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Unraveling Alzheimer's: The Pathobiome Connection - Episode 353 · Gladden Longevity Podcast

0:00
Certain undetected infections,
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we call them stealth infections,
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even if they're incredibly common in certain people under certain circumstances
0:07
can be disease drivers that contribute to immunosinescence and indeed
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in impact longevity, as well as the ability to live,
0:15
you know, a healthy and enjoyable life.
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Today I'm talking with Nikki Shultek.
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you're gonna find this a really fascinating conversation.
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She's involved with a project called the Alzheimer's Pathobiome Initiative.
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And it has to do with the fact that ~ a lot of chronic diseases,
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including Alzheimer's, heart disease,
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et cetera, have an infectious component to them.
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And she's been going down the rabbit hole in this regard.
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And the conversation we have is,
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I think.
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One of the most intellectually stimulating and somewhat far ranging conversations
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~ we've had on the podcast. I think you're really going to enjoy
0:53
the interaction back and forth.
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~ she's a wonderful, wonderful guest.
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And ~ I think she and I are gonna end up doing some collaborations together,
1:02
which you'll hear about as you listen to the podcast.
1:06
So enjoy this. I think you'll really like it.
1:09
We went from saving hearts as a cardiologist to rewriting the entire aging playbook.
1:14
Dr. Jeffrey Gladden believes 100 is the new 30,
1:18
and he's got the science to back it up.
1:19
This is the Gladden Longevity Podcast.
1:23
Welcome to the show.
1:25
Thank you for having me.
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Yeah. I was excited when I saw the ~ topic that you're gonna speak be speaking
1:32
to us about, ~ Alzheimer's and the pathobiome.
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~ and that's a really interesting topic.
1:39
But before we get to that topic,
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I'm curious how you got to be interested in that topic.
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Tell us a little bit about how you got to into all this.
1:47
Yeah, thank you for asking. So ~ I got interested in broadly kind
1:53
of understanding how infections or our immune responses to infections
1:57
in the body can drive autoimmune states
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Mm-hmm.
2:00
in general. ~ really with particular interest on neurodegenerative disease
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and zeroing in on Alzheimer's over a course of time,
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but I kind of got recruited to it.
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I got really sick in my early thirties.
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I'm very thankful now to be in my mid-40s.
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So it was like nearly 11 years ago.
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Yeah. ~
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And I contracted Lyme disease.
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living in Connecticut, in the state where the disease is named,
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Lyme Connecticut. Yeah. And ~ I was misdiagnosed for a year,
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which I actually consider myself fortunate.
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that's kind of short in the grand scheme of Lyme misdiagnoses.
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What the infection does is
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a number of things that are undesirable in certain people.
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~ it can impact your immune system broadly.
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And it also oftentimes if you get a tick bite,
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which is one of the main routes of transmission,
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you may also get co infections,
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other things that the ticks carry.
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It's sort of nature's dirty needle.
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~ on top of that, I had had another factor in my case that I didn't realize
3:02
was pertinent until I became unbelievably ill for an entire year with multisystem
3:06
autoimmunity was that
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I also likely harbored a chronic respiratory infection,
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~ a bacterium, actually not one but two that are unbelievably common
3:16
in the human population, transmitted from inhaling when someone coughs on you.
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~ some people it can present like just a normal upper respiratory tract infection.
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In other people it can become a full blown pneumonia requiring hospitalization.
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And in many people the infection is never cleared.
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It actually becomes chronic. Wow.
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This year of illness, ~ where literally at points I feared that I would
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not get to see my three and five year old kids grow up.
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I was diagnosed with so many different conditions spanning from my GI tract,
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my heart, my joints, my brain.
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~ my physicians thought I could have multiple sclerosis.
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I do not.
3:54
no.
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~ although at the time it was interesting when I went to the neurologist,
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they said, We really can't tell you that you won't get lesions in your brain.
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Right now you have a lot of symptoms that are very concerning and your
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MRI at this current point in time is clean.
4:08
It was sort of just like this terrible like looming feeling.
4:13
This axe hanging over your head.
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Yeah.
4:15
Yeah, literally. ~ so so this all happens to me in a year.
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I also developed a terrible bladder pain disorder called interstitial cystitis.
4:23
And I'm going and terrible breathing problems,
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air hunger, my asthma that had been previously well controlled on steroids,
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inhaled steroids, basically became totally out of control.
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And I was immunosuppressed. So the ~ you know,
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I had a dozen specialists. I had previously worked in pharma and biotech,
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so I could
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navigate the healthcare system and I was advocating for myself.
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But what I noticed was everything was siloed.
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So I'd go see someone about a symptom in one part of the body,
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even though I had multi-system complex chronic illness,
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my physicians were thinking about their area of expertise.
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And when I would pause it, hey,
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I have, you know, this all came on with joint pain,
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brain fog, fatigue, you know, d ~ air hunger was a new symptom.
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That's not typical for asthma.
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It's a different sensation.
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A wheezing, what could this be?
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And they're like, I'm here to talk about your cystitis,
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or I'm here to talk about your arrhythmia.
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So we so it went. I was ~ the human hockey puck,
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I call it. Like difficult cases like mine,
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because now after eleven years,
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~ you know, I'd fast forward I I became a collaboration architect
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and scientist to help bring people together globally,
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studying more broadly.
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Not just Lyme disease, not just this respiratory bacteria that initially introduced
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me to these concepts, but really to put ~ some serious force behind
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a concept that is so logical. And it's that certain undetected infections,
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we call them stealth infections,
5:56
even if they're incredibly common in certain people under certain circumstances
6:00
can be disease drivers that contribute to immunosinescence and indeed in
6:05
impact longevity as well as the ability to live,
6:08
you know, a healthy and enjoyable life.
6:10
~ so yeah, my my experience for that year with complex chronic illness,
6:16
though, will likely continue the rest of my life.
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~ like a lot of other patients that have later stage neurological Lyme diagnoses
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where there are multiple coinfections involved,
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you know, they're it's very difficult to eradicate these organisms.
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So
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We really don't have wonderful solutions,
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is the truth, you know, to a lot of these problems yet.
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But the good news is that with enhanced advocacy and,
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you know, some of the efforts that research teams like ours and others around
6:48
the world are, you know, basically grasping and launching forward,
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really a lot of spearheading by patients and people personally impacted.
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~ we're starting to see some serious momentum.
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You know, the concept of
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Targeting diseases, and this probably resonates with you given your your specialty
7:06
and then your your background is waiting until the horses are already fully
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out of the barn is not a good solution.
7:14
Yeah. Right. It's figuring out how to keep everything in in the first place.
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You know, what was the upstream event,
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for example, with Alzheimer's that led to the formation of a beta plaque or Tangle?
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And that's really what
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the premises behind our work is looking at one potential factor
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in the human exposome or it's,
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you know, the word exposome, we use it a lot.
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it's everything that you come in contact with.
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And that can be a lot of toxins,
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mold, pathogens, certainly, air pollution.
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That's right. Well, it's we've highlighted several different things here.
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~ you know, one is let's just talk about the medical system for for
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a second because the audience has heard about this,
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but it's it's so disjointed, it's so reductionist in the way that it's constructed
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and the w thinking that goes on inside of it that it's very difficult
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to get the solutions that people intuitively want to have,
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which is really a systems approach,
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a systems biology approach, right?
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that's one thing. Then the other thing that you're bringing up is just
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the somewhat occult, ~ and very tricky ~ nature of some of these infections that
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like to ~ have a host to hang out in and ~ they will either
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play with the immune system or kind of trick the immune system or
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do things to disguise themselves or activate the immune system in ways that
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if people have genetic predispositions and you know maybe some other things going
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on, ~ can lead to a whole host of manifestations that are unrelated
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to the directly unrelated to the,
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you know, the the infecting agent,
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but it's the immune system that now is out running kind of wild in the streets with,
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you know, in reaction to some of these things.
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So it's ~ it's really interesting ~ not to try to unravel
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Right. ~ and to get to the bottom of it to your point.
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So, yeah.
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Yeah, I mean, it it's sort of like a combination of the pathogens directly impacting
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and also the immune system running wild,
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like you said. So so our research and others indicate that it's a
9:26
bit of a combination. That's right.
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And that it's different from patient to patient.
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So as you pointed out, like a systems level approach to comprehensively looking
9:36
at patients that have multi-system autoimmunity,
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for example, like
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When patients indicate to me, ~ because I've shared my story so widely,
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~ and I was treated with antimicrobial drugs ~ for my Lyme disease
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and ~ continue to, you know, have to take medications in order to stay well,
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unfortunately, due to the prolonged nature of my illness.
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~ thankfully I have specialists that know how to do that.
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The main issue is that many patients won't
10:08
Be identified as having a chronic infectious process,
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they'll be labeled as, you know,
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various things, fibromyalgia, different types of arthritis.
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They'll these patients will have tons of specialists,
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they'll be on multiple biologics,
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mostly aimed at disarming the immune system.
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And in those patients that don't really respond favorably to biologics,
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you name the condition, whether it's Crohn's,
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RA,
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You know, they really should be screened for stealth pathogens that
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can drive chronic inflammation and result in some of the very processes that
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we call a disease when you look at blood work.
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~ you know, one of the stunning examples of this being you're
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an interventional cardiologist,
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is the bacteria that I was mentioning that is very strongly associated with asthma,
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chlamydia pneumoniae.
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Uh-huh.
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People have never heard of it,
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even though the majority of the population has come in contact with
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it by middle age. It is
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A really interesting bacteria because it has to live inside a human cell.
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It literally can't live outside the cell.
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It requires our energy and our lipids in order to survive.
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So essentially it's like a little pirate.
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It gets into the cell, it takes energy from the mitochondria,
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and many diseases of aging are linked with mitochondrial dysfunction
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or characterized by, as well as oxidative stress.
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dyshomeostasis of metals and lipids,
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meaning all of these changes and many of these changes are inducible
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by this particular pathogen. And so I thought it would be cool to bring up
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~ a neat sort of connectivity between the study of that organism,
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which is a respiratory bacteria,
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right? Or not the sexually transmitted chlamydia.
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And the connection that was discovered with heart disease,
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atherosclerosis. Do you remember by any chance the trials that took place
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in the early two thousands with antibiotics?
12:01
Yes. Yeah. It was when people figured out that actually,
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~ if you were looking at plaque,
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I think if you there was a study done where they looked at plaque under
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a microscope and they found that,
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you know, at least half the plaques,
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you know, had active organisms in them and a lot of the organisms were actually from
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the oral microbiome.
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Yeah, so so this this ~ was a really compelling field of study that died
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on the vine, unfortunately, because of poorly designed clinical trials,
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which were largely financially motivated,
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the way the trials were designed.
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~ at the time when researchers were showing,
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this chlamydia organism can be in the cells,
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lining the vessels, right?
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causing issues and u utilizing lipids,
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causing foam cell production, right?
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Like it could you could induce the hallmarks of the disease using animal models.
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You would repeatedly find organisms like you said,
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oral pathogens, ~ things like porphyremonis gingivalis,
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but also this respiratory bacteria,
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chlamydia, became a intense agent to study.
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And a lot of funding went to it from the NIH for a period of more than a decade.
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But then when the pharma companies came in and studied it,
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~ they attempted to treat it using a single therapy,
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which is a very tricky thing when you have a highly resistant organism
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by nature or an obligate intracellular bacteria.
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Typically, those require more extensive long-term multi-drug regimens.
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~ they did relatively short trials and they also looked at patients that were very,
13:36
very sick. Many of the trials were for secondary prevention,
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so the people had already had events.
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And so they didn't
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They didn't show any meaningful results with antibiotics.
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And basically the whole field dried up.
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But at the same time, and this is important history for our group,
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the Alzheimer's Pathobiome Initiative,
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Dr. Brian Balin at the Philadelphia College of Osteopathic Medicine with Dr.
13:57
Alan Hudson from Wayne State in Detroit had a really historic conversation about
14:04
their curiosity, given the fact that this C pneumoniae organism.
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Could get involved in atherosclerosis and infect immune cells and endothelial cells,
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could it be in the brain in Alzheimer's?
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So this led to the very first publication
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in 1998 demonstrating using a multitude of different techniques,
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viable chlamydia organisms in postmortem brain specimens,
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where the plaques are in Alzheimer's disease.
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And relative.
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Relatively absent in the controls.
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So this was one of the first studies,
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the first study in the United States of America.
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~ previously herpes viruses had been linked by Dr.
14:44
Ruth Atsaki and others in the UK.
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But
14:47
huh.
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interestingly enough, the reason I wanted to talk about a little
14:51
bit about heart disease and atherosclerosis is the porphyromonus gingivalis organism
14:55
that shows up in atherosclerosis is also being studied.
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in relation to Alzheimer's disease.
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And the National Institute on Aging has given a $49 million grant to study
15:06
a drug that would essentially target the virulence factor for the the P.
15:11
gingivalis. So it's something that at one time,
15:16
the idea that organisms could be involved,
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microbes could be involved in Alzheimer's and really involved
15:22
in any chronic disease, it's sort of been a hotly debated topic for a long time.
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But
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now more than ever we're seeing that because it's so sensible,
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plausible, and, you know, from other areas of medicine,
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we know ~ you know, that these things can be drivers of inflammation.
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You know.
15:39
Yeah,
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the way I think about it is that they're kind of accelerants.
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I don't know that they're the primary causes per se,
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because I know that there's underlying genetic predispositions
15:51
for Alzheimer's and things like that.
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You've got different pathways for amyloid processing,
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whether it's the alpha or beta pathways that it goes down,
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and they're you know, the Apo E4 plays a role there,
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you know, plasmalogens play a role,
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reverse cholesterol transport plays a role.
16:06
~
16:08
And then, you know, many other lifestyle factors end up playing a role.
16:11
But I do think that once you once you have a ~ a plaque,
16:17
whether it's ~ in a coronary artery or in the brain,
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I think what happens is when you add the infectious agent in,
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now it's you've got something that's actively stirring the pot,
16:29
right? In terms of ~ augmenting inflammation and augmenting
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the oxidative stress that comes from inflammation.
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So to me it seems like it's it's i I'm sure it's it's pathogenic on some level,
16:43
but it also seems to be an accelerant to an underlying process that somebody
16:47
had a predisposition for whether they'd been exposed to that ~ pathogen or not,
16:53
if that makes sense. So
16:55
It does make sense. ~ it's one way to look at the situation and ~ you know,
17:00
many of the different things that you address.
17:03
So the first thing I'll say is we can't uncouple genetics and the pathobiome.
17:08
They're extra inextricably tied.
17:11
One of the most powerful forces on human evolution have been pathogens that we've
17:16
had to battle. And so even ApoE4,
17:19
which you know, people commonly refer to as the Alzheimer's gene.
17:23
Having two copies drastically increases your risk of developing the disease,
17:26
can be modifiable with lifestyle factors,
17:28
and we believe also prevention or treatment of certain infections.
17:32
ApoE4 enhances susceptibility of AD associated pathogens,
17:37
and these mechanistic models have already been done.
17:40
~ as well as we now understand that the PLACs,
17:44
two of our different teammates within our consortium have
17:48
demonstrated that amyloid beta plaques are in fact antimicrobial
17:53
in nature or antimicrobial responses.
17:55
They're a part of the innate immune system and they are recruited
17:59
in response to herpetic viruses and other infectious agents.
18:03
So I actually think it I have a slightly different view than you,
18:08
slightly divergent, which is always a good thing in our book.
18:11
That is the whole purpose of building a global consortium of different
18:14
Experts so that people can respectfully disagree with one another
18:17
and debate these topics. But I think what we are finding in the work that
18:22
has happened already and as well as in the work that we're currently doing
18:27
is that the root of the inflammation itself is pathogenic.
18:32
And then, yes, certain other factors in your life can predispose you
18:37
to risk to being ~ basically.
18:40
affected in a negative way to things that may be commensal in somebody else's body.
18:44
So that's why we really liked the word pathobiome,
18:47
because it captures something that I think you're trying to grab the essence
18:50
of when with what you're saying,
18:51
which is some people walk around and have chlamydiaan moniae
18:56
or porpheromonis gingivalis and they harbor it and it is part
19:00
of their commensal ecosystem. And it may not be harming them,
19:04
but at some point, either in time or never in a lifespan,
19:08
There may be a tipping of the scales in which the immune system decides,
19:12
okay, we've had enough, or you no longer have enough beneficial commensals,
19:16
~ for example in the gut. That's a great example of this,
19:20
that you have a disproportionate number of the bad guys.
19:23
And and this can be is an overlooked,
19:27
I think our team thinks, factor in terms of longevity and aging.
19:31
And ~ you know, it could be something where certain individuals have
19:35
an enhanced susceptibility.
19:37
to the ~ immune response and also to the burden of infection.
19:43
Yeah. No, I I I I I would agree with that.
19:46
the other thing I would just say is that what I was positing earlier
19:50
was really more of a a thought than I'm not I'm not married to what I just said,
19:55
but it seemed to me that it it could be acting as an accelerant
19:59
to some underlying predisposition.
20:01
Because with ApoE four, we know that there was a survival benefit to ApoE four.
20:06
Everybody was Apo E four for like,
20:08
I don't know, ten, twenty, thirty thousand years ago.
20:10
I forget the number.
20:11
Right, because it there was a survival benefit.
20:14
And what was the survival benefit?
20:15
Well, they mounted a a greater inflammatory response to,
20:18
you know, whatever whatever they were,
20:21
you know, facing, right? So ~ right.
20:24
Malaria, whatever else, you know,
20:26
~ tetanus or, you know, whatever else happened,
20:28
right? So ~ so you now have ~ something that was beneficial in one context,
20:35
right, where it's helping you survive because you got an inflammatory response
20:38
to kill off a bug that would have killed you otherwise.
20:40
So that's helpful.
20:42
But then later on, when you get into a world where that's less the case,
20:46
now it's ~ it's being activated by these other pathogens in
20:50
a way that's accelerating another process,
20:52
right? Or so it's it's it's a really interesting interplay between genetic survival
20:59
timelines for survival. ~ you know,
21:02
like Apple V four was good for short term survival,
21:05
but not so great for long term survival,
21:07
right? So ~
21:09
It just depends on what challenge the organism's trying to overcome in the moment.
21:13
~ but back to your point, I do think that there's a really fascinating interplay
21:17
between the gut, the commensals in the gut.
21:20
What we've been excited about recently is we finally got a hold
21:23
of anaerobic commensals that we can actually give as probiotics that actually have
21:28
the ability to almost function like a fecal transplant for people,
21:31
which has gone very, very exciting,
21:33
right? So that's kind of cool.
21:35
And ~ and then I think
21:37
You know, one of the things that one of the reasons I didn't go
21:40
to an into infectious diseases was because,
21:43
you know, I trained in internal medicine before I went to cardiology,
21:46
right? But of course we have exposure to ID all the time,
21:49
infectious disease all the time.
21:50
And these are incredibly knowledgeable people.
21:52
But it just seemed to me like there was just this morass of stuff that
21:57
you could never quite get your arms around,
21:58
right? And we're always trying a different antibiotic combination and you know,
22:03
then now you got a co infection.
22:04
It just seemed like, my gosh, this is like a
22:07
a nest of stuff that I don't know we you know,
22:09
cardiology seemed more straightforward.
22:10
Back to where we are today, however,
22:13
I think with with the advent of AI and the ability to kind of deconstruct
22:18
the rat's nest, ~ and look at it,
22:20
I think it becomes infinitely more fascinating in terms of what we can actually do.
22:25
So
22:26
Absolutely. Yeah, there were it's funny that you brought up FMT.
22:30
So one of the ~ one of the brilliant innovators in ~ you know
22:34
the gastrointestinal space, the late Dr.
22:37
Thomas Barodi, had a ton of ~ interesting patents and ~ you know,
22:43
innovations. He was out of Australia and Sydney.
22:46
He had he was one of the early adopters of FMT and worked with teams here
22:51
in the United States.
22:52
But then he also became incredibly fascinated by the possibility
22:56
of reversing atherosclerosis. So he had actually,
23:00
you know, designed a clinical trial and ~ gotten funding to study this issue,
23:06
looking though with a much more aggressive antimicrobial regimen.
23:09
But to your point about playing whack a mole with the bugs,
23:13
~ in the long term, what I would love to see as a patient is better therapies,
23:19
maybe ~ enhancing the immune response.
23:23
enhancing commensals that can be harmful to things that you don't want
23:28
in your microbiome. You know, there are so many brilliant scientists
23:32
and innovators in the world. And if people begin thinking about this as a facet,
23:38
you know, with regard to longevity,
23:41
with regard to chronic disease,
23:42
begin thinking about the path biome,
23:44
we'll start to see better solutions than,
23:46
you know, what we currently have,
23:48
which what we currently have has
23:51
took me from being basically non functional to I get to sit here today,
23:54
eleven years later, chatting with you,
23:55
which is a gift. But it it's imperfect,
23:58
right? It's not great
24:00
That's right. Yeah. It's a it's a little messy still.
24:03
You know, one of the things that I like about ~ being able to
24:08
use these commensal probiotics,
24:09
they're from a company called Designs for Health.
24:12
There's one called Anterostipes,
24:14
and there's another that's refrigerated,
24:15
and another one that's five commensals.
24:17
But the thing I like about it is that to your to your point there about getting
24:23
microbes that actually drive other microbes out that you don't want to have,
24:26
~ when you
24:28
When you put these into the into the gut,
24:30
what they've been able to show with their research is that it sort
24:33
of changes the soil in the gut,
24:35
so to speak, right? Because they're anaerobic.
24:37
They're not sitting up where the air is passing over them.
24:39
They're down in the in the wall of the gut.
24:42
And when they actually take hold and are doing well and healthy,
24:46
then the bad bacteria that sit on the surface,
24:50
like the weeds in the garden, naturally get pruned away.
24:53
And, you know, as long as you're putting
24:57
good food and other things to feed the good bacteria,
24:59
you know, not sugar. Now you're you're actually getting the garden to grow
25:03
in a very healthy fashion. And I think I love solutions like this where
25:07
we can actually ~ you know, change the soil,
25:10
change the environment, if you will,
25:12
internally to help it be in a very healthy place.
25:15
~ I think coupling that concept with the idea of going in and killing
25:21
off the bad guys that are, you know,
25:22
actually harming us today.
25:24
There's some mix of that, right?
25:26
That's that's gonna work. So yeah.
25:28
Absolutely. Yeah. I mean, ~ in my own case,
25:31
like during the course of the year before I knew what was actually wrong with me.
25:34
It was funny. I I had always lived the way you should live.
25:38
I never smoked. I was a runner,
25:41
avid runner, weightlifter, yoga,
25:43
healthy eating. I was intrigued by it from the age of fourteen.
25:46
I picked up a Mediterranean cookbook that was sitting in my house and began cooking.
25:49
I love to cook. when I fell ill,
25:53
I leveled up the general health,
25:55
right? But I couldn't
25:57
like exercise or curcumin or, you know,
26:01
~ meditate or or probiotic myself out of that one.
26:05
It was, you know, totally degenerative in my case.
26:08
And so the burden was and I do have a copy of ApoE four,
26:11
which is fascinating. And I I have spent a lot of time ~ you know,
26:16
researching it because it's been conserved,
26:17
right? So it's not that it serves no purpose.
26:20
It's
26:21
You know, like you s you pointed out,
26:23
it helped us survive enteroviruses and ~ the ancestors withstood malaria.
26:29
But it ~ it does do other things that may ~ beget certain risk factors that
26:36
that are for those of us that now we live longer,
26:38
right? We're living when beings live longer.
26:41
And so we were at one time, you know,
26:44
the road was shorter. Now that the road is longer,
26:46
maybe, you know, this this active immune response can be damaging.
26:50
you know, in the face of certain infections or a pathobi,
26:53
you know, that you develop as you age.
26:55
But yeah, we we've really felt that one of the solutions to kind of all of
27:00
it is not to work in silos, but to build bridges between the different silos.
27:05
So working with clinicians, working with ~ people that have
27:11
one area of study that's completely distinct from the next person.
27:14
people in immunology, we have experts in fungi,
27:18
bacteria, viruses.
27:20
~ neuroscientists, you know, people focused on PEDs,
27:23
neuropathologists, biostatisticians,
27:27
people looking at epidemiology.
27:28
So because essentially what I felt about it,
27:31
and I felt the same way about my case,
27:33
is that whether it's a complex disease or one complex patient,
27:37
a team approach to looking at the problem is going to be a much better
27:43
way of handling it because, you know,
27:46
the it we're at a point where
27:48
For a lot of chronic diseases,
27:49
~ you know, with really healthy lifestyle,
27:53
a lot of it could be avoided, right?
27:55
Plain and simple. Just to keep the to the facts.
27:58
Sorry. Like most people, you know,
28:00
it's ~ related to lifestyle. The majority of of chronic illnesses can link back
28:05
to ~ you know, not eating properly,
28:08
not taking care of oneself. But in the case of people that already do that
28:13
and then get devastating illnesses,
28:15
~ you know, just dis
28:17
discerning other disease mechanisms that are,
28:19
you know, taking place in certain individuals and then having a precision approach.
28:24
So we've really advocated for in patients that have new onset memory issues
28:30
or neuropsychiatric disease or neurological complaints,
28:33
regardless of age, ~ to have testing for various infections.
28:38
And some of the strongly associated pathogens are,
28:41
you know, Lyme bacteria, Abrellia Birdorfry,
28:44
and some of the other newborn pathogens.
28:46
like babesiosis and bartanella.
28:48
And then of course, you know, herpes viruses,
28:52
the good old cold sore, ~ may not be so innocent as it appears.
28:56
And then another important one appears to be Epstein Bar virus,
29:00
with a very, very strong association with MS.
29:03
~ you know, with military database study that revealed that in this very large
29:09
cohort over an extended period of time,
29:12
essentially if you didn't get Epstein Bar virus,
29:14
you didn't go on to develop MS.
29:16
And that for many people, ~ you know,
29:19
they some people will use the word causation,
29:22
you know, Epstein Bar causes MS.
29:24
And there are mechanistic studies highlighting that it could be a potential driver.
29:28
But to your earlier point, ~ there's likely to be like a complex array
29:34
of things that occur that result in a tipping point,
29:37
including the genetics. So, you know,
29:40
it's ~ we believe it's an important area of study,
29:43
but we also believe that
29:44
You know, we have to really diversify how we examine chronic diseases where there's
29:49
been little massive progress.
29:52
Yeah. Well I I applaud your thought process here and I ~ I align with your
29:57
aspiration a thousand percent.
29:59
So one of the ways that we've come ~ to think about this is to and
30:05
I'm gonna push your your construct a little bit further,
30:08
which is that yes, it's important to have multiple ~ specialists in the room,
30:15
but we think that what's actually missing is a systems biology construct.
30:21
Because when you get a lot of specialists together in a room,
30:24
they still are working inside their own silo together.
30:28
And in a systems biology approach,
30:31
you actually create a construct where,
30:33
particularly with AI, you can actually have all the different pieces.
30:37
For us, there's a life energy circle,
30:39
right? Which is a psychospiritual space,
30:41
which is, as we know, a big driver when that's out of alignment,
30:44
drives aging, disease, you know,
30:46
chronic
30:47
illness, pain, all those things,
30:49
right? So that's a big one. Then there's longevity itself,
30:51
which is the hallmarks of aging.
30:52
Then there's health, which is basically all the organ systems,
30:56
subsystems. Then performance, which is how we stay fast,
31:00
agile, strong, quick, balanced,
31:01
etc. And then the environment we reside in,
31:04
right? So when you have a system like that,
31:06
then every disease will arise from within that system.
31:12
And when you have a whole system
31:17
You may have specialists that come in at different points,
31:20
but they're working inside of a system that's also pulling in other data.
31:24
~ because they're they're only aware of what they're aware of.
31:28
And in a systems approach, you can actually bring in all the information
31:32
and then get their input as well,
31:34
but realize that, hey, well, we need somebody over here that actually
31:37
can speak to us about something environmental or something psychological
31:41
or something, you know, immunological or whatever it is,
31:44
right? And
31:45
So that's what we're working on now with in the longevity space is
31:50
and the health space, human optimization space,
31:53
if you will, is a systems biology approach to bring all this together
31:57
and then leverage AI to help us actually understand where where's the where
32:01
are the points for the highest leverage?
32:03
Because that's really what we're after,
32:06
sort of what I call the elegant solution,
32:07
right? So we know there's Epstein Bar,
32:09
we know there's this, we know there's that,
32:10
but where's the elegant solution,
32:12
right?
32:12
When we apply leverage here, here and here,
32:15
how do we actually coax the system back into health?
32:18
~ so anyway, just to let you know,
32:20
~ it's a little bit of an extrapolation from ~ the concept of reaching
32:25
out across disciplines to pull people together because it creates
32:28
a construct everybody can come under ~ and and work together.
32:33
So anyway, I don't know if that resonates.
32:36
I you know, I think you would really ~ resonate with how we do science within
32:41
our consortium. So it's not like a typical consortium where everybody does their
32:46
separate thing. We've been convening weekly for years.
32:49
Some of the people like a decade.
32:51
Yeah. And we have data sharing,
32:54
specimen sharing implemented, even ~ a new enhanced sterility autopsy program.
32:59
So we are working in a very integrated fashion as you describe.
33:02
And in in our grant submissions,
33:05
there
33:06
all team science grants, meaning it's never going to just be one investigator
33:11
or two investigators. It'll be an entire team.
33:13
And then I'm typically involved and some of our other leadership is involved
33:17
to be sort of the hub and to maintain that connectivity with the consortium.
33:21
And that's actually one of our longer term goals.
33:24
Well, really short term. But it it can be long term 'cause it's aspirational.
33:28
But
33:29
We have an incredible research template and plan that we've begun to work.
33:33
It involves multiple centers, different types of expertise,
33:36
you know, with a main data core,
33:38
~ leveraging many of the things you mentioned.
33:41
But obviously those are very expensive and costly,
33:45
right? So we have identified various government mechanisms to support team science
33:50
and innovative research programs that take a systems biology approach.
33:54
And we're finding, you know, still there are great challenges federally
33:58
to get funding for this sort of thing.
34:00
So we've really relied very heavily on philanthropy funding to launch the program.
34:05
~ but our our desire is to be able to point to mechanistic pathways through which
34:11
certain polymicrobial infections or infections alone,
34:15
unlikely that they act alone, ~ can be disease drivers,
34:20
triggers and or worsening.
34:23
diseases in various patients with first emphasis on the brain.
34:26
But, you know, the the research platform is intended to be something that
34:30
is a framework that's reusable.
34:32
So in other words, the data core and then all of the different teams doing
34:35
mechanistic studies, population studies,
34:38
~ you know, various ~ different detection methods for pathogens,
34:43
the people looking at the immunology side of things.
34:45
~ we are all
34:48
basically convening as much as we can without having an institute.
34:51
You know, would I love someone to come forward and say,
34:54
Wow, what a cool concept. You know,
34:56
do you guys would you want an institute?
34:58
The answer is yes.
34:59
Mm-hmm. Yeah. Well you've kind of created a virtual institute,
35:02
but ~ I realize the advantages of having something,
35:05
you know. Yeah, down the hall exactly.
35:06
Down the hall. Down
35:09
the hall and and talk to the T yeah.
35:11
But ~
35:13
Yeah, it's very cool. You know,
35:14
as I'm hearing you talk, I'm actually desirous.
35:19
I'll use that word. I'm actually desirous of being able to take your data
35:24
and plug it into the AI that we're developing,
35:26
because we're developing the systems biology AI ~ in the longevity and health space.
35:32
And the smarter that that is, ~ the more elegant the solutions will
35:38
be that come out, right? And so we're looking at
35:41
When you think about the AI, it's it's it's a couple of interesting things.
35:47
We're we're working to make it deterministic and also ~ also inferential.
35:54
And so it's a combination of being able to put in things that we know to
35:59
be true and s keeping it to basically color inside the lines,
36:03
but then to be able to see relationships across things and ~ work towards,
36:09
you know, what I call the elegant solution again.
36:11
So
36:12
~ I think you're working in a space where
36:16
by definition you're curating and cultivating data that fits
36:23
perfectly into a systems biology approach,
36:25
because that's actually what you're doing.
36:26
This is your own systems biology approach.
36:28
So it'd be really interesting to see ~ what could come
36:35
of that because we're looking at it through additional lenses that most doctors
36:38
aren't, right? From the longevity side,
36:39
the hallmarks of aging.
36:41
probably we have we have full omics inside this,
36:43
right? Genomics, metabolomics,
36:45
proteomics, all of it, right? So we have massive amounts of things
36:49
to leverage against this that could really accelerate,
36:53
you know, what we all learn, quite honestly,
36:56
and how we help people. So that would be pretty interesting.
36:58
Yeah.
36:59
Yeah, we've seen some really great you know,
37:02
collaborative efforts taking place around for just to take Alzheimer's
37:06
for a second just to pick one field.
37:08
Yeah. ~ you know, where consortia are formed and they'll be using Omics approaches,
37:14
a variety of them, you know, and leveraging neuroimaging
37:18
and biomarkers and tracking lifestyle.
37:22
one of the things that's frequently and pretty I mean always across
37:27
the board omitted.
37:28
is any kind of nod to the microbiome or the pathobiome.
37:33
You're starting a little bit more with the microbiome,
37:35
~ which I think is a related but sort of distinct subject,
37:41
right? ~ when we talk about pathological organisms,
37:45
it it's very different than the idea of,
37:47
you know, a resident microbial community,
37:50
which sort of has just a neutral or even beneficial tone to it.
37:55
~ but yeah, absolutely. I mean,
37:56
it sounds like what you're developing is really fantastic and could
37:59
be highly applicable to, you know,
38:01
serve as ~ you know, something that data like teams like ours and others,
38:07
you know, as as that accumulates ~ mechanistically pointing in various directions,
38:13
highlighting certain genetic traits,
38:15
~ you know, highlighting certain pathogenic states that that are taking place
38:21
in certain people.
38:22
~ for example, one thing we're really curious about is two-thirds
38:26
of Alzheimer's cases are women.
38:27
And for MS actually.
38:30
Both are infection associated chronic diseases.
38:34
so we're deeply curious about the changes that take place through
38:40
a woman's lifespan hormonally and how those may play into susceptibility to
38:47
~ neurodegenerative processes andor vul vulnerability to pathogens or as you said,
38:53
the immune system, you know, mounting a defense against something that
38:57
is inappropriate and harmful.
39:00
Yeah, I think I think ~ I think it's a really fascinating field.
39:03
Right. you know, when you think about aging and you think about women aging,
39:10
men have their own issues, of course,
39:11
but when you think about women aging and you think about ~ how important estrogen
39:17
is for the brain, ~ you know, there was a really interesting study that
39:21
was done by Kaiser Permanente ~ a while ago now where they looked
39:26
at five hundred thousand women.
39:27
It was kind of a retrospective study.
39:30
They looked at 500,000 women and they looked at women that got any form
39:33
of hormone replacement. And by that it could have been they got testosterone
39:38
for a month, they got estrogen for two weeks,
39:40
they got, you know, estrogen, progesterone,
39:42
testosterone for six years, they got whatever,
39:46
right? And what they showed was that there was a 50% reduction in in dementia
39:52
in the group that got any form of hormone replacement therapy,
39:55
which is
39:57
I thought was fascinating because my gosh,
39:59
I mean, if you just got testosterone for two weeks,
40:02
really, that's gonna have any kind of impact.
40:03
Or you got estrogen for three months or whatever,
40:05
right? Unopposed estrogen, which we know is potentially dangerous.
40:08
So I think I think it's an interesting piece of it,
40:11
but when you think about it, there's ~ you know,
40:15
the hormones, they in they basically ~ create a lot more robustness in the tissues.
40:21
~ they also are immune modulating in many respects when they're balanced,
40:25
right?
40:26
So the combination of immune modulation,
40:29
~ tissue resilience and robustness,
40:31
you know, the many factors that go into play here.
40:33
And then you bring in the pathogens and all this.
40:35
You can see it's just this incredibly complex morass.
40:38
But I think for the first time we're actually gonna have enough compute power
40:42
to actually get our arms around it and and be able to say,
40:45
okay, here are the here in this individual,
40:48
that's what I'm thinking about for the individual.
40:50
In this individual, here are the eight or nine factors that are the most critical.
40:53
If we correct those, this should
40:55
steer the ship, right? So
40:57
Absolutely. And that's really one of the you know,
41:00
that's ~ what you mentioned about estrogen is something we've really zeroed
41:04
in on because with in females with estrogen depletion,
41:08
you know, some of the barriers become more permeable in a bad way.
41:11
~ because membranes, the gut b barrier.
41:14
But a lot of people don't really think about the blood brain barrier.
41:17
And I don't think it's been studied ~ really effectively,
41:21
you know, to look at
41:22
Is there enhanced permeability of the shield that's supposed to protect the brain?
41:27
If you're also seeing increases in translocation of gut bacteria with depleted
41:32
estrogen, you're seeing enhanced UTIs,
41:34
urinary tract infections, vaginal yeast infections,
41:38
and then tissue thin. So it's very fascinating,
41:41
understudied. and so we're very privileged to be able to help work on that
41:46
and get to that, you know, space of research in the context of ~ aging.
41:52
in females as it pertains to neurodegeneration and Alzheimer's.
41:55
Because I do believe there's something there,
41:57
as you're pointing out. it's just likely to be it's gonna need to be precise,
42:01
precise approaches, right? That take into a lot of factors into account.
42:05
And as you mentioned, AI, what an incredible tool to help us do that.
42:10
Yeah. ~ so excited about it really.
42:12
You know, I think the other thing to think about is to bring
42:15
in the functional medicine physicians,
42:17
~ and the the true longevity physician everybody's a longevity doctor now,
42:22
but bring in the actual people that are,
42:24
you know, working at the the root cause of the root cause kind of area.
42:28
and the functional medicine approaches which ~ may not have as many studies behind
42:34
them and many times have many studies that just aren't,
42:36
you know, widely referenced, but ~
42:40
There's a lot of information there that when it's aggregated together,
42:44
I don't think we're that far away.
42:46
I I have told people two years ago I thought we were going to crack aging
42:50
in three years, and I still think we're on on course to crack it in
42:54
the next twelve months. And the reason I say that is because,
42:57
you know, kind of the work that you're doing,
42:59
the way that
43:01
That AI is really facilitating this rapid integration of information that
43:05
can be very precise. And I think if we get a little bit of quantum computing
43:08
on top of it to ask the optimization questions,
43:11
we're not far away from actually being able to to crack it.
43:16
And so if you can crack the code on aging,
43:18
then I think you can really crack the code on health.
43:20
~ and health optimization, diseases start to fall,
43:24
like dominoes also, I think. So pretty interesting.
43:27
And some of the diseases that we study also manifest in childhood.
43:32
So we are also examining ~ while we're called the Alzheimer's Pathobiome Initiative,
43:38
~ we are looking at the whole human lifespan because we acknowledge that some
43:43
of the neurodegenerative, neuropsychiatric diseases that get diagnosed early bear
43:47
a lot of similarities, whether you're talking about symptomatology
43:51
or biomarkers from blood or CSF neuroimaging.
43:57
And even brain specimens, postmortem brain specimens.
44:00
So one of the things that our team is digging into are ~ cases of pans and pandas.
44:06
~ the pediatric neuroimmune disorders linked with infection
44:12
as a trigger or a continual simmering pot,
44:16
~ either in the consoles in the case of pandas,
44:19
~ or it can even be, you know,
44:22
from a tick bite, something like Lyme disease or COVID.
44:25
SARS-CoV-2 can be a trigger. But these disorders bear some striking similarities
44:30
to neurodegenerative diseases associated with advanced age.
44:33
And so you're okay, well, if neuroinflammation is present,
44:37
if autoimmunity is a factor, ~ enhanced blood-brain barrier permeability,
44:42
mood alterations, sleep alterations,
44:45
~ urinary, you know, so there's so many different things.
44:48
And so we're stepping outside the bounds of specialties,
44:52
but also across the lifespan. And
44:55
I love it.
44:56
you know, due to really external inspiration,
45:00
honestly, Dr. Gladden. It's like my own experience with complex chronic illness,
45:04
but then also talking to patients around the world.
45:07
And a lot of patients can become extremely knowledgeable.
45:10
Like we're talking they
45:11
Very knowledgeable.
45:12
can become thought leaders.
45:15
Yes.
45:15
Yeah. And so those of us that have had to take the pain and turn it into a solution,
45:21
you know
45:22
because there wasn't one, because we feared we'd lose our lives or our ability
45:27
to to thrive and be with our families.
45:29
You know, th those things can really accelerate and inform research and also,
45:33
you know, things like what you're doing.
45:35
and it's interesting. There was a there have been,
45:38
you know, points in time where obviously with all of
45:40
the sophisticated diagnostic approaches that we have now to evaluate patients,
45:45
something that gets lost is at times,
45:49
especially in the context of
45:51
People that have chronic Lyme disease that drift from one doctor to the next
45:55
is just that that patient-physician connection,
45:59
you know, like the person across from you listening to your story,
46:03
piecing together the clues and digging a little bit deeper,
46:07
you know, because a complete blood count on somebody with chronic Lyme looks pretty
46:11
unremarkable oftentimes. And so,
46:14
you know, that next level of curiosity,
46:17
that next level of interpersonal connectedness at the soul level.
46:21
between a practitioner and their patient has to come back into the space because
46:25
the more sophisticated we get,
46:26
the more disconnected we can become.
46:29
Yeah. No, that's that's I mean,
46:31
I think you're bringing out something about the healing connection really,
46:34
the therapeutic connection, the therapeutic relationship,
46:37
the therapeutic ~ trust and construct that goes between ~ you know,
46:42
somebody that needs help and somebody that wants to provide help.
46:45
~ yeah, you're never gonna move away from that.
46:48
You know, I I also keep in mind the fact that while the body can be exposed
46:55
to a million different insults,
46:56
maybe ten million different insults.
46:59
It only has a finite number of responses.
47:01
Right. And so right.
47:04
It only has a finite number of responses.
47:06
So if we can actually ~ understand the way in which these external
47:12
imp you know, agents or whatever are well how they're triggering
47:16
the finite number of internal responses,
47:18
which is typically inflammation,
47:20
oxidative stress, you know, leaky gut.
47:22
I mean, it's really fairly finite,
47:23
right? then we should actually be able to ~
47:29
have some interventions that actually go in and stop these things,
47:32
right? And so so you're it's two prongs.
47:35
One, you're stopping the reaction to what happened,
47:38
and two, you're clearing whatever the the insult was that came in.
47:42
Right. So you have two two sides to that,
47:44
right? Yeah.
47:45
So do you want to know the reason,
47:46
one of the reasons why I believe that the amyloid clearing antibodies
47:51
are not demonstrating a whole lot of efficacy?
47:53
It's that it's there for a reason.
47:57
~ it's not to say it's not ~ problematic.
48:01
It is. but what happens,
48:06
even if you took away the amyloid in from the research that's already been
48:10
published, if you have a confluence of organisms that
48:13
By nature of being alive, they have to steal energy from your mitochondria.
48:17
They have to dysregulate metals,
48:20
lipids, they have to drive oxidative stress as a part of their whole thing,
48:24
right? They cause the release of heat chalk proteins and cytokines.
48:27
You haven't actually handled, you've taken the batteries out of
48:31
the smoke detector while the fire is raging.
48:33
So, you know, the the drug situation
48:38
has undoubtedly delayed progress because,
48:42
you know, and I
48:43
I worked in pharma and biotech.
48:45
~ I'm not, you know, against ~ drug development.
48:49
We need we need innovation. We need people that are actually creating solutions
48:54
to the problems. We need better testing for infections is one great example.
48:58
We need better precise treatments,
49:00
things like phage therapy that could potentially have promised to
49:04
be more widespread use someday.
49:06
But you know, until somebody really
49:09
develops a solution around these problems,
49:12
and it may not have to be a a therapeutic solution,
49:14
it could be preventative ~ or something else.
49:18
I think it the economic d thrust is missing.
49:20
And the economic thrust also informs and exerts pressure
49:26
on the federal thrust for funding.
49:29
Yep. I'm just gonna say something for your audience.
49:32
A phage is basically a virus. So you can use a virus to go kill other things,
49:36
right? Just so if that slipped past you,
49:39
we use something called ecofage actually to kill off things in the gut.
49:42
It'll go in and kill off all the bad stuff,
49:44
right? So we're familiar with use of phage.
49:46
but that's an interesting thing.
49:48
I think to your point about economic incentives is one of the biggest
49:53
~ problems in medicine, right?
49:56
Because
49:57
Chronic disease, it makes more money than ~ curing disease on some level,
50:01
right? And so there's there's lots of ~ financial incentives that
50:07
I think are misaligned with health.
50:08
It would be nice if we could get those straightened out.
50:11
~ but in the meantime, I'm not gonna try to change systems that are.
50:16
I just wanna find the answers that we need to find and then let those speak
50:20
for themselves, right? So that's Absolutely.
50:23
Absolutely.
50:23
Yeah.
50:24
We're we're right there with you.
50:25
Exactly. We're not focused on,
50:27
you know, what hasn't been done or,
50:30
you know, like looking in the rearview mirror.
50:32
We're trying to look ahead and say,
50:34
okay, well, what can we do in the context of the funding we have,
50:38
with the information we have, with the resources we have today to make
50:41
the most of it. And one of the things we felt is so important
50:45
is collaboration and doing so in a very intentional manner,
50:49
not just
50:51
consortia that show up every once in a while and yeah,
50:53
we're on a email distribution list together,
50:56
but true collaboration, you know,
50:57
saying, hey, I ran this specimen of the same region.
51:01
Did you what did you find? Here's what I found.
51:02
And then, ~ I didn't pick that up.
51:05
You know, so this whole idea of rigor and reproducibility in science,
51:09
which ~ Dr. Jay Bodhicharya, the new director of the NIH,
51:13
speaks about all the time, that's exactly what we are doing with
51:17
the Alzheimer's Pathobiome Initiative.
51:19
We're leveraging
51:20
preexisting testing that is, you know,
51:23
some of them perhaps not even commercially available,
51:25
but are in academic labs, looking at the most reliable ways
51:29
of detecting neuropathogens that can become prob very problematic and that
51:34
in and of themselves can trigger disease pathology.
51:37
Yep. No, I think that's right.
51:39
I think it's good to look outside the allopathic model or even
51:43
the osteopathic model, right? And look at there I mean,
51:46
there's a lot of wisdom in ~ traditional medicine practices,
51:50
you know, Aerobedic medicine, Chinese medicine,
51:52
things like that. They've been dealing with this stuff a long time.
51:54
What goes on in Japan. I mean,
51:57
I th I'm really I'm agnostic to where the solution comes from.
52:00
I really don't care where it comes from.
52:02
I just care that it works. So
52:05
I agree. I I have to admit, like ages ago,
52:08
you know, because right out of college I worked for Pfizer.
52:11
And ~ you know, I think that the allopathic medical community sort
52:16
of looks down upon some of the more traditional,
52:19
longer standing even, you know,
52:21
leveraged by humans for so much longer than our modern medical machine.
52:26
~ but during, you know, my own ~
52:30
Chronic illness journey, learning,
52:31
you know, with the working with a functional doctor or naturopath as a part
52:35
of my team, you know, there is it's a big world.
52:38
And there are abundant solutions and ideas.
52:41
And I'm like you, I feel like,
52:42
boy, if the if the solution could be,
52:45
you know, tucked away, hiding.
52:46
I mean, I was pretty excited. There was this ~ seaweed extract derivative
52:51
by a company called Shanghai Green Valley Pharma.
52:53
they went and got approval in China.
52:57
I do not know where they stand as far as US approval,
52:59
but they were giving it for patients with leave mild
53:02
to moderate Alzheimer's disease.
53:03
And their proposed mechanism was modification of the gut microbiome.
53:07
Okay. But as you said, there there are so many natural compounds that have
53:13
themselves evolved defenses ~ against pathogens and have anti inflammatory
53:19
properties too. ~ so yeah, it it's ~ once we grasp as you're saying.
53:25
that you keep going back to like the systems biology way of thinking.
53:30
And if we can actually do it, which is challenging 'cause people tend
53:34
to like form factions and groups,
53:36
right? And and then kind of hang out with that that group.
53:39
~
53:40
Tribal. It's tribal, right?
53:43
Yeah. Not that it's a bad thing,
53:45
but I think we we need to be sort of talking to one another because
53:48
we have big problems that deserve faster solutions and more accessible,
53:53
right? Because a lot of what we are talking about,
53:56
the precise approaches that even I've had the benefit of receiving,
54:00
they're out of pocket expenses,
54:02
right? They're not these things are not covered by insurance.
54:04
And so the current model really is to go after sick people
54:11
and they're already sick.
54:12
~ but in the future, if you know,
54:16
reimbursement would allow for longer precision medicine visits,
54:20
you know, like my Lyme disease specialist spent four hours with me the first visit.
54:24
Can't really do that within the bounds of insurance.
54:28
No, you can't. ~ it's a combination of insurance and the health care system won't
54:34
allow it, those two together, right?
54:36
So I think a lot of the solutions are gonna come
54:40
out of the alternative approaches because people are able
54:46
to take more time. I think the incentives are aligned around
54:50
Not how do we make a drug that we can make a billion dollars off of,
54:54
but how do we actually find a solution that's gonna work?
54:56
I think there's I think in some sense there's more intellectual integrity
55:01
in in some of those areas and there could be when someone's really aligned with the,
55:06
you know, with the financial bottom line,
55:08
so to speak. And I realize drug discovery is expensive and I understand
55:12
all that and I understand there's lots of reasons for it.
55:15
There's also a lot of AI stuff now that's coming along to really
55:19
you know, rapidly speed up drug discovery also.
55:22
~ like I've been looking at some stuff where,
55:24
you know, they w they spent I don't forget ~ how many months trying
55:28
to find four molecules that could do something.
55:30
They ran AI for three minutes and came up with fifteen hundred.
55:33
You know, it's just like it's crazy,
55:36
right? So I mean the the rate of innovation this is why I say Asian will
55:39
be cracked in a year, because the rate of innovation is is right high five,
55:44
right?
55:46
Right. I mean this would be very good.
55:49
I'd be thrilled.
55:50
Yeah. But the rate of innovation is so ~ beyond exponential that it's almost hard
55:56
to comprehend. So that's why I think if but I l I love the idea
55:59
of trying to collaborate with you on this in some way,
56:02
shape or form.
56:03
We are always ~ you know, right at at our website,
56:06
alspi.org. we ~ right there it says,
56:09
you know, there's always a link to reach out.
56:11
You and I obviously are connected now.
56:13
Yeah, we're always keen to collaborate with other people that have open minds,
56:17
a deep curiosity and a desire to see change like within the lifetime,
56:21
right? Yeah. I think there's so much ~ that can be harnessed.
56:25
And ~ we wrote a paper in the last year with a team,
56:29
~ the ~
56:31
gentleman who helped to co-found VIOME,
56:33
the gut microbiome testing company.
56:35
Yep. Moho Vusich. We wrote a paper ~ that we essentially called attention
56:41
to the chronic disease epidemic needing a Manhattan project style approach
56:46
and not to build a bomb, but to leverage the existing solutions that are there.
56:50
And I think that's a lot of what you're saying and what your concepts
56:54
are hitting on is that we already have tools that can help us
57:00
address the various issues that we are aware.
57:02
And you're you made this point before that I wanted to really agree with,
57:05
which was that the biological mechanisms are finite,
57:09
right? So engaging in various inflammatory pathways,
57:13
like even if, for example, we're able to say,
57:16
okay, this certain set of pathogens in this particular individual,
57:20
~ you know, that has a Poe4, for example,
57:23
~ and then other genetic traits,
57:25
you know, I will result in
57:28
increases in IL seven and you know,
57:31
so where you could begin to paint a picture and then once the machine learning
57:36
or AI is involved, you know, you can then start to draw inferences if
57:41
you have large data sets, right?
57:43
Like if you accumulate enough information about enough people.
57:45
That's right. So I think I think it's it's just a very exciting time.
57:50
And I love your timeline of a year.
57:52
I feel like I'm gonna I'm gonna hang my hat on that.
57:55
I like it. Yeah.
57:56
All right. Well we'll we'll reconvene next August,
57:59
sounds good. Okay. Beautiful. Well,
58:02
Nikki, it's been such a pleasure chatting with you.
58:04
I really appreciate you taking the time.
58:06
Thank you.
58:07
I appreciate you, Doctor Gladden.
58:08
Thanks for you know, I was very informative.
58:10
I learned a lot from you about what you all are doing and look forward
58:13
to continuing to talk.
58:15
Yeah, beautiful. All right. Well thank you.
58:18
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