Welcome to the Dr. Gundry Podcast. So 7.2 million Americans are living with Alzheimer’s right now, but by 2060, that number is expected to nearly double. If I was a betting man, I bet you it’s gonna be even higher. Now, for decades, medicine has been chasing the same theory to stop it. Clear the amyloid plaque, stop the disease. Drugs are FDA approved. Billions of dollars have been spent to develop them, but according to a just release co-trained review of 17 trials and over 20,000 patients, they don’t work. And they may actually be making things worse. Today’s guest, my good friend, Dr. David Permeyer, is a board certified neurologist and six-time New York Times bestselling author. His new book, Brain Defenders, makes the case that we’ve been targeting the wrong thing in Alzheimer’s, and that the real answer lies in a set of immune cells most people have never heard of.

(01:02)
In a bit, David and I will talk about why Alzheimer’s drugs have failed, what microglia are, and why they may be the most important cells in your brain, not neurons, and what the latest research says that you can actually do to protect your brain for the long haul. We’ll be right back.

(01:25)
Brought to you by the online healthy marketplace, Thrive Market. Make healthier swaps without the overwhelm. Visit thrivemarket.com/gundrypodcast for 30% off your first order, plus a free $60 gift. You and I have been saying this for years, and now the data is finally catching up with this. I mean, 17 trials, over 20,000 patients, and it says that FDA-approved amyloid clearing drugs deliver no meaningful benefit and raise the risk of brain swelling and bleeding. So what does this c – recent confirmation mean to you?

What it means to me, I think, is, uh, again, it, a confirmation’s a great word. It pretty well confirms what we have been talking about for an awful long time. Even before there were drugs that, uh, there was this amyloid-centric view of Alzheimer’s disease caused by one thing, the accumulation of this beta amyloid in the brain, end of story. And it’s called the amyloid hypothesis. And I think that’s a great term because a hypothesis is something that we will. It’s an idea that we will then test. And what’s happened is the testing has shown that this is not the cause of Alzheimer’s disease, but it’s a monotherapy approach. Getting rid of the amyloid should be presto changeo, the brain is fixed, everything’s good, and go on about your business. Well, the reality is, because the hypothesis, uh, is flawed, that getting rid of the amyloid has proven to be completely, uh, ineffective.

(03:04)
You just mentioned a cochrain analysis. And, you know, for people in the field, uh, that is the gold standard. There’s nothing better. This is an unbiased look at as much data that c – one can find to come up with an answer for a question. The question they asked in this case was, do the amyloid targeting drugs work in the treatment of Alzheimer’s disease? And what they came up with was no. And as you well mentioned, you know, this is 20,342 patients in 17 different studies over 18 months per study looking at all the data. And there’s no real benefit to using these drugs at all in the face of what you well characterized significant risk with 20 to 25% of people having brain hemorrhages and swelling, uh, with the statement from, you know, the drug manufacturer that we don’t know if this is gonna be a long-term problem or not.

(04:02)
One would think, just on the outside, uh, that bleeding into your brain and swelling might not be the best thing for you. Nonetheless, I mean, the whole scenario under which these drugs came under FDA, uh, evaluation and then subsequent approval, uh, if we had time, and maybe we will, we can talk about how that process occurred, because it’s, it’s worrisome how that even happened. But that said, we have to ask ourselves, what is upstream of the amyloid accumulation that’s really at play here? And as you said in your setup, it is the activation of the brain’s immune system, the inappropriate activation and persistent activation of the immune system that leads to a, a good brain going south. And I think that what is so empowering for our time together today is that we can control that. That so much, Dr. Gundry, of what you’ve been talking about for so many years is at play here, meaning the metabolic issues that, you know, really beleaguer the human body are what is targeting these brain immune cells called microglia to turn their backs on us and to shift to a form that is threatening.

(05:15)
It’s the same process that’s underlying, uh, coronary artery disease, uh, generally heart disease, uh, immune dysfunction throughout the human body. And the good news, uh, that what we will certainly unpack is that our choices determine whether the immune system in the brain is friend or foe. When it’s foe, when it’s working against us, then it sets the stage for the destruction of our brain cells, the destruction of the connection between those brain cells called synapses, and even, uh, disruption of the very important blood-brain barrier. So I think the, you know, the synopsis here is that we can give you the keys to the kingdom, and it’s all about reigning in the function of our brain’s immune cells by targeting their metabolism. And here’s the home run. Their metabolism mirrors your body metabolism.

Actually, just a few weeks ago, I had the honor of addressing the Alzheimer’s Association here in Southern California. And, uh, the way I set it up, and I, I think you explained it very well, most of us remember nine eleven, and I actually made a joke that if you don’t remember nine eleven, you’re here at the right place at the Alzheimer’s Association. But after nine eleven, we began putting barriers against terrorists, uh, in front of important structures, uh, airports, government buildings. And these barriers were designed to prevent a terrorist from taking a car or whatever and ramming through. I said, “Imagine, if you will, that the barriers in your brain, such as amyloid plaques, are actually barriers to prevent terrorist access to these important structures, the neurons.” And we assume that the barriers were the cause of the problem, but they’re just a living example of we’re trying to prevent something from getting to the brain.

(07:16)
And you and I agree that those some things are things that are coming from the gut, like lipopolysaccharides, just to name one, like living bacteria to limit, name another. You’re right. We’ve been targeting the wrong thing. We don’t – Yes. Taking down the barriers didn’t work.

No. And in fact, it’s been a couple of decades that we’ve, uh, seen the research of Dr. Rudolph Tanzi at Harvard who has characterized beta amyloid as being what we call an antimicrobial peptide. The barrier that you just referred to. In other words, it’s there as a response to the threat of the terrorist, i.e. Some sort of bacteria or virus. So in a very real sense, uh, the enemy un – of my enemy is my friend. We shouldn’t be getting rid of the beta amyloid. That isn’t the issue here. The issue is what is causing it to accumulate? And, you know, one very important thing that you, that you raised just now is this gut-brain connection. Who knew, right? That things from the gut can make their way through the systemic circulation and ultimately get into the brain. And I’ve puzzled over, okay, now that they’re in the brain, w- why is there a threat?

(08:28)
What do they do there? And it turns out that there are receptors on these microglial cells that sense these products, the lipopolysaccharide that you mentioned, the LPS, or even inflammatory cytokines, or particles of viruses or bacteria that then shifts them from being supportive and nurturing and allowing us to grow new brain cells to what I call in the book, the evil twin. The evil twin destroys our synapses, creates an environment that is less favorable for the neurons, and destabilizes the blood-brain barrier. And this sets the stage for, really, the brain to ultimately decline. And, you know, the issue is that I think the biggest factor a- at play in our modern world is the metabolism of these immune cells being challenged. Normally, their mitochondria are working quite efficiently, cranking out that ATP that allows them to stay on our side, to stay supportive and nurturing of everything going on in the brain.

(09:30)
When the metabolism of these cells shifts away from the mitochondria, in other words, the mitochondria become less effective in producing these ATP molecules, these energy molecules. What happens is these cells shift to a different form of energy metabolism called glycolysis. And when they do so, again, they become the evil twin. And that evil twin is, uh, again, an immune cell that would otherwise be very supportive. It goes around through the brain and digests away the synapses that are the connection between one brain cell and the next brain cell, and really the fundamental for us to remain connected to ourselves and to each other and to the world around us. So, you know, that is really central to what goes on, uh, making the brain ultimately degenerate. And again, the empowering part of this story, uh, is that these microglial cells, in terms of their metabolism, that dictates whether they are friend or foe, that metabolism mirrors our body metabolism.

(10:35)
Things like threats to the, the gut barrier that you’ve been so eloquent in talking about for years, uh, really set the stage for these cells to shift, uh, and turn their backs on us. And the really empowering good news is that we can bring things back.

We know now, I guess, uh, that, uh, you know, our immune system was designed to defend us from, from bacteria, from viruses, uh, from other assaults. Uh, years ago, when the Plant Paradox came out, I, uh, was honored to talk at Harvard at a neurology conference and actually saw, uh, living pictures of what you described, that these microglial cells are literally like Pac-Man that take the dendritic processes of neurons and literally eat them away. And I mean, you can watch this in real time when they sense a threat. Now, I’ve described it in a, in a slightly different way. I, I look at it, the, the neuron is the castle. And these dendrites where they make connections with synapses are forts in the hinterlands. And the invaders are attacking the forts. And the castle says, “Oh my gosh, we gotta get everybody back in the fort.

(11:59)
Pull up the drawbridge and this’ll be our last line of defense.” And so these guys have been nibbling away these dendritic processes as a, as a bad method of defense. But then we pull up the drawbridge and the poor neuron, uh, among other things, starves to death. And you’re right, can’t communicate to any other neuron.

It’s all about loss of connection. But I, I, I wanna take a step back and for your audience, ask the question, why would Dr. Steven Gundry, a cardiologist who’s now spending a lot of time exploring what’s going on in the gut, why would Dr. Gundry be invited to speak to a neurology, uh, conference? Think about that. It is because of these exact shared mechanisms that you described that, yes, the gut is magically related to the brain. Who knew? I mean, many years ago, I wrote a book, uh, called Brain Maker talking about the gut-brain connection. And my colleagues really, uh, to be fair, gave me a bit of a hard time because, you know, how could the gut, for example, be related to the brain or the heart or the immune system or cancer risk, all of these issues that you have, again, so well described?

(13:11)
So you’re exactly right. I mean, we have had this neuronal-centric kind of view of the brain. It’s all about the neuron. Uh, for really most of my professional career, that’s for sure, for 40 years, that’s really all the attention, uh, was directed at the neuron, the brain cell. And the reality is, the neuron is the workhorse. And what’s directing the show, what’s keeping things going are these microglial cells, these immune cells. Really expands our view away from just thinking about immunity as a response to a threat to really more of the housekeeping, uh, kinds of tasks, keeping things in tip-top shape, keeping those synapses working that you well described, keeping the neurons functional, making sure that debris is removed, making sure that that vital blood-brain barrier is actually patent or functional. Because w- when any, uh, link in this chain gets weakened, then basically all hell breaks loose.

(14:08)
And, you know, the numbers that you quoted at the beginning of our time together today are staggering. When we recognize that right now, not in 2016, but right now, one in nine Americans over the age of 65, that includes you and me, uh, is already diagnosed with dementia. To not call that a, an epidemic, I think is underselling it. It is an epidemic. And what is so incredibly valuable is for your viewers to gr – get their arms around the fact that everything Dr. Gundry’s been telling them for years of watching this podcast and writing your books is spot on as it relates to the brain. That we’ve gotta keep our blood sugar in check. We’ve gotta keep our waistlines in check. We’ve gotta keep blood pressure in check. We’ve got to exercise, get a good night’s sleep, and socialize with other people. These are the simple keys to the kingdom.

(15:01)
There is no magic drug. And I will tell you, if there were some miraculous drug, I would have prescribed it. Uh, I would’ve prescribed it to my own father who died of this very disease.

Yeah.

But I, I, one other point I, I’d like to make, and well, I’ll make many more points in our time together, is that what’s really exciting for me is that we, we now understand that this role of the immune system in neurodegeneration or the degeneration of the brain extends far beyond Alzheimer’s disease. Involves Parkinson’s and multisystem atrophy and frontotemporal dementia and progressive supranuclear palsy and all of the various types of neurodegenerative conditions and even neurodevelopmental conditions like autism spectrum disorder. Yeah. And even mood disorders like, uh, major depressive disorder are all really now, uh, seen to re – uh, be a representation of this activation of the immune system away from being what we call M2 supportive to being M1 destructive. And so it’s throwing a very, very large net. And, you know, we’ve known for several years that metabolic issues like having elevated blood sugar significantly increases risk for having, uh, major depression, for example.

(16:17)
What we’ve not recognized, but certainly need to recognize, is that being a type two diabetic is associated with as much as an 85% increased risk for developing Parkinson’s. And as high as a threefold increased risk for developing Alzheimer’s. So this idea of this change in the brain’s immune system being influenced by our metabolic state, I think, is now having a huge amount of traction. And we’re already seeing interventional trials whereby the metabolism is targeted even in existing Alzheimer’s patients with really in – amazing, uh, outcomes in terms of improvement, not just slowing their rate of decline, but stabilization and even improvement. One study came from, actually, I mentioned his name already. Dr. Rudolph Tanzi

(17:09)
Working with Dr. Dean Ornish, a cardiologist, published a- at Harvard, where they took, uh, a group of 51 individuals who were diagnosed with Alzheimer’s disease and put them on a lifestyle modification program, changing their diets, getting them to exercise, managing stress. And over the 20 weeks, 70% of these individuals either had stabilization or improvement in their cognitive function. These are people, uh, you know, who went through a program. The side effects were lowering of their blood sugar, losing weight, and, you know, basically improving their cardiovascular function. That was the side effects. And these weren’t people taking a beta-amyloid targeting drug, risking themselves, uh, with respect to brain hemorrhage or brain swelling. So, you know, you can’t patent that kind of intervention. And you can’t sell it on TV as an advertisement. And yet, look what these guys did. You know, I think your mission, my mission is to get the word out that we all have the tools in our hands.

(18:15)
It’s just, you know, about guidance to, to really learn how to implement these tools. That’s why I wrote this book is to really let people understand that there is no magic bullet out there. Again, I wish there were. When it becomes available, you and I will both talk about it. We’ve dedicated ourselves to expanding the, the number of tools in the toolbox. Yep. Looking, looking at risk-benefit ratio.

(18:37)
And, uh, you know, that’s the mission here. E- empowerment through knowledge is what was really what we do.

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(20:48)
Well, you, you mentioned this throughout the book, but you and I, uh, are just slow learners. I mean, Hippocrates, the father of medicine, 2,500 years ago said all diseases begin in the gut. And I guess I’m a slow learner. He was right. And then we now have the tools to show why he was right. And you, you spend a lot of time in the book talking about those tools and using those tools to modify without drugs with, you know, with really fairly simple steps that you can have a tremendous impact. You know, our, our good friend, Dale Bredesen, has just published a paper doing, looking at very much the same thing, the lifestyle intervention. Uh, he makes a point, which you do in the book as well, that besides diet and exercise, we’re, we’re in a toxic environment. Uh, whether it’s pesticides, herbicides, whether it’s microplastics, whether it’s noise.

(21:52)
And that was actually a good point in your book, that noise in itself is traumatic to the brain. So what do you do to improve things step by step, simple steps that you can take to stop this process? Or at least. Well, I think you can reverse it as, as you think, but at least stop it.

I think step number one, and it supersedes everything else one might do, is to reframe your thinking on exactly what we are talking about to the extent that you begin to embrace the idea that you can make these changes and that they’re going to be valuable. Because if you don’t do that, then nothing else matters because you won’t do anything else. You know, we can talk about why sleep is important, why reigning in metabolism through dietary approaches and exercise, and I might add sleep again, uh, are very, very important. But again, step one is you gotta get your arms around the fact that you are, uh, empowered here and the ball is in your court. Because until that happens, we are living our lives at the mercy of, uh, hoping that something is developed. And as the, uh, film director James Cameron once famously said, hope is not a strategy.

(23:14)
We can hope that there’s a, a miracle drug. And I’m, I, I hope that too, because that’s going to help a lot of people who are really not, uh, able to, I think, embrace the idea of lifestyle change. And it offers up yet another tool. And, and let’s be clear, in the new book, uh, I discuss where drugs may play a role. We talk about GLP-1 agonist drugs.

Yeah.

I, I’m not saying that’s what we should be doing for one and all right now, but I am, uh, certainly open to drugs that are incredibly effective in terms of changing metabolism. And that’s really the ballpark in which we find ourselves that there may be some, uh, you know, studies that demonstrate effectiveness. The first real interventional trial using drugs, GLP-1 drugs, orally semaglutide, uh, to target Alzheimer’s really did not reach the endpoints that they wanted. Although, interestingly, C-reactive protein, a marker of inflammation, uh, in the intervention group was reduced by some 30%. There’s, there’s some noise there in the background. I think we have to pay attention to it. But that said, we have seen, uh, incredible results with, uh, injectable GLP-1 agonist drugs in the treatment of, uh, Parkinson’s disease. One study in the New England Journal of Medicine actually, uh, showed that in the group receiving a GLP-1 agonist drug versus placebo, the, the placebo group over the, uh, period of the study declined as one would expect over the couple of years.

(24:42)
Whereas the, um, interventional group actually stabilized or slightly improved. We’ve never seen that, uh, in Parkinson’s. That’s treating the fire, not just the smoke. And this is a little tangential, but let me say that in Parkinson’s, it’s reasonable to treat the smoke, the tremor, the rigidity, gives people some functionality, but underneath all that, they continue to decline. So this idea of, you know, treating the underlying disease is rel – is new. And that is certainly not what’s happening as we target, uh, beta amyloid in Alzheimer’s. So the keys to the kingdom, again, are reigning in our metabolism. That’s where sleep and exercise and, uh, diet are so fundamentally important. The simplistics of the diet, they could, we could do a deep dive. But all I really want is people to be on whatever diet for them keeps their blood sugar, uh, intact, keeps their blood sugar from spiking, uh, over 40, uh, if you’re using a continuous glucose monitor, keeps the fasting insulin low, the A1C low, not just below the level of dia- diabetes, but low to the extent of 5.3, maybe 5.4.

(25:54)
That’s not in the normal range, that’s in the ideal range as it, as, as for our conversation. You know, that’s one of the most important things about diet. There are so many diets out there, one name or another. Uh, e- every week there’s a new diet, whether it’s Primal Paleo or Atkins from the old days, uh, Mediterranean, Mediterranean Plus. You can, you can name off a hundred mind diet. But I, I really tried to simplify, uh, what the recommendations are in this book by metricizing, by looking at the outcome of the diet, through looking at the markers of blood sugar and insulin, uh, functionality. I’d like a lot of plant, a lot of color on the plate. We wanna have those polyphenols. We wanna have a lot of dietary fiber, uh, to nurture our microbiome, to reduce the leakiness of the gut and that LPS, uh, from making its way to the brain, and it does.

(26:48)
I think that we’ve really gotta reassess the type of fats that we are consuming. Uh, there is a fat that’s called olive oil. Uh, my friend, Dr. Steven Gundry, has been talking about it for years, and he’s right on target as usual. Uh, so dietary fat, we need to stop castigating it, but we need to have a bit of a discussion as to what makes for a good fat versus a bad fat, especially in the, the context of the brain being 70% fat. We’ve gotta make, build a brain, make a brain from the good fats that we are consuming. We have a discussion about the omega-3s and a discussion about protein as well. But the mission here is to simplify. The mission here is to really recognize that the gut is playing a huge role, and that we’ve gotta reign in metabolism through our dietary approaches, and then move on to recognizing that metabolism, here’s the new headline, is highly influenced by the quantity and quality of the sleep that we get.

(27:49)
Well, how would you know? Well, I guess I got four hours of sleep last night because I go to bed until 2:00 in the morning, or whatever it may be. Okay, you would know that. But if you think you’re sleeping eight hours a night, you might not be. You might be, uh, w – nearly waking up or actually waking up several times. And beyond that, we’ve gotta understand the quality of sleep. Are you getting enough deep sleep, for example, to activate the brain’s cleanup system called the glymphatic system, which we’ve just learned is also activated by movement during the day. But we’ve gotta understand this. And, you know, it was only just a few years ago when the only way we would know that was by undergoing a sleep study in a laboratory with a bunch of wires connected to your skull and an EKG monitor and a pulse oximeter and somebody watching you with a camera all night.

(28:38)
And then

They tell you, “Go to sleep.” <laugh>

Yeah, and go to sleep. But that we’re watching every move. Uh, I actually underwent one because I was telling everybody back in the day, “You should get one because we need to understand your sleep.” So I, I underwent one. And before I went to sleep, the technician who was watching me, uh, was telling me this horrendous story. I don’t wanna go through it, but it was very destabilizing for my sleep. Plus, you’re in a, a lab. But anyway, these days you can wear your Apple Watch, your whoop, your Oura Ring, whatever it may be, and really get wonderful metrics, uh, as it relates to not only the quantity of your sleep, but I think as important, the quality. How much REM are you getting? What was your latency? What is your heart rate variability during sleep? Which is an indication of the activation and activity of your parasympathetic nervous system.

(29:27)
The rest and digest part of your nervous system. When you’re always in sympathetic overload, it increases your cortisol production. That does what? It damages and threatens your microbiome, leads to increased gut permeability, and that is bad for your body. And yes, the brain is part of your body. And your microglial cells, getting back to our original topic, can sense that. And when they sense that, they shift from becoming supportive to being destructive. So, you know, those are, are the fundamentals. And I, I will say that I wanted to pave the way for, uh, the idea that A, uh, there’s some really cool things coming down the pike that aren’t really readily available yet, but, uh, you know, science is really taking a leap forward in this idea that the brain’s immune system holds the keys to the kingdom, uh, and B, that, you know, we’re gonna remain open to that.

(30:20)
And I, I presented some really forward-thinking ideas in the book, you know, based upon what some really cool guys or, and girls are doing, uh, research-wise that I think, uh, in, in the short term are gonna be available soon, some of which is even available right now, things as, uh, seemingly out there as flashing a light in your eyes at 40 hertz. I mean, uh, you know, at first blush, you’re thinking, “Yeah, you know, what are gundry and pearl mutter, uh, smoking now, flashing a light? How could that be, uh, good for your brain?” Well, it turns out that Dr. Li Wei Sai at the Massachusetts Institute of Technology, that’s MIT, uh, has done incredible research showing that light at that specific frequency, first in rodents and now in humans, and now in humans with Alzheimer’s disease, is dramatic in terms of its effects o- on the brain’s immune system.

(31:17)
Why it happens, I don’t know. I mean, what Dr. Li Wei Sai has come up with is that it restores a background frequency called gamma oscillation, which is a normal, beautiful sinusoidal kind of wave background music in the brain, if you will, that keeps these immune cells in check and doing good things.

You know, you mentioned, uh, in the book about microtubules, and I, I bring it up because you talk, you have a whole chapter on exciting new advances like flashing lights, and, uh, and you didn’t mention, uh, transcranial ultrasound. And I just though I’d throw it out there because the theory is that this will actually promote microtubule growth. Um, what say you?

Interestingly, the, the latest news on transcranial ultrasound, which of course came out after I submitted my manuscript as members, as did the, the cochrain analysis, uh, is that, uh, it is being looked upon, uh, right in line with what I just mentioned with the 40 Hertz light. So transcranial has become, uh, looking like a powerful tool to reestablish this beautiful background music, this gamma oscillation, which will allow these microglutal cells to reconvert back to being, uh, supportive. And as you well mentioned, support the function and formation of microtubules. So microtubules, uh, are the way, uh, interestingly, let me just talk about one aspect of what they do. Uh, they actually allow the transfer from one cell to the next of functional, healthy mitochondria. Can you imagine that? That one brain cell finds that its neighbor has deficiencies in the mitochondria and says, “Hey, I’ll send you a few or however many you need through these microtubules.” And where the story becomes really interesting is because the maintenance of the microtubules, uh, is the task of a specific protein in the brain called tau.

(33:25)
Tau 217. The function of Tau 217 is to keep those microtubules functioning. When we have. I love this story. It’s really, uh, it just floats the boat. When we have metabolic issues like elevated blood sugar, insulin resistance, or inflammation in the body, what happens is that this tau protein becomes phosphorylated. That becomes something called ptau, phosphorylated Tau 217. And that is an indication then that the microtubules are not working as effectively. It turns out that nowadays, this is one of. You can measure it in the blood. Yeah. And you can do that without a prescription. We talk about it in the book. And nowadays, this has become, uh, the darling of laboratory blood analysis for Alzheimer’s risk and even the progression or lack thereof of existing Alzheimer’s disease. We talk about, uh, the idea that you can go to your local laboratory, even without a prescription now, and say, “I would like to have my P Tau 217 measured.” And, uh, you know, we put in the book what are a good levels of P Tau 217.

(34:38)
I just had mine measured. It was less than 0.1, which is a good thing. Uh, uh, and meaning that, uh, my metabolics are intact to the extent that I am not threatening to change my functional tau protein into phosphorylated tau protein. That’s what this test means. Therefore, my risk right now for developing Alzheimer’s is seemingly low. It all comes together when we look, uh, even through the lens of these microtubules. When microtubules are threatened and not working appropriately, it is associated with shifting our brain’s immune cells, these microglial cells, away from being friendly to being threatening, away from what we describe. Well, what has been described, not just by me, the M2 configuration into the threatening M1 configuration.

I think women really ought to know that, at least in Alzheimer’s, they are not the stronger sex. They’re by far the stronger sex in most, uh, most things, uh, as my wife reminds me all the time, and my two daughters. But women are far more susceptible to Alzheimer’s than men. And I, I think that does not get enough clarity, clarification from, from all of us. Um, any thoughts on that? Well,

Actually, I dedicated a section in the book to that. I think, uh, m- most importantly is the fact that women are, represent two-thirds of the Alzheimer’s patients here in America. And I put in the book, uh, a comment, because I think it’s very valuable, that women have not been the subject of research to answer the question why. And, you know, books have been written. Dr. Lisa Musconi wrote a wonderful book, XX Factor or XX Syndrome. I forget what the title was, but her name is Lisa Musconi. Yeah. Uh, wrote this beautiful book, uh, and it, uh, unpacks a lot of, uh, explanations. From my perspective, what I really dwelled on in, uh, Brain Defenders

(36:42)
Is the idea that when this manifestation begins, uh, it really is around the perimenopausal time. And what happens during perimenopausal time is that levels of a particular hormone, estradiol, which is E2, a form of estrogen, uh, plummets dramatically. And when estradiol plummets, drops dramatically, it marks the synapses with a certain type of protein called complement protein. And when these synapses or connections between brain cells are tagged with complement protein, then the microglial cells see them, uh, as prime for digestion. So this tagging of the synapses, the connection of one neuron to the next neuron through their dendrites, uh, when they are tagged because estradiol levels plummet, it sends, uh, what’s called an eat me signal to the microglia. So, uh, interestingly, uh, again, what’s happening is that we are seeing a very powerful connection here through the hormone system, uh, of activation of these microglial cells, such that I came out very much in favor of hormone replacement therapy, uh, as it relates to a, uh, a technique of keeping this particular mechanism from happening.

(38:06)
Y- you know, there are other aspects of hormones that I think are very valuable, acting as trophic hormones or nurturing, uh, hormones in the brain as well. But, you know, I think when my mission was to really, uh, vet where is this brain immune system playing a role, and how are these various inroads being explained through the lens of these microglial cells? And through that lens, we get a great understanding about what’s going on in the female brain. Uh, there, there are other, uh, things that have come to light really very recently. One, a researcher, a Dr. Sarah Marzi at the Marzi Institute, uh, in the, uh, in England, uh, Neuroscience Institute has really identified that there are different epigenetic markers in neurons, uh, in men versus women. Uh, some of which are induced, uh, these epigenetic markers by, uh, not just gender, but we induce these epigenetic markers.

(39:05)
In other words, uh, changing of gene expression, uh, in men and women through toxic exposure, for example. Yeah. That, and that’s, uh, varies depending upon the part of the brain that, uh, is involved. Uh, different epigenetic changes happen, for example, in the area of the brain that makes dopamine for the motor system, that area then being involved, as she identified, uh, so eloquently in, when she describes it, in Parkinson’s. So we’re really in a very, uh, exciting time, uh, in determining what it is that activates these immune cells to then digest away neurons and digest away synapses. And, you know, as it relates, again, back to your, uh, question, the, the gender differences, my, my bullet points would be, number one, that women need more attention, being two-thirds of Alzheimer’s patients. And, and I think, uh, research needs to be more directed to your question.

(40:01)
And secondly, that, uh, hormones, I think, uh, are playing a pivotal role, and now we understand why.

In your book, uh, you make a, uh, and thank you for doing this. Um, there is probably a window of opportunity in perimenopause and menopause to start hormone replacement. And it’ll help. And I totally agree with that. But, uh, you make a good point, and I totally agree with you that if you kinda miss that window of opportunity, and the European data would suggest that it’s three to five years. If you miss that window, then you kinda are playing Russian roulette. And, and sadly, I see that frequently with my patients with increased risk of cancer, increased cardiovascular disease risk, even increased risk of bone loss. And you point this out, and, and thank you for doing that, because sometimes I feel like I’m not completely on the bandwagon that hormone replacement, uh, started at age 70 is a really good idea.

I think, uh, it gets to timing. Uh, actually, Dr. Misconi, I mentioned her just a moment ago, is at present carrying out an interventional trial. And again, what you said is so on point that it is all about timing. So <laugh> I had a though this morning, I was thinking, you know, we had dinner with a couple last night, and, uh, people that we’ve been friends with for many, many years, and one of the, uh, individuals is dev – has developed Alzheimer’s. And, uh, you know, ultimately, the, the tragic part was that she’s aware of the fact that her mother ended up, with the same situation, ended up in a memory care clinic, uh, or s – or s – a center. And I thought, what a strange thing to call it, a memory care center, because what I’m doing right now is memory care – Yeah. Is really bef- before there’s an issue.

(42:01)
Preventive care. Uh, that’s what memory care should, should be all about. And that is to say, getting back to our, our current point. Uh, I mentioned in the book, uh, and no, I didn’t hold back. I said, so are you. Uh, to make it very clear where I stand on hormone replacement therapy, I am in favor o- of. I mean, I think the whole idea of the breast cancer risk, et cetera, you and I both know that that data was, was really very flawed and really derailed the medicine and healthcare a- away from the notion of h – of, of hormone replacement being po – you know, having some possible, uh, positive aspects, which I, I believe it does. So, uh, you know, the idea of, of getting back to that memory care, I, I want memory care to start in our 40s and 50s when we have a memory and we wanna care for that memory because that is when the seeds of our metabolic mayhem begin in our 40s and 50s when the seeds for Alzheimer’s are planted, not when we are becoming forgetful.

(43:04)
So it’s very heartening for me to see that there is now a journal of prevention of Alzheimer’s. That is, uh, it’s breathtaking that there’s a journal, a peer reviewed journal dedicated to the idea of preventing Alzheimer’s disease, which is, you know, a fundamental shift in just the whole, uh, approach of medicine and healthcare, uh, here in America, certainly. You know, call it like it is. It’s not healthcare, it’s illness care. We don’t do anything for people until they are ill. In my world, it’s until they develop a neurodegenerative condition. Then we hope we’re gonna do something when it’s really, you know, fourth and long. There’s three, three seconds left on the clock. No, I, I think the time, uh, as John Kennedy said in his inaugural address, the time to fix the roof is when the sun is shining. Yeah. And that’s, that’s my message.

(43:55)
And, uh, you know, I, I’ll, I’ll keep repeating this message until it, it takes hold.

You kind of finish up, um, with, you know, this, we talk about all this doom and gloom. Uh, but there is, you know, honest hope. And, uh, you lay it out. And does it take some work? Yes. Uh – It

Does. And is it worth it? You bet.

Yeah. You know, as I tell my patients, “You’re probably gonna hate me for about six weeks, and you’re probably gonna start liking me after that.” Um, I, I think it’s the same message here. You, you gotta work at this. Uh, but the alternative is, as you and I know, is disastrous.

Call it like it is. You know, our options, once it’s happened, uh, once that diagnosis is made, are slim and none. I mean, uh, you know, I, I, a- as you would’ve expected, put a section in the book dedicated to our friend, Dr. Dale Bredesen. ‘Cause as you well know, he is developing, uh, an interventional approach that is showing success in, in, in some patients. Yeah. By targeting these triggers that force our microglial cells away from being friend to being faux. It’s a fundamental of this book. It’s a fundamental, I think, of where the science is going now, which is very heartening. I mean, we’re seeing researchers do microglial transplants into the brains of humans, not just laboratory animals, doing, uh, mitochondrial

(45:26)
Transplants, uh, into humans, not just rodents. So this is very, very exciting. It’s very exciting time when now we focus on this idea that, uh, this is, you know, really where the money is. And, you know, for me, the fact that this book is coming out now and is, is already going to be published in, in 16 countries around the world, you know, at the same time it’s published here in America. Normally, as you know, you get your French version and your Spanish version, you know, a, a year later when they say, “Yeah, it did pretty well in America.”

Right.

This is getting out early a- across the world, and I couldn’t be happier because, uh, this is, is so important, not just for the general public to appreciate, but also I think to validate the, the researchers that are doing this work around the world that, yeah, you guys are on the right track, and it’s, it’s all about the simple stuff. It’s all about eating right, getting exercise, socializing. I mean, uh, you know, the Blue Zones told us a f – a few important, uh, levers to pull. And I think that the, the idea of the fact that people who are socially connected have a lower risk of heart disease, a lower risk of cancer, and yes, a lower risk of developing Alzheimer’s disease. The question is why? Well, interestingly, we can deconstruct and say, well, socialization is associated with better metabolic health. We know that. Uh, lower levels of inflammatory cytokines in the blood, that’s been demonstrated as well, better insulin functionality.

(46:57)
But interestingly, when we are together with other people, even virtually, even what’s going on between you and me right now, you create higher levels of the love hormone in your body called oxytocin. I mean, just because you and I are friends and we’re hanging out together, more oxytocin in our, in our bloodstream, and it makes its way to the brain. Uh, and that oxytocin, well, you know, that’s originally where it came from anyway, targets our microglial cells. Our microglial cells have oxytocin receptors on their surfaces. When that, uh, receptor is stimulated by higher levels of oxytocin, they stay in their supportive, loving, nurturing role. And you wonder, okay, I know I’m supposed to socialize. I’m supposed to play bridge with people or botchy ball or whatever it is. You know, meet in the public square and that’s good for my body, good for my brain.

(47:49)
Uh, but now if you have to deconstruct it and you need a mechanism, that’s very powerful. Uh, oxytocin. And in fact, there’s been an interventional trial now that showed some interesting findings, some of which were positive. Very small trial of only five Alzheimer’s, but gave them intranasal sprays of oxytocin. Uh, so I think, um, it’s, it’s there for the asking. You can do intranasal spray of oxytocin if you choose. But you know what? Uh, maybe get off, uh, the internet and stop doom-scrolling. You go outside and talk to your neighbor. That’s powerful therapy. Who knew?

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(49:30)
Well, that’s why I tell everybody to get a dog, uh, because it forces you to go walking twice a, twice a day, and you will more than likely run into another dog walker, and your dogs will have to socialize, and it’ll force you to socialize. So just another reason. Plus, your dogs bring a great microbiome to you. And who knows? Maybe socialization. You and I. Well, we can’t do it here, but among groups of people, we exchange bacteria all the time.

I seem to recall that you and I may have talked about this once before. Uh, I think that was the last conversation I had about this, that’s actually good for us. Certainly having pets, you know, it, it, uh, it helps stabilize immune function and resets immune function. We know that kids who grow up with pets or living on a farm are exposed to dirt, uh, and, and – Yeah,

Do much of it. Germs.

Germs in a good sense, who knew, and their risk for food allergies, et cetera, and atopic dermatitis, et cetera, remarkably reduced. So, so you’re right. You know, I, I think we’re coming into a time when we are really re-contextualizing the whole notion of the immune system. Again, you know, moving away from it, just being involved as a response element against being threatened, uh, to being, you know, really deeply involved in maintenance and nurturing and keeping things functional. And there’s a new term, uh, that is gaining a lot of traction that marries, uh, the immune system to our metabolic, uh, functionality. And it’s called, oddly enough, immunometabolism. And that has become my watchword, immunometabolism. The idea that our metabolism is so deeply intertwined with the regulation and activity of our immune system. It relates diabetes, hypertension, obesity, uh, hyperlipidemia to the functionality of the immune system.

(51:27)
And now, we get it. We understand this relationship between metabolic issues in coronary artery disease and risk for cancer and in, in neurodegenerative conditions as well because of how these metabolic issues, uh, are interpreted and reprogrammed. In, in our case, our discussion did the microglial cells, nurturing and supportive of even the very synapses that connect one neuron to the next, uh, to, uh, shifting because of our metabolic issues to being the evil twin, as we talked about in the book. So the tools are very straightforward. And the tools are now totally validated and allow us to understand the associations between metabolic issues and brain degeneration. I mentioned those relationships earlier. And now, you know, we’ve connected some very important dots. We’re getting the corner pieces of our jigsaw puzzle put in place now. The rest of the pieces now are gonna come, uh, be put in pretty easily.

(52:29)
Uh, but most importantly, these are tools, as I, I’ve said a couple times today, uh, when, uh, in our time together. These are keys to the kingdom. The fundamental message I think I’d like to give to your viewers is don’t wait. Don’t wait. Don’t be under this misguided, uh, ideology that you can live your life come what may, and that modern science and medicine is going to have some miracle magic bullet, uh, to help you through this. We don’t have a way of cleaning out your coronary arteries once they’ve become significantly narrowed. I wish we did. We don’t have a way of, uh, uh, generally available of really putting your brain, uh, back on track. So it’s all about, uh, prevention. It’s all about metabolism. And through this wonderful new term, immunometabolism, the relationship of our metabolic health that is dictated by our choices, the relationship to the brain’s immune system, the microglia, being supportive or destructive.

(53:34)
And yes, uh, like your patients who hate you for the first six weeks until the things, things turn around. Yeah, I’m not saying that people are gonna, you know, wonderfully embrace these dietary changes or my call for exercise or getting to bed earlier and turning off the TV and making the room colder. All of these things m- may not, you know, sit well with everybody. But, uh, by all means, it’s, it’s a better choice, uh, than asking yourself, “What am I gonna do now when I’ve come back from the doctor’s office? And she has told me that I am suffering from mild cognitive impairment, MCI, which is a harbinger for the next, uh, diagnosis, which is full-blown Alzheimer’s disease. It doesn’t have to happen. I am pleading with your audience.

No, you’re absolutely right. Getting back to Hippocrates, all disease begins in the gut. I have a patient who’s a Sanskrit scholar, and we were talking about this. And he said, “You know, I’m gonna go back because the Buddha and Hippocrates were contemporaries.” And he came back and he says, “You’re not gonna believe this, but the Buddha said enlightenment comes from the intestines. And I’d like to keep this enlightened. So I think if we can take care of our intestines and our microbiome, uh, we can keep, keep our brain in pretty doggone good shape.” You bring up, again, the oral microbiome and the oral cavity is so, so important, uh, in all of this. Um, maybe before we go, uh, should we brush our teeth? Should we floss? Uh, or who cares about all that?

You know, our discussion of the gut, uh, absolutely needs to in- include the mouth, uh, because it’s all the digestive system. It begins at the lips. Yeah. Uh, and, and makes its way all the way through. And I mean, all the way through. And, uh, I, I think there’s this sense that we need to sterilize our mouths because of germs. Yeah. And, you know, I, I think that we’ve gotta recognize that the oral microbiome, those organisms that live in the mouth, are, are there to do good things, uh, to keep the mouth healthy, uh, and have dramatic systemic effects. In other words, throughout the body, including the brain. We can, uh, look at one mechanism where the o – uh, oral bacteria do good things. They convert nitrates in our food into nitrite. Uh, we eat nitrate-rich foods like beets, for example, and then these wonderful bacteria are there to serve us and convert that into nitrite.

(56:15)
That forms the basis by which our bodies are able to manufacture nitric oxide, nitric oxide or NO, just say yes to no. Uh, nitric oxide is very important. We know, uh, for allowing our blood vessels to relax, to get good blood supply throughout the body, and yes, good blood supply to the brain. But I think a lesser known, uh, and equally important role of nitric oxide is to enhance how insulin does its job. Who knew that nitric oxide was really fundamentally important for the function of insulin, uh, throughout the body? So, uh, these are good things that our oral microbiome does. One wonders why there is such a significant increased risk for both type two diabetes and metabolic issue, and elevated blood pressure, a metabolic issue, both of which threaten the brain’s immune system, uh, in people who routinely use, uh, antibacterial mouthwashes. Yeah. So, uh, interestingly, both of these studies, uh, demonstrated that.

(57:18)
And, you know, this, uh, c – uh, idea that we’ve gotta be killing 99% of germs, that’s what the commercials will tell us. That’s a good thing because we might get bad breath, uh, halitosis, give it a name, uh, and that’s gonna be very offensive to ourselves and to others, is we need to rethink that. So I, I really welcome the idea that this idea has come to light. And number two, uh, that we are seeing the development of products that nurture the, the oral microbiome, various toothpastes, uh, that are designed to both strengthen our teeth, to reduce our exposure to fluoride, reduce our exposure to fluoride, and nurture the oral microbiome. So, uh, you know, I’m really welcoming this new idea that these bacteria are not just there to be destroyed by the next time we, you know, we’re in the bathroom and we see the pump thing and the little cups, and off we go.

(58:14)
It’s a habit that is associated with significant risk to our metabolic state, metabolic health, and therefore to the function of the brain’s immune system. It seems like a long way off, doesn’t it? The idea, and I talk about this in Brain Defenders, that sterilizing your mouth with, uh, these mouthwash preparations is bad for the brain. Uh, it’s something we, we need to rethink. Now, uh, that said, you mentioned flossing and brushing and, uh, what I think is really very handy and important, and I use a, a water flosser. I use a water pick. And what, what’s great is, you know, the amount now make them USB rechargeable. You stick it in your, in your luggage. Uh, and then you have it when you, when you travel, which you should. Uh, I think this is a very valuable tool because we really do need good oral health.

(59:02)
That doesn’t include sterilizing the mouth. It means periodontal care. Uh, it means brushing, uh, twice a day, using a water flosser, uh, and, uh, uh, using dental floss if, if you so choose, I think it’s very important. Because when we get periodontal disease, then we can have overgrowth of certain bacterial species that are bad for the body that can increase inflammation throughout the body and can even make their way to the brain. Uh, what won’t be on the quiz is the name of one particular type of bacterium called porphromonous gingivalis. Uh, but, you know, the idea that we can, uh – Yeah. Uh, see this bacterium or fragments of the bacterium that still have biological activity in the brain at higher levels in Alzheimer’s patients provides an important clue that periodontal disease may be playing a role. We certainly see research that shows an association between periodontal disease and And inflammation throughout the body, as well as a risk for Alzheimer’s disease.

You might believe this, but most people wouldn’t. Um, 21 years ago, I gave a paper at the American Heart Association. I made people, uh, floss, uh, every other day and looked at their HSCRP, highly sensitive CRP. A, a good marker of generalized inflammation. Why did I choose every other day? I hate to floss. Uh, my wife flosses twice a day. She’s a nut.

Yeah, get a water flosser and, and just travel with it.

But it turns out that if I could get people to floss every other day, their CRPs dropped dramatically. And the more they flossed, the lower it went. And that was literally 25 years ago.

I can only imagine, uh, how your colleagues must have responded to that presentation. I mean, I know what it’s like. I, I have been there giving these talks, uh, you know, about the things that you and I know are important. And, uh, afterwards, you know, people just nodding their heads. And I, I didn’t say back then, “Just wait.” Uh, but I knew that the research was going to ultimately make their way to their journals. And it has, as, as you’ve seen in cardiology journals and certainly neurology journals. Uh, it’s really quite breathtaking that, uh, even in the, the most well-respected mainstream neurology journals, we’re seeing, you know, indications of metabolism, its effect on the brain, uh, even, you know, even diet. Uh, even in JAMA, there was a study last year called the POINTER Study. And the POINTR study looked at, uh, 20,111, uh, individuals and followed them, uh, for 12.7 years.

(01:01:51)
And it, it, it, uh, was an, an interventional trial. What they did with these, uh, folks was they had two groups, uh, and they, they followed these, uh, individuals. Uh, and actually it was, it was followed them for two years, my mistake. But again, 20,000 people. They had two groups. One group was given a dietary intervention, lifestyle intervention in terms of physical activity and stress alleviation, et cetera, and met over the two-year period, not 12.7, either virtually or, uh, real-time, uh, counselors to guide them through. That was one half of the group. And these are people in their late 60s with metabolic issues already, uh, insulin resistance, et cetera, overweight. So at great risk, right? Uh, in whom you would expect cognitive decline over a two-year period. The other group got the same information, but had only, I think, three interventions or meetings with people over the two, uh, each year for two years.

(01:02:52)
So a total of six versus, I think, 34 or 36 interventions. So what did they find? The group that had the very vigorous counseling to work through diet and lifestyle, et cetera, they didn’t stabilize their cognitive decline. They actually improved. They improved their cognitive function during the end of the two-year, uh, trial. But what about the group that just got, basically got the information, a little pat on the back a couple of times a year? What happened to them? They dramatically improved as well. That’s the part of the pointer, uh, study that doesn’t really get as much attention. But the point is, these, uh, uh, people were just basically given information and their cognitive function should have declined, but it improved. It shows that these are very powerful inroads to better brain health, better brain function, number one. And number two, it says that you, Dr.

(01:03:41)
Steven Guntry, are on track doing the right thing, even though it was 25 years ago and your colleagues were nodding their heads for you saying floss, uh, every other day. Uh, so it’s, it, it validates this idea that we’ve been putting forth for decades that guess what? Hippocrates was onto something. Buddha was onto something. That lifestyle choices are hugely important as it relates to your general health and as it relates to your brain health. And again, we are the architects of our brain’s destiny. That’s job one, is to embrace that. And then hopefully the rest of what we’ve talked about today, those things are gonna fall into place.

Yeah. And, and look, if your brain defenders are, you know, right there, and all you gotta do is read the book, and he doesn’t have to call you every other day to, uh, to read the book like you just pointed out, pointed out. Uh, that’s why this is so important and I wanted to have you on. Uh, before I let you go, I like to have an audience question. Okay. And we’ve got from Anon on YouTube, “My doctor mentioned some of the new Alzheimer’s drugs that are getting a lot of attention. Are they worth it?” That’s a great question. And, uh, recently, I have, uh, two patients who are very educated individuals. Uh, one, uh, is in their late 70s, ones are in their early 80s, who have recently been diagnosed with Alzheimer’s disease. They both carry a single copy of the APOE4, and we didn’t talk about that today, but we have in the past.

(01:05:18)
And they’ve decided to get this exciting new Alzheimer’s drug. I’ve counseled them. Uh, how would you answer this question, and how would you coun- counsel my patients?

Well, first, I would offer up the disclaimer that I’m not their doctor, but I would say if a drug works and it’s not that risky, I would absolutely take it. These drugs carry a great risk and do not work. And I would say the simplest thing would be to Google Cochrane amyloid drugs, and you’ll get your answer. Because what the Cochrane analysis, uh, found was that the drugs, the, the term they used in terms of describing their effectiveness was trivial. I didn’t make that up. And they described the real clear and present danger of using these drugs. And not to mention, $40,000 a year in expense. Yeah. Though it’s covered now, which is, makes, that Medicare’s covering. Uh, I had this discussion with the, uh, director of Medicare and Medicaid, uh, Dr. M- M- Mehmed Oz several weeks ago, uh, and asked, uh, why is Medicare paying for these drugs that are ineffective as per the Cochrane analysis?

(01:06:35)
So, um, the, the answer to the question is that if, if they were my patients, I would absolutely recommend that they steer clear of these drugs with full understanding that Dr. Perlmutter is, would absolutely be in favor of a drug intervention if it were safe and it worked. Let me add one more thing, because I think it’s desperately important for these individuals that there’s a, a warning on the label of these drugs that they should not be used in people carrying the APOE4 allele. So the idea that they’re both carriers of APOE4 allele and they’re going to receive this drug is very worrisome. They are at much, much higher risk for brain hemorrhage –

Yes.

If they’re exposed to these drugs. Uh, it’s right there in, uh, the information about this drug that they are absolutely contraindicated, meaning they should not be used in anyone carrying the APOE4 allele. That was not known at the beginning of the use of these drugs, uh, until somebody, uh, did a stratified study to try to figure out who are these people that are at such high risk for brain hemorrhage, and it turns out it’s the APOE4 carriers.

Again, uh, you’ve given, in the book, a lot of honest hope for people. And I think that the takeaway, particularly with this question, is th- these drugs are not the honest hope. Um, there are far better ways. And you’re right. Prevention, uh, uh, it’s such a ugly word, but it’s, it’s how we, how you stop this. Oh,

As you mentioned, APOE4, which is a r- risk, uh, multiplier for Alzheimer’s. The pointer study that I mentioned a, a, a little moment ago about, you know, over the two years with people who had the very vigorous intervention or even just got the information didn’t really have the interaction, that included APOE4 people who improved. So it’s a real testament to the power of these seemingly simple, uh, lifestyle interventions to really right the ship and really, you know, redirect, uh, the brain’s destiny. So I would encourage those individuals and anyone who’s, you know, been able to listen to us today, uh, that even carrying the APOE4 allele is a predisposition. It is not a determinant. It is no way a determinant for getting Alzheimer’s. You

Know, I got interested in the APOE4 because a lot of my coronary artery disease patients carried it. And I go, “What, what’s with that?” Um, so, but it is not a, a determinant. In fact, most people who get Alzheimer’s aren’t carrying that allele.

That’s right. I mean, APOE4, uh, it, you know, represents about 23% of Americans will carry at least one copy of the APOE4 allele. And so that’s, that’s right. And, uh, and, and interesting, get, uh, getting back to our beta amyloid, uh, discussion, uh, 75% of people who have a lot of beta amyloid in their brains do not develop dementia. So the idea that this is the cause of Alzheimer’s, uh, is really quite, uh, unfounded. And the idea of targeting it then for therapy, for the reasons that we’ve discussed, really makes no sense. So, uh, uh, again, where we will see wonderful developments is in the idea of immunometabolism. And, uh, I am open to the idea that maybe there will be a time for using a GLP-1, an Ozempic-like drug, uh, in the treatment of Alzheimer’s disease in the future. I, I really will keep the door open because, you know, we have to, again, look at risk-benefit ratio, and we know what the risks are, uh, at least some of them.

(01:10:19)
We don’t know fully what the risks are. That’ll play itself out over the next few years. But face it, Alzheimer’s, which has been kind of thematic of our conversation today, is pretty much a fatal condition. May represent about the third leading cause of death amongst, uh, adults, uh, in America today. And we don’t normally think about it like that. Well – Right. You know, this person’s in an institution now because he or she is having cognitive issues, but it causes people to die. And, uh, therefore, the idea that there could be a drug intervention, like using a GLP-1 or who knows what else may be developed with a low risk profile that could help stabilize or improve the situation. I will keep you posted. I will absolutely keep you posted and, you know, do the outreach on social media and, and all the things, because I think people need to keep their finger on the pulse of, of these developments.

All right. I gotta let you go. So Brain Defenders is out August 18th. Dumb question. Where can listeners find it?

Oh, it’s good question. So it’s, it’s available everywhere. But I would direct your, uh, listeners to braindefenders.com. Oddly enough, that’s the website. Because yes, you can buy the book wherever you want. Uh, but we have all kinds of, of nice things for people, perks and discounts and various things when they buy the book wherever they buy it, and then just go on to braindefenders.com to register and get all the things that our, our wonderful partners have offered up.

All right. Well, it’s great to see you. Uh, for folks who are watching on, uh, video, you are on your boat somewhere up near, um, Seattle or Vancouver or

Where – I’m in downtown Vancouver, Vanc – in, uh, Coal Harbor, for anyone who knows. And, uh, yeah, it’s, uh, it, it’s nice to be in the northwest in the, in the heat of the summer, that’s for sure.

Very good. Well, thanks, uh, for seeing us again and updating us. And thank you for writing this book. And, uh, en- enjoy your, uh, sailing. Now it’s time for the question of the week. This from Colleen O’Connor, 1319, over on YouTube on my episode about statins. She asked, “What blood tests should be requested? What’s the medical lingo?” Well, at the very least, you wanna make sure you get total cholesterol, LDL, HDL, and triglycerides. Preferably, you should ask for an OX LDL, oxidized LDL. And my favorite is one run by Boston Heart called OXPL-APOB. That stands for oxidized phospholipid ApoB. To me, it’s the most accurate way of predicting whether your cholesterol is sticky. And if they can run it, ask for a plaque test, PLAC or LPPLA2. That looks at how sticky your blood vessels are, and quite frankly, you have to have both to make plaque.

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Great question. Now it’s time for the review of the week at Heddy Turner over on YouTube on my episode about coffee mistakes. They said, “Thank you so much. I’ve had enough things happening to me in hospitals. I pay close attention to making the right decisions for my health now.” Well, you’re right. Hospitals in Germany long ago were called Cronkenhaus Sick Houses. And quite frankly, it is not a healthcare center. It is a sick care center. And the object of the game is to try and stay out by eating properly, exercising, sleeping, and socializing. Thanks for the review.

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That’s a wrap on today’s episode. And before you go, I wanna leave you with one task. If anything you heard today made you think, made you wanna dig deeper, or gave you something you’re going to pass along to someone you care about, please take 15 seconds and leave a five-star rating and review on Apple Podcasts or Spotify. I know that sounds small, but those reviews are how Apple and Spotify decide which shows to surface to new listeners. And this show only grows when people who’ve never heard of it suddenly find it. That person finding this podcast today could hear something that genuinely improves their life or the life of someone they love, maybe even saves one. Everything I share here comes from my research when writing my next book and my clinics, where I’ve been seeing patients six days a week for over 25 years, working with nutrition and supplements as the primary treatment.

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This is real world medicine. Help me get it to more people. And thank you. Truly thank you. I’m Dr. G, and I’m always looking out for you.