Name: Joe Rogan Experience #1870 - Max Lugavere
Uploaded: 2022-09-14T00:00:00.000Z
Description: Watch the stand-up comedy video 'Joe Rogan Experience #1870 - Max Lugavere' from PowerfulJRE on Comedy Buff. Published 2022-09-14. Transcript available.

Watch the stand-up comedy video 'Joe Rogan Experience #1870 - Max Lugavere' from PowerfulJRE on Comedy Buff. Published 2022-09-14. Transcript available.

Joe Rogan Experience #1870 - Max Lugavere

Joe Rogan podcast, check it out.
The Joe Rogan Experience.
Train by day, Joe Rogan podcast by night, all day.
What's up, Max? How are you?
What up? Thanks for having me.
Pleasure to meet you.
Same.
I've enjoyed your content online, so it's exciting to meet you in person.
Thank you. I'm glad to hear that.
So you were telling me before we got rolling, I said save it.
Let's just talk about it.
What is this Alzheimer's thing that you're doing?
What are you doing?
Yeah, so I've been deeply immersed in the Alzheimer's dementia prevention world
for the past almost decade at this point.
I'm not a, just to lay it out up front, I'm not a medical doctor.
I didn't take the academic route.
I started college sort of on a pre-med track, but what ended up happening was I
ended up going into journalism straight out of college,
and I ended up working for a TV network in the U.S. that was backed by Al Gore
back in the day.
And so I got to hone my storytelling chops there, but I'd always been really
passionate about health, nutrition, medicine, things like that.
But in 2011, my mother started to display the earliest symptoms of what would
ultimately be diagnosed as a form of dementia called Lewy body dementia,
which is a rare form of dementia.
Robin Williams had that.
Yeah.
Yeah.
Terrible condition.
It's described as feeling like you have both Alzheimer's disease and Parkinson's
disease at the same time, and certainly that's what I observed in my mom.
And so when she started to display those symptoms, it had taken me and my
family completely off guard.
I had no prior family history of any kind of neurodegenerative condition.
My mom certainly wasn't old at the time.
She was 58.
She was still, you know, a spirited, youthful woman in middle age.
She had all the pigments in her hair.
And for me, I was in between jobs, and I really had the opportunity.
I was grateful to have had the opportunity to go with her to different doctor's
appointments.
And I grew up in New York City, so we had access to, you know, cathedrals, to
medical advice and examination.
And in every instance, we were met with what I've come to call diagnose and adios.
Basically, a physician would run a battery of esoteric tests on my mom, scribble
down a few notes on a prescription pad, and send us on our way.
But we had to ultimately take a trip to the Cleveland Clinic in Ohio, which is
known for taking on really complex medical cases.
They build a team around the patient, and it was there that for the first time,
my mom was diagnosed with a neurodegenerative condition.
She was prescribed drugs for both Alzheimer's disease and Parkinson's disease.
It wasn't until a few years later that she actually received the Lewy body
dementia diagnosis.
But at that point, I started to dive into the research, because I had been
trained as a journalist, which, you know, you're not trained as rigorously as a
PhD scientist, but you're kind of taught similarly to investigate things, to
maintain skepticism, to, you know, ask questions.
And I started to look into the literature and just generally get a sense of
what it was that my mom had been diagnosed with, what this, you know, what this
entailed.
And I realized that in most cases, dementia begins in the brain decades before
the first symptom, 10, 20, 30 years even, by some estimates.
And so for me, this became something really important to explore as a
potentially preventable condition, because I realized for the first time that I
had a risk factor, that my mom, you know, was my risk factor, essentially.
I didn't, I hadn't even yet looked into my genes at that point, but, um, but so
I, uh, I started looking into it and I came across all of these like
fascinating insights, which, which we can talk about.
But I decided at that point, um, that I, to, to sort of do what I could to help
push the, you know, move the needle with this condition, um, that I would use
my skills, which at the time were, uh, filmmaking.
Cause I had just come off, you know, I was like producing content for TV and I
was on camera.
I was a communicator as well.
And so I decided to do a documentary, um, on the topic of dementia prevention,
the first ever, uh, documentary on dementia as a potentially preventable
condition.
We've all seen dementia documentaries on, you know, HBO and networks like that.
And they're always, they always push this, this very like doom and gloom, um,
mentality about the condition, which I, which I understand.
It is a very difficult condition.
It's America's most feared condition after all.
Um, and this is a condition that, you know, 90% of what we know about Alzheimer's
disease in particular, which is just one form of dementia has been discovered
only in the past 15 years.
So it's a very rapidly evolving field of science.
But I felt like if we know that this is a condition that begins in the brain
decades before the presentation of symptoms, then to me, what that is, that's a
very empowering insight.
That means that we have agency to change our cognitive destiny.
So I started shooting with my mom, which was very hard to do, um, because, you
know, I mean, my, the person who I love most in the world, I was watching, um,
decline right in front of the camera.
Um, but also, um, I decided to exploit my media credentials at the time to then
talk to researchers and scientists around the world.
Um, and I was doing my own research in the primary literature as well, but I
decided to, um, to, yeah, to go to these labs and clinics where they're really
ushering in dementia as a potentially preventable condition.
And I actually signed myself up to become a, uh, uh, uh, uh, uh, study subject
in one actually at Weill Cornell in New York.
And, um, and I actually became, ultimately I became, um, a collaborator with
the, uh, principal investigator there who's become my mentor over the years,
Richard Isaacson.
Um, and I got to, uh, coauthor a paper in a clinician's textbook, uh, on the
clinical practice of, of dementia prevention.
Cause, you know, uh, after all this time I've learned so much about, um, about
the condition, the etiology and so forth.
Uh, but this documentary, I'm super excited for it.
It's, um, it's called Little Empty Boxes and we have a trailer up at littleemptyboxes.com.
Why Little Empty Boxes?
Well, it's a, it's a nod to something that my mom says in the film, which is
actually something it did, you know, my mom's condition.
It seemed like her cognition had just severely downshifted almost, almost
overnight.
Um, and so my mom never, my mom never like forgot who I was or anything like
that.
The presentation of Lewy body dementia is different from Alzheimer's disease.
And once you've seen one case of dementia, just generally speaking, you've seen
one case of dementia.
Every, every dementia is, is different.
But in my mom's case, it led to her often losing her train of thought soon
after, uh, beginning to express an idea.
Um, and she would often say things that just, you know, didn't, didn't make
logical sense.
So it's sort of a nod to what, um, to something that she, you know, that she
says in the film.
But, uh, I'm super excited because we, we inked a partnership with a, uh, a
wonderful foundation called the Alzheimer's Foundation of America.
And, um, and, um, yeah, I'm just super excited to, uh.
Is dementia purely genetic or is it caused by environmental factors or any
other things that people consume?
Great question.
Um, so though dementia, though Alzheimer's disease was coined in 1906 by a
physician named Aloise Alzheimer, the brain has long been thought of to sit in
sort of the ivory tower of the brain guarded from what happens down below by
what's called the blood brain barrier.
But we now know that the brain is influenced by everything that happens down
below.
And the, the dogma, especially with regard to Alzheimer's disease fundraising
over the past couple of decades has really been that this is the, this is a
condition that you can't treat, prevent, or slow.
But we now have really solid data to say that we actually, that it is a, it is
a potentially preventable condition.
So when it comes to, uh, our risk for developing Alzheimer's disease and other
forms of dementia, there are basically two categories of risk.
You have your non-modifiable risk factors of which there are three.
So you've got your age, your genes, and your gender.
So your age, age is still the number one risk factor for developing Alzheimer's
disease, right?
You can't change your age yet.
You, um, you have your gender.
If you're a woman, your risk is double that as compared to a male's.
And you have your genes.
Now genes is something that we can actually talk about because though you can't
change your genes, making them therefore a non-modifiable risk factor.
You can change the expression of your genes, how your genes express themselves
moment to moment.
So for example, if you live in the United States and you carry a copy or two of
what's called the APOE4 allele.
So it's basically a polymorph, polymorphism, meaning it's not a mutation.
It's actually a very common gene variant.
About one in four people carry the APOE4 allele.
In the United States, that increases your risk anywhere between two and four,
14 fold, depending on whether you carry one or two copies.
I think that's also the same genetic expression that makes you have CTE.
So CTE, yeah, it, it, it, it makes everything more, it makes your brain more
vulnerable in general to insult, whether that is from TBI, uh, exposure to
pollutants, exposure to unhealthy ways of eating.
Do we know why it does that?
Well, it's interesting.
Yeah.
So the APOE4 allele is thought to be the ancestral version.
So it's the first version.
All, all non-human primates are APOE4, four.
So they carry the APOE4 allele, not just one copy, but two copies.
And yet they don't develop Alzheimer's disease.
When you look to people, we've evolved, uh, these different isoforms of, um,
the APOE gene.
So we have APOE2, three and four.
And just to reiterate, APOE4 is the ancestral allele.
So cultures that have, um, longer exposure to modern agriculture, actually
there's lower frequency of the APOE4 allele.
The thinking is that, that agriculture, right?
Like when we became domesticated, when we started basing our diets around
grains, when we became more sedentary, less, uh, generalized in terms of our,
um, cognitive, the, the, the daily cognitive tasks that our ancestors would
have undertaken, that it's selected against the APOE4 allele.
So it's possible that that allele, which again is very common, one in four
people carry it, carry it, is sort of the canary in the coal mine for the, for
the Western way of life.
That if you adopt a Western way of life and you eat, you know, today, 60% of
calories that adults consume come from ultra processed junk foods, right?
We're more sedentary than ever before in human history.
We've got more stress.
We're exposed to more environmental pollutants.
That that is what dramatically is what pulls the trigger, right?
Because genes load the gun.
It's our diets and our lifestyles that pull the trigger.
But if you were to take somebody with that same genotype, right?
And move them to a less industrial, a less industrialized part of the world,
like say, Ibadan, Nigeria, where the frequency of the APOE4 allele is just as
common.
It has no, it has little to no association with Alzheimer's disease.
So just to put that another way, what that suggests is if you're genetically at
risk for developing Alzheimer's disease in the United States, you might simply
move to Ibadan, Nigeria or another less industrialized part of the world and
see that risk abolished.
So with this consumption of processed foods that is responsible for a large
percentage of the calories that people consume today, is the human body
adapting to that?
Is that why this APOE4 is less prevalent than it is in other cultures?
You know, it's possible, although with age being the primary risk factor, it's
unlikely that that has