Brain Doctor: The Foods Quietly Raising Your Alzheimer's Risk (It's NOT Sugar) | David Perlmutter
By Dr Rangan Chatterjee
Summary
Topics Covered
- Ultra-processed foods triple your Alzheimer's risk
- Microglia shift from brain friend to foe
- Inflammation rewires you toward impulsive choices
- Uric acid tells your body winter is coming
- APOE4 is predisposition, not destiny
Full Transcript
What is the effect of a high ultrarocessed food diet on the health of our brains?
Well, that's a great place to start. So,
what we know uh with respect to these ultrarocessed foods is that uh they lead to metabolic mayhem. And I think you know you and I can unpack all of the
pathways uh with which this metabolic mayhem is destructive in the brain. But
you know the bottom line is there's a metabolic underpinning for Alzheimer's disease. When you look at what people
disease. When you look at what people eat there's a relationship uh to evaluating what people eat and their risk for a disease for which we have no meaningful pharmaceutical treatment. And
interestingly in the journal of prevention of Alzheimer's let me pause right there. Think of it. a journal of
right there. Think of it. a journal of prevention of Alzheimer's. For me,
that's a huge a huge step that they would dedicate an entire medical journal to the notion of Alzheimer's prevention when, you know, so much in our world is really focused on the treatment of
particular diseases. Anyhow, in January
particular diseases. Anyhow, in January of 2025, published an article that really evaluated over a 12-year period of time uh in 1,375
people followed them for 12 years as part of the Frammingham Heart Study and basically followed what they ate. And
what they found was really quite uh important I think for our discussion today that for every one serving of uh ultrarocessed foods whatever they were
these patients had an associated increased risk of Alzheimer's of 13%.
And for those who were eating 10 or more servings per day of these ultrarocessed foods which you know here in America make up 60% of adult calories. Think
about that. But if people consume 10 or more servings per day, their risk for Alzheimer's went up about threefold.
Now, is this meaning that ultrarocessed foods are causing this risk? You know,
this is a, you know, a retrospective study. Uh, it's a correlation, not
study. Uh, it's a correlation, not causation. But if you ask me, and I
causation. But if you ask me, and I think you are asking me, yes, I and I'll I'll break it down as to why I think uh these ultrarocessed foods are so darn threatening. So, you know, I've been
threatening. So, you know, I've been thinking about this for an awful long time and writing about it and lecturing about it because I think people need to grasp the fact that Alzheimer's doesn't
just happen, you know, it's not a genetic thing by and large. It is a manifestation of our lifestyle choices and beyond food. That's for sure. The point is that
food. That's for sure. The point is that should be empowering news for people that this disease which people fear more than cancer uh is something over which
they have a a significant degree of control in terms of being basically the architect of their brain's destiny.
Yeah, thank you David. There there's so many empowering messages that I think exist in 2026 about brain health compared to
even 10 years ago in 2016. Right?
there's so much science. There's so much research. And the reason actually I
research. And the reason actually I started off this conversation asking you about ultrarocessed foods is because I think there's been a growing
awareness for some time that heavy ultrarocessed food intake is not a good thing for health. I think a lot of people know that there's a relationship
between your rate of intake and obesity and things like type 2 diabetes and maybe your risk of heart attacks. But I
still don't think it's common knowledge that the overconumption of these types of foods has a detrimental impact on the health of our brains. And your new book,
which I thoroughly enjoyed reading over the past 24 hours, uh, brain defenders in the chapter on diet, I'll be honest, there were some pretty
alarming statistics. You quote some
alarming statistics. You quote some research, David, that was published in Jamama Neurology in 2022 where they followed more than 10,000
individuals for an average of 8 years.
And this is what you wrote in your book.
Compared with the participants who ate the least amount of ultrarocessed foods, those who consumed higher amounts
experienced a staggering 28% increased rate of global cognitive decline. meaning all areas of decline
decline. meaning all areas of decline including memory, language and attention. That is a staggering increase
attention. That is a staggering increase in risk, isn't it?
It really is. And again, you know, critics would say, well, that's correlation. It's not causation. And I I
correlation. It's not causation. And I I understand that you cannot say that uh you know, the ultrarocessed foods are causing dementia based on the study. I
can say it and I believe it but you know from a strict scientific perspective this is a correlation but when we add these studies together in the aggregate the study I just quoted you on
ultrarocessed foods I don't think is in my book because it it's quite recent uh but having said that um you know I I think we understand that when type 2
diabetics manifest a 3 to 4x increased risk of of developing Alzheimer's and even pre-diabetics we make we see the relationship ship to insulin resistance
and even mild elevation of blood glucose. Uh and then we see what people
glucose. Uh and then we see what people absolutely understand and that is the relationship of consumption of these ultrarocessed foods to type 2 diabetes
and as you mentioned obesity then and obesity as a risk for Alzheimer's as well. Everything really kind of falls
well. Everything really kind of falls into place. The puzzle pieces are
into place. The puzzle pieces are absolutely falling into place. Still in
a world that would like us to believe that we should live our lives come what may and then when we develop an issue there'll be a magic drug to fix it.
That's the messaging in the western world. Uh I mean I don't know how it is
world. Uh I mean I don't know how it is in the United Kingdom but here in America we have uh television commercials for one drug after another.
And it's interesting because when you when you take a look at what the drugs are doing, many of these drugs are what we call monocclonal monoconal antibodies or antibodies that are directed against
inflammatory proteins used in lot of autoimmune and inflammatory conditions. And it's quite
inflammatory conditions. And it's quite clear that metabolic disturbances increase these autoimmune and inflammatory conditions through
something called imuno metabolism.
Meaning there's a direct relationship between our metabolic health and how balanced our immune system really is. I
gave a lecture on that this past weekend uh in Chicago. How does imunomabolism this notion that our metabolism plays out in our immune system? How does that
manifest in the brain? And it is the the exactly what brain defenders is all about. The fact that we have in our
about. The fact that we have in our brains immune cells called micro gal cells and they can be friend or foe.
They can be supportive of our bloodb brain barrier and help us make new neurons and new synapse connections between the neurons or they can shift and become the evil twin where they
destroy our synapses. They reduce our rate of growing new uh neurons and they damage the important bloodb brain barrier. That shift between being the
barrier. That shift between being the good twin or the evil twin is dictated by their metabolism. And their
metabolism reflects our total body metabolism. Now, I've just said a lot,
metabolism. Now, I've just said a lot, but the let me collect the two outline dots. They are that our body's
dots. They are that our body's metabolism determines whether our brain's immune system is going to support a good, wonderful, healthy brain or is going to set the stage for our
brain to be destroyed based upon our metabolism. And here's the empowering
metabolism. And here's the empowering part about what I just said. Our
metabolism, each of our metabolisms, your metabolism is based upon choices that you make every day. So that's darn
empowering that you have the choice to make lifestyle uh changes to increase the the value of your metabolism to ultimately affect your brain's destiny.
So you know I know we have a lot of time together today to uh chat about a lot of different things but having said that what a message I mean that flies directly in the face of what we are
being messaged. What would be message is
being messaged. What would be message is as I mentioned earlier, just live your life however you want and we will fix it. That doesn't work. Uh we need to
it. That doesn't work. Uh we need to have the ball hit across the net to our side of the court so that our destiny really depends on how we return that serve.
Yeah, David, I've been thinking a lot about brain health over the past few months.
I've had multiple conversations on this podcast with people like Professor Dale Bredesen, Dr. Tommy Wood, all kinds of professionals and researchers like
yourself who are showing us from multiple angles that there is plenty we can do about this. This is not our fate.
Even if our mom and our dad or our auntie had Alzheimer's, it doesn't mean it's going to happen to us. Now, what's
really interesting though as I talk about this with my friends and colleagues and perhaps this is my age.
I'm, you know, in my mid to late 40s, David's, but a lot of people I speak to will say back to me, I'm worried about
my mom. I'm worried about my dad at the
my mom. I'm worried about my dad at the moment. It it very much feels as though
moment. It it very much feels as though this is reaching epidemic levels, right?
The amount of people who are struggling with cognitive decline as they get older is becoming so common that I believe many people think it is the norm. But
it's not, is it? It certainly doesn't have to be the norm.
Yeah. I mean, it, you know, people laugh away the idea of senior moments and instead of Alzheimer's disease, they call it old-timers disease. Well, I will tell you, uh, I'm not planning on being
there, and I know Dale Bredesen's not planning on being there. And, uh, it it's interesting. Let me take take you
it's interesting. Let me take take you back a moment to what you just said. And
you said, you know, my friends in my 40s are telling me about they're worried about their parents. My statement is that your friends in your 40s should be worried about themselves because we know
that the seeds are sewn for Alzheimer's in terms of the metabolic threats to the brain in our 30s and in our 40s. So this
is when we really need to start concentrating on an Alzheimer's prevention program because the metabolic changes that occur in the brain happen
2, three, four decades prior to the clinical manifestations. When I say
clinical manifestations. When I say clinical manifestations, I mean the the issues that people begin to recognize.
Loss of sense of smell being something that happens very early, a loss of certainly memory, cognitive function, uh executive function, etc. But those those things are late players. Uh you know,
they're late to arrive at the party. And
you know, my outreach now, you know, my outreach has really been to those people who are suffering and uh you know, and hopefully their family members might, you know, get tight clued in on what I'm
talking about. But I realize now that to
talking about. But I realize now that to really have an impact because of the very epidemic that you describe, uh we've got to be targeting uh uh individuals at a lot younger age and
make them realize that yes, what you just said is true that this is an epidemic in older people. But the way to prevent it is to target those individuals earlier in life. We know
that well at least here in America that you know we have uh 30 uh million uh Americans adults with pre-diabetes and you know the staggering thing about
that uh fact is that 90% of them don't know it.
So I really welcome and uh applaud the idea that there's direct to consumer laboratory testing now available here.
And that means that people can't blame their doctor and say, "Well, my doctor told me I needed a fasting blood sugar every year and it was pretty good and he or she says I we we'll see what you're
doing next year." No, the people can be again uh in charge and can get their own fasting blood sugar, but beyond that get much more detail as it relates to their metabolism.
A fasting blood sugar is interesting, especially if it's really high. You know
you've got a problem. But a predictor of fasting blood sugar elevation even before it's elevated is a fasting insulin test. And you know I'm very
insulin test. And you know I'm very deeply uh involved in uh getting that message out that we should all know our fasting insulin levels and our hemoglobin A1C's. And you know if you
hemoglobin A1C's. And you know if you really want to take it to the next level, wear a continuous glucose monitor.
Believe it or not, even if you're not diabetic, these are available without prescription. Yeah. and not only shows
prescription. Yeah. and not only shows us what our blood sugar is in the morning when we awaken but also gives us a sense as to the dynamics of our blood sugar control during the course of the
day during uh the times during which we exercise what happens during a meal after a meal etc. These are very in uh valuable inputs for us in terms of
understanding our metabolism.
And I would say if we want to re in our metabolism that that keeping blood sugar where it needs to be is absolutely job one. Why do I say that? Because all the
one. Why do I say that? Because all the other lifestyle inroads play out in terms of blood sugar, not getting enough sleep, exercise, uh stress. Uh I don't
know that lack of social connection is necessarily threatening blood sugar, but I bet it is. Uh I'm I'm certain if we were to to you know look at for a study about that we would see it because you
know a lot of people talk about it as it relates to reduced risk of alzheimer's visav you know the blue zone studies etc. And I think it it it sort of yeah
okay you know social connection is important but let's talk about sleep and exercise. That's usually the
exercise. That's usually the conversation, but you know, this it's one of the important pillars, so I want to make sure we don't uh overlook that.
Yeah, thank you. I I completely agree.
Um social connectivity is absolutely huge.
I think you raised a really good point, David, about this idea that we should be paying attention to our brain health in
our 40s, not just in our 70s when things start to go wrong or we forget our grandchild's name or whatever it might be. I think I want to come back to that
be. I think I want to come back to that point. Testing for sure. Before we go
point. Testing for sure. Before we go into those areas though, one of the things I enjoyed the most about your new book, Brain Defenders, is that you
really set the stage at the top of the book about this one fundamental mechanism that potentially underlies virtually all neurodeenerative
conditions. You've already mentioned the
conditions. You've already mentioned the microglea immunomabolism, but I really want us to just really [snorts] understand that because this kind of
balance between M1 microglea and M2 is something I hadn't come across before.
And once you get that in your head, you can look at every single lifestyle intervention through that lens and go, what is this doing to M1 and M2 book's all about? You you hit the nail on the
all about? You you hit the nail on the head. It's exactly what we're talking
head. It's exactly what we're talking about. And you know the polarization uh
about. And you know the polarization uh of these microgle cells from being M2 supportive to being M1 destructive is is a theme now that we're actually seeing
elsewhere in the body. We've known that macroofagages uh the immune cells in you know in the rest of the body go through the same sort of shift when they are metabolically challenged. We even know
metabolically challenged. We even know that condondraittes that are involved in either nurturing or destroying our joints have an M2 supportive or M1
destructive configuration. So you know
destructive configuration. So you know uh but when you we see through the lens that you describe the part the the take-home message is it empowering
because we control the levers that determine whether these microgle cells are going to be on our side or setting the stage for brain destruction. And you
know I'm thinking of a slide that I use when I when I um in my presentations in fact with who you mentioned Dr. Dr. Dale Bredesen 3 days ago in Chicago and it is
a a type of brain scan uh that is called TSPO and it's actually a brain scan u that allows us to image activated
threatening M1 micro GA when people are alive in vivo and when I show the image in Alzheimer's you know the brain lights up but then I list the diseases in which
this TSPO imaging is positive in other words Microg GA have been shifted to being the evil twin and the list is really every major neurodeenerative condition you can think of including
Parkinson's fronttotemporal dementia multiysmaty progressive super super nuclear paly uh long covid PTSD major depression you know there are a lot of
things included uh that are manifestations of this shift in the immune system and you know that said it it sheds light not just on the neurodeenerative issues, but in the mood
disorders as well, which we we've known for many years are characterized by increased inflammation in the brain. But
now we understand why there's destruction, why there's uh destruction of the synapses, for example, in particular parts of the brain like the prefrontal cortex because we're turning
on these immune cells that are damaging the synapses. Yeah, just to check I've
the synapses. Yeah, just to check I've got this clear so far, David.
The microglea are the brain's resident immune cells. When they become damaged
immune cells. When they become damaged for a variety of reasons, you know, insulin resistance, toxins, infections, whatever it might be, they change shape
and function. Ultimately that causes a
and function. Ultimately that causes a disruption in mitochondrial function and that then leads to neuroinflammation
which sits at the heart of many of these different kinds of neurodeenerative conditions. Is that an
conditions. Is that an oversimplification or have I rushed?
No, I'm going to actually I'm going to actually simplify even further.
Okay.
When there's a shift from M2 to M1, as you correctly stated, there's a phenotypic shift a shift. In other
words, they change their shape. There's
a functional shift as you describe and there's a metabolic shift away from using the mitochondria to produce energy to another type of energy production
that we call glycolysis.
But importantly, one of the major inroads or uh threats that shifts the mito uh the microglea is inflammation.
The chemicals of inflammation called cytoines target the M2 microglea and shift them to becoming the evil twin.
Those inflammatory cytoines can come from anywhere in the body. When you get your arms around that, you realize then, oh, they can come from a leaky gut. When
we have a bowel disturbances, for example, that leads to increased inflammation in the body. These
chemicals make their way to the brain.
and now help us understand why there is such a constant correlation between neurodeenerative conditions like Parkinson's and bowel disorders
further and here's where the story gets really interesting these inflammatory cytoines are produced once those microglea shift to becoming the evil twin so once we shift from
being supportive and loving M2 microglea to the threatening M1 configuration it as you mentioned increases neuro inflammation. What does that
inflammation. What does that neuroinflammation do? It further targets
neuroinflammation do? It further targets those good M2 micro glea and shifts them over to being zombies. Think about that.
So this explains now we understand why a football player who no longer is playing football but yet has been diagnosed with CTE, chronic traumatic encphylopathy,
gets worse over time. Why Alzheimer's
patients worsen over time. Why
Parkinson's patients continue to worsen over time. long after they've had their
over time. long after they've had their head trauma, long after they've had their exposure to a toxic chemical. We
can talk about that a little bit later.
I think we're we're we're teeing up an awful lot to talk about. But that said, it's because this spreads to through the brain like a cancer. These M1
threatening microgle cells target the support of M2 microgle cells and with time become dominant. So, uh what you said is very true. But I think the
important thing is that there is a shift in their metabolism away from the mitochondria doing the heavy lifting as it relates to energy production to a
different form of energy production called glycolysis. So in a very real
called glycolysis. So in a very real sense, we should be targeting mitochondria as we talked about in brain defenders uh if we want to do something very very important and that's the
take-home message of our time together today and that is that the microglea can shift back to being good and that's our mission.
Yeah.
Most of the messages are deeply empowering. The message is it's never too late. Having said that, going back to your chapter on diet when
you were, you know, quoting some of the research that exists out there on the relationship between diet and brain health, I mentioned one of the studies that you wrote about um there was
another one you spoke about this 2024 study published in neurology led by a researcher from Harvard Medical School where they investigated the relationship between ultrarocessed food consumption
and brain health outcomes. And [snorts]
yes, you know, as many other studies, that study, you know, concluded that there was a significant association between higher ultrarocessed food intake
and an increased risk of cognitive impairment. But I tell you what was
impairment. But I tell you what was really striking for me, David. A couple
of paragraphs later, you write that interestingly when some of those patients adopted the Mediterranean diet, the DASH diet, that dietary approach to
stop hypertension or the Mediterranean DASH diet after the initial survey, the brain altering effects of UPFS
persisted. This means switching to a
persisted. This means switching to a healthier diet can't always reverse the damage done. You just mentioned there,
damage done. You just mentioned there, didn't you, that we want M2 microglea.
If for a variety of reasons they start to shift to M1, that's problematic for our brain, but then it's a feed forward cycle where those M1 microglea
themselves start to cause more M2s to go to M1. Could that be one of the reasons
to M1. Could that be one of the reasons why when we change our diet, eat let's say after 20 or 30 years of a poor diet that actually some of those brain
altering effects might um might have persisted.
Yeah. And I think you know when we look at what has been the goal of pharmaceutical intervention for Alzheimer's disease their goal I mean in an ideal world would have been
improvement in cognitive function.
But then they settled on, well, let's just see if we can stabilize people so they don't decline. You know, that's a reasonable goal for a patient with early Alzheimer's. Uh, but they even failed at
Alzheimer's. Uh, but they even failed at that. So, I I think that uh the idea of
that. So, I I think that uh the idea of reestablishing cognitive function and and and improvement is going to require a a much more comprehensive approach.
And we outlined a lot of things in the book uh that need to be added. Diet is
certainly one important pillar. diet is
really critical as it relates to reducing inflammation. But if we want to
reducing inflammation. But if we want to really boost uh the growth of new brain cells and the the formation of new synapses, we have to target exercise as
well such that we will increase the production of brain derived neurotrophic factor in the brain or fertilizer if you will that helps also nudge these micro gal cells back from being M1 destructive
to being M2 supportive.
You know if you look at Dr. Dr. Dale Resen's work he talks about 36 things uh that need to be at least considered if not targeted to bring about uh actually
improvement in brain function. So you
know the mission here is to indicate that there are multiple inroads that threaten these microgle cells. We know
that their metabolism is key. So
metabolic health is certainly important.
Inflammation is very important as well.
infections need to be considered. Toxic
uh uh issues like metals etc need to be considered. All of these things uh
considered. All of these things uh attack the M2 microgle. So there are receptors on these microglea uh that then uh instigate the change in their internal metabolism that leads to their
shift to becoming M1.
Yeah. But I think your point is well taken that uh and Dale Bredesen makes it very clear that we need a multi-pronged approach if we're going to do more than
stabilize but if we're going to uh lead to improvement. Now as we say that uh
to improvement. Now as we say that uh that is something that can be achieved.
I actually quote his work in the book and uh present a couple of his case studies where in uh in which patients clearly improved uh and demonstrated not
only improvement in their cognitive function but improvement in the size of their brain's memory center the hippocampus on brain imaging that is
black and white. These are read by independent uh radiologists who didn't know that there was an intervention and clearly described enlargement post
treatment of the hippocampus in these treated individuals. So the idea that
treated individuals. So the idea that the brain can't improve and cognitive function can't improve I think is outdated. Uh I I think it takes a lot of
outdated. Uh I I think it takes a lot of work. But I think the beauty of what we
work. But I think the beauty of what we are talking about now is it takes us away from hoping and relying upon something called monotherapy.
Western medicine is built upon this idea of one drug for one illness. And in
Alzheimer's, it just doesn't hold up.
Yeah.
And you know, in Parkinson's, it doesn't hold up. We don't have any medications
hold up. We don't have any medications right now to treat Parkinson's disease.
And that may be surprising for some of your viewers, but the reality is all of the medications that are approved for Parkinson's treatment are treating the symptoms. They're treating the smoke.
They're not treating the fire. I think
these medications are excellent. I think
that the ability of using leodopa to help an individual with their rigidity in Parkinson's and some of the antiolinerics uh as it relates to uh addressing the
tremor are valuable allow people to continue on with their lives. But the
disease continues to progress underneath that uh symptom-based approach uh readily and uh maybe this sounds a little bit divergent but uh in 2024 a
fascinating study and I talk about it in the book uh was published in the New England Journal of Medicine uh 135 Parkinson's patients were randomized to
receive a GLP1 ompic like drug or placebo for one care and the results
were dramatic. Uh the group receiving
were dramatic. Uh the group receiving the placebo uh continued to decline as we would see in Parkinson's, but the group receiving the GLP-1 drug stabiliz
slightly improves on what is called the unified Parkinson's disease rating scale, a a standardized way of assessing how a Parkinson's patient is able to
function uh in their daily life. So this
is the very first time uh well I'm going to actually say it's the second time it's I'll tell you the first time in a moment that uh that the actual underlying metabolic issue uh in
Parkinson's was addressed and look what they found. Now I'll tell you about the
they found. Now I'll tell you about the first uh was actually our study uh in the 1980s using introvenous glutathione published in the journal movement disorders. Introvenous glutathione was
disorders. Introvenous glutathione was given also to improve mitochondrial metabolism and our patients demonstrated pretty dramatic improvement on the very
same scale used in the more recent GLP-1 study. Let's be clear, I'm not saying
study. Let's be clear, I'm not saying that, you know, ompic is the treatment for Parkinson's. That's not the
for Parkinson's. That's not the take-home message from what I just described because this um GLP-1 was specifically chosen uh because of its
ability to make its way into the brain.
And in fact, now it's not available uh on the market here in America because it's been associated with uh some changes in the pancreas. But that said, what do GLP-1 drugs do? Well, they don't
just lower our appetite. They don't just control our blood sugar. the blood sugar control being why they were originally developed and now we're seeing uh you know a variety of other outcomes in
people taking the GLP-1 drugs but one study that I did describe uh in brain defenders uh mentions how in type 2 diabetics mitochondrial function is
improved in people using these GLP-1 drugs that is huge because mitochondrial dysfunction is at the heart of what is going on in the Alzheimer's and
Parkinson's brains and in all neurodeenerative conditions. I gave a
neurodeenerative conditions. I gave a talk at what's called the Institute for Functional Medicine, IFM, I know you're familiar with that group, 20 years ago where I said Alzheimer's is an acquired
mitochondopathy means, you know, by and large it's not inherited. We could talk about what that means in a moment, but a a a problem with our cells energy making
machinery, our mitochondria.
And again we mentioned earlier when the mitochondria become dysfunctional that shifts our microgle cells from becoming supportive to becoming destructive. So
we need to then take a step back and ask ourselves.
Again thinking about what I just said about the GLP1 drugs targeting mitochondria. Again I'm not saying this
mitochondria. Again I'm not saying this is our answer. I did say in the book and for those who read the book the language I use was pretty strong. I'm open to it.
I am absolutely open to it. I mean, you know, a lot of what my work is all about and yours too really are the lifestyle issues that are people are are getting
wrong and people can improve because that's very empowering. That's the
take-home message. People do these things and can and have better health.
But you know, as are you, I am open to anything that is uh fulfills the notion of risk benefit ratio. And if the
benefit of GLP-1 drugs in an Alzheimer's patient seem to be uh very favorable in the face of uh not such a significant risk, I'm all in. You bet I am. That's
going to be part of the toolbox. Uh I I think it's, you know, our duty as physicians to keep an open mind and put in our toolbox whatever uh is satisfies
risk benefit ratio. So uh that said, we will see uh what happens with JLP1s and the brain. We know that uh recently the
the brain. We know that uh recently the study on oral ompic semiglutide was published in Alzheimer's patients interventional trial and did not meet
its end points uh in terms of improving uh or slowing their rate of decline.
That said, perhaps it was because it was oral and uh semiglutide uh coupled that didn't make its way to the brain, but we will see. You know, researchers are hard
will see. You know, researchers are hard at it. Uh not just certainly looking at
at it. Uh not just certainly looking at GLP1s, but at a variety of ways of targeting not only mitochondria, which will help our microgle cells, but the microgle cells themselves.
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20%. Or click on the link in the description box below or scan the QR code on screen. So many things you've touched on there, David. Just to
summarize to make sure everyone's sort of in the same place as we are in our heads.
Number one, metabolic health is crucial.
Right? You mentioned that maybe these GLP-1 agonist trials are demonstrating that actually when we address metabolic health and of course you can address metabolic health with lifestyle as well
as with drugs actually the impact on brain health is profound. You mentioned
that often if we want to optimize our brain health there are multiple things we have to do not just one thing not just two things but we have to address
it from multiple different areas.
You also mentioned about um Dale's work and you know I I've like you been a friend of Dales for many years and I I went I think it was in 2016 I went out
to America to Palm Springs and I worked with Dale for about 10 days on this deep immersion with patients and I met some of his patients who have had their cognitive decline reverse and we worked
on patients together for a few days. It
was very very inspiring to look at that research. This is 10 years ago now. So
research. This is 10 years ago now. So
this is not as new as people think. This
idea that actually there is something that you can do about Alzheimer's particularly early stage Alzheimer's.
You also mentioned David that there are cases of reversal or at least reversal of symptoms. Of course it's much easier to do that at
the earlier stages in the later stages.
you know, it can get harder, but I have seen it, David, like you have with patients in early cognitive decline. And
yes, we want to get involved way before that stage, but even at that point, there are things that you can do that make a meaningful difference in that
person's life and their family's lives.
We're going to talk about these things.
We have touched on diet and how important it is to take out ultrarocessed foods as much as we can from our diets. So I guess the question
I have for you, David, is how have your dietary recommendations evolved over the years? And are there some sort of core principles that you
can share with people to say, listen, if you want to keep your brain well for as long as you possibly can, this is what you should do when it comes to diet.
I've done my very best recently to simplify the the notion of dietary recommendations because there are so many diets. There's probably a diet for
many diets. There's probably a diet for every letter in the alphabet. Uh whether
it's paleo or primal or mind diet or med diet or green med diet. Uh and I think it's it's very challenging for patients to think they need to adopt a certain
diet and follow it to the letter uh in order to achieve an outcome. So in this time around and this is uh book number 16 I looked not at the diet but at the
outcome and I said uh that really I don't care what diet uh you want to what name you want to attach to your diet let's look at what that diet should do and to be you know to be very simple
about it because I think that's what people really need because you know when you try to adopt a certain diet and you have to have an app or follow a book it's very challenging so I said I want
you to be on a diet that keeps your blood sugar under incredibly tight control, that offers up your body a lot of dietary fiber. In other words, is mostly plantforward,
a diet that is colorful, so we're going to get lots of different polyphenols.
And that emphasizes not only adequate amounts of protein, but good fats as well. Leave it at that. And I describe
well. Leave it at that. And I describe what adequate amounts of protein are in terms of grams per kilogram, ideal body weight. And I also described in depth as
weight. And I also described in depth as you as you saw what are the good fats.
That's it. So uh I I wanted to open the door uh to people to embrace their uh ethnicity in terms of their food choices or not whatever they they choose. Um you
know thinking about that the idea of a Mediterranean diet. If you when you
Mediterranean diet. If you when you travel around the Mediterranean you really see that they're not doing the Mediterranean diet anymore. Uh I just got back from there and it's it's you
know this uh we originally called it the standard American diet the SAD diet which became the western diet. Face it
it's the global diet now you know just dramatically emphasizing ultrarocessed foods. You know your theme for our time
foods. You know your theme for our time together today. So this is a global
together today. So this is a global issue and it you know it explains why there's 53 million uh Alzheimer's patients um you know in the world right now and that number will triple by you
know by 2050. [clears throat] So, uh, you called it out as a an epidemic and it is and it's it's something over which we have control. The fact that it's
increasing so rapidly argues against it being genetic because our genetics have not changed. Our metabolism has changed
not changed. Our metabolism has changed and I would, you know, I would add to that our epigenetics have clearly changed as well. As a matter of fact, we could talk about the work interestingly
of a Dr. Sarah Marzy. She's actually uh in the United Kingdom. I had her on my podcast recently who's talking about how epigenetic changes are really underlying, you know, a lot of what's
going on in the brain. We we'll put a pin in that and deal with that later.
But, uh, you know, getting back to to what you've been talking about. So, I I I'm trying my best to simplify these dietary recommendations, uh, such that
people can look at their diets in terms of how I am metricizing my body. In
other words, what's the outcome of the food I'm eating on my blood sugar?
Yeah, that is a leap that takes you away from chapter and verse following a specific recommendation that a doctor has developed to actually looking at
outcome. What is it doing to my blood
outcome. What is it doing to my blood sugar to me and you might agree? I think
that's one of the most important issues that goes ary when people are eating it appropriately. So
appropriately. So yeah, you know, I really emphasize for people the idea of knowing what your blood sugar is. Even if you can't get a
sugar is. Even if you can't get a continuous glucose monitor, go to the the pharmacy and buy a finger stick that diet, it's available to anybody. And I
know it's not pleasant sticking your finger, but do it once a month and see where you are. But um it's it's really that important. Again, the fiber for the
that important. Again, the fiber for the microbiome, the polyphenols, we should have a we could talk about that in terms of why that's important for the brain.
uh the right kind of fat gets back to your original question. What has
changed? I think one of the biggest change uh that uh I emphasize now that really was not emphasized earlier in very very early in my career
frankly respectfully before you were born. Uh and that is you know the the
born. Uh and that is you know the the position on fat. I mean there there was a time when fat was uh not the right thing to be eating in any form. And you
know that was what the science was telling us. And I you know in mainstream
telling us. And I you know in mainstream medical training was paring that and that changed obviously and for good reason uh over time uh in my outreach
that you know fat is a fundamental player uh for metabolism for inflammation for structural integrity of the neurons you know a variety of things that that the right fats do in our
bodies.
Yeah.
I really like the guidelines you provided for food there, David, because ultimately whatever diet you follow, there's a
certain outcome that we're looking for, right? You know, one of those outcomes
right? You know, one of those outcomes is a wellontrolled blood sugar, right?
So, you can get that outcome in a variety of different ways. So, I I kind of feel this is a good time to talk about testing. Um, one of the things I
about testing. Um, one of the things I really enjoyed reading at the start of Brain Defenders was this idea that there are two wars that we're fighting at the moment. One is, I think, the war as to
moment. One is, I think, the war as to why are millions of brains around the world, as you say in the book, on fire.
But then you also said the other war we're fighting is on our attitudes, our attitudes about illness and expectation.
And I [snorts] thought it was a really provocative thought, but a very important thought because that's what we're up against, aren't we? We're up
against a medical system that has made amazing inroads in to certain conditions that many of us have grown up with and
absorbed the idea that if you get sick, the medical system will be there to take care of you. And
as we're realizing, for many of the conditions that now are affecting a majority of the world's population, these are chronic diseases that take
years to build up in your body. As you
said earlier on, David, maybe 20 to 30 years before you get a diagnosis of Alzheimer's, that process has been going on and causing havoc in your body. You
know, the diagnosis is the end stage, right? That's right. Of a long process.
right? That's right. Of a long process.
And that really ties into what you're saying about what diet you want to follow is the diet that gives you a certain outcome on certain biomarkers.
Now, David, one thing early on in my career, I did back in maybe 2012, 2013,
2014, I would go to America a lot in my vacation time to go to conferences and to learn stuff that I felt I didn't learn at medical school. A lot of the
good conferences back then was certainly in America. And what I noticed from
in America. And what I noticed from chatting to a lot of uh American physicians is that the American medical system is fundamentally very different from the
UK one. And it's very obvious now as I
UK one. And it's very obvious now as I look back. But what that led to is for
look back. But what that led to is for many years, David, I was hoping that the NHS, our national health service, would really take on the mantle of prevention.
And unfortunately a few years ago I realized that you know what I I actually don't think that's ever going to happen because the DNA of the NHS is to manage
disease. And I think often it does that
disease. And I think often it does that very very well. And the NHS's idea of prevention is once you hit the age of
40, maybe every now and again go in and get your blood pressure checked and maybe once every 5 years get some bloods done. That to me seems like prehistoric
done. That to me seems like prehistoric prevention compared to what we know. So
what I did about a year ago, David, um I don't think you know this yet actually.
About a year ago, I thought in the UK we're in a position where people who are interested in health might listen to my podcast or your podcast or or read books
and go, "Yeah, you know what? I need to check my fasting in. I need to check my homocyine, my uric acid, the topic of your last book." Right? Who knew?
Yeah, Ben, we'll we'll tie this all up in a minute. But actually, they would listen to these conversations or read our books or other people's books and then they weren't able to get that
certainly in the UK from their NHS doctor. You just can't get for most
doctor. You just can't get for most people a fasting insulin or a homocyine on the NHS. Now there are private providers where if you were really
motivated you could put together the correct panel but you know there's a lot of work on your shoulders in order to do that. So I teamed up with some amazing
that. So I teamed up with some amazing tech guys and created something called do health which I don't think there's anything like it in the UK and basically we don't do like a you know test
hundreds and thousands of biomarkers. We
started small and test the 11 biomarkers that I believe are the most impactful when it comes to metabolic health. And
we give daily and weekly lifestyle advice on what you can do around them.
Like all of these 11 biomarkers we know impact your metabolic health, your short-term health, and your long-term risk of disease. But at the same time, they are 11 biomarkers that are all
amanable to change. Right? Those are the criteria.
It's only been live for 2 and a half months, but the feedback, David, is absolutely incredible because a it's very very cost effective for what it is, but we are basically gone I I think
talking about the sort of stuff you're talking about, right? We're checking
stuff like fasting insulin, homocyine hbaw1c alt, B12, uric acid, you know, and I I I won't do
the whole list, but I would say that your book, your last book, heavily influenced my decision to put uric acid in this panel of 11. So, first of all,
thank you. Um but I think what it means
thank you. Um but I think what it means then is whatever diet you follow to you know as long as it's you know generally a whole food minimally processed food
diet as much as you can if you are getting these biomarkers in the correct range right a low fasting insulin an
HBA1C maybe under I don't know 5.3 5.2 to whatever whatever it is you know if you're homoyine in the normal range then actually you know that whatever
lifestyle you're following the key markers that influence metabolic disease are actually you know in good shape and we've decided to recheck twice a year well three times a year so it's like you
test you do four months of lifestyle change and then we recheck because of course this isn't just a one hit so first of all I want to get your take on that David do you think this is the kind
of approach that we now need if we really want to get on top of our brain health. Um, and then I guess secondly,
health. Um, and then I guess secondly, you know, from what I've said, are there any downsides to this kind of approach?
Well, let me answer the second question first. I I can't imagine the any
first. I I can't imagine the any downside. You know, cost will have to be
downside. You know, cost will have to be considered, but I mean everything that you mentioned on that short list uh has huge uh play in terms of brain health
and you know it it it impacts metabolic health in the body and the brain isn't distant from the body. It's part of the body. It's going to be the same impact
body. It's going to be the same impact on the heart, on the liver, on bone density for which is reflective of metabolic health. Who knew? And you
metabolic health. Who knew? And you
know, my only time in visiting your country was several years ago when I when we met. And it's interesting because I was asked I was summoned to
visit with um then Prince Charles and we sat uh at in uh at Highrove I guess it's called. And um he he asked me the
called. And um he he asked me the question, what is the reason that our health is deteriorating? And the answer was very simple.
ultrarocessed foods. And I looked at him straight in
foods. And I looked at him straight in the eye. I said, "That's what's going
the eye. I said, "That's what's going on." Uh, and that's what you need to
on." Uh, and that's what you need to address. And he said, "Well, I don't
address. And he said, "Well, I don't know how I'm going to address that." And
I don't think there was really any outcome of that meeting, but uh I I think that's what we're up against. And
I think um you know, the food industry has no interest in health and healthcare really doesn't spend uh any time in involving itself in food. So this is a
huge disconnect that has never been present in humanity. Yeah.
Traditionally uh food and health have always been linked and it's uh I remember years ago I was uh somebody accused me of my practices being
non-traditional because I was talking about nutrition and the brain said that's really non-traditional and actually interesting it was a time when I was supposed to be the chairman of
neurology at our local hospital. It was
my turn. Nobody even wanted the job. And
one of the individuals in the group said, "Well, we can't have Dr. Pearl Mutter do it because he's doing these non-traditional things like nutrition."
And I, you know, I'm thinking, you know, humanity has always valued the food that we eat and its relationship to our health and its relationship importantly
to our connection to the planet as well, which uh is really something I think that we we no longer value and even recognize.
Well, not we but uh you know generally in the world there's no connection between the fact that the the planet is giving us this sustenance. All food
comes from the earth whether you're vegetarian or not you know because ultimately plants are the source of food even for the animals that people eat with the energy ultimately coming from
the sun uh for all of it. So um you know I think I was a little bit divergent on my response to you but I think that um it is very challenging. I honor what you're doing because I think what you're
doing is simplifying. You know, there are uh organizations here in America that offer 400 different labs and uh it's overwhelming in my opinion.
Well, yeah, David, you you raised a key point there. So, I I I'll be honest with
point there. So, I I I'll be honest with you, I never had any uh plans or desires to launch a health app, right? But I
just thought there are so many people out there who want to know their biomarkers so they can make changes and see what changes are working and which
changes are not working. Which is why I think tracking biomarkers and rechecking them is so important because a you can be making some changes to your diet and
not getting the drop that you might want to see in your HBA1C. I accept there are other factors like movement and stress and sleep, but it might be that oh,
maybe the diet you're trying at the moment isn't the right one for you.
Maybe, you know, maybe you're really insulin resistant and actually you need to so personalized. I I'm just loving what
so personalized. I I'm just loving what you're saying. It's so personalized
you're saying. It's so personalized because maybe that diet isn't the right diet for you.
Yeah. Maybe you heard it about the evidence on the latest podcast you listened to and thought great, but when that diet interacts with your biology,
what is the outcome on these key biomarkers? And so I kind of feel that
biomarkers? And so I kind of feel that this is not a slight on the NHS. It's
basically saying, look, let the NHS do what the NHS is really good at. Let's
create something that I hope is the future of preventative health in the UK.
And I specifically insisted on small amounts of biomarkers, right? Because I
think it can become overwhelming over time. David, I'm sure we'll add to these
time. David, I'm sure we'll add to these biomarkers. But we've we've started
biomarkers. But we've we've started where there's 11 biomarkers. There's
damn good evidence for all of them. I I
I think that's a home run. I mean, look what I did in this book. I said one biomarker. I mean, we we look at a lot
biomarker. I mean, we we look at a lot of biomarkers as in the book. talked
about homocyine and and GFAP uh pal 217 you know other things but uh in terms of your diet I just wanted to control your
blood sugar and having said that and you make the changes and your blood sugars recalcitrant uh it's still not coming around you know you might need metformin
you might need a medication so that that's the point here and I think what what you alluded to is the notion of personalized medicine that this person may have adopted a specific
diet and it's not yet controlling her uh blood sugar. So what you know the
blood sugar. So what you know the uniqueness there is this notion of personalized measurement based perhaps on her genetics and other aspects of her lifestyle as
well the variables like exercise, sleep etc. that you know that is is just not enough and she would not know it's not enough unless she is testing. Exactly.
We have that ability now. We we should uh you know welcome it and and use this information that we have and we can through guidance like you're offering be
our stewards of our own health. Yeah.
And really adopt more cubrious lifestyle choices based upon the input from this information. So I I think what you're
information. So I I think what you're talking about is an absolute home run.
David, I've heard you previously talk about the fact that your homocyine was previously elevated and that you take B vitamins to manage that. I know you
write about homocyine in the book as an important biomarker we should all be looking at. I wonder if you could just
looking at. I wonder if you could just touch on why you think homoyine is so important, but also if you could remind us for those people who didn't hear my first conversation with you. Why is uric
acid an important biomarker to look at as well? Okay, let's start with homoyine
as well? Okay, let's start with homoyine and my homocyine as of yesterday was 8.2 and that makes me very happy. So,
you know, it's been said that why should I take supplements? After all, I can't measure that they're doing any good. And
I always, you know, people have asked me that question when I give a lecture, whatever. And I and I I always challenge
whatever. And I and I I always challenge that because um, you know, the notion of a supplement means it's it's something added to to supplement because of a
deficiency or a need. That's why we take certain supplements. And and so in my
certain supplements. And and so in my case, I had a need. I had an elevated homoyine. I'll describe what that means
homoyine. I'll describe what that means in just a moment. But the reason that I have an elevated or had an elevated homoyine is because of my unique genetics. I carry something called an
genetics. I carry something called an MTHFR polymorphism. Now, that's a mouthful. It
polymorphism. Now, that's a mouthful. It
simply means that I don't handle B vitamins in a good way when I consume B vitamins either in a supplement or getting them in food or perhaps even the
ones created by my my gut bacteria such that I'm not able to methylate. It's
it's a biochemical change that activates let's say and makes them work worthwhile the B vit certain B vitam B6 B12 and folate folic acid. So I have to add and
that is the reason that my homoyine level is elevated. So I take these I take uh folate I take uh rather uh methylated folate uh B12 sublingually
and a B complex and every once in a while a B12 shot and lo and behold my homoyetine level has come down. I don't
feel any different. I feel happier, right, and more confident, but I don't I can't feel. So, like, oh gosh, I I been
can't feel. So, like, oh gosh, I I been taking these vitamins now. I have more energy and, you know, my life is great.
That's not what you're looking for.
You're again getting back to the idea of looking at your biometrics like you described with your testing. So,
homoyine has been elevated homoyine has been directly correlated with dramatic increased risk for Alzheimer's, uh, even cardiovascular disease as well. We've
known for a long time that homocyine poses a threat because it is converted in the body to something called homocyic acid. Homocyic acid does two things that
acid. Homocyic acid does two things that are very important. It damages the lining of blood vessels. Hence the
cardiovascular risk from elevated homoyine and it is a mitochondrial toxin. Home run. So elevated homocyine
toxin. Home run. So elevated homocyine is threatening mitochondria and therefore threatening whether your micro gal cells are friend or foe.
Yeah, that's why Dr. Chattery is adding homocyine to his very short panel of critically important blood markers and I
applaud you for it because I went to a cardiologist yesterday. I do see a
cardiologist yesterday. I do see a cardiologist. I had atrial fibrillation
cardiologist. I had atrial fibrillation in the past. Did well after a cardioversion after a ablation procedure. Home run. But um we I
procedure. Home run. But um we I mentioned homoyine and uh he said I'm going to have to send you to a different cardiologist who knows about that kind
of stuff and I was grateful that he would refer me. Uh but homoyine is a player. I mean it really is a player. If
player. I mean it really is a player. If
28% of people in western cultures have this MTHFR
genetic uh variant like I do, 28% of people are at great risk for having an elevation of this homoyine that is a brain threat,
then darn it, they they need to know about that and fix it by taking simple B vitamins.
Yeah, David, I just want to comment on a couple of things there.
First of all, there's this idea that well, you may have checked your B12 levels, right? But in some ways, it
levels, right? But in some ways, it wasn't necessary in the sense that your homocyine was elevated. We know that an elevated homocyine increases your risk
of dementia and as you say, other conditions as well. So therefore you need to do certain things like take
methylated B vitamins to bring the homocyine down irrespective of your B vitamin levels. Right? It's it's a it's
vitamin levels. Right? It's it's a it's a subtle difference there. You're you're
taking the nutrients to drive the biomarker down and by driving that biomarker down you're reducing your risk of getting sick.
Yeah. Let me let me simplify that if I can. Sure. If you have your B vitamin
can. Sure. If you have your B vitamin levels checked and they're normal, it's not good enough because you're not you might not be deficient in those B vitamins. You might
be deficient in the methylated B vitamins which you can't really test for, but the homocyine is a proxy for that. Maybe that made it more
that. Maybe that made it more complicated. I don't
complicated. I don't No, no. I I think it's great because
No, no. I I think it's great because it's not the way I think people think about nutrients, right? So, I think that's really useful. I do want to talk about uric acid, but a thought just came
up for me, David, which is I believe that you are in your 70s now.
Is that correct?
71.
You're 71. Okay.
I remember meeting you in London two or three years ago. You were sharp, bright, right? Right on the money. You gave a
right? Right on the money. You gave a great talk. We we did a lovely podcast
great talk. We we did a lovely podcast together.
I see you now at 71 having written I think you said what is it? 18th 16th
book you know this is number 16 correct your 16th book I think for many of us it's inspiring I think a lot of us would go if I could have the sort of cognition
and brain that David Pilmut appears to have at the age of 71 I'd be very happy with that and I think that's very relevant in the context of what we're talking about which is our brain health
getting worse as we get older what do you attribute your apparent exceptional brain brain health, too.
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I think you just mentioned it uh a moment ago. You said curiosity. And
moment ago. You said curiosity. And
curiosity has been powerfully motivating for me throughout my lifetime. Really
trying to understand okay you know there's a paper written that shows this correlation but why what's underlying it? And I think satisfying that
it? And I think satisfying that curiosity has been the development of this idea that all of our inputs for things like Alzheimer's risk converge on
the brain's immune system. So that's you know connecting dots has been something really central in my life as has been uh the idea of compassion that I learned
from my father uh a a brilliant neurosurgeon brain surgeon who uh as fate would have it died uh of Alzheimer's. Uh that was um that was a
Alzheimer's. Uh that was um that was a powerful uh event in my life and it solidified
my desire to learn more. uh Robert
Kennedy senior uh said years ago that some people see things as they are and ask why. Others see things as they could
ask why. Others see things as they could be and ask why not. And I love it. I
just I just love it because you know medicine puts has traditionally puts constraints on outliers like you and me and you know many of the people who've been on your
podcast and on my podcast. And I think we're starting to get to a place where we're starting to value a little bit uh the idea that, you know, maybe people are on to something. And I think the
notion of lifestyle influencing brain health is really gaining a lot of traction right now. So um I keep my my
brain uh aggressively engaged, not as uh I I don't do that as I exercise for. I
mean, in other words, I dedicate time to exercising each day. I don't say I'm going to do x amount of reading and writing each day because it's good for my brain. That's just part of my what I
my brain. That's just part of my what I do. So that it it's not one of my
do. So that it it's not one of my lifestyle choices. I I don't know if I
lifestyle choices. I I don't know if I made that clear.
As are the foods I eat, the sleep I get, you know, metricizing, all these things.
So, uh I'm I'm grateful to hear you say that. You you still you think I'm still
that. You you still you think I'm still in the batters box. That that's
encouraging.
Let's get together when I'm 81 and we'll reassess where we are.
Yeah. David. David, what what I hear from you there uh are so many sort of beautiful things about curiosity, compassion. Thank you for sharing about
compassion. Thank you for sharing about what happened to your father and how influential that has been in terms of what you do today.
But it sounds to me as though so much of what you do is an expression of who you truly are. And I think this
is where we often go wrong with behavior change. My philosophy on behavior change
change. My philosophy on behavior change is that yes, at the start it can be tricky right?
But I think the missing link in behavior change for many people is that at some point I actually think behavior
change or adopting healthy behaviors becomes quite easy and effortless when it truly is an expression of who you are. When there's full alignment with
are. When there's full alignment with the person who you are and the person who you are being out there in the world are one and the same. I kind of feel
that your behaviors follow suit. So I
obviously don't know the intricacies of your life, but you write about empowering us uh to have better brain health. You've treated so many patients
health. You've treated so many patients and help them. And it strikes me as though you can't really write about this stuff and be curious about this stuff
and not also do it yourself. There would
be a complete misalignment between what you were writing and your behavior. So
it strikes me though you you do have a wonderful lifestyle and you're engaged, you're curious, you enjoy what you do. And so it all kind of
fits together instead of it being that I'm trying to make lifestyle change in conflict with the person who I believe myself to be.
Well, I I I really want to be not be that person. It's do as I say, not as I
that person. It's do as I say, not as I do. and uh many of the things that I
do. and uh many of the things that I choose to do then I I uh articulate uh if they're effective and achieving a goal. But going back to what you were
goal. But going back to what you were speaking about earlier, I would I I focus not on who I am as much as who I
want to be. And so there's still plenty of work to be done. And that's what life is about is doing that work and focusing on those goals. You know uh
the Daly Lama said uh if if you want somebody to be happy want others to be happy treat them with kindness
and if you you want to be happy treat others with kindness. So I I think that uh maybe it's self- serving then uh and
that's okay uh that you know if you do this work and uh you see the outcome that it's good for you and it therefore you know that's self- serving and I'm the first to admit that.
Yeah.
We wrote a book my son and I two or three books ago uh called Brainwash and it really focused on something you just touched on
and that is our decision making. what do
we decide to do once we have information? Are we able, you know, you
information? Are we able, you know, you said then it gets easier? Um, and we we focused on the the the hardware of decision-m if you will. what are the mechanics of decision-m and really tried
to distill that down to two important brain areas. The amygdala
brain areas. The amygdala uh which leads to our rapid uh decision-m that is really pretty um self-centered doesn't look at future
consequences doesn't look at impact on uh other people on the planet etc. I want to do it. I want to do it now. And
that's it and a story versus bringing into the decision-m process an area of the brain called the prefrontal cortex which for our discussion can be looked
upon as the adult in the room that uh is measured says hang on a second how is this going to play out in terms of your life moving forward? How does it affect
other people? Is empathy involved? Etc.
other people? Is empathy involved? Etc.
The prefrontal cortex as we reach our teenage years begins to exercise control over the more uh impulsive amydala type
brain activity. It exercises what we
brain activity. It exercises what we call top- down control or what I like to say the adult comes into the room. the
pathway that connects and allows that top- down control called the anterior singulate uh is threatened by inflammation and that
has huge implications.
What causes inflammation in the human body that would then lead us to be more impulsive, less empathetic and more self-centered? Ultrarocessed foods. So
self-centered? Ultrarocessed foods. So
the pervasive consumption of pro-inflammatory foods globally is segregating us away from the gift that we have of this wonderful prefrontal
cortex allowing us to conceive of the future and consequences and be empathetic beings and locking us into being this narcissistic self-centered uh
instantaneous decision-making apparatus called the amygdala. It has its upsides.
We need to make rapid decisions at times instantaneously and not think about things when you're backing up your car in the rearview mirror in the camera. I
used to use something called the rearview mirror for some of you younger people that was anyway um but you see a kid on a tricycle. You don't think about it. You step on the brake instantly.
it. You step on the brake instantly.
That's an amydala response.
But to live your life in fight or flight and making decisions based upon the amydala doesn't have good outcomes even as it relates to your lifestyle choices.
So what I've just done is created a feed forward process whereby when we eat what you are so focused on these ultrarocessed foods increase inflammation in the body. It takes us
away from better decisionm what does that do? We continue to eat those foods.
that do? We continue to eat those foods.
We continue to stay up late. We continue
to lack exercise sedentarity and that just builds a situation whereby we're paving in my world the way for brain degeneration. But the simple part that
degeneration. But the simple part that you I think touched upon is that any inroad that can allow us to reexplore
and value and utilize this prefrontal cortex as playing a role in our decision-m and exercise this top down control will ultimately allow many other
lifestyle choices to come online and pave the way for for a better life. So
it really does come down to the nuts and bolts of our decision-m apparatus.
Yeah, that is so interesting as to the impact of inflammation and ultrarocessed food consumption on our ability to make the right decisions. So maybe it's yeah
at first it might be a bit tricky whilst you're changing over your behaviors but as the inflammation starts to come down you know your decision-m will start to
improve and you may well find it easier and easier over time to make certain changes. David let's go back to uric
changes. David let's go back to uric acid. Um that was the topic of your your
acid. Um that was the topic of your your last book. Why
last book. Why is uric acid an important marker for us to look at when we're trying to assess our metabolic health?
The next sentence I think is very important.
Uric acid tells your body winter is coming.
What does that mean? It means that uh elevation of uric acid does things to pave the way for your survival during times of caloric scarcity. meaning
increased fat production, downregulating mitochondrial function, increasing blood pressure as a a hedge against not even
finding water. So this is a a a genetic
finding water. So this is a a a genetic change that happened in proconsul, our one of our primate ancestors around 8
million years ago. a change such that uric acid would be increased when our ancestors, our primate ancestors ate a certain food that would be present in
the late fall when winter is coming.
Something is in the food in the late fall that triggers the body's production of uric acid that sets into motion this survival pathway. And what is that
survival pathway. And what is that trigger? It is fructose, fruit, sugar.
trigger? It is fructose, fruit, sugar.
When does fruit ripen? It ripens in the in the fall before winter. It's a
beautiful uh bit of chronobiology, isn't it? That, you know, we're in harmony
it? That, you know, we're in harmony with the planet. The plants finally ripen their, you know, the starch turns to sugar. Fruit gets sweet. We love
to sugar. Fruit gets sweet. We love
sweet. We're hardwired to love sweet. We
eat the fructose and fructose is directly metabolized to uric acid. That
is a powerful signal to our metabolism to prepare us for winter.
There would be selection of those uh individuals who had higher uric acids for survival because they made more body
fat and they had a depot for caloric achloric reservoir so they could survive during times of caloric scarcity when others who didn't have high uric acid
would die. Well, where are we today?
would die. Well, where are we today?
We're in that same situation where we still have the lack of uricase enzyme, the enzyme that breaks down uric acid such that we as humans uh accumulate
uric acid higher than any other mammal.
And that uric acid is directly leading to fat formation uh by changing cellular metabolism. It's directly involved in
metabolism. It's directly involved in damaging mitochondrial function. uh it
is elevating our blood sugar and elevating our blood uh pressure as well.
Uh inhibiting nitric oxide and as such uh leading to inability of blood vessel to relax. By its inhibition of nitric
to relax. By its inhibition of nitric oxide it it is uh downregulating the effectiveness of insulin. So where is the fructose coming from? Well fructose
is the number one natural additive sweetener to food. You know, more than 80% now of foods in America's grocery stores have added sweetener. And by and
large, that sweetener is fructose or a combination of fructose with other sweeteners. Why? Because it's really
sweeteners. Why? Because it's really sweet and it's really easy to make and it's cheap.
So, we make fructose from corn, high fructose corn syrup that is just, you know, across the board ubiquitous in in foods to make them palatable. and
tapping into this ancient desire survival mechanism that we have uh for sweet foods. So we recognize that uh
sweet foods. So we recognize that uh uric acid when elevated is a powerful metabolic destabilizer that higher uric acid levels are linked to all cause
mortality. They're linked to development
mortality. They're linked to development of dementia and they're certainly linked to development of metabolic issues like diabetes. So I think it's reasonable and
diabetes. So I think it's reasonable and to understand what is your uric acid level and I think you mentioned you're going to include that in your 11 item panel and you absolutely should
uh you know people it takes us to an interesting discussion of in the normal range. What does that mean?
range. What does that mean?
Oh I got my labs back and everything was in the normal range. Oh but the the labs I got last time I had something that was out of range and my doctor said I should be careful. It was my B12 level was too
be careful. It was my B12 level was too high and you know I don't know why I'm focusing and vitamin D level was out of the normal range. Well, I I think that
clearly what you're going to do if you're not already doing is is recontextualize this notion of normal range. Normal range is average. It's two
range. Normal range is average. It's two
standard deviations from the mean. Uh
looking at large population sets, large data sets and what is average? And what
is average is not necessarily what is best. We want people, you want people to
best. We want people, you want people to be in the optimal range. In other words, what is best? Blood sugar of 100 is not good enough. No way. That's just not
good enough. No way. That's just not good enough for for your messaging and my messaging. We want people who are
my messaging. We want people who are listening to us today and will continue to listen to you and pay attention to your app to really focus on what is optimal, not just what's good enough.
Yeah, absolutely. Thank you for sharing the importance of uric acid. And I
completely agree. you know, there there are normal ranges, there are optimal ranges, and certainly with Do Health, we're helping educate people as to where they are now, where they could get to,
and we're going to help them along the way to get there. David, I want to go back to the central message of Brain Defenders, which is we want to as much
as possible keep our microgle cells in the M2 form and not have them go to the destructive M1 form. We've touched in
terms of practical applications to people. We we've spoken about some
people. We we've spoken about some dietary principles. I wonder if we could
dietary principles. I wonder if we could go through some sort of practical takehomes for people, but through the lens of M2 and M1. So, for example,
people know that exercise is good for their well-being. How exactly is
their well-being. How exactly is exercise good for the brain? And what
does exercise do to our microgle cells?
I'm going to answer that question in one moment, but I just want to get a little bit broader perspective because I'm often asked, what is the one thing, the number one thing you can recommend for
people uh to help them chart their brain's destiny for the for the better.
And that one thing is to embrace the idea that you are in charge with regard to the these choices with with respect to your lifestyle choices. Yes, sleep,
yes, exercise, yes, diet. These are all connection, social connectivity, important, but the most important thing is to recognize that you're in charge.
You control your brain's destiny. Now,
as it relates to exercise, uh we've known for an awful long time people have said, "Yes, exercise good for your heart, good for your brain."
And u it it brings to mind just one other thing that's I think divergent, and that is that nobody talks about a brain smart diet. But for h how many years have we heard about hearts smart
diet, right? There's even I think a
diet, right? There's even I think a label that goes on certain foods. This
is a heart smart food.
Why not the brain? It's the same thing.
We're talking about inflammation, free radical stress. Uh and you know, it's
radical stress. Uh and you know, it's it's the very same diet. It's no it's no different. But let's get back to
different. But let's get back to exercise. I've had a cup of coffee as
exercise. I've had a cup of coffee as you can see. We have to look upon the muscles which are the active player in exercise obviously and the brain but look upon the muscles as being an
endocrine gland and that will raise eyebrows. You know people consider the
eyebrows. You know people consider the endocrine gland well the adrenals you know the pituitary uh the ovaries these are our endocrine glands and by
definition the endocrine gland is is a part of the body that creates messengers that go elsewhere in the body and do certain things right uh the pituitary
sends out things like growth hormone uh that do certain things adrenal uh cortropic hormone from the pituitary challenges our adrenal glands to do certain things but the muscles indeed
They do exactly that. They secrete
chemicals when they are active that do really good things throughout the body.
Uh they are, you know, cathpsin uh B irrian 6. Oddly enough, we tend to think about
6. Oddly enough, we tend to think about that as being a pro-inflammatory cytoine, but actually does some some great things. These chemicals go
great things. These chemicals go throughout the body and even into the brain and do uh good things for us. uh
importantly something called irri gets into the brain and stimulates the brain to produce something called BDNF. I
spoke about BDNF brain derived neurotrophic factor earlier.
You really want to have a lot of BDNF in your brain because BDNF nurtures the neurons nudges the microglea back to being supportive and therefore nurtures
the formation and preservation of our synapses and yes even the bloodb brain barrier. So, we want this BDNF to be
barrier. So, we want this BDNF to be present. We know that there are higher
present. We know that there are higher levels of BDNF when we exercise. And
that was demonstrated uh way back in 1988 by a Dr. Ericson, University of Pittsburgh, who correlated exercise in a one-year interventional
trial versus simply just doing some mobility work, but actual aerobic exercise with not only increased BDNF, but also increased size on MRI scanning
of the brain's hippocampus showing that it exercise caused growth and also improved memory performance as a consequence of exercise. Since that
time, multiple multiple studies have come out. Studies demonstrating a
come out. Studies demonstrating a correlation between the number of steps you take on a daily basis and your risk and/or rate of cognitive decline. Simply
taking steps. The magic number was oddly enough close to that 10,000 that we often hear uh batted around as being the ideal uh amount of steps to take in a
given day. I think there are benefits to
given day. I think there are benefits to both aerobic exercise uh as it relates to producing that BDNF and also resistance exercise
simplistically to increase the the size of the pharmacy. So there's more muscle mass there to create these really supportive chemicals for total body
health and for brain health as well. So,
and I actually describe this in the book that really what has been demonstrated in research that looked at what is best aerobics or resistance answer both both
all the above that you really want to have I actually say there should be three and um just to be kind of conjectural and that is I think we
definitely want to have flexibility uh exercises as well. Why? because I think we need to remain flexible so we reduce our risk of injury. If you become injured then all bets are off. You're
not going to exercise anymore and you know that whole program uh is postponed.
So I think flexibility stretching really important. I like balance exercising as
important. I like balance exercising as well keep you from falling again hurting yourself. But the main players are the
yourself. But the main players are the aerobic and the uh resistance training.
So what do I do? I I go to the gym three times a week and do weights. Uh I I tend to like the machines, but I do some free weight uh work as well with dumbbells uh
on a incline uh board, incline bench. Uh
I'm particularly fond of the ab machine.
Um and uh and then I I use a variety of other machines, but I stretch first and I actually use a power plate. I think
their data is solid in terms of improving flexibility and yes, balance.
On the other days, I either run or walk or uh use an elliptical machine, but right now I've gotten a new stationary bike that I am totally thrilled with. Um
it it gifies exercise. In other words, I'm on the stationary bike and I'm having to do these various games which are fun and I want to win. And at the end they show you the leaderboard and you know I've gotten up to I think
number three on the leaderboard for no number four and I'm the old man. And so
I did an Instagram post saying, "Hey, for you who are using the Avon uh stationary bike or treadmill, that David P, that's me. I'm number four on the leaderboard. Don't let the 71y old guy
leaderboard. Don't let the 71y old guy catch you." But anyway, so for me,
catch you." But anyway, so for me, gamifying uh has been very helpful cuz 30, 40 minutes go by quickly cuz you know, a machine like that can be boring.
That's why I like to be outside and run because then I can see things, breathe fresh air, you know, see people, wave at them, and uh experience nature. But u so that's what my program looks like and I'm sticking to it.
Yeah, David, thank you for sharing what you do. I think
you do. I think obviously I can't know this for sure, but I would imagine there are going to be some people listening to this conversation
who are thinking, I wish my mom or dad in their 70s was doing what David is doing. And the reason I say that, I just
doing. And the reason I say that, I just want to really highlight this point that yes, we've used some technical language at points during today's conversation,
right? really tried to help people
right? really tried to help people understand the science that exists behind your recommendations and everything you talk about in brain defenders.
But on a human level, this is very very real. People's lives
are being so devastated by family members having cognitive decline. A, you
know, on a on a sort of individual interocial level, it can be very frustrating to see that happen to a loved one. There can be significant
loved one. There can be significant financial implications for families when it comes to how do you look after people with cognitive decline? Do they need to sell their house, go into some kind of
facility?
These things are incredibly worrying for people. Yet the central message behind
people. Yet the central message behind so much of what we're talking about today and frankly what both me and you have covered on our various platforms
for many years is that it really doesn't need to be that way. There are things it's not as difficult as you think it is. There are things that you can do
is. There are things that you can do that are going to really make a difference. But I do think David, there
difference. But I do think David, there may be a generational issue here in the sense of you said before, right? We spoke
about this war on our attitudes. I saw a good mate of mine this weekend and his mother unfortunately is starting to decline cognitively and
she's going to see her conventional doctor and really you know as well as I do that you go to your conventional doctor you you're generally told that there's not much you can do about this.
There is an inevitable decline. you
know, yes, they might put you on a waiting list for things and check your blood pressure and your blood sugar, but there's not much practical guidance. And
I was chatting to my buddy and he said, "Rangan, everything you're talking about, I'm I'm trying to share with mom, but she's not listening. You know, she
drinks half a bottle of wine every night and hasn't [clears throat] for many years. That's just part of her
years. That's just part of her lifestyle. She's unlikely to change
lifestyle. She's unlikely to change now." And I think David, there's a
now." And I think David, there's a there's a really key point here, isn't there? Which is
there? Which is look, I'm learning this information at an earlier stage in life than perhaps you did because the science is there,
right? So I'm able to really implement a
right? So I'm able to really implement a lot of this stuff in my 40s and hopefully that will continue for decades, right? Well, there is a
decades, right? Well, there is a generation and maybe you're part of that generation, but perhaps because of the way that you think, your curiosity, your
practice, you've ended up in a different state of health compared to many of your peers. But I think my friend's mother,
peers. But I think my friend's mother, there are so many people out there like that. They think this is inevitable.
that. They think this is inevitable.
And you know, what advice would you give like to people like my friends who say, "Ran, I'm listening to this information.
I'm reading the stuff, but I can't get my parents to put the advice into action.
I think it's very challenging because my generation and his his mother uh again, we were brought up to think that our lifestyle choices didn't matter. Do
whatever you want that you like, you know, cater to your your desires. And
modern medicine's got the fix. And don't
worry about it. They they'll fix your heart. to fix your brain, you know, and
heart. to fix your brain, you know, and and that's just an incredible uh mis messaging that uh, you know, really characterizes what you're you're talking about here. You're right in your
about here. You're right in your observation of people in my generation because they uh they're very difficult to convince uh to to prevail upon in terms of um you know what your friend is
up against with his his mother and uh you know that's that's pervasive. Uh
what I would say to that individual is look do the best you can but let's talk about you because I I really uh am think
that it's uh the the bigger play here is the 40 and 50 year olds 30 year olds uh that uh you know John Kennedy President Kenny said during his
inaugural address that the time to fix the roof is when the sun is shining. Not
to say we ignore these individuals. We
do the very very best we can. But
frankly, you know, a lot of times there's just not going to be any response from the child to the parent on the part of the parent because the
parent's going to go, like you say, to their trusted doctor who may likely not be dialed in in terms of what you and I have have discussed today and the value
of what we've talked about today.
It's incredibly valuable. It is the top tier ahead of any pharmaceutical or other type of intervention. What we've
discussed today are the keys to the kingdom.
Yeah.
And it's not monetized. That's why we don't hear about it very much.
Yeah. I mentioned alcohol there with my friend's mother. What does chronic
friend's mother. What does chronic alcohol consumption do to that M2M1 balance? Well, the threat of Alzheimer's
balance? Well, the threat of Alzheimer's with respect to alcohol consumption is a U-shaped curve that those who do not consume any alcohol have a slightly higher risk in comparison to women who
drink one glass of wine per day or men consuming two glasses of wine today. And
then the risk goes up with uh more alcohol consumption. So there's a
alcohol consumption. So there's a U-shaped curve with an ideal range of alcohol consumption. think more recent
alcohol consumption. think more recent literature would indicate that really isn't true uh globally as it relates to alcohol that you know call it what it
is. Alcohol is a neurotoxin
is. Alcohol is a neurotoxin and it threatens brain cells. Is there
an upside to the polyphenols in red wine? Yeah, there is. But there's also
wine? Yeah, there is. But there's also non-alcoholic uh red wine and other wonderful sources of polyphenols that you know don't require alcohol. But I
get that, you know, there's an upside to alcohol in terms of what it does for people socially been part of their culture, but it's not a half a bottle, it's a glass. So, um, you know, I I
think it's making these subtle adjustments so that you can still feel good about life and participate and minimize a risk.
Yeah, David, one thing we've not talked about is genetic testing. And again, I think a big theme throughout our
conversation today is how our approach to medicine has changed over the years, right? There's normal blood test versus
right? There's normal blood test versus optimal. There's getting involved when
optimal. There's getting involved when you have symptoms versus practicing true prevention. And when I was at medical
prevention. And when I was at medical school at Edinburgh Medical School between 1995 and 2001, I'm pretty sure we were told about APOE4
testing, but the general view was you don't do it, right? There's no point knowing your genetic status because there's nothing you can do, right? So
why would you want to live your entire life with fear when there's nothing you can do? Now, of course, our
can do? Now, of course, our understanding has moved on dramatically since then. So, I wonder, you know,
since then. So, I wonder, you know, David, if you could first of all explain what is APOE4, what does having one or two alals do to your risk of getting Alzheimer's? And then I'd love to get
Alzheimer's? And then I'd love to get your perspective as to whether you're a fan of getting tested or not.
Let me first answer that I'm absolutely a fan of being tested. We know that individuals who carry APOE4 alil. So
this is a genetic alil that comes and you have two shots at it. It comes in three varieties. APOE2, APOE3 and APOE4.
three varieties. APOE2, APOE3 and APOE4.
As it relates to Alzheimer's, APOE2 is protective. APOE3 is about neutral and
protective. APOE3 is about neutral and APOE4 is associated with increased risk.
And as I mentioned before, you have two shots at this. So that you can have any combination you can think of between 2, three and four. Uh you can be a 44 which
poses a significant is associated with a significant risk for Alzheimer's disease through multiple uh pathways that we'll I'll mention in just a moment. But it's
been indicated that carrying APOE44 uh and there are you know a significant number of people in in America who uh are carriers of APOE44
uh that your risk may increase for Alzheimer by as much as 8fold even as high some reports as high as 12fold risk but not determinant. It's a
predisposition but not a determinant.
I'll double click on that in just a moment.
um having one alil, in other words, having a 34 or a 24 combination is also associated with a an increased risk of Alzheimer's by anywhere between three
and fivefold. So, a really significant
and fivefold. So, a really significant increased risk. Now, why is AP APOE4
increased risk. Now, why is AP APOE4 um associated with such an increased risk? What does it do? We know that it
risk? What does it do? We know that it involves multiple pathways. Uh it
involves down reggulation of mitochondrial function. uh and as such
mitochondrial function. uh and as such seems to target microgle cells. But in
work done by a British researcher Dr. Sarah Marzai at what is called the Marzai Clinic. I had her on my podcast
Marzai Clinic. I had her on my podcast recently. She actually created
recently. She actually created micro gal cells that expressed either no APOE, APOE 2, three or four, and then
injected them into the Alzheimer's mouse model brain who lacked microgal cells and demonstrated dramatically that those
who had uh APOE2 and had dramatic reduction of inflammation, sort of middle-of the road inflammation, APOE3, but dramatic increase and cell loss in and beta
amaloid accumulation in those carrying the apoE4 alil the micro gal cells that she had engineered and injected into their brains. So again, while we've kind
their brains. So again, while we've kind of labored over what are the exact pathways by which APOE4 is ultimately increasing risk of Alzheimer's, um it
looks as if now it's converging on the micro gal cells, which is really uh kind of interesting because we can offer offsets to that through the techniques
that you and I have talked about today.
What I'm saying is people can have APOE4 alil and then engage these various other lifestyle changes and other practices
beyond lifestyle to actually offset and i.e reduce their risk that would
i.e reduce their risk that would otherwise have been significantly amplified. Again I want to say that we
amplified. Again I want to say that we should look upon carrying the ApoE4 alil as not a determinant but as a predisposition. It is clearly a risk
predisposition. It is clearly a risk marker. It's it's a risk marker like
marker. It's it's a risk marker like MTHFR again 28% of people like me like like I am have this MTHFR and therefore elevated homocyine another risk factor
for Alzheimer's that similarly can be offset in my case by taking methylated B vitamins. So I think there's been a huge
vitamins. So I think there's been a huge change in the messaging of of well not not necessarily with respect to mainstream but with people who
understand that notion of this APE4 being a predisposition but not a determinant that okay these are the cards you've been dealt how are we going to play the hand. Yeah, it it's such a
it's such a key point, David. This idea
of knowing your risk. I mean, look at this a different way, right?
The amount of times in my career, let's say a middle-aged man would not pay attention to their lifestyle until they came in for a check and their
blood pressure was found to be significantly elevated. Right? And often
significantly elevated. Right? And often
that might happen at a time when maybe their own father had a heart attack or a buddy of theirs from school, you know, had some angina or something like that,
right? So getting the right test for
right? So getting the right test for some people, yes, it makes them anxious, but for a lot of people it is the stimulus that they need to then engage
with changes, right? So someone might hear this podcast and go, "Yeah, yeah, it's important. I look after my brain
it's important. I look after my brain health, you know, but my life's pretty good, you know, I don't feel I've got any symptoms yet. My lifestyle is generally okay. If they did a genetic
generally okay. If they did a genetic test and came back as a let's say a three four, maybe they don't have two APOE4 alals, maybe they just have one,
they then know if they're educated in the correct manner that oh, okay, if I look at all my risk, I have a genetic
predisposition here, which means it's even more important that I lock in on these lifestyle changes. if I've got APOE E44 like double, you know, yeah,
you don't want to get anxious about that. You want to go, okay, right,
that. You want to go, okay, right, there's nothing I can do about that.
What can I do to reduce my risk? And I
think that's an empowering message. Now,
could one argue, David, that the recommendations that we would make to you for your brain health are the same irrespective. So for example, if someone
irrespective. So for example, if someone was listening and they said, "David, listen, I'm going to get brain defenders and I'm going to do everything in that book, why should I go to the trouble and
expense of getting an APOE4 test?" You
know, does getting that alil back practically make any difference in terms of what I do?
Well, I I think the answer is that I cannot imagine uh anyone doing everything I talk about in the book. So
there's a hierarchy and I think that uh if you were carrying APOE4 you would be much more dedicated and really be involving yourself not just in the standard recommendations that I made
that people are probably aware of but I wanted to reinforce but even some of the leading edge things that we talk about in the book and beyond that I think being much more aggressive in terms of
following your cognitive function. you
know, we have the ability uh to look at cognitive function in very sensitive ways these days and that would guide you in terms of at what level should I be engaging this program that I describe.
Yeah, there's so much you've covered um in the book, David, but we haven't even scratched the surface today. I really
appreciate the stuff at the end where you talk about some of these novel therapies, but also where you think this field is going. I also just want to say
I read a lot of health books and this I think is beautifully written. It's very
concise. It's to the point as to where the science is and there's so many practical tips in it that I think people could just pick it up, scan and immediately know what they have to do.
So, thank you for once again writing a wonderful book for that person who has realized throughout this conversation that
they've neglected their brain health for the majority of their life. They've not
paid attention to their diet, their exercise, their sleep, their stress, but something shifted within them and they want to make a change, but they're
worried that it's too late. What would
you say to them? If
if anybody is cognitively intact enough to have that mental conversation, I'm worried that it's too late. They're in
great shape. They are in great shape and and ready to take full advantage and and redirect their brain's destiny. So,
absolutely have at it.
Yeah, great advice, very empowering.
David, the book's called Brain Defenders. Thank you so much for coming
Defenders. Thank you so much for coming back on the show.
My absolute pleasure. Thank you. If you
enjoyed that conversation, then I think you are really going to enjoy this one that I picked out especially. [music]
When you consume sugar, you are poisoning your mitochondria. Sugar and
cyanide do the same thing. This is the toxin.
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