicated, right?

You have a lot of different root causes that you have to look at, you have to synthesize so much data, and I know that many practitioners in our community have started off, you know, trying to do this work, trying to reverse cognitive decline, and they’ve ended up being stumped by either tricky patients or just not being able to work quickly enough because of time. You know, time is brain, and you actually have the clock is running. And so we’re really excited to have TruNeura as one of our partners.

Essentially, TruNeura is a clinical implementation tool, clinical implementation program that, on one hand, is synthesizing the data, organizing the data, and visualizing the data to make it easy for you to track the outcomes and to understand what is driving the cognitive decline in the person in front of you. So that’s a very big, important part in making an impact in it, but it’s also keeping track of what the patient is doing. And you can push your recommendations to the patient, both lifestyle and clinical, so that they can then take up and use those tools, and we can track what did each patient do, and what outcome Did it have, not only on their biomarkers, but also on their wearables.

And there’s wearable integration to make it easy, as we spoke about a couple of episodes ago. You know, we need tools like this to be able to compete with these other organizations that have data that are consumer focused, and so we’re really excited to have true neuro in the mix. So if you go to
goevomed.com/truneura , I can get yourself a demo. And I would love to chat with you, because one of my goals for 2026 the year of the brain, is to get 500 clinics, 500 clinics across the country, to launch a brain health program so that we can build capacity of the brain health, cognitive decline reversal network.

If that sounds appetizing, get in touch. I’d love to speak with you. There’s both a massive economic opportunity, an impact opportunity and a society transformation opportunity by doing this. And we’d love to hear from you if you’re interested in doing that. So continuing on that theme for the clinical corner here today, what I wanted to do is to showcase what I think that Eric Topol is missing. What is the clinical information that Eric Topol is missing that if you understood it, you would then understand how to prevent and reverse neurodegenerative diseases, particularly, let’s start with Alzheimer’s and dementia, and there’s many places you could go for that education.

But I’m super grateful to the personalized Lifestyle Medicine Institute for giving me access to Dr Burke’s talk from last year’s session. And what we’re going to jump into here today is some of the very specific diagrams. Now if you’re listening to this audio, I highly recommend that you get onto the YouTube channel and watch this, because Dr Burke has some of the best slides, the most sophisticated, the most clinically interesting slides that I’ve ever seen.

And in this session section of the of her talk last year, you will see the mechanisms of action that are defining and facilitating the prevention and reversal of cognitive decline. And so you know, if you know doctors, if you’re watching this, and you know doctors that have told you that this is impossible, you can’t reverse it, there’s nothing to be done. This is the segment to show them, because you see that deep within the science, deep within the physiology of the body are the clues to the prevention and reversal of cognitive decline. And so we’re going to take a segment of Dr Burke’s talk for our clinical corner, and we’ll come back to wrap up in a minute. Enjoy.

So this slide really lays out the story of how gut problems turn into brain problems. So on the left hand side, in a healthy gut, we have a nice, dense mucus layer and intestinal glycocalyx. We have intact epithelium, and all of the things that are supposed to stay in the gut, like LPs, lipopolysaccharide, our microbes, amyloid, are all in the gut, and then we have this nice balance of immune conversation with the immune cells, the astrocytes and the microglia and through the enteric nervous system. There in the middle, our HPA axis is balanced. And then our cytokines, I’m sorry, our neurotransmitters are being circulated from the gut up to the brain, everything is happy, but on the right hand side, that’s where we see what happens with a leaky gut and how leaky gut directly leads to neurodegeneration.

So we have the loss of the structural barrier. So now we have LPS coming in, triggering an immune response. We have cytokines and bacterial metabolites, leading to a disruption of the blood brain barrier, which is the little pink cells along the middle of the slide. We have that blood brain barrier disruption now leading to activation of the microglia, that leads directly to our neuro inflammation and neurodegeneration. So you cannot have a healthy brain without a healthy gut. They’re inexorably linked.

So what does all this mean in the context of the pathology that we often see in Alzheimer’s disease? And I say often because I actually even had this conversation earlier today, we see people late in life, in their 80s, 90s, with robust amounts of amyloid, who did not have cognitive decline at autopsy, obviously. And then we see people that have symptoms consistent with an Alzheimer’s type presentation, who don’t end up having a lot of plaque. So it’s a piece of the puzzle. It’s a strong contributor, but it isn’t an If This Then That there, as always, there’s more complexity to the puzzle.

So let’s look at how it unravels. So in the middle, we have our common pathways of chronic disease. We have chronic inflammation, oxidative stress, cytokine imbalance, and we see those commonly lead to things like diabetes and to rheumatoid arthritis or inflammatory bowel disease. And in the brain, we see that lead to things like amyloid plaque, tau tangles, and then the cognitive decline and neuroinflammation pathways.

So how is amyloid beta actually formed? What? What is it that triggers that process? So on the left side, we have in the healthy state, normally, we have amyloid precursor protein, which is a transmembrane protein, and that middle transmembrane section, the red section, that’s the amyloid beta peptide. So in a healthy situation, Alpha secretase cleaves the A,P,P at the membrane, I’m sorry, at the middle, so that the amyloid beta peptide is divided and that.

Doesn’t clump together, but in situations of either the inherited ones like the AP, P or the P senilline mutations, or in the setting of chronic inflammation, beta and gamma secretase Get upregulated and they cleave amyloid precursor protein at the membrane level, and leave that amyloid beta fragment to then clump together, and that leads to the oligomers that lead to the amyloid beta plaques. So that’s how inflammation is related to the formation of amyloid just one way, then outside the neuron, we have the amyloid beta cascade leading to those plaques that then accumulate and interfere with the neuronal, synaptic signaling and inside the cell, the amyloid beta stimulates the hyperphosphorylation of tau, so excessive phosphorylation of tau and that stimulates the formation of the tau tangles. So that’s how those things are happening.

And when you look at it this way, that the tau tangles, the amyloid plaque, the hot microglia and the toxic astrocytes, those are the pathological characteristics that we see. But what really leads to the activation and the creation of all those things are the things that we’re used to dealing with, like inflammation and infections or dysbiosis, toxins, some genetic components. So all of those pieces are what are contributing to the environment that’s creating the pathology that we want to change.

And importantly, amyloid beta is actually an antimicrobial peptide, so just let that sink in for a moment. So if amyloid beta is our innate immune response to microbes that have gained access into the brain or into the enteric nervous system, because we can see Alpha synuclein tangles there, then it’s really a defensive response, not a pathologic response. And so that changes the whole conversation about what we want to do with amyloid. And then it makes sense that when you give people an amyloid binding antibody, and you rip amyloid out of their brain like ripping off a scab, but those brains bleed,

and you’re taking away the protection. So this is one of my favorite slides, but it’s it’s busy and a bit complex, and without my pointer, I’m hoping you guys will stay with me on this one. So this study, basically, we know that we have this rich microbiome, and we know that we have it in multiple areas of the body, but now we are learning that the brain actually also has a biome. And so this study was rapid post mortem analysis, tissue analysis using next gen sequencing, and they looked only at the bacterial geniuses that were present.

They didn’t look for fungi or viruses. They looked only at bacteria. So the so first of all, let me, let me put so the far left bar, that’s the blood biome. So blood also not sterile, just not infected, right? It’s this whole homeostasis thing, where there’s just a little bit there doing whatever role it’s supposed to be doing, but when it gets to be too much, then we have an infection, so you have the blood biome, and then the very next one over is the initial control area of the brain, that’s the enter rhinal cortex.

And what you can see is that that has a completely different microbial structure, like you can just see the colors are all different than the blood. So the brain biome is not just passive passage of bacteria from the blood into the brain. It’s actually much more closely matched to the nasal, sinus and oral biomes. That’s why the mouth is so important in cognitive health. Then we have the do those, there’s our controls. Then we have the hippocampus. The green arrow is pointing to the hippocampus of an Alzheimer’s patient.

The yellow arrow is pointing to the control hippocampus. So hippocampus where memory is stored, atrophies with Alzheimer’s disease. So in the control group, we have a big amount of green, which is lactobacillus, and we have a pretty large amount of the bright green, which is streptococcus, and then a little bit of the purple. But when you shift from there to the next bar, which is the hippocampus and the Alzheimer’s patients, we lose the lactobacillus. We have the big increase in the now I’m drawing. Blank on it. Let me see. Let me look at my notes in the Thank you.

The Cutibacterium, cutibacterium, so cutibacterium, which is a common nasal colonizer, has, that’s the purple that has. There’s almost twice as much cute of bacterium in the Alzheimer’s hippocampus, as there is in the control outpaced only by the amount of acute of bacterium in the Parkinson’s disease patients, which is, I think, the fourth or fifth line over So, in the interest of time, I won’t go through all of these, but there’s really fascinating differences that occur through the blood biome and the, I’m sorry, the brain biome.

Okay, so now let’s turn our attention to tau protein, the other supposed Alzheimer’s disease villain. So the microtubules are a structural component, that’s the scaffolding that supports the axon we transport nutrients through like a little highway, and tau acts like a structural bolt that holds those in place. And tau is meant to be able to be removed and replaced, because it’s that restructuring of the microtubules that allows us to have neuroplasticity and also for the brain to grow when we’re when we’re children. And so when we have hyperphosphorylation of tau, then the tau starts to stick together, and the microtubules start to unwind, and we have loss of axonal transport.

Now tau is also an innate immune response protein, and there are a variety of ways that tau can be moved from one place to the other. We used to think that tau only ended up in the blood because the axon degenerated and the tau leaked out, but now we know that tau can be spread at the synapses, it can be released in B from the dendrites. Once it’s scavenged by the microglia, it can then also be packaged into an exosome and sent back to the neuron. So there’s a whole cycle of tau. But when the microglia are activated, and we get into this detrimental loop with il one beta and TNF alpha. Then that’s when we start to get the pathological tau increasing.

So Tau has a lot more jobs than just its structural protein role, we can contrast that stabilization to these emerging roles that we’re learning about that seem to be mediated through another group of enzymes called the thin kinases. So tau now has been found in both the T and B lymphocytes, which is really interesting, and brings it back to that innate immune response in the cell signaling loop that we just saw with the neurons and the microglia, and also it’s been found in the mitochondria and in the nucleus. So tau moonlights in a wide variety of other roles. So it’s not a pathological protein. It’s a protein that has specific roles that then get hijacked when the body is out of balance, right, when we have chronic inflammation, when we have a huge inflammatory burden, when we have a dysbiosis, perhaps in the brain, that’s what stimulates these dysfunctional environments.

Now, if fin is if the ability of fin to act is taken away. So this is a study using fin knockout mice so they remove the ability for fin to be active. On the bottom the black dots are neurofibrillary tangles, which we see in the presence of fin in the normal mice, but when you take the fin knockout mice, there’s no black because now without fin, tau doesn’t tangle. So the story just keeps getting more and more complicated. But I really just want to emphasize that there’s just a lot more going on than just stuff gumming up the works.

So lastly, tau also mediates T cell driven neurodegeneration. And so here in the healthy brain, again, on the left, we have our happy little environment, and then on the right, where we have the amyloid and the extracellular tau on the bottom left, activating the microglia, which are producing pro inflammatory cytokines, which are causing direct inflammatory damage to the neuron. Then on the right side, they can also present antigens to the T cells. Ulrich create T cell clonal expansion with antibodies against tau, and that can attack the neuron as well, so much more than folded proteins.

All right. So that brings us to our newly available blood brain biomarkers. So now that we have a little bit of a deeper understanding of where each of these proteins is coming from and what they signify, we’re better equipped to be able to use these and understand the information that we’re that we’re getting from them. So first we have p, tau, 217, this one is highly specific to Alzheimer’s disease. It’s more specific than p tau, 181, so it has supplanted that. It can be measured in both blood and CSF.

But of course, for our purposes, most people don’t want to have a lumbar puncture and have their CSF sampled, so it’s nice that we can measure it in the blood. Then we have the amyloid beta 4240, ratio. This is also highly specific to Alzheimer’s, and together, they make the diagnosis. So amyloid beta 42 is the one that gets more sequestered in the amyloid plaques. So as more amyloid plaque is forming, the ratio of 42 to 40 in the blood is falling. So I don’t know why they couldn’t have put the ratio the other way. So high p tau was bad and high amyloid ratio was bad, but they didn’t. So now we all have to remember that high is bad for one and low is bad for the other one.

Then we have neurofilament light. Now neurofilament Light is really a measure of axonal damage, so it’s not specific to the specific type of neurodegenerative disease. It’s just telling us that there’s axonal damage occurring. So it’s going to be elevated in a wide range of conditions, and it can be really excellent for tracking, both tracking after things like concussion, like someone’s had a moderate or severe concussion. We can use NFL to follow their recovery. And then when we’re working with people with our cognitive decline interventions, then we can see whether or not we’re making a difference in the rate of injury.

And the last one is GFAP, or glial fibrillary acidic protein, that’s an indicator of the astrocyte activation glial damage, and so it’s elevated in more than just Alzheimer’s as well, but it may be a potential marker for distinguishing Alzheimer’s from Frontotemporal dementia, because FTD has less astrocyte activation. So it might be helpful in that, although I can just say, in my experience of using these over the last couple of years, I don’t often see GFAP elevated, and so I don’t know that I would really feel confident that it could differentiate, but that’s what that’s what people are hoping for.

Okay, so back to our unified barriers. So now that we know everything that’s going on behind the curtain, behind the scenes in the neurodegenerative process, let’s go back out to our barriers and think about so now we know the glial cells, the endothelial cells, the neurons, these are the cells that are producing the inflammatory cytokines, that are signaling the gating, the barrier integrity of the brain, and that signaling is going to signal the immune cells to migrate into the brain, because, remember, the Brain is supposed to be an immune privileged environment, normal, normal white cells, T cells, lymphocytes. They’re not supposed to be in the brain unless disaster is happening and so that that level of signaling is going to start a whole inflammatory cascade.

Wait, I need to go back. Okay, so this article was published in 2021 and the quote that I think is super important for us is this damage to the fragile glycocalyx can lead to increased permeability of the blood brain barrier, tissue edema, glial cell activation, up regulation of inflammatory chemokine expression, and ultimately, brain tissue damage is that not what we just went through as the pathology of Alzheimer’s disease, right?

So this protecting the endothelial glycocalyx is the most important first step in preventing cognitive decline. We’ve known for a while now that the EGX is an important factor in the blood brain barrier. But really, this information just started coming out in about 2010 between 2010 and 2015 a few studies were trickling out, but from 2020 to the present, we’ve had an exponential increase on the number of studies looking at the glycocalyx and its role in neurodegenerative disease.

And once the EGX and the blood brain barrier are damaged, we have a whole host of diseases that we see as a result, and they’re not just neurologic like diabetes. Okay, so here’s our big picture view. This slide really captures the whole story. So in the. Central area. The central concept is that the microbiome, gut brain connection, is central to the health of the organism, the system, the brain, the gut.

On the left, we have what happens when things go wrong, the factors at the bottom, like leaky gut, dysbiosis, Western diet, antibiotics, stress, those are going to lead to imbalances in all the things we see in that bottom list, increases in LPs, increases in the translocation of LPs across the gut, intestinal barrier, alterations in the gut microbiome, gut inflammation, all of that leading to increases in peripheral oxidative stress, and then the cascade of events at the top, with the blood brain barrier disruption, neurodegeneration and so on.

But on the right is where we have the thread of potential control over this whole disease process, because all of our healthy lifestyle choices create that section, the paragraph in the middle, with high diversity, with lots of lactobacillus feces, like we saw in the normal brain, and all, of course, of the nutrients that we need, and then everything in the brain, the neurochemical production, the neurogenesis, the blood brain barrier integrity, are all up regulated, and neuroinflammation is down regulated, that is how we stop the tsunami of Alzheimer’s that we are facing.

Wasn’t that great? Wasn’t that some of the best graphics? Wasn’t that yes, complex, but making it easier to understand, it’s easier to see now, how we can intervene and make an impact in reversing and preventing cognitive decline, and whether you are treating patients with these kind of issues, if you’re treating mental health disorders, or even if you’re treating some of the subsets of root cause, whether that be, you know, hormonal patients, gut patients, cardiovascular patients, biotoxin illness patients, toxic patients, there’s something to Learn in there for everyone, because this is the physiology, and this is what is happening in the bodies and the brains of your patients.

So let’s talk a little bit. I’ve got a couple of other things that I want to bring in. I want to talk about a couple of the other mission partners. You know, one of the things that is mission critical today is that we start to think about how to expand the footprint and impact of the clinics that are already in the network. Look around the network, and you will see that most clinics are one or two practitioner clinics, because scaling functional medicine has proved harder than getting started with functional medicine in general, we have very passionate clinicians like yourself, and we need to find a way to make it easy for them to grow their practice and grow their capacity in each and every zip code of this country.

And so I’m going to highly recommend that if you go to goevomed.com/fpc, you can take the scalability assessment and you can find out what is holding you back from growing your practice. What is holding you back from reversing more chronic disease in your community? And it doesn’t matter whether you’re doing you know what your focus of your practice is, whether you do cash, fee for service, whether you do membership, whether you do programs, you can learn from this 20 minute investment in your time what’s going on in your practice, and it’s completely free.

So goevomed.com/fpc, you can find this scalability assessment, you can take it, and you can learn so much about the future of your practice. All right, we have a lot of cool things coming up as well from one of our mission partners, fullscript, and I don’t want to share too much, but they’ve got some exciting things coming down the pipe, and we talking about that in future episodes. Thanks so much for watching. If you can share this with someone that you know, like and trust, we’d love to bring more people into the community. If you want to get in touch with us, you’d like to set up a time with me.

You can go to goevomed.com/concierge, you can book a concierge call with either me or my team. I’m going to be taking a lot of these calls in the next couple months, because I want because I want to hear from you. I want to hear what your needs are. I want to understand what we can do to make it easy for you to be successful in your practice and grow the capacity of your clinic and the network. Thanks so much for tuning in. I’m your host. James Maskell, this has been the evolution of medicine podcast, and we’ll see you next time you.

 

 

 

 

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