Latest / Biohacking Autism with Nadia Elkhatib. / Autism Brain Development: The Building Blocks Behind Myelin, Plasmalogens and Alzheimer's | Dr. Dayan Goodenowe

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Autism Brain Development: The Building Blocks Behind Myelin, Plasmalogens and Alzheimer's | Dr. Dayan Goodenowe · Biohacking Autism with Nadia Elkhatib.

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Welcome back to Biohacking Autism.
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Welcome back to Body Packing Autism.
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I'm Nadia Elkhatib In my recent solo episode,
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I'm Nadia Al Kati. In my recent SO episode,
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I talked about why I now want to understand baseline biology before chasing
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I talked about why I now want explaned biology before chasing
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the next treatment. One piece I only touched briefly was lipid biology,
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the next treatment. One piece I only touched briefly was lipid biology,
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and that is why I wanted today's guest.
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and that is why I wanted today's data.
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My guest today is Dr. Dayan Goodenowe,
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My guest today is Dr. Dangao,
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PhD.
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PhD,
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Neuroscientist, biochemist, inventor,
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neuroscientist, biochemist, mentor,
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and clinical research expert whose work in
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and clinical research expert.
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human biochemistry spans more than three decades.
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And human biomes response within the day.
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He
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developed advanced mass spectrometry and metabolomics technologies
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for studying biochemical patterns in health and disease.
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And he has also authored or co-authored more than 50 medical publications.
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His published work includes research on plasma phospholipid biomarkers in autism.
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plasmalogen deficiency in Alzheimer's disease and dementia,
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and also targeted plasmalogen precursor supplementation in people with cognitive
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That the interesting information people.
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impairment.
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He is the founder of ProDrome Science,
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the author of Breaking Alzheimer's,
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and the founder of Dr. Goodenowe's Dietary Therapeutics,
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which is advancing plasmalogen precursor therapeutics through
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an FDA-regulated development pathway.
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I've had the chance to meet.
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Had the
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chance to meet ~ Dr. Goodnow several times and hear him speak many times.
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Dr. Goodenowe several times and hear him speak many times.
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And every time I come away thinking differently about brain biology,
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Every time I come away thinking differently about brain biology,
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lipids, and how we define health.
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lipids, and how we define health.
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Today we're going to use that biology to look at two different tracks.
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Today we're going to use that biology to look at two different tracts:
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Autism and early brain development,
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autism and early brain development,
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but also Alzheimer's cognitive decline and caregiver longevity.
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but also Alzheimer's cognitive decline and caregiver longevity.
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Dr. Goodenowe welcome to Biohacking Autism.
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Dr. Goodnow, welcome to Biohacking
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Autism. Well, thank you, Nadia.
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Good to be talking with you again.
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Wonderful. Well, I'd love to start where you often start when we teach this with
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the fall. Well, I'd love to start,
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we often start when we teach this,
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the brain itself. Before we ask what goes wrong,
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the brain itself. Before we ask what goes wrong,
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I'd love people to understand what is being built.
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I'd love people to understand what is being built.
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So before we split this into autism and Alzheimer's,
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So before we split this into autism and online,
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can you walk us through the basic architecture of the brain in the sense that
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can you walk us through the basic architecture of the brain in the sense that
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the gray matter, the white matter,
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the brain matter, white matter,
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synapses, myelin, and where do plasmalogen fit into it before we define plasmalogen?
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synapses, myelin, and where do plasmalogen put into it before
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we define plasmologist, where do they fit into
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Where do they fit into all of this?
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all of this? Certainly.
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So the thing is the brain itself is just,
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if you're not intimidated or awestruck by the human brain itself,
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you really aren't paying attention to it.
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And we have not even scratched the surface of the understanding of it.
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And quite frankly, we probably never will.
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The human brain is really a quantum mechanical simulation.
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And if you think about, if you go back to quantum mechanics and Richard Feynman,
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the two-slit experiment of a photon,
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whether it's a wave or a particle,
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basically you have to think about how do you make a thought.
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Right? How do you choose to have chicken salad or a burger for lunch?
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Like the things that you we don't take we take this stuff for granted,
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but the ability of the human brain to simulate this ~ this creation
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out of nothingness of of a thought is something we don't really
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pay enough attention to, and that's our consciousness.
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And where does this all begin and how does the brain get built to create that level
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of infrastructure? Because you're dealing with people think of the brain like
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a computer with zeros and ones,
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but it's not.
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It's far, far more complicated than that and far more subtle than that.
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Because what you're dealing is with a complex wiring diagram.
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There's 300,000 plus fibers connecting different areas of the brain.
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Then these fibers end on what's called synapses or the you know
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the the presynaptic boutons which which release neurotransmitters to connect
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to the next ~ neuron. So it's like the wiring in your house,
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like one wire.
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Connects to another wire and it turns the lights on,
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so to speak, right? But it's not a zero-one game.
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And so the the basic structure of the brain is a wiring diagram.
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Like think of wiring of your harness of your car,
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for example, where you have this bundle of wires that connect different parts.
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And then they terminate at a synapse,
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which connects, which decides whether or not the signal is going to enhance
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the next neuron or suppress the next neuron.
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So we're not dealing with a zero to one event.
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We're dealing with
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You know, a scaled event. And this is where it gets really more
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and more exciting because we have some core neurotransmitters.
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And this is what also gets people in the weeds about human brain,
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because they get into, it's a neurotransmitter imbalance or it's this
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and that and all these things.
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And so we we try to outthink God,
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which is really not wise, because we really can't outthink our own brain,
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because that would be like the robot trying to figure out itself.
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It's not really happening. And so when you take a look at if you look
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at the actual physical structure of the brain.
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We're dealing with billions and billions of neurons,
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and each of these neurons store neurotransmitters in a little vesicle.
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And the vesicle is like a little,
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you know, sphere, if you will,
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that contains within it thousands and thousands of actual neurotransmitters.
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And people hear about GABA or glutamate,
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serotonin, noradrenaline, dopamine,
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all these different neurotransmitters are stored in that kind of fashion.
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And then the neurons release those neurotransmitters through this.
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process of vesicular fusion and release.
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Those little beads, those little,
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you know, vesicles, the number of those vesicles in your brain are about
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the same number of grains of sand in the Hoover Dam.
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Okay, the entire Hoover Dam, if you take the entire Hoover Dam and took every single
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grain of sand that in the entire concrete building of that building,
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of that device, you would have that number of boot the the vesicles.
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But people don't realize that the human brain operates at between 50 to 100 hertz.
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Which means fifty to a hundred times per second,
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per second, the entire Hoover dam breaks apart and reforms itself.
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Breaks its apart and reforms itself.
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Okay? And it's not a zero to one event.
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So now when a for a neurotransmission event to happen,
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what's called is a it's called I know we're getting in the weeds here,
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but it's kind cool. ~ it's it's a action potential threshold.
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And I tell people it's like a child trying to get the attention of their mother,
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right? And the mom's doing something and the child's harassing them,
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saying, Mom,
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Mom, mom. At some point, when you get to the fourth mom,
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the mum reaction says, what? And you've reached the action potential that you've
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you've you've created enough of an event that you're going to
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get an all-or-nothing event afterwards.
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And that subtlety of the human brain is what makes
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it still outperforms all computers manufactured on Earth in a given year.
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One human brain outperforms that because it's not a zero-to-one event.
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So first of all, you have to understand that type of aspect of it.
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Yeah.
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And then you have to think of what does a brain do for us?
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Like why why do we have a brain?
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What's what's a and it's really adaptive.
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It's not smart. It doesn't think,
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it doesn't know if you're gonna have pineapple juice or if you're going
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to put yourself in a cold bath or if you're gonna be out hot in the summertime.
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Like it has no idea what the heck you're gonna do with your body in a given day.
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And it's got to adapt to whatever you choose to do.
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You get in a fight with your spouse,
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you know, you're or you're in love,
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it's gonna have all those types of interactions.
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And so it adapts to our environment.
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And so the question is, what is its ability to adapt?
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When does certain circumstances occur that we can no longer adapt
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to our environment? Okay, if I take you,
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you know, throw you outside at minus sixty degrees naked,
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you're not going to survive. Like it's just not within your realm
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of of tolerability, right? And so we're dealing with autism and Alzheimer's
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and when brain function gets to a point that it can no longer perform within
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~ a window of tolerability, then we have dysfunction.
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So then we talk about how does the brain get resilience from the beginning.
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And the brain starts with a basically raw set of wires.
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Like there's really no programming.
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People think there's programming,
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but it looks like programming,
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There's no problem like this.
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but there really isn't. So it starts in the third trimester,
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is when the brain starts myelinating it.
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This is the so you're all these wires of your brain are basically raw wires.
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So during development in the womb,
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you have the basic neurological structure,
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the connections of different sections of the brain connect to each other.
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But they don't really know the the brain doesn't really know how works yet.
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It doesn't really know what a toy feels like.
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They don't really know what a sound of the bum sounds like.
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They don't really know, you know,
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what movement looks like. They have no way of knowing that because they have
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no prior knowledge of that. They have to learn all of that from the very get-go.
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And so they start learning some of it in the third trimester.
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And as the brain learns things,
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as these wires connect and cr and cause some sort of signal,
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the brain says, ~ I want to keep that thought.
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I want to keep that signal.
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This is, you know, this is what this is my finger.
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Okay, when I move my finger, okay,
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this neuron is active. And so it says,
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okay, when this so now that I've figured out where my fingers are,
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I'm gonna myelinate those axons that drive my fingers.
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And these raw wires get myelinated.
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And this is the protective coating around our wiring.
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And so just like the wiring in your wall,
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you have a plastic coating around those wires.
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And what happens too is different wires require different
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strength of protection. Now if you're a guy,
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if you if you work with electrical things,
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you'll have different if you, you know,
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the wires in your computer, really little thin wires,
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will have a a very, very little bit of of plastic coating,
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but a big thick wire that's that's connecting your house is going to have a big,
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you know, thick myelination sheet.
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So you're going to have this protective coating depending upon the strength
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of the signal that's going to be passed through that wire.
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And the brain adapts and adjusts for that using cells called oligodendrocytes
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and it myelinates it, right? So this starts in the in in early ~ third trimester
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and this it this starts building and in the first two or three years
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of life is where the brain does you know a majority of its learning.
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So we have this massive myelination process over the first three years.
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And that's a very critical neurodevelopmental stage.
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Then it kind of tailors a little bit between age three and eight.
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And then there's different phases,
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but it continues to myelinate way up until ever,
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like we myelinate now, right? And so that's kind of how the brain develops.
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And it's it connects the dots on those things.
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And it's a very powerful system.
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But people should think about it as an adaptation.
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So we talk about autism or talk about neurodevelopmental disorders.
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Sometimes we think about the causation.
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Something is actually attacking the body and causing something.
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But what's really what's happening is the brain is trying to adapt and
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is trying to find the best possible.
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~ outcome given its ability to to adapt to the environment.
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And that's why autism will have certain you know,
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you're gonna have a diversity of symptomology because different children
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are going to have different ways of adapting to the you know their their
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neurodevelopmental challenges.
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That kind of and so plasmalogens are a critical component.
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So the the
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so now your brain and your body is not made of wood and plaster like your house
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and glass. It's made of living material.
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Like your body is making it. So
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There are cells that do those particular things.
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Like your the the myelination process is done by cells called oligodendrocytes.
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And the synapses, of course, are part of the neuron system.
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And so there's building blocks.
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So the build the bro the body has to actually build that.
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It has to take material that you eat.
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If you eat a hamburger and a milkshake,
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somehow it's gonna have to make you know membranes and bone and hair from that
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stuff, right? So it takes all that stuff that we eat and it converts
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it into building block materials,
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and then it builds.
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Using those building blocks, it builds your body.
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And the ability of it to actually perform that is a functional issue.
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So that's kind of where so plasmalogens are a critical building block that your body
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makes to make membranes and synapses.
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And they're critical for a couple things.
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They're critical for the vesicular fusion.
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If you're low in plasmalogen, you vesicular fusion doesn't work.
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And if you're low in plasmalogens,
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you can't make enough myelination.
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And you can have
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You know, the brain's compartmentalized,
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so those different areas will have different ~ effects.
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So plasmalogen is a critical part,
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plasma phosphatidylcholine. And there's certain things,
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cholesterol, there's certain molecules that your brain just doesn't trust
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you to eat, right? It says, you know,
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I can't trust you to eat the right stuff.
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So I'm just gonna make it myself.
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Just give me the b give me the bare bones material,
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and I'll take it from here. And a couple of those things
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are plasmalogens and cholesterol are the two big ones.
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Your brain actually makes.
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More cholesterol than it needs,
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it actually donates cholesterol to the rest of your body.
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And same thing, most of all the plasmalogens in your brain are fundamentally made
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in your brain, except for some dietary supplements that happen ~ from
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the mom during through the placenta and during early childhood development through
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breastfeeding. So breast milk has certain plasmalogen precursors as well.
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I kind of went in random roundabout way.
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I don't know if that answered any questions or created
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No,
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ten times more.
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Well no, it definitely answered all the the the question,
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Definitely answered all the the the question,
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but it also yes opened up by the way new concepts that I I didn't
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but it also, yes, opened up by the way,
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new concepts that I I didn't I didn't realize that myelination was in that book.
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I didn't realize that myelination was adaptive.
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I thought it was the same across the board and that you myelinate everything
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I thought it was the same across the board and that you myelinate everything
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at the same time on an ongoing basis.
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at the same time on an ongoing basis.
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But you're saying myelination is actually adaptation.
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So you
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So
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is learning. And this is what w I did a
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Right.
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big lecture on sleep.
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So there's two aspects of your sleep that people forget about.
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You have REM sleep, which is basically the reenactment of activity during your day.
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And then you have deep sleep, okay?
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And that deep sleep is the myelination phase.
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So when you learn, the reason why the body,
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human brain, has to sleep is that you can't not learn if you don't sleep.
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And so it during your sleeping period is when you decide what memories
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of the day you're going to keep and what memories of the day you're going
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to throw away. And so if you don't sleep,
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you can't remember. ~ Memory goes away.
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So what happens in our REM sleep,
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we reenact, like our body becomes kind of ~ frozen,
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but our brain is active. So you're actually reenacting activities.
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And it could be the activities of that day,
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it could be previous activities,
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you're reliving things. So this is important.
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So if you wanna if you want to remember good things,
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you've got to remember good things.
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Okay, like so your brain again is not smart.
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It can actually, it will, it will program what you tell it to program.
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So if you want to program fear,
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if you go to bed every night afraid,
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okay.
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You're going to get strong, your fear responses are going to
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get stronger and stronger and stronger.
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But it does it through that process.
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So one, the REM sleep, it does your acetylcholine system,
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like basically like an Alzheimer's system,
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like the it actually relives all your activities.
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And that programs the broad the brain to say,
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okay, here is a here is a like a song,
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basically. Like a song would be 20 different neurons firing in sequence,
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right? It's a it's a it's a sequence.
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And then the brain says, okay,
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I like that sequence. And then
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So as you go through the REM cycle down to deep sleep,
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REM, deep sleep, REM, deep sleep,
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you actually lock in memories through that process.
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And so the myelination is that and so that's why babies sleep so much,
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right? So they're sleeping a lot because they're myelinating.
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So the more you like the deep sleep is really where the myelination
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of the brain happens. And so as we get older,
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okay, we sleep less or we have a harder time getting into deep sleep.
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And so the ability to like if you can you can you can think of your sleep pattern
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like an accordion.
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You can either have a condensed according or you have strong relapse,
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you know, stretched out according.
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So it takes deep the longer it takes you to go into deep sleep and into REM,
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the the the the less time you actually have to actually myelinate
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and and create memories. And so that's kind of where that all happens.
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Amazing. I I love that.
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I love that. So this is the way I'm picturing a test.
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So this is the way I'm picturing it.
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Yes. So we're not we don't have any pre programming,
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So we're not having reprogramming or really good at adapting as long as
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but we're really good at adapting as long as we have the raw materials.
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we have raw materials.
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Correct.
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In a nutshell. Okay.
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And it adapts
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at the at the subconscious and the conscious level.
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Like your brain adapts to how your heart functions or how your lung is functioning.
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So it still does all that stuff behind the scene.
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It's still, whether it's a conscious activity or an unconscious activity,
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the brain doesn't care. Okay? It doesn't really it doesn't differentiate between
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Yeah.
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what we consider conscious activity and unconscious activity.
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Yeah. Amazing.
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To the brain, it's the same thing.
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And so the same way it adapts
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to how your heart's working. So when you talk about exercise and muscle memory
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and other things that you may
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~ adapt to your baroreflex, like a lot of your gut function and brain function
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are still going to be regulated ~ behind the scenes.
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Okay, this is great. So ~ so my next question is ~ just going back in history,
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Great. So so my next question is just going back in history.
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so you came to all of this through metabolomics because that's where you started.
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So you can't do all of this through metabolomics because that's when you started.
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So what did you start seeing in the data when you were looking
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So what did you start seeing in the data when you were looking
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at metabolomics that led you towards plasmalogen?
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at metabolomics that led you towards cosmologens?
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So I started my scientific career like anyone starts a scientific career,
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learning from all the different scientists before me.
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And based upon their hypotheses,
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you kind of retest them. So I've always been interested in how the brain works
17:48
bec and then
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When you take a look at, you know,
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biology versus physics versus chemistry,
17:53
you know, the world we live in is really chemistry.
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It's the transformation of these chemical molecules.
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So I really got enamored with how chemistry works and how that's
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the actual biological basis of the world that we live in.
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And then trying to understand how we can measure chemistry in real time with
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interactions, because clearly whatever is happening is happening
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at a biochemical level.
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Not at a physical it you know,
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it's clearly it's biophysics as well.
18:21
If you want to get deep into, you know,
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magnetic fields and, you know bilateral symmetry,
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stuff like that. There's absolutely there's there's field situations going on.
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There's there's no question about that.
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But back to, you know, c some of t kind of the nitty-gritty that you can kind
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of see and measure. So metabolomics,
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a lot of people were enamored with the genomics revolution in the nineties
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and and early two thousands, and there wasn't really a counterpart
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to the biochemical side. Like how do we
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measure all these biochemicals because,
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you know, our biochemistry is the same.
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Like glucose in a plant is the same as glucose in your body.
18:56
Right? And so when you take olive oil out of your book when you take olive
19:00
oil out of your pantry, that's exactly the same molecule that's in your blood when
19:04
I measure triglyceride levels.
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And so chemistry is not really dependent upon your genome.
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Your genome interacts with it,
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but it's still different. So so I depended a technology called Ioncyclotron mass
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spectrometry
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That measure thousands and thousands of molecules that could allow us
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to measure in real time how the biochemical systems were were adjusting
19:24
to each other. And at that point in time,
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I was still in the typical biotech pharma mindset saying,
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this is great. I can use this to diagnose disease.
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Because clearly I should be able to biochemically differentiate bipolar disorder
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from schizophrenia because they're clearly different people,
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and so they're they're being behaving differently.
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So there's got to be a biochemical counterpart.
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you know, one sister with ovarian cancer versus a sister without ovarian cancer.
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And in autism, I did a longitudinal study looking at parents of autistic children,
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children with autism, and then their non-affected siblings,
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or what the parents often will call them autism light,
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right? They'd be something quirky,
20:01
but they're really not, you know,
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they wouldn't be diagnosed that way.
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And we could find that there was an actual correlation and ~ a trend
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in terms of like the the autism light individuals
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Would biochemically fall between the completely unaffected children
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and the autism children. And it clearly identified that there
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was this mitochondrial ~ stress occurring in children with autism.
20:27
And I was looking at diagnostics at the time.
20:28
Then as you dig deeper into this thing,
20:32
and as time goes on, and that's when I my you know I patented,
20:35
you know, we 100% diag like autism is technically diagnosable with 100% accuracy
20:40
biochemically. It's it's and it's part of our biochemical.
20:43
Scan technology, you know, we don't do diagnoses anymore,
20:46
but those those molecules and those those patterns are available for people
20:50
to to measure themselves. But the question is,
20:53
okay, that's fine. It's ~ you know,
20:55
we can label people, but I think as we as we learn more,
20:58
it's not about labeling somebody,
21:00
it's about okay,
21:01
Yeah.
21:01
now that we understand something,
21:03
how do we intervene? Like what what's what's going on afterwards?
21:07
So there's mitochondrial stress,
21:08
but is that you know what's causing it?
21:11
But also what is the effect of that?
21:14
And what happens now as you as you dig deeper and you and we have done more
21:17
and more studies in different diseases is understanding when the brain
21:22
is under stress, in autism it's a mitochondrial dysfunction mostly,
21:27
then what it does is it impairs the ability of the brain to do the things
21:31
it wants to do. Okay, so it's basically running on less than high functionality.
21:36
So it's gotta do these Sophie's choices.
21:38
It says, okay, I have enough, I can do certain things,
21:41
but I can't do all things.
21:42
So what things am I going to do and what things am I not going to do?
21:46
So the brain has to make these choices,
21:47
right? And so we start chasing the bad guy,
21:50
because there's enough bad guys out there to chase.
21:52
But ultimately, we have to start asking the question and saying,
21:55
well, what is the brain trying to do?
21:57
Why don't we just help the brain do what it's trying to do?
22:01
Like we don't have to go chase every bad guy down.
22:03
We don't want to chase every glyphosate molecule and every,
22:05
you know, vaccine and every, you know,
22:07
you know, flu, virus, or whatever.
22:10
Because it's look, we had
22:12
We've had autism before we started spraying all the crops with glyphosate.
22:14
We had off autism before the vaccine schedules got changed.
22:18
So we can say, there was less then,
22:20
sure. So there's an association,
22:22
fine. But it's not like these things created the world of autism.
22:27
We've been studying autism for decades and decades and decades.
22:29
So what that's told us though is that if you have a mold infection or
22:33
if you get Lyme, anything that actually stresses a child during that developmental
22:37
phase, depending upon that child.
22:39
Depending on the the level of resilience that child has,
22:42
okay, it increases the risk that you're going to have a disruption
22:45
in that child's ability to develop and the brain to develop robustly.
22:49
Okay. I try not to use the word normally,
22:51
but it's ri just robustly. It's like saying and a resilience.
22:55
And the so that's kind of where now we've gone saying,
22:59
okay, well, what is the critical component?
23:02
What are what are the what are the imaging or what are
23:06
the other physiological components?
23:08
That we recognize with children with autism.
23:10
Okay. Interesting things, like they typically have visual acuity,
23:13
which is better than average. Like they actually,
23:15
interestingly, they have better vision than average,
23:17
but they'll have hypotonia, right?
23:19
They'll have less muscle function.
23:20
They're often a little more clumsy than normal.
23:22
And they'll so you can actually say,
23:24
okay, there's some muscle issues and there's some other issues with ~ you know,
23:27
obviously ~ tactile sensitivity,
23:30
sound sensitivities, you know,
23:32
the ability to interpret social cues becomes impaired.
23:36
Like they can't.
23:37
really understand as well. And so then you can start asking yourself,
23:41
okay, once we start digging into this in more detail,
23:44
these are things that clearly the brain wants to do,
23:47
but it can't quite do them fully.
23:49
And that's where the myelination process comes in and the fact that they're just
23:53
not robustly myelinating these axons that allow them to clearly separate signals
23:59
from each other. Like I tell people like,
24:01
you and I, we can go into a you know a wedding reception and there's
24:05
a hundred people talking
24:07
loud and all over the place. But you can still carry on a conversation
24:10
by focusing on one person. You can focus on that person,
24:12
have a conversation, and tune everyone else out.
24:14
Well that it's the myelination of your brain that allows you to do that.
24:18
Okay. It allows you to say I can take one wire and hear that signal and
24:22
I can tune out the rest of the wires.
24:24
Right? But when your wires are not fully myelinated,
24:28
then you can't separate the sounds.
24:29
They all kind of come together.
24:31
And so people want they want quiet,
24:34
right? They want less noise, less light.
24:36
less, you know, more structured social environments,
24:40
all these things that they have more control over,
24:42
because they can't really and it just it all starts making sense.
24:47
And so when we start re reinforcing those core biochemical systems
24:52
and biological systems, all of a sudden they start interacting with
24:55
the world around them. And so when I'm talking about autism a lot,
24:59
because it's not their ability to emote,
25:02
it's their ability to receive.
25:03
And this is what people really miss this point a lot.
25:05
It's we learn not by doing, we learn by receiving.
25:09
And I say this to everyone, right?
25:09
Yeah. The mirror neurons. Yeah.
25:10
If I if I want to tease my sister,
25:12
right. Well,
25:13
Mm-hmm.
25:13
if I want to tease my sister, I want to be able to I I I need to know her reaction.
25:17
Right? I need to say, okay, if I do this,
25:19
that what kind of reaction do I get?
25:20
Okay, well I'm gonna well I'm gonna modify modify my behavior.
25:23
Sooner or later I'm gonna get something to get a reaction.
25:25
And then I'm gonna remember, okay,
25:26
now but the only way I can do that is by watching her.
25:29
And and and it's it's her re it's reception back,
25:32
right? And with autism, it's it's
25:35
their receiving part becomes blurred.
25:37
So they can't really they they want to get a hug from their mom,
25:39
right? How do I get a hug versus,
25:41
you know, a yell? And these type of things.
25:43
And so once they start learning that,
25:45
then the world becomes a playground.
25:47
Then it becomes fun. Because then now it's now they can go and do these things
25:50
and say, ~ and they start experimenting like we all do.
25:53
And then you start seeing a whole different transformation because they they're very
25:57
observant. They they haven't missed anything.
26:00
These children and adults with autism,
26:02
they haven't missed anything. And
26:04
Once they start getting stronger on the myelination and and the world becomes less
26:09
frightening and actually becomes fun to play in,
26:11
then they what happens is you get ~ yeah,
26:15
it's just they're they're just just amazing.
26:17
First of all, their their sense of humor is like no other type of group of people.
26:22
They have the driest, quickest wit.
26:24
and so when the when the autistic children and adults start really kind
26:28
of coming alive, like they just kind of they always end up surprising
26:32
you with their with their their quick wit.
26:34
So it's it's really rewarding to see that happen in individuals.
26:37
And it's amazing. And I'm hoping everybody listening can feel this nuance
26:37
It's amazing and I'm hoping everybody listening can feel that new walls
26:41
and more than nuance, a reversal of the way that we see things.
26:42
~ more than nuance a reversal of the way that
26:45
So, Dr. Goodenowe, basically you're talking about resilience and adaptation.
26:47
What we've always done
26:51
What we've always done is we've taught this kid how to talk to his sister.
26:54
is we've taught this kid how to talk to his sister,
26:57
And if she says this, this means that,
26:58
and if she says this, this means that,
27:00
and we're treating this. What you're saying.
27:00
and we're treating this. What
27:02
you're saying is no, this kid's body is able to do this,
27:02
Is no, this kid's body is able to do this,
27:05
it just doesn't have the building blocks.
27:06
it just doesn't have the building blocks.
27:07
So, how about we enable the body to do its job instead of trying
27:08
So, how about we enable the body to do its job instead of trying
27:14
to do it for them?
27:14
to do it?
27:15
And this way they can also learn other things and have that sense of humor
27:15
them and this way they can also learn other things and have a sense
27:19
of humor and give the body the tools to be able to do it by itself on
27:20
and give the body the tools to be able to do it by itself on its own.
27:24
And that's where the word plasmalogen comes in.
27:24
its own and that's where the word plasmalogen comes in.
27:30
For someone who's hearing this word for the first time,
27:30
And for someone who's hearing this word for the first time,
27:32
so can you tell us what plasmalogen are and why are they different from which
27:33
so can you tell us what plasmalogen are and why are they different from which you've
27:38
we talked about cholesterol, phosphatidylcholine,
27:39
talked about cholesterol, local DHA or any other lipids that
27:41
even DHA or any other lipids that people may
27:44
have already known?
27:46
So plasmalogens are are phospholipid.
27:48
So all the phospholipids in your body are based on upon a glycerol backbone,
27:52
which is like a three-carbon. Think of a fork basically,
27:55
and you get a fork with noodles hanging off of it.
27:57
So you have these two noodles called fatty acids,
28:00
and then you have a polar head group.
28:02
And these phospholipids create a ~ a phospholipid bilayer.
28:06
So these these noodles are, they like to organize with each other.
28:10
So they create this phospholipid bilayer.
28:12
And that's how your body creates walls.
28:14
Okay, and then all the membranes of your body are made by these phospholipids.
28:17
And you have 30 trillion cells in your body.
28:20
30 trillion. Okay, every single one of these things is differentiated.
28:23
It's a very massive apartment complex with 30,000 apartments.
28:27
~ And within the in the walls that separate one apartment from another apartment
28:32
are membranes. And then the body makes these membranes.
28:35
And phospholipids are what make these membranes,
28:37
phosphatidylcholine and plasmalogen.
28:39
And then inside each of these cells,
28:41
you have the subcellular compartments.
28:43
So you have your nucleus and mitochondria and peroxisomes.
28:46
And this is how the body compartmentalizes its its functions.
28:49
It's how you have a you can you can have your kitchen separated from your bedroom,
28:54
right? But then in your kitchen,
28:55
you can have a your stove right next to the refrigerator.
28:58
And so you have one spot in the in your kitchen that is at minus 10 degrees,
29:03
whatever it is, and one that you can have really,
29:05
really hot. And the reason why you can
29:07
Compartmentalize this is because you've created these barriers,
29:10
these compartmentals. And your body does the same thing.
29:12
And the ability to compartmentalize these functions is made
29:16
by living material called phospholipids.
29:18
Plasmalogens are a critical component of that.
29:21
And what plasmalogens do,
29:24
so like they're they're everywhere.
29:26
Like 50% of the lipids of your heart are plasmalogen,
29:28
high degrees in your lungs. So children who are born prematurely that'll have
29:32
bronchial dysplasia, they're typically plasmalogen deficient.
29:35
The myocarditis that we're suffering from right now is typically from plasmalogen
29:39
depletion of the heart, for example,
29:41
kidney function. And in the brain,
29:43
these plasmalogen are made, though there's two,
29:46
there's multiple types, but two main limes.
29:48
One is the omega-9 version, and the omega-9 version creates these really,
29:52
really tight ~ packing material,
29:55
like your electrical tape, if you will,
29:57
that wraps the axons. So the omega-9 is used to make the myelin.
30:01
And the omega-3 is
30:03
is used to make really highly flexible membranes.
30:05
So these when I told you about the all the vesicles bursting and forming back,
30:10
that's dependent upon these omega-3 plasmalogens.
30:13
And also why children with autism actually have actually higher levels.
30:17
That's why you'll see this hypersensitivity in certain areas.
30:20
So people say there's a connectivity issue,
30:22
right? So areas of the brain have hyperconnectivity and areas of the brain will have
30:27
reduced connectivity. And that's just that's just how the the brain is adapting
30:32
To its resource development. So these plasmalogens are made from scratch.
30:36
They're made in an organ now called proxisomes.
30:39
And that's why, you know, as we get older,
30:42
proxyomal function with muscular development.
30:45
So in Alzheimer's disease, as we get older,
30:48
our proximal function can decline,
30:49
our oxidative stress levels can get elevated,
30:52
plasmalogens get depleted, and that's how plasmalogens and their association with
30:57
aging and Alzheimer's disease was determined.
31:00
Use using this mass spectrometry technology,
31:02
and then you know we we we can restore them.
31:04
So the question is so we can see these problems,
31:07
and in in autism, there's advanced MRI called diffusion tensor imaging
31:13
or neurite orientation dispersion and density imaging ~ that allows us
31:18
to look at the microstructure of white matter.
31:19
So we know unambiguously in autism,
31:22
this white matter development is delayed.
31:25
Okay, so they're having a hard time myelinating.
31:29
And the myelination process is highly,
31:31
highly dependent upon plasmalogen levels.
31:33
So we know by by default that there is an insufficient plasmalogen supply
31:39
for myelination in autism. There is an excess plasmalogens in their synapses because
31:45
they have this hypersensitivity.
31:46
So you have this inflammatory syndrome,
31:49
which is causing this mismatch in their brain.
31:52
And so providing plasmalogen precursors is one of the only real ways that
31:57
we can restore plasmalogen, because they're not.
31:59
dietarily available. They're the other thing that makes them special
32:03
is this little bond called a vinyl ether bond.
32:06
And it's like a fuse. And it is probably,
32:10
well not probably, it is the most oxidatively sensitive molecule in the human body.
32:17
It's the body uses it for reducing oxidative stress.
32:20
So peroxides and any kind of oxidative stress that occurs in the body,
32:23
the body dumps a bunch of plasmalogens on it,
32:26
like a fire blanket, and it douses the fire.
32:29
And it's not like a coq10 or some antioxidants like a you know,
32:35
like a flavonoid, for example,
32:36
like you know, your fruit your fruit and vegetables.
32:39
Those molecules kind of hold oxidative stress,
32:42
they they kind of hold an electron like a hot potato,
32:44
and they kind of sequester it for a little while,
32:47
but eventually it has to go someplace.
32:48
Plasmallogens break apart. They're they're they're destroyed in
32:53
the process of neutralizing oxidative stress.
32:57
And so the body uses it.
32:58
To get ~ under massive inflammation events because it can make them again,
33:03
right? So it says, okay, I'm going to dump a bunch of plasmalogen
33:05
on this oxidative stress or this inflammation.
33:07
And if I get rid of it, fine, then I'll gradually rebuild my plasmalogen up.
33:11
And as long as that inflammatory event is relatively short lived,
33:16
that works perfectly fine. But under situations of really chronic inflammation,
33:20
then all of a sudden your reservoir gets depleted.
33:24
You can think of the plasmalogen like a
33:26
You know, we're here in Southern California,
33:28
so people have fires and they'll have lakes that they'll draw and you know
33:32
see the airplanes come in and go in and grab the water and dump the water
33:35
on the fire. And that lake is being fed by streams,
33:39
by water runoff from the mountains or wherever the case may be,
33:42
right? And that lake has accumulated water over several years of this trickling
33:48
in of water. So if you have a big fire and you go in,
33:52
you have a bunch of water reserves.
33:55
And that's fine if you use up half the water and the fire's out.
33:57
Great. The fire's out and you can take a couple more years for that that lake
34:01
to rebuild. But if you have to use up all the water in the lake to fight the fire,
34:05
then you're out of water. Then you're stuck with just a little trickle
34:09
of water that comes like whatever water is coming into it is your trickle.
34:12
And this is kind of how what what happens with these plasmalogen deficiency
34:16
situations is that the reservoir gets drained and the body just can't refill
34:21
it fast enough.
34:22
And so all autism has this neuroinflammatory component.
34:25
So they have this high consumption or breakdown of plasmalogen because
34:31
of neural inflammation. So the so if you take a look at autism brains,
34:36
biochemically and and neurologically,
34:40
there are a few things that are just ubiquitous in every single child.
34:43
Whether they're three years old or they're 45 years old with autism,
34:47
okay, they're going to have neural inflammation.
34:49
And neural inflammation is
34:51
microglial inflammation, which means there's going to be
34:53
an excessive inflammatory load and the body's constantly fighting it.
34:57
It's constantly trying to put these fires out.
34:59
And it depletes many things. It depletes energy,
35:03
but it also depletes these plasmalogen levels.
35:04
So there's always an inflammation event.
35:06
There's always a ~ an impaired myelination.
35:09
Like the myelination, like reproducibly study after study,
35:13
has shown that the white matter density in autism is is is reduced.
35:18
Okay. You know, you can often see
35:20
The corpus callosum is a bit thin,
35:21
which is the big fiber network between the hemispheres.
35:24
And then you see these biomarkers of of mitochondrial dysfunction
35:30
are very commonly ~ observed. And so then we want to rewind that and we say,
35:35
okay, how do we deal with rather than fighting autism like a disease,
35:38
why don't we talk about restoring health?
35:41
What we want is a resilient child.
35:43
Okay, we want a resilient brain.
35:44
We want a brain that can adapt to a changing environment.
35:47
We want a child to be able to go into a new job.
35:50
Okay, and not be stressed out about it and and actually handle
35:53
the circumstances that are coming to them.
35:54
So the question is how do we build a resilient brain?
35:56
What is it biochemically and physically that creates a resilient brain?
36:00
And also we deal with our elderly patients.
36:03
As you get older, right, we all know have our parents,
36:05
and so all of a sudden their world gets smaller and smaller and smaller,
36:08
right? They less they like less,
36:09
you know, less novelty, they like less ~ you know,
36:12
they want things in a struct in a structured way.
36:15
Anything new causes them stress.
36:17
Same exact concept happens
36:19
late in life as it does early in life when people have when we lose
36:23
the resilience of our brain to handle new things.
36:26
And so so we won't once we understand how resilience is built,
36:30
and it's built slowly, right? Like all of us.
36:34
Like, you know, the things that stressed me out when I was 17 don't stress
36:36
me out now. I've ha it's happened to me a few times.
36:38
So I've been there, done that,
36:40
lived that, and so I've built up resilience.
36:42
And so every time you you are faced with a circumstance that is overcomable.
36:47
That's the critical thing.
36:49
Okay, that you have to have a stress event that you can actually overcome.
36:53
And you slowly build up resilience through that and through experience.
36:57
However, if you are put in a circumstance that is beyond your capability
37:01
to overcome, then you get depression and anxiety.
37:04
Okay, and we create this in animals.
37:05
So if I if I want to create a depressed animal,
37:08
it's very we have a very standard mechanism.
37:10
It's called so what you do is you take ~ a pool,
37:15
right, and you make it opaque,
37:17
like you make it milky so.
37:18
the the mouse or the rat can't see the pads and say you make nine a square
37:23
of of nine squares and you put electricity in all those squares.
37:27
And what you do is you you leave one square without any electricity,
37:33
a safe square. And the animal will gradually find the safe square.
37:36
And they'll get better at it. And so they'll learn.
37:37
Okay, they'll get faster and faster.
37:39
They'll still they'll get zap,
37:40
zap, zap, they find the safe square.
37:41
And then you you wait a day or you do it again and they find it faster and faster.
37:45
Well then what happens if you do that?
37:48
And then you finally take away the safe square and you make them all electrical.
37:53
And so it's unavoidable stress.
37:54
And so when you create an unavoidable stress situation,
37:57
you create depression. And your brain shuts down ~ because it
38:02
it learns how it it puts itself into a protective forgetting mode.
38:08
And this is what post-traumatic stress will do and and these things will people,
38:12
you know, people think, you know.
38:14
memory is good, but our ability to forget is just as important as
38:17
our ability to remember. Like we have to if we if we can't forget certain things
38:20
in our life, we would totally destroy ourselves.
38:22
So anyways. What a wonderful So resilience is what we want to talk about.
38:22
Yeah. No, absolutely. my God. What what a wonderful kind of again changing.
38:28
Yeah. What a wonderful way of like looking at things from from
38:28
Yeah. Yeah. What a wonderful way of like looking at things from from different
38:33
a different angle again. And and we're gonna be focusing on building the resilience.
38:34
people again. And and we're gonna be focusing on focus.
38:37
And that's
38:37
the other critical last thing on that point is like we forget,
38:40
like we we we start mothering or
38:42
we're par overparenting our children and our adults.
38:44
Yes, sure. Yeah.
38:45
Okay. Because
38:46
then once you start fixing the brain and you start getting resilience,
38:49
you gotta let them go play with their brain,
38:51
right? And you got the the the when you're a caregiver of a dementia patient,
38:55
right, and you start restoring their resilience,
38:58
well you gotta let them go make a cup of coffee and make a mistake every
39:01
now and then. Like you actually have to put them in an environment
39:03
to to relearn these things. And sometimes we get ~ so protective that when
39:08
we start r restoring resilience,
39:11
then
39:11
we're so scared that we're we're overly protective.
39:14
And so we wanna kinda it's our job to carefully manage their,
39:18
you know, reentry into the world around them.
39:23
And as they do that, ~ they get stronger and stronger and stronger.
39:27
Absolutely. As long as they have the raw materials to build adaptation,
39:29
does they have all materials to build adaptation.
39:32
which in turn will
39:33
give them that resilience. So we're going back again to you know
39:35
So we're going back again to maybe downstream
39:37
the downstream reasons to
39:39
be able to even build that that which is amazing.
39:41
But just before we go a little deeper into autism specifically,
39:43
A little deeper into autism specifically.
39:45
I'd love to give everyone listening the same reminder I give
39:45
I'd love to give everyone the same reminder.
39:48
on every clinical episode
39:48
I guess every clinical.
39:49
biohacking. Autism is educational.
39:51
Nothing in this conversation is medical advice or a treatment plan for your child
39:52
Educational, nothing in this conversation is medical advice or treatment
39:56
for your child or
39:56
or for you.
39:57
for you, use it to ask better questions with your own practitioner.
39:58
Use it to ask better questions with your own practitioner.
40:02
So this is where I'd love to spend some more time because our audience
40:02
So this is where I'd love to spend some more time because our audience
40:06
has heard a lot about acute inflammation,
40:07
has heard a lot about inflammation,
40:09
mitochondria, but much less about myelin and white matter.
40:10
mitochondria, but much less about violin and white matter.
40:13
So can we talk and you mentioned it a little bit for 2009 autism research?
40:13
So can we talk? And you mentioned this a little bit,
40:16
2009 autism research.
40:18
~
40:19
what did you find? And you talked about finding some patterns.
40:19
~ what did you find and you talked about finding some pattern.
40:22
So what did you find in the phospholipid?
40:23
Right. So what did you find in the phospolipid
40:25
patterns and how did that lead you to the mitochondrial dysfunction hypothesis?
40:26
patterns and how did they lead you to the mitochondrial dysfunction hypothesis?
40:31
So did you first find the phospholipid patterns and then extrapolate that into
40:32
So did you first find the phospolipid patterns and then extrapolate that into
40:38
mitochondrial dysfunction?
40:39
mitochondrial dysfunction?
40:40
Correct. So the mitochondrial dysfunction part.
40:42
So you have in your cells you have these two main energy organelles.
40:47
One is your mitochondria.
40:49
And the other one's peroxisomes.
40:50
So your peroxisomes are basically anabolic.
40:53
They bake they make things. They make plasmalogen,
40:55
they make your cholesterol building blocks,
40:57
and so on and so forth. Your mitochondria are your energy cells,
41:01
and they are supposed to be clean energy.
41:03
Hydrocarbons go in, carbon dioxide,
41:06
water, and ATP come out, basically,
41:08
right? It's supposed to be this super clean energy.
41:10
And so what happens then is it's a closed system.
41:13
So if mitochondria function gets impaired,
41:16
Then other parts of the cell have to start picking up the slack
41:18
and things get moving into other areas.
41:20
And so we had we went through a whole big chain train of thoughts.
41:23
Like, so there's certain diseases of children that have virtually
41:28
all genetic diseases have autism-like symptoms.
41:30
So children with a mitochondrial,
41:32
like a genetic mitochondrial defect,
41:34
will often have mitoch autism symptoms.
41:37
X-linked ALD. Okay, so again, autism is highly male-dependent,
41:41
right? There's a three-to-one ratio of boys versus girls.
41:44
And so we have certain genetic diseases that only affect male children,
41:48
like X-linked adrenal liquid dystrophy,
41:50
right? And those children can't,
41:52
as a proxomal disease, they can't make they can't process these very long chain
41:56
fatty acids. So very long chain fatty acids are elevated in autism,
41:59
for example. So we started looking at,
42:01
well, maybe there was a partial gene suppression of XALD,
42:06
which turned out to be not the case in autism,
42:08
by the way. So so you look for a lot
42:10
Yeah.
42:10
of things and some things work and some things don't.
42:13
So it turned out to be this really this environmental,
42:16
you know, generic mitochondrial stress,
42:19
probably caused by inflammation.
42:21
And so we can see, so we can track our way backwards.
42:24
So what metabolomics allows us to do is versus genetics.
42:28
So metabolomics is reading, is actually measuring the cars on the freeway.
42:32
It's not actually
42:33
Okay.
42:33
measuring the freeway. It's like when you're when you're on Google Maps
42:36
and you're driving and it's showing the traffic jam up ahead,
42:40
it's doing that by measuring how many.
42:42
car how many cell phones and how how fast the cell phone signals are moving.
42:46
So it's actually doing exactly that thing.
42:48
And so Google Maps is exactly so Google Maps was telling,
42:48
So that's metabolomics.
42:52
okay, there's a there's a blockage up ahead because these cars aren't moving.
42:56
Metabolomics works the same way,
42:58
but using biochemical markers.
43:00
And so then you can say, okay,
43:01
so if there's a if there's a traffic jam,
43:04
sooner or later people stop taking the freeway and they go on side streets.
43:07
So all of a sudden you see a whole bunch of cars on streets that
43:11
normally don't have cars on them.
43:13
And so, well, what's going on with these things?
43:15
And so you can trace your way back to where this ultimately where where
43:19
the actual ~ damage is to the the freeway structure.
43:24
So in autism, these ~ very long-chain fatty acids,
43:28
elevated DHA levels, so this these molecules very clearly indicated that
43:33
mitochondrial function was impaired.
43:34
And that the body was shifting a whole bunch of molecules into peroxisomes.
43:39
And so
43:40
It showed that there was a mitochondrial defect because we there
43:43
was this disproportionate ~ molecular flow through peroxisomes.
43:48
So that's how that molecu that was that was designed.
43:50
Disproportionate as in too much.
43:51
Too much. Well, it's gotta go
43:51
Too much.
43:54
in, right? Like what like your your body is somewhat closed.
43:59
Like it's gotta find a these the the molecules that go into your cell have
44:02
The right. Right. Mm-hmm.
44:03
to find a place
44:04
to go. And so that's how that was able to track down
44:07
to the mitochondrial perspective.
44:08
Then you say, okay, what's causing this mitochondrial dysfunction?
44:11
Which is the next phase, right?
44:12
It's like, is it a genetic disease?
44:14
Is it, you know, obviously, you know,
44:16
there's some trend through through the through the maternal lines,
44:20
because you know, all your mitochondrial DNA is maternal DNA.
44:23
Yeah.
44:24
And then the but ~ but no, it really was so now we get to what's causing this
44:30
mitochondrial stress is most likely neural inflammation.
44:34
Okay, so neural inflammation, so what allows you to
44:38
So, multiple sclerosis is probably the most classic ~ white matter neuroinflammatory
44:43
disease. And you'll notice that the gender bias in multiple sclerosis
44:47
is the opposite of that of autism.
44:49
Yes. It's more women. Yeah. Mm-hmm.
44:50
And so basically,
44:53
girls who don't get autism get MS.
44:55
So beta-esterdiol is an incredibly powerful ~ neuroprotectant.
45:01
And it's primarily a mitochondrial enhancer.
45:05
It's why women
45:07
Have much less diseases
45:07
Real.
45:08
than men until they get to menopause.
45:10
Then after menopause, all the things that kill us men start killing the women.
45:14
And it's because they lose the estrogen protection that they've had over that that
45:17
Yeah. You get heart disease and Alzheimer's.
45:18
th those decades. Right.
45:21
Yeah.
45:21
Exactly.
45:23
And so those are the things that we deal with.
45:24
So back to this concept now. So okay,
45:26
so there's mitochondrial stress.
45:27
Where is this mitochondrial stress coming from?
45:29
Okay, there could be some inherent inability,
45:32
there could be nutritional deficiencies,
45:34
and there could be environmental stress loads.
45:36
Okay, so all these things add to one one level.
45:39
And then this mitochondrial this this inflammatory syndrome is creating a load.
45:44
So for example, all of you, all of us,
45:46
anytime you have fatigue, it's mitochondrial related.
45:49
So when you get a flu, for example,
45:50
and you're tired, right? You say the flu wears you out.
45:53
Well, that's because your body,
45:55
the mitochondrial capacity of your body is being used to fight
45:59
and support your immune system and your your inflammatory response.
46:03
And it doesn't have enough left over.
46:05
For all the other things of your body.
46:07
And so that's kind of what happens with autism in the brain.
46:10
You don't notice it that way. So it's the brain fog,
46:12
other issues, and so it's just not able to do two things at once.
46:17
It can't actually perform the function.
46:20
So that's why neural inflammation is ubiquitous in autism.
46:24
And now the question is why does neural inflammation persist in some children
46:28
and not in others? Because clearly everyone gets some neural inflammation.
46:32
Even healthy children are going to have.
46:34
a bad reaction to something and then they recover.
46:36
And the question will be then,
46:38
the children who recover have mitochondrial resilience and they have other,
46:42
you know, ~ ways of overcoming it.
46:45
So I take, you know, you get a mold infected school and say,
46:48
wow, there's a school, there's a high rate of autism in this school,
46:51
and it was linked to mold infestation.
46:53
Well, not every child got autism in that school.
46:56
So many children with this exact same exposure level are getting better.
46:59
And this is what what what is my pet peeve is we we always focus on the bad thing.
47:04
We always focus on here's the child with autism,
47:05
here's but what about the individuals that are experiencing the same level
47:09
of environmental stress, but they're surviving and thriving in it?
47:13
We should be learning from those individuals,
47:16
okay, and and applying the knowledge from those that level of resilience and say,
47:20
how did how why is that person performing so well versus someone else?
47:24
And then can we transfer the knowledge of resilience from resilient individual
47:30
to people that are susceptible?
47:32
Because the susceptibility is is simp is not it's not an inherent thing.
47:37
It's it's just ~ it's biochemical math,
47:41
it's biochemical engineering. So that's what we're basically biochemical engineers
47:44
at this point in time. So we can restore the body's ability to
47:47
to perform its function. And every person is different.
47:50
So that's why we've created this whole model of self-directed research.
47:53
Like you can't and this where our our neurosupport program with autism
47:58
and and and other programs, where families,
48:01
they
48:02
can evaluate how they're doing.
48:04
Because each child is going to be different,
48:05
circumstances are unique. And as we build communities of individuals who
48:09
are able to discern these optimal outcomes is better.
48:16
And we've learned as a you know scientist,
48:18
and I fall in that category, I get that trap,
48:21
we overthink things sometimes.
48:22
Sometimes we, you know, too much knowledge can drive you crazy sometimes.
48:27
So sometimes the simple solutions really work.
48:30
And what we found a lot
48:31
Is that this myelination, you know,
48:33
clearly eliminates many negatives.
48:34
Yes. Okay.
48:35
You know, the methyl transfer
48:36
system is another big thing for kids,
48:38
you know, but clearly what we're noticing is when you give them myelination support
48:44
in the form of plasmalogen precursors,
48:46
it it it's quite beneficial. And sometimes children all they need is that.
48:50
And sometimes they'll need more.
48:51
And so we've kind of I've learned over the years to not overthink as much anymore
48:57
start with the simple stuff and then gradually get more complicated as you need to.
49:01
Yeah, build on success, cumulative success.
49:01
Yeah, build on success, cumulative success.
49:04
And because other than of course the mitochondrial issues,
49:05
And because other than of course the mitochondrial issues,
49:08
what you've seen is impaired myelination probably as a result
49:08
what you've seen is impaired myelination probably as a result.
49:13
Well, and let's see,
49:13
of the mitochondrial issues.
49:15
and we look at but and we look at all these different studies that have been done.
49:18
The ones they all have different levels of work.
49:20
Like acetylcarnitine. So carnitine has success rates in autism,
49:23
right?
49:24
What does it do? It improves
49:24
Yeah. Mitochondria
49:25
mitochondrial function. People think it improves the transfer of fatty acids into
49:29
the mitochondria, but it also actually sucks out excess acetyl-CoA.
49:34
So it acts as a buffer. And acetylcysteine imp improves your glutathione levels,
49:39
your B12, methylfolate, betane,
49:42
trimethylglycine, these things all have had positive effects because that those
49:46
are issues that are are generally affected.
49:48
So you can see from this smoke,
49:51
there's a fire in the center.
49:53
And the in the the fire in the center of the smoke is this mitochondrial function.
49:56
And then the question is, what is this,
49:57
what is this, what is this impaired mitochondrial function stopping
50:02
the brain from doing? And so what we're doing is basically saying,
50:04
okay, let's just help out and carry and and add some load on the back end.
50:09
And ~ and then sometimes if you just do that,
50:12
you've you've you've reduced the load and they have more than sufficient
50:17
mitochondrial function for everything else.
50:19
No, that that's amazing. And that brings us to something that I would love
50:21
Amazing. And that brings us to something that we'd love to look
50:23
to look at from two different angles.
50:24
at from two different angles. One is preconception health and the other
50:25
One is preconception health, and the other one is an explanation of what happened
50:28
one is an explanation.
50:30
to people with autism. So you connect early brain development,
50:32
So you connect early brain development,
50:35
but also breastfeeding and plasmalogen precursors.
50:36
also breastfeeding and plasmalogen and precursors.
50:38
So what do you think the data is telling us?
50:39
So what do you think the data is telling us and what should we hear that without
50:41
And what should parents hear that without without turning it into blame?
50:45
without turning it into blank and now we're talking about mitochondria
50:46
Because now we're talking about mitochondria coming from the mom.
50:49
something long and of course breastfeeding?
50:49
And of course breastfeeding as the mom also.
50:51
Well
50:52
it's basically health. I it's common sense if you think about it,
50:55
right? And so you're gonna have not all mothers are gonna be same,
50:57
okay? Not all mothers gonna have the same environmental,
51:00
you know, diet.
51:02
background and so on and so forth,
51:04
clearly, okay? ~ either e during during during the the ~ the pregnancy phase
51:09
and during early childhood development.
51:11
And so one of my big passions on this is once we understand the development
51:14
of the brain, we have a community program in Moose Jaw,
51:17
Saskatchewan, Canada. I I provide free services to the entire city.
51:21
And the pro one of the projects we'll be launching early in fall,
51:24
we just got a big clinical tri clinical study approval.
51:28
So we have a large epidemiological
51:31
tracking study been approved just last week and we'll be able
51:35
to track changes across the spectrum of health.
51:37
But my personal belief is that if we focus on maternal health,
51:42
okay, especially in so that the the the child during development in
51:46
the womb has sufficient materials,
51:48
like the plasmalogen ~ precursors in pregnancy,
51:52
for example, because we know it's a it's a heavy metabolic load.
51:55
And obviously maternal health is is critical for that.
51:58
And then
51:59
Also early childhood development,
52:01
then the breastfeeding support.
52:04
So children moms that take plasmalogen precursors will have more plasmalogen
52:08
in the breast milk and improves brain development in children.
52:11
I strongly believe if we do these basic things,
52:13
we can reduce, if not eliminate,
52:15
most ca most autism cases. And what I want to be able to prove,
52:19
you know, epidemiologically, is that if we can interact with a community
52:23
of 35,000 people that have a couple hundred kids per year being born,
52:27
that we can actually within a couple years show that.
52:29
If we do basic things, that there are no new cases of autism in in a whole city.
52:34
Okay. So we can show people that this is not that complicated.
52:37
We've created comp we've created the complications because we've we've
52:41
we strayed away from just restoring health and we're we're focusing
52:44
Right. That's it. That's it.
52:45
on fighting disease. And that's
52:47
kind of where we're at. So in terms of maternal health,
52:50
then that's also gonna help the moth the the health of the mother because
52:55
you know supporting a developing infant is metabolically demanding.
52:59
know, mentally and physically demanding of of that of the mom.
53:03
And so I think anything we can do to more scientifically and more strategically,
53:09
because clearly maternal health,
53:10
we all know it's important, right?
53:11
And every mom knows that. And so they're already they're already doing certain
53:15
things. But are we doing enough?
53:18
Are we are we applying enough scientific knowledge?
53:20
We we have more scientific knowledge about personal health and infant health than
53:26
we're actually applying into the field.
53:29
And this is one of my I say this all the time.
53:31
We don't lack scientific knowledge.
53:33
Like I'm I'm a scientist, but I'm just one of thousands and thousands
53:36
of scientists who've who developed,
53:38
invented, observed, you know, published amazing results over decades
53:43
and decades and decades. It's not that we don't know what's going on.
53:47
We just don't apply this knowledge effectively.
53:49
And this is what we need on the community model of actually understanding
53:53
how do we take the knowledge that we actually have and actually start using it and
53:59
engaging communities in a manner that they see the benefits from it,
54:02
right? Because people need to see it can't be just some theoretical project.
54:06
They actually have to feel better and see positive outcomes
54:10
and get reinforcement through that process.
54:13
And so I think that's kind of what my personal mission is at
54:17
the Moose Jaw Vitality Project is to understand how can we make change
54:23
in a community that's that's that is lasting.
54:26
~ and that's
54:28
You know, because then that's dealing with real people.
54:29
Like, you know, we're on a podcast,
54:31
like we're we're already like the the people that we reach on a daily basis,
54:36
that's not everybody. Okay, people are busy with doing their own things
54:39
in their own world, and they're localized.
54:41
And so we we do need to be in local environments and and really interacting with
54:46
people at the community level to to really get
54:52
the the educational change ~ and then the observational change in time.
54:57
Yeah,
54:57
and and thank you for going into application because frankly we can't wait.
54:58
Thank you for going into application because frankly we can't wait.
55:02
I mean, yes, science is great and we can definitely go into the art of the science.
55:03
I mean, yes, science is great and we can definitely go into the art of the science.
55:07
It's wonderful. But we're here with these kids and their lives are moving
55:08
It's wonderful. But we're here with these kids and their lives are moving
55:12
on and and they're just not adapting.
55:13
on and and they're just not adapting,
55:14
They're not resilient. So yes,
55:15
they're not resilient. So yes,
55:16
thank you for doing that and talk about the proof of concept.
55:17
thank you for doing that and talk about the concept.
55:19
Congratulations about the the approval for the trial.
55:20
Congratulations about the the approval for the trial.
55:22
That's amazing. And also
55:23
That's amazing. Also
55:25
Yeah, my God, that's so great.
55:26
Yeah, my god, that's so great.
55:27
We'll we'll definitely keep up with that.
55:28
We we'll definitely up with that.
55:29
And you also have a NeuroSupport program.
55:30
And you also have a neural support program.
55:33
~ and it's a strong parent reported ~ program
55:34
~ and it's a strong parent reported ~ program
55:39
and we've had amazing responses to ~ that program.
55:39
and we had amazing responses to ~ that program.
55:43
So what outcomes were tracked in that program?
55:44
So what outcomes were tracked in that program?
55:46
How was improvement defined? What have you seen so far?
55:47
How was improvement defined? What have you seen so far?
55:50
Because you had all kinds of different ages and are you planning another study
55:51
Because you had all kinds of reasons.
55:53
Exactly.
55:53
of court?
55:55
Well, again, what I I always like to the scientist in me
56:01
and the clinical researcher in me looks at these validated scoring systems.
56:06
Okay. And I think everyone has to realize that when you enter
56:09
an actual formal trial, like our trial is a observational trial.
56:13
So we're we're basically watching,
56:15
okay, and we're interacting, but we're not dictating.
56:18
We're not saying, hey, take this supplement or take this drug.
56:22
Okay, it's not an it's not an inter interventional trial.
56:24
It's an observational trial, right?
56:26
And so people make their own decisions about their their life and their involvement.
56:30
And we're just, we're we're the bookkeepers.
56:33
Okay, we're tracking that information and drawing associations between these things.
56:36
Because what we do is restoring health versus back my old life
56:42
in the pharmaceutical industry,
56:43
where we're actually humans are basically lab animals to test my drug,
56:46
right? Like you're not, we're not really,
56:48
and this is hard for people to understand this.
56:49
Like when you when you enter a clinical trial,
56:52
It's not about you. Okay? It's about you know creating a very structured inclusion
56:58
and exclusion criteria to validate a particular molecule or drug
57:03
for a particular purpose, right?
57:05
And people are chosen very specifically to meet a certain endpoint.
57:09
So you are nothing more than a lab rat in a clinical trial.
57:13
Sorry to say that. That's just that's just the way it is,
57:15
right? So but we're in the when we're dealing with restoring health,
57:18
it's different. It's not about
57:20
the drug or the intervention anymore.
57:22
It's about the person and their health and the restoring their health.
57:25
And so we like to start with open-ended questions.
57:27
So what is, you know, my first thing I always ask parents is if there's
57:31
a couple things that would happen in your world,
57:34
okay, what would make your life better?
57:36
Okay. One would say, well, if I could just get my child in the car seat
57:40
in the morning, my life would be dramatically better.
57:42
Right. And so or or you know, there'll be actual things.
57:46
If I if I can get him to stop beating me up and my and his sister up.
57:50
that'd be great. So the aggression,
57:52
sleep, you know, outbursts, those things,
57:55
~ you know, so social emotion back.
57:58
So those, you know, man, if if my son would just give me a hug,
58:02
that would change my life, right?
58:04
Like those are the things that I want to hear about,
58:06
right? And so those are things that cause and then they're subtle.
58:09
You can't really put them on a score card,
58:11
right? And that's kind of what that's what I want parents to talking
58:15
and thinking about. So when we see our biggest observations are
58:19
Sleep improves dramatically, is generally speaking.
58:21
So sleep is a dramatic improvement.
58:23
We typically see gut function and their immune system gets better.
58:26
But sleep, aggression is one of the first things that go down.
58:29
Very quickly, they stop being aggressive.
58:32
Because the aggression is frustration.
58:34
It's mental frustration, right?
58:36
And they can't interact with their world.
58:38
The world is just driving them crazy.
58:40
And it's neural inflammation. And so we see aggression reduced.
58:44
And then we eventually start seeing ~ this
58:48
More social interaction. They start becoming more aware of things
58:51
in their surroundings. They start noticing the cat.
58:53
They start noticing things in their environment more.
58:56
Things that they just normally just walk by and don't even pay attention to.
58:59
And so they start seeing, ~ they're interested in things that they weren't
59:02
interested in before. And then they start having some interactions with
59:06
and they start wanting social feedback.
59:10
Okay. And so they start looking at it.
59:12
And then eventually they start doing,
59:13
depending upon and because each child is going to have different levels of.
59:18
of like it's a very large spectrum as we all know.
59:21
And often what happens then is people they start doing role playing,
59:27
which is a big deal, right? Which is the hard thing with children with autism.
59:29
You would
59:29
They don't they don't play
59:31
in a certain way. They don't they don't mimic and they don't you know
59:33
and so once they start mimicking things,
59:35
and then they start, you know,
59:37
there'll be some and they start doing some testing.
59:40
So sometimes you get a little bit of acting out,
59:42
but more the acting out is really them typical,
59:44
Typical. Normal,
59:46
exactly.
59:47
Those are the things that we start seeing in in families going forward.
59:47
yeah. Mm-hmm.
59:50
And then they start,
59:51
you know, getting more involved in the world around them.
59:54
And they think it's important
59:55
that's fun.
59:57
for the parent to recognize what's important in their world rather than because
1:00:01
often when we do a lot of this clinical research,
1:00:03
we force the parent into our square peg,
1:00:07
okay? Very specific things. And r we
1:00:08
Agreed. Yeah.
1:00:11
don't want to do that. We want to basically say,
1:00:12
you know, and
1:00:15
Because I don't know a lot of papers they've been they've been through the ringer,
1:00:17
right? They've been through ten doctors,
1:00:18
they've been here and there trying to get diagnosis.
1:00:20
And it's important to get a diagnosis so they can get certain,
1:00:23
you know, support services and a bunch of other things,
1:00:24
Yeah. Right.
1:00:25
right? So there's just there's some logic to that.
1:00:27
But then they'll
1:00:28
often come to the situation with the with a medical mindset.
1:00:31
Okay, I've got a diagnosis of my child.
1:00:33
I've got ~ I've got they come with their their their pseudo-doctor cape on,
1:00:39
right? Which they've actually become an expert,
1:00:41
right? All these parents have become experts.
1:00:43
in their child's health, which is great,
1:00:46
and especially with our rare disease program,
1:00:48
like that's another on the more extreme side of situations.
1:00:51
But really try to bring it back to,
1:00:54
you know, what are the what are what are the things that are improved quality
1:00:57
of life? And if you start there and you start building upon that,
1:01:01
~ then first of all, you're not labeling anyone,
1:01:04
you're just trying to get resilience.
1:01:05
You're just trying to improve the outcomes in in their daily lives.
1:01:08
And then then and then you take a change.
1:01:12
And I always
1:01:13
The other thing I tell people,
1:01:14
ultimately it's about time and the trajectory of time.
1:01:18
And if we can change the trajectory of your life to where things
1:01:23
are getting better versus getting worse,
1:01:25
then as things get better, you calm down and let time take its place.
1:01:29
I can't turn a two-year-old into an eight-year-old without six years
1:01:32
of brain development. Okay, so the question is is getting a child back onto
1:01:36
the neurodevelopmental pathway,
1:01:37
okay, the brain can only develop at a certain rate.
1:01:39
And our challenge is to change that trajectory.
1:01:44
Then then time is on your side.
1:01:45
Okay, so you say, okay, this is I'm I'm seeing slow,
1:01:48
steady improvement. And if I just keep doing what I'm doing,
1:01:52
I'm gonna be I'm gonna be adding to my my my psychological savings account over
1:01:56
time. And in and get to a point where ~ life
1:02:01
is livable as is, and then each time you you you know you set your baseline
1:02:07
and you reset your baseline and you reset your baseline,
1:02:10
and not ~
1:02:12
put it not to put a judgment scale of anyone else but your own child
1:02:16
and say what what are the what are the different steps.
1:02:18
And you know most parents are of course are in that headspace anyways.
1:02:21
Yeah. Yeah. No, no, this is great.
1:02:21
So that's exactly great.
1:02:24
And this is giving parents, I'm hoping that everybody can see
1:02:25
And this is giving parents, I'm hoping,
1:02:27
that everybody can see it sounds complicated when we're talking about
1:02:28
it sounds complicated when we're talking about it like this,
1:02:31
but it's
1:02:31
actually very simple. It's just again giving the brain the raw materials
1:02:34
Just again giving the brain the raw materials to do all these very complicated
1:02:36
to do all these very complicated things
1:02:39
things
1:02:40
on its own.
1:02:41
on its own, basically. And then the brain can start building pathways
1:02:41
Basically, and then the brain can start building pathways
1:02:44
and resilience and adaptation,
1:02:45
and resilience and adaptation,
1:02:46
which is amazing. So I would love to move now to the second track
1:02:47
which is amazing. So I would love to move now to the second track of this podcast,
1:02:50
of of this podcast, because this part is about the parents too.
1:02:53
because this part is about parent too.
1:02:55
And I always want the parents to remember that.
1:02:56
And I always want the parents to remember that I need my brain to lie.
1:02:57
So I need my brain to last. A lot of the people listening to this show
1:03:00
A lot of the people listening.
1:03:03
are in their forties, fifties,
1:03:03
This show are their 40s, 50s, 60s,
1:03:04
sixties, and beyond, raising and supporting someone who may need them
1:03:06
and beyond. Yeah. Raising and supporting someone who will need them for decades,
1:03:09
for decades who will.
1:03:10
We'll need them for decades. So can you take us through the aging brain
1:03:11
who will need them for decades.
1:03:12
So can you take us through the aging brain and what have you learned from data about
1:03:15
and what have you learned from the human data about plasmalogen plasmalogen
1:03:19
ethnology and and cognitive
1:03:19
and and cognitive decline?
1:03:21
decline? Yeah, so so on the brain decline phase.
1:03:26
So at w at our center in Moose Jaw,
1:03:29
Canada, we have a a a f a facility that people actually come
1:03:32
And stay there for several months at a time.
1:03:34
And our we call it basically boot camp.
1:03:37
It's a rehab model where people come,
1:03:39
their caregiver and the patient,
1:03:41
you know, their their the the the the dementia person and their caregiver would come
1:03:45
together because people create this codependency over time.
1:03:49
And we want to create a novel environment.
1:03:51
So when people their homes, they they know where their coffee machine is,
1:03:54
they know where everything is.
1:03:55
So everything is actually too comfortable and too normal.
1:03:59
And we want the caregiver to get some separation from the dementia
1:04:03
c ~ client for their own health,
1:04:07
restore their own health because they're gonna be in that stage age category
1:04:10
as a general rule, whether or whether slightly younger if it's you know,
1:04:14
like if it's a ~ a child. Then once they get some space,
1:04:20
then we we s restore the health of both.
1:04:22
We find a lot of people that are just at that stage,
1:04:25
they're like I'm you know, we're
1:04:28
I'm one month, two months before putting my my wife or my husband into long-term
1:04:32
care, because I just can't take it.
1:04:33
I'm I'm I'm almost killing myself right now,
1:04:36
right? They're at that stage, right?
1:04:37
And they don't want to do it, but you know,
1:04:39
they're they're they're dying on the vine themselves at this point in time.
1:04:43
And so we bring them in, ~ create some separation,
1:04:46
gets get the caregiver back into more of a healthy routine,
1:04:51
their brain health improved. And then the dementia patient.
1:04:54
Okay, or client, we we obviously we we we're not we're not a medical facility,
1:04:58
so our our individuals are clients of ours.
1:05:01
The they then get the restorative program,
1:05:06
but also other tools in their environment to start working on.
1:05:10
And they get some independence,
1:05:11
and then there's a novel environment.
1:05:13
So they have to kind of learn where the bathroom is and where the room
1:05:15
Adapt, right? Mm-hmm.
1:05:16
is and where and so you're
1:05:17
actually forcing their brain into this waking up adaptive space.
1:05:20
And that
1:05:21
Mm.
1:05:22
the combination of the biochemical support.
1:05:24
Plus the the environmental stimulation really enables them
1:05:29
to start improving dramatically.
1:05:31
~ and we see that quite extensively.
1:05:33
Same thing on the on the on the family side.
1:05:36
So obviously on the autism, there's a lot of aut you know,
1:05:41
adults with autism, right, that are in relationships in their with their parents
1:05:45
and their parents are now getting older because you know their their their autism
1:05:49
child is in their thirties, for example,
1:05:50
right? And ~ and kind of build that independence.
1:05:54
And find ways in which the autism client can gradually
1:05:59
get more tasks that they can overcome and they become more independent
1:06:06
and get some separation between them.
1:06:08
And that's the hardest part because this codependency kind of creeps
1:06:10
in and people get frustrated, they don't have time,
1:06:13
they don't have you know, it's they've kind of created a a
1:06:18
a structured environment that is survivable.
1:06:20
And I treat each of these things as trauma.
1:06:24
Right. The dementia patient knows they're losing their memory.
1:06:27
Okay.
1:06:27
Yeah.
1:06:28
They understand it. They they they are frustrated by it.
1:06:30
They know they need they're becoming dependent and they haven't been dependent
1:06:34
before. Same thing happens with ALS.
1:06:36
We do we we just did a big ~ open house on ALS last Saturday.
1:06:41
It's the same thing. And it's even worse in ALS because it's it's happening with
1:06:45
people much younger, but they realize they're becoming dependent.
1:06:48
And the person who's caring for them,
1:06:49
there's gonna be guilt associated with you know how much work someone
1:06:52
has taken care of them for them.
1:06:53
And vice versa. And so you want to get that create this mutual independent
1:06:58
relationship again. Each person needs to feel valued in that relationship.
1:07:02
Okay, the caregiver needs to be respected for what they're doing,
1:07:05
but also have they can't be comp their their entire human identity can't
1:07:09
be tied up in their in their caregiving status.
1:07:13
And then the the dementia patient also has to start creating some level
1:07:17
of independence of what they can contribute to the relationship and
1:07:20
and feel valued and useful in that situation.
1:07:23
Of
1:07:23
course. Yeah. It's traumatic.
1:07:23
We'd able to it's a it's traumatic.
1:07:25
It's also traumatic when people start remembering traumatic Yeah,
1:07:27
Yeah, it's traumatic, but it also complicates things if now the caregiver
1:07:29
it's traumatic but it also complicates things that the caregiver is
1:07:32
is the one that ends up with Alzheimer's.
1:07:33
the one that ends up with Alzheimer's.
1:07:34
Now you have somebody that's starting to develop Alzheimer's
1:07:34
So you have somebody that's starting to
1:07:36
caring for someone with autism.
1:07:38
I mean, talk about a horrendous situation,
1:07:41
but you know, it's not that impossible.
1:07:44
It's very, very much possible,
1:07:47
unfortunately. But
1:07:49
That's why I wanted to talk about Alzheimer's.
1:07:51
And and right now, the only things that we typically hear about
1:07:54
for Alzheimer's are two things.
1:07:57
Two two things. One is genetic that equal e4.
1:07:57
One is genetic, the ApoE4. ~ and then the other thing that we always hear about
1:08:00
~ and then the other thing that we always hear about there Lloyd Black and then Tao.
1:08:03
are amyloid plaque and then tau.
1:08:06
What are your thoughts on on these three things and also their connection or yeah,
1:08:07
What are your thoughts on on these three things and also their connection or yeah,
1:08:12
their relationship with plasmalogen and phospholipids?
1:08:13
their relationship with plasma and phospholipids?
1:08:17
Yeah, so this is where science really messes with people's minds.
1:08:20
Okay. When it comes to dementia and reduced cognition,
1:08:24
there really is only one thing.
1:08:26
None of them matters. It's age.
1:08:28
Age is it's the aging brain. Okay?
1:08:32
And this is we so typically we start seeing dementia you know creeping
1:08:36
up in one percentage of people in the 60s,
1:08:38
then it gets to 3, 4% in the 70s,
1:08:40
and up to 30% of people in the 90s.
1:08:43
But if you actually cumulate it,
1:08:47
if everyone who had dementia in their 60s and 70s and 80s lived to age 95,
1:08:52
and so all everyone made it to age 95.
1:08:56
Eighty percent of the population would have dementia.
1:08:59
Eighty percent. Only twenty percent would not have dementia.
1:09:02
So so how can you actually talk about a disease that is
1:09:07
the preponderance of the entire human population?
1:09:10
Okay, so and so you get in so we stick about,
1:09:13
it's amyloid, it's plaque, it's whatever.
1:09:16
No, it's the aging
1:09:17
It's aging
1:09:17
brain and shrinkage. Okay, so and so these things so these worse.
1:09:19
My God. Okay. That's worse. Doctor Goodenowe,
1:09:21
Right.
1:09:22
because now you're saying that it's happening.
1:09:24
Okay, I'm
1:09:25
listening.
1:09:25
Okay. Dementia
1:09:26
dementia is a default. Okay. If you live long enough,
1:09:29
you basically get dementia, unless you have some mechanism.
1:09:32
So let's understand the aging brain and how the aging brain loses
1:09:36
its ability to function. And dementia is not a bacterial infection,
1:09:40
it's a functional activity. It's the ability to run a hundred meters.
1:09:44
Okay, so if I'm 30 years old and I can run a hundred meters at 15 seconds,
1:09:48
you know, not 10 seconds,
1:09:49
Okay.
1:09:49
you know, and then I'm and as I get older,
1:09:52
okay, instead of 15 seconds.
1:09:54
It's now twenty seconds, then it's twenty-five seconds,
1:09:56
then basically I need and so what you've you've lost the actual functional ability
1:10:00
to perform a task. Okay, cognition is a functional cap capability.
1:10:05
You can lose it, okay, early in life with with surgeries and in you know
1:10:10
pe women with breast cancer, right?
1:10:12
We call it chemo brain. So cognitive dysfunction,
1:10:14
okay, will happen in ~ multiple areas.
1:10:17
So so cognition is a functional capacity of the brain,
1:10:21
not a pathological issue.
1:10:24
We do have these pathological associations.
1:10:24
So that's why you lose. Okay.
1:10:26
Yeah.
1:10:28
And this loss of cognition is fundamentally the cholinergic system.
1:10:32
So the acetylcholine system of the brain loses its ability to perform properly.
1:10:37
And this cholinergic system has a couple critical components that require
1:10:41
cis you know the vitality.
1:10:44
One is the phosphatidylcholine,
1:10:47
the ability to make the the methyl transferase system,
1:10:50
and the other one is plasmalogens.
1:10:51
And ironically,
1:10:54
The methyltransferase system, when it gets dysfunctional,
1:10:57
the methyltransferase system causes phosphorylated tau to accumulate.
1:11:01
Okay, so all of the tau, the neurofibrillary tangles of the brain,
1:11:04
are caused by methyltransferase defects.
1:11:06
And all of the amyloid in the brain is caused
1:11:07
Which is called by yeah. Mm-hmm.
1:11:10
by plasmalogen deficiencies. Okay,
1:11:11
so these are a couple weak, these are a couple of the weak links
1:11:14
in in human biochemistry as it goes forward.
1:11:16
So when we want to again understand the functionality of the human brain,
1:11:20
cognition requires
1:11:23
couple things. requires the the colonergic system to work,
1:11:26
requires plasmalogens, you get the physically from the brain,
1:11:30
you get cortical thickness, cortical volume,
1:11:32
the the volume of the brain, prevent the shrinkage of the brain.
1:11:35
And so we now have advanced MRI technology that can clearly articulate these
1:11:39
changes. So people when they scientists when they look at dementia patients versus
1:11:44
they they try to do age matching.
1:11:45
So you're gonna have this decline phase in the average population
1:11:48
and then you're gonna have this decline phase in the dementia population.
1:11:51
And the dementia population will have this minor accelerated decline.
1:11:55
So people, when we we call someone with dementia,
1:11:57
what we're calling is accelerated aging.
1:11:59
The ApoE4 genotype doesn't
1:12:00
Okay. Okay.
1:12:02
change how many people get dementia.
1:12:04
It changes when you get dementia.
1:12:06
So if you have an ApoE4 genotype,
1:12:08
you're you and so the curve gets shifted.
1:12:09
Early. Yes. Got it.
1:12:12
And so then when I say,
1:12:13
okay, if I draw a line at age 70,
1:12:15
I say, ~ because these people with ApoE4 were getting dementia five years earlier
1:12:19
than everyone else.
1:12:20
Well, when I go to seventy-five,
1:12:22
there's gonna be more of them.
1:12:23
So we can say, ~ and and and statistically it's absolutely true.
1:12:26
Statistically speaking, if you have an ApoE4 genotype,
1:12:29
you're gonna have twice the risk of Alzheimer's.
1:12:31
Okay, that's a mathematical certainty.
1:12:33
Yeah.
1:12:33
And same thing we talk about w women,
1:12:35
we'd say w women have a higher rate of dementia.
1:12:37
Well, they don't really. Okay,
1:12:39
they they get it earlier because of post postmenopause,
1:12:42
right? Because
1:12:42
Menopause
1:12:42
so a couple things with women.
1:12:43
So women have inherently lower levels of plasmalogens than men.
1:12:46
So if I if I take average levels of of of of
1:12:50
Plasmalogen levels in men versus women,
1:12:52
men will have higher levels. Same thing with muscle density.
1:12:55
Men will have typically higher muscle density.
1:12:56
So the creatin levels are higher.
1:12:58
And these are all protective in certain areas that men have protection
1:13:02
on muscle densities and other things that women ~ don't have as much of.
1:13:07
And so plasmalogen, but women have this other superpower,
1:13:10
which is called ~ estrogen. And so and the and it's been protecting them
1:13:14
in different areas. And so as they get older,
1:13:17
Men still maintain their plasmalogens for a little bit longer.
1:13:20
~ they never had estrogen in the first place,
1:13:22
so they never became dependent upon it.
1:13:24
Women who were became dependent on estrogen,
1:13:26
then they lose that dependency.
1:13:28
And everything else that happens post-menopause ~ creates this accelerated thing.
1:13:33
And so we see all these diseases in women,
1:13:35
like multiple sclerosis, you know,
1:13:37
relapsing or remitting, the transition from relaxing remitting into secondary
1:13:40
progressives happens post-menopause.
1:13:42
A lot of these things happen when ~ the
1:13:45
the human body, the female body has been used to a certain environment
1:13:50
and you've basically put it into a whole different environment all of
1:13:53
a sudden and said, you know, sink or swim basically.
1:13:56
And it it takes a while for it to figure out how to swim in this new environment.
1:14:00
So anyways, back to this whole concept.
1:14:02
So amyloid is caused pri by membrane dysfunction.
1:14:06
So when when you get lower levels of plasmalogens in your membranes,
1:14:08
amyloid levels accumulate. So we've I've published all this stuff
1:14:13
extensively on on on this issue.
1:14:15
So back to the d you know, restoring cognition in individuals
1:14:20
or preserving cognition in individuals,
1:14:22
we need to preserve these core systems that we've known since the seventies.
1:14:25
Like this is not new information.
1:14:27
Okay, we've known the critical component of the phosphatidylcholine system.
1:14:31
We've known the critical component of plasmalogens and this ~ membrane structure
1:14:36
for ~ many, many, many years. And so we just need to restore the resilience
1:14:41
and then your brain has a muscle.
1:14:42
We call like when you look at the muscles in your arms and your legs,
1:14:45
the brain muscle is called cortical thickness.
1:14:48
Okay, when you look at your head,
1:14:49
~ the the the outer edge of your brain is is your your cortex is so your
1:14:55
the gray matter is on the outside next to your skull,
1:14:57
which is where the largest surface area is.
1:14:59
Then we have gray matter inside these subcortical ~ structures inside.
1:15:04
But basically the outside of your brain is where all the activity is happening.
1:15:07
And it's it's six layers of cells called this cortical thickness.
1:15:11
So we measure 600 layers of cortical thickness.
1:15:14
And so we can see which areas are thinning.
1:15:16
Okay, so basically, if your biceps are thinning,
1:15:19
then your arms are going have less strength.
1:15:20
Well,
1:15:21
Right.
1:15:21
if the area of your brain, so different areas of your brain that start thinning will
1:15:25
correspond with different areas of your brain that have reduced function.
1:15:28
If my occipital cortex starts thinning,
1:15:30
I'm gonna have reduced fission.
1:15:31
And so we can map these things and we can understand where we're we're losing actual
1:15:36
physical structure of the brain.
1:15:38
And so we can start now we've
1:15:40
get to the point when we restore brain health biochemically,
1:15:43
we restore the resilience of the brain through biochemical interventions with
1:15:48
plasmalogen precursors phosphatidylcholine,
1:15:50
mitochondrial support, you know,
1:15:52
muscle support, the brain will regrow.
1:15:54
It it the the the you
1:15:55
So
1:15:55
can re you can rebuild the muscle of the brain.
1:15:59
So can you re-uh increase cortical thickness then?
1:16:01
Increase oracle. absolutely. Highly reproducible observation.
1:16:02
Re-increase it? that's amazing.
1:16:05
Okay. Okay. So all of this to me,
1:16:06
Okay, so all of this to me,
1:16:09
the the thing that I'm thinking right now is that basically everybody should
1:16:09
the the thing that I'm thinking right now is that basically everybody should
1:16:13
be working on their prevention of dementia,
1:16:14
be working on their prevention of dementia,
1:16:17
cognitive decline, Alzheimer's.
1:16:17
cognitive decline, Alzheimer's.
1:16:19
that's number one. But even better,
1:16:20
~ that's number one, but even better,
1:16:22
yes, is that there is a solution.
1:16:22
yes, is that there is a solution,
1:16:24
There is a way to restore that health.
1:16:24
there is a way to restore that health.
1:16:26
And I think it should
1:16:27
And I
1:16:27
think it should always start with some.
1:16:27
always start with some form of
1:16:29
measurement and testing. ~ so if somebody wants to know whether their brain
1:16:30
measurement and testing. ~ so if somebody wants to know whether their brain
1:16:35
is actually getting healthy, or actually everybody should get a baseline
1:16:35
is actually getting healthier actually everybody should get a baseline
1:16:38
and then see if their brain is getting healthier.
1:16:39
and see if their brain is getting healthier.
1:16:40
So which blood biomarkers but also imaging measures do you find most useful now?
1:16:41
So which blood biomarkers then also imaging measures do you find most useful?
1:16:46
Like
1:16:47
a Prenuvo, is that something you would recommend?
1:16:49
Yeah, so the
1:16:49
Prenuvo, which is a full body brain full body scan,
1:16:52
which is great for you know looking for peripheral,
1:16:54
you know, cancers and things like that.
1:16:56
It's pretty cool technology for sure.
1:16:58
We have a very specialized brain MRI scan.
1:17:01
We'll look at 10 different ways of looking at the brain,
1:17:03
full digitization of brain. So there's a couple things,
1:17:06
back to your point. Is the first thing you have to remember though,
1:17:09
is you have to eliminate this idea of age-appropriate function.
1:17:14
You got to get that out of your head.
1:17:17
Okay.
1:17:18
It's supposed to work no matter if you're 90,
1:17:20
whether you're 10 years old or you're 90 years old,
1:17:22
function is function. Okay. I don't want to hear people say,
1:17:24
well, I have a great brain for a 90-year-old.
1:17:26
Well, that's doesn't help. Okay.
1:17:28
And so you so you you have to believe function is function.
1:17:33
And you should be able to maintain function indefinitely.
1:17:36
The heart is supposed to work in a certain way.
1:17:39
It should stay working that certain way every single year of your life.
1:17:41
You shouldn't say, you shouldn't accept a 70-year-old heart functioning less than
1:17:46
a 30-year-old heart.
1:17:47
And that's the and that's the concept of resilience.
1:17:49
If you maintain it, if you if you understand w how it's built and what
1:17:54
it requires for preventative maintenance,
1:17:56
okay, you want to take a look at say I have a 1957 Chevy and it runs
1:18:00
as well today as it did in 1957 because I I it it I know how it works.
1:18:06
I make sure all the components of this car work.
1:18:09
And your body works the same way.
1:18:11
And it's biochemical, so the body will actually regenerate itself if
1:18:15
you provide it with the right materials.
1:18:16
So, first and foremost, you have to think of that way.
1:18:18
Then, if once you believe and understand that concept,
1:18:21
then you have to do preventative maintenance.
1:18:23
But how do you know what's fix what's broken?
1:18:25
Okay, in your house, when your baseboards get all scuffed,
1:18:28
you can see it and say, my goodness,
1:18:29
my baseboards look like they're 20 years old.
1:18:31
I'm gonna go paint these things,
1:18:32
right? And then you can fix them.
1:18:34
But so but you fix them because you visually saw my baseboards
1:18:37
are getting scuffed up. Well, your body's biochemical.
1:18:40
So you need two things. You need to look at the biochemical
1:18:43
and the physical structure. So the brain emoride.
1:18:45
will tell you as a baseline, okay,
1:18:47
where your brain is today. And you basically is drawing a line in the stand saying,
1:18:51
okay, here's my brain today. I will age no further than this line.
1:18:54
Okay, that's your benchmark for for the rest of your life.
1:18:54
Yes, yes. Mm-hmm. Yeah.
1:18:57
And
1:18:58
then you do biochemical analysis,
1:19:00
which is what we do with the bioscan technology,
1:19:02
and you measure your mitochondrial function,
1:19:05
methyltransferase, plasmalogens,
1:19:06
phosphatidylcholines, and so on and so forth.
1:19:08
And the system is supposed work.
1:19:09
And you can now say, okay, which of these systems are not working
1:19:12
the way they're supposed to work?
1:19:13
Doesn't matter what disease you have,
1:19:15
disease is completely irrelevant.
1:19:15
Mm-hmm. Exactly. Yep.
1:19:17
Okay, you're saying health is health.
1:19:19
Your health,
1:19:20
my health, health is the same for every single person.
1:19:22
Okay, disease is different. Disease differentiates us,
1:19:25
but health is unifying. It's a singularity.
1:19:28
And so we say, okay, it's like the dipstick on your car.
1:19:31
When the oil is low, you put the oil in.
1:19:33
You don't wait for the engine to start knocking.
1:19:35
Say, well, you know, that's which is what basically our medical system is now.
1:19:39
But we need to know all the dipsticks.
1:19:41
Right? And so and what functionality they are.
1:19:44
So that's where the bio scan technology comes in.
1:19:45
And then once you have this, it's not about diagnostics.
1:19:50
It's not like saying you're not in this the sucks to be you business.
1:19:54
Okay, what I tell people. So this is what diagnostic right now is you
1:19:57
you label it and you can't fix it.
1:19:59
Well the cool thing about biochemistry and metabolomics and this neurology
1:20:04
of the brain is that everything we measure,
1:20:06
we can move, we can we can modify because it's biochemical.
1:20:10
And so now you say, okay, now I know what it's supposed to do.
1:20:13
So I make changes and I restore that physiological function.
1:20:17
And this is where we use the advanced biochemical engineering with the what
1:20:21
we call BioNutrix. It has plasmalogens and other biochemical intermediates.
1:20:24
But they're basically, there's no drugs involved.
1:20:27
It's basically saying it's a you're you're cooking and the pantry
1:20:32
is biochemical intermediates instead of you know flour and sugar.
1:20:36
And so you have these molecules that you say these are the things that
1:20:39
Body works on. I don't need a drug to do this.
1:20:41
Okay, I don't need to redesign what God created.
1:20:44
Okay, I just need to make it work.
1:20:45
Okay, it it's I I gotta find out.
1:20:48
I don't have to outdo what was done.
1:20:51
I just say it was designed to work.
1:20:53
Let me monitor it and do the best I can to when it deviates from health,
1:20:59
I just restore that health without thinking about it.
1:21:02
And that's the critical part. And then then we then we can start reducing some
1:21:06
of the health anxiety. We don't need to overtest ourselves.
1:21:09
Okay, we're we're overtesting ourselves and we're we're we're we're obsessing
1:21:13
on everything. When and I tell this story,
1:21:15
like you know, my first car was a little Triumph TR7,
1:21:18
which was fun to drive, but every time I got the gas,
1:21:21
I had to check the oil because it would just,
1:21:22
it was, it was, it was completely a disaster of a car for
1:21:23
Yeah.
1:21:25
maintenance, right? And so the maintenance schedule was like every day.
1:21:28
Now the cars I drive now, I don't check the oil every time because I've learned
1:21:33
that, okay, this is in good shape,
1:21:35
and so you have this maintenance schedule.
1:21:36
Your human body should be the same way.
1:21:38
Once you've got certain things figured out,
1:21:40
you should check them on a regular basis,
1:21:42
but not in but
1:21:42
Mm-hmm.
1:21:43
not in a in an obsessive way. And
1:21:45
Yeah.
1:21:46
that's the that's the goal of future.
1:21:48
It's amazing. It's so simple. You give the raw materials
1:21:51
and then you check a little bit upstream that the raw materials are giving
1:21:53
bit upstream than the raw materials like if you think that you're trying to cook.
1:21:55
you this thing that you're trying to cook.
1:21:57
And if it is great. If it's not,
1:21:57
And if it is worth if it's not,
1:21:59
well, give more raw materials or different raw materials and check
1:21:59
well give more raw materials or different raw materials and check
1:22:03
and rinse and repeat. Right?
1:22:04
and then some repeat. Correct.
1:22:06
Right? Yeah, and then that's the and that's
1:22:07
So of course.
1:22:08
the other part people think forget w when you're doing biochemical engineering like
1:22:11
this, it's food. Okay, people say,
1:22:14
when do I have to stop taking supplements?
1:22:15
Well never. Okay, so so the human body is designed to
1:22:21
survive under periods of deficiencies.
1:22:24
Okay. Remember, we we you
1:22:25
Yeah.
1:22:26
know we weren't we weren't created and we weren't we didn't live thousands
1:22:29
and thousands of years with being able to go down to the drugstore and
1:22:32
get a niacin supplement or or or riboflavin.
1:22:35
Like that was never available to our predecessors,
1:22:38
right? But they're available to us now.
1:22:39
So we can actually get those precursors.
1:22:41
So we get these different levels of nutrients from our diet,
1:22:44
but there's no way we can get the complete nutrition all the time.
1:22:48
So you're gonna have periods of time like
1:22:50
30% of the population is riboflavin deficient.
1:22:52
Okay, B2, okay, absolutely.
1:22:57
Mineral absorptions, niacin deficiencies,
1:23:00
thiamine. So your body is gonna have periods where you're deficient.
1:23:04
But you accumulate that over years.
1:23:06
So you start by the time you get 70 years old,
1:23:09
you're probably deficient in riboflavin for 10 of those years,
1:23:12
right? Because you know, you're not eating the same diet.
1:23:14
Your diet changes. So sometimes you're getting lots of something and
1:23:17
not enough of another, and sometimes you're getting
1:23:19
And and so on and so forth. So when you when this bioengineering approach that
1:23:22
we take is no, the you want to say,
1:23:25
here are the core systems that I need,
1:23:27
and you take it every day or every week or whatever it is,
1:23:29
but certainly on a regular basis,
1:23:30
Exactly. Yeah.
1:23:32
it's not you you're not fixing a bacterial infection.
1:23:35
This is actually your your biochemical physiology indefinitely.
1:23:40
And then if you get these core components,
1:23:42
~ it also frees up your dietary,
1:23:46
you don't have to be so obsessive on your diet as well.
1:23:48
Like you still
1:23:49
have, you know, I'm I'm an advocate of a high protein,
1:23:52
high fat diet. Like you want to be,
1:23:53
you know, high you know, fat and carbohydrates,
1:23:57
one or the other. Like don't take both.
1:23:59
Like so high protein, high fat or high protein,
1:24:01
high carb is fine. Okay, to a certain degree.
1:24:03
Like I'm a high protein, high fat person.
1:24:06
~ we can talk about fasting
1:24:06
Right. Me too.
1:24:08
and muscle wasting and all those other things,
1:24:10
you know, get more details. But that's kind of where philosophically thinking,
1:24:14
you know, we we do have this
1:24:18
th this disease mindset, like cure the disease.
1:24:21
Okay, like, you know, take something,
1:24:23
cure it, then I'm done with it.
1:24:25
And we have this this sense of,
1:24:28
~ my grandfather ate and smoked and drank and you know,
1:24:34
we have this concept that we can abuse ourselves and we're proud of
1:24:38
the abuse that we put on ourselves and saying,
1:24:40
I've I've been able to do this abusive behavior and survive,
1:24:43
which is typically not what we should be doing.
1:24:47
totally agree. Of course.
1:24:47
And you wouldn't do that to your car or anything else you own,
1:24:50
right?
1:24:51
Yeah, or your house. And totally agreed.
1:24:53
And totally agreed. And also to add to all of this,
1:24:53
And also to add to all of this,
1:24:56
our nutrients now, our food is not as nutritional as it used to be before.
1:24:57
our nutrients now, our food is not as nutritious as it used to be before.
1:25:01
So that's why we have to supplement.
1:25:02
Absolutely. So that's why we have to supplement again.
1:25:03
And again, the supplementation is the raw materials and then your body
1:25:05
Supplementation is the raw materials and the body can do its job.
1:25:07
can do its job. So alongside plasmalogen precursors,
1:25:09
So alongside plasmalogen precursors,
1:25:11
Which lifestyle variables matter to you for preserving brain structure and function,
1:25:12
which lifestyle variables matter to you for living brain structure and function,
1:25:17
as we as you talked about muscles?
1:25:17
as we talked about
1:25:18
muscles. Maintaining muscle mass is critical.
1:25:21
Okay.
1:25:22
Your muscles are the critical,
1:25:23
you know, consumers of fatty acids in your blood supply.
1:25:29
Virtually all diabetes is curable by improving muscle densities,
1:25:33
fundamentally. And I did a big lecture on diabetes basically talking about people
1:25:38
talking about ins
1:25:38
It was great.
1:25:38
type two diabetes, right? When people say insulin ~ sensitivity issues.
1:25:43
But really what happens is the body can't process fat and sugar at the same time.
1:25:48
And or you get reduced
1:25:51
metabolic capacity. So your muscles process fat.
1:25:56
So maintaining skeletal muscle mass is a critical thing as you get older.
1:26:00
So that's one thing. So and then your basic eating habits and patterns,
1:26:05
you know, like kind of an intermittent fasting is fine.
1:26:09
Okay. And y pick one that matches your lifestyle.
1:26:13
Not everyone can fast for longer periods,
1:26:16
but you want to go through this cycle.
1:26:18
Okay. Just like
1:26:19
We talk the sleep, right? You have a REM period and you have a deep sleep.
1:26:22
And that cycle, your body's always cycling.
1:26:24
There's no such thing as homeostasis.
1:26:26
Okay, your body's always changing.
1:26:28
It's either going from morning to night,
1:26:30
and it's it's changing. Either you're fed or you're fasting.
1:26:33
So you want to basically create those patterns in your body
1:26:36
and maintain those patterns. It's got to be able to change from the fed state
1:26:40
to the fasting state. And if you're always snacking,
1:26:43
then your body doesn't get into the fasting state.
1:26:45
It doesn't mean you need it doesn't mean you need to go through a three
1:26:47
day fast or something like that,
1:26:49
unless you you know, you want to for certain things and you should,
1:26:51
you know, get other nutrition while you're doing such a thing.
1:26:54
But you should have peri like you you should get those good twelve hour fasting
1:26:59
periods in your day. ~ you know,
1:27:02
and good sleep hygiene, for example.
1:27:03
Like don't eat late at night and snacking.
1:27:06
Those th so there's basic things that you wanna make sure of.
1:27:09
And then psychologically, you need to deal with stress reduction in our world.
1:27:13
~ is is and
1:27:15
Have meaningful personal relationships.
1:27:18
Like, you know, we are human. We get you know,
1:27:21
have connectivity, be involved with and be,
1:27:24
you know, engage in your community,
1:27:25
engage with people around you.
1:27:26
And that and all these things are they they give you a reason to get up the morning.
1:27:30
And under all that umbrella, the number one thing is purpose.
1:27:33
You need a purpose in your life.
1:27:34
And I I I talk a lot about this,
1:27:36
especially for longevity research,
1:27:38
right? We're talking about extending human life,
1:27:38
Yes. Mm-hmm. Why?
1:27:40
decades, maybe a century or more.
1:27:42
Yeah.
1:27:42
Like
1:27:43
so if you're gonna live indefinitely,
1:27:45
well
1:27:46
Humans have not been programmed to to do things in their seventies
1:27:51
and eighties and nineties. Like we don't have a plan.
1:27:54
Okay. You know, it's not saying,
1:27:56
~ I'm gonna go my my third university degree starts at age eighty.
1:27:59
Like my all I'm gonna go to university with all my eighty year old pals.
1:28:00
Mm-hmm. Cool. That sounds amazing.
1:28:03
Right? We don't have that type of social
1:28:05
I love that.
1:28:06
right. So we don't we we don't have any socialization to deal with it.
1:28:09
Yeah. Yeah.
1:28:09
Like what what are you
1:28:09
gonna do with an extra fifty years of your life?
1:28:11
So creating purpose is really critical.
1:28:14
So
1:28:15
Because you need a reason to get up in morning,
1:28:16
to get dressed, brush your teeth,
1:28:18
do the things that you need to do.
1:28:19
you're gonna eat better, you're gonna be engaged in the things around you.
1:28:23
But that's the next trick, is and you we have to learn not to retire.
1:28:27
~ this retirement mindset also,
1:28:29
you know, you can change your life,
1:28:31
you can change
1:28:31
Yeah.
1:28:31
what you do, but you have to have a reason to be here.
1:28:34
Yes.
1:28:34
And we all know this, right? You know,
1:28:37
you know, you have these long term relationships where someone loses their spouse
1:28:41
and then soon thereafter they die themselves because they lose purpose,
1:28:44
right?
1:28:44
And so purpose is always critical for health and vitality.
1:28:48
Yeah, no, that's amazing.
1:28:50
And these are free things that everybody should be doing,
1:28:51
These are things that everybody should be doing,
1:28:54
have to be doing, because it's also based off the ~ part of
1:28:55
have to be doing because it's also based on the ~ part of
1:28:58
the foundational things that you need to get your body to do its job.
1:28:59
the foundational things that you need to get your body to do it.
1:29:02
So now yeah, it's unique to you,
1:29:03
Exactly. And it's unique to you.
1:29:04
You're right. It's it's no one no one no
1:29:06
exactly.
1:29:07
one decided no one decides what what is right for you except you.
1:29:10
Yeah, absolutely, absolutely. So I'd love to now put these two tracks together.
1:29:10
So absolutely, absolutely. So I'd love to know put these two tracks together
1:29:15
And I would love, love, love to hear what you have to say about this autism,
1:29:16
and I'd love, love, love to hear what you have to say about this autism.
1:29:19
neurodevelopmental,
1:29:20
neurodevelopmental Alzheimer's neurodegenerative,
1:29:21
Alzheimer's, neurodegenerative.
1:29:23
They're not the same condition,
1:29:24
they're not the same condition,
1:29:25
but you keep coming back to some of the same cellular systems.
1:29:26
but you keep coming back to some of the same cellular systems.
1:29:28
~ so where do you see the underlying biology overlap?
1:29:29
~ so where do you see the underlying biology overlap?
1:29:33
So across the membranes, but also mitochondria,
1:29:33
So across the membranes, but also microproprio oxidative stress synapses,
1:29:36
oxidative, stress synapses, myelin,
1:29:38
and where are they?
1:29:38
myelin, and
1:29:39
where are they fundamentally
1:29:39
fundamentally different.
1:29:41
different? Well, if you think of optimal human health development,
1:29:46
okay, we start with nothing.
1:29:48
Right. You're you're in the third trimester,
1:29:50
you have raw wires in your brain,
1:29:51
you have basically no myelin. You don't know anything,
1:29:53
right? You don't know your fingers from your toes for the most part,
1:29:56
right? And so you have this developmental phase that goes up.
1:29:59
I don't know how well this looks like.
1:30:01
And then that you have the slope of increasing neurodevelopment.
1:30:05
And you reach kind of sort of I will say a plateau,
1:30:07
but at some point you become mature and your brain is kind of mature.
1:30:10
It's full. Like your skull can't grow beyond its out,
1:30:13
you know, so it's gonna be full.
1:30:15
And then we we create that.
1:30:16
plateau and we want to maintain that now forever.
1:30:19
Okay. So what happens in autism is that slope to get to that optimal that gets
1:30:26
deviated from. Okay. They're developmental.
1:30:28
So you get this that's so when you reach your middle age,
1:30:31
you've you're not, you haven't got a fully developed brain.
1:30:34
Like you've you've missed certain pieces.
1:30:35
Like your nevel neurodevelopment is is lacking a little bit,
1:30:38
right? And typically with Alzheimer's and dementia,
1:30:40
what happens at this plateau, we start going downward.
1:30:44
And so the issue is when you start going down at later on in life,
1:30:48
okay, you have the same kind of myelination,
1:30:50
brain shrinkage, impaired functionality that you'd have if you were off
1:30:55
the chart on the front end. Right?
1:30:57
So ultimately for autism, bipolar,
1:30:59
all these a lot of these neurodevelopmental disorders,
1:31:02
like these other are also related to the white matter development issues.
1:31:05
And so improving that white matter development and obviously,
1:31:07
you know, social interactions,
1:31:09
the that's there's there's an optimal path of development,
1:31:13
right? And that's just
1:31:14
~ within a relatively narrow range.
1:31:16
And then we want to maintain that.
1:31:18
So immortality is basically saying,
1:31:20
okay, how do I keep this functionality indefinite?
1:31:22
And that's what we're not doing.
1:31:24
So we we've kind of we don't know we've human socialization
1:31:29
has not really been optimized for that.
1:31:33
There's been no real selection process.
1:31:35
There's really no reason for us to be living,
1:31:38
you know, over 100. Right. And
1:31:38
Reason. Purpose.
1:31:40
so since we there's since there's been no real reason to do it,
1:31:42
there's been no real
1:31:45
selection ~ of that process. And so we have to kind of create that reason
1:31:49
and then obviously the biochemistry.
1:31:51
So that's that's why they they have similar characteristics.
1:31:54
They're just different aspects of of development.
1:31:57
Sides of the same coin.
1:31:59
Yeah, no, no, that's great. Okay,
1:32:01
wonderful. So now I would love to
1:32:01
Okay.
1:32:02
move from the biology into the tools that you have built around it because this part
1:32:05
Into the tools that you have built around it,
1:32:08
because it's part a lot of people are going to want to hear about this.
1:32:08
the a lot of people are going to want to hear about this.
1:32:10
Can we talk about Prodrome Glia?
1:32:11
Can we talk about Prodrome Glia?
1:32:13
What exactly is it? Why is it the plasmalogen precursor rather than a plasmalogen?
1:32:14
What exactly is it? Why is it the plasmalogen precursor rather than the plasmalogen?
1:32:18
And how do you make it?
1:32:19
And how do
1:32:20
you make it? Yeah, so the plasmalogen precursor,
1:32:23
so the your body has lots of plasmalogen.
1:32:26
And the final step in making plasmalogen is creating this vinyl ether bond,
1:32:29
which is highly sensitive to acid for a purpose of neutralizing.
1:32:34
pero other things in your body.
1:32:36
Unfortunately, when you eat an animal product that has plasmalogens in them,
1:32:40
they get digested by the hydrochloric acid in your stomach.
1:32:44
So you can't actually eat fully intact plasmalogens and get intact plasmalogens
1:32:49
in your blood supply. You need what's called a plasmalogen precursor,
1:32:53
which is called an alkyl-acyl-glycerol.
1:32:54
That's what's present in human breast milk,
1:32:57
an omega-9 version. And then so so we manufacture
1:33:01
These plasmalogen precursors, an omega-9 version and omega-3 version,
1:33:05
that gets absorbed, it doesn't get digested by the stomach acids,
1:33:08
gets absorbed into your blood supply,
1:33:09
enters into the brain and all the cells of your body,
1:33:12
and once it gets into the cells of your body,
1:33:14
your body makes the final two processing steps to make the final final molecules.
1:33:19
So those those are the nutritional plasmalogen precursors.
1:33:22
We also make ~ an animal based,
1:33:26
like an egg yolk oil, so to get phosphatylcholine from an animal source,
1:33:30
like your brain.
1:33:31
needs an animal based phosphatidylcholine.
1:33:33
Your periphery can use plant based,
1:33:35
but your brain cannot. And so we we make a special egg yolk oil version
1:33:40
of you know the the the omega nine omega three plasmalogen with with
1:33:45
egg yolk oil and other other nutrients like vit like coQ10 and vitamin D three,
1:33:50
K two and you know vitamin E you know make make a bigger ~ brain food,
1:33:55
if you will, for that. And so those those are the
1:33:59
Nutritional components. We also have a muscle water that we use,
1:34:02
my 2O for clients, that prevents muscle wasting.
1:34:05
So it's used to restore muscle mass.
1:34:07
~ is pretty dramatic. And we have a nutrient drink that we make artificial milk
1:34:12
for children with rare diseases,
1:34:14
and we'll be incorporating that later.
1:34:15
So there's some other nutritional components that we we have at our disposal.
1:34:20
And then we have our advanced laboratory analysis work that measures plasmalogens
1:34:24
Yes.
1:34:24
and phosphatidylcholine and all these critical things that I've been measuring over
1:34:27
the last decades.
1:34:28
of human health. So we can measure,
1:34:30
you know, the critical aspects of human health.
1:34:32
And then we have advanced MRI technology for measuring the brain.
1:34:33
So yeah. So can can you tell us real quick also about this?
1:34:36
Yeah. So can can you tell us real quick also about this?
1:34:38
Because so you have two types of measurements.
1:34:39
So you have two types of measurements.
1:34:40
You have the prodrome scan, the blood test,
1:34:41
You have the Pro drome scan, the blood test,
1:34:43
but you also have a BioMetrix NeuroMRI.
1:34:44
but you also have the BioMetrix neuroMRI.
1:34:46
So what does each one measure at a high level?
1:34:47
So what does each one measure at a high level and how to use them together
1:34:49
And how do you use them together to understand whether someone's biology
1:34:52
to understand if there's someone's biology or that the brain is changing
1:34:53
or that the brain is changing or what even the patient needs or the client
1:34:55
or what even patients
1:34:57
Well, so
1:34:57
needs?
1:34:57
the BioMetrix bioscan or the Prodrome scan.
1:35:00
So under Prodrome Science, through our doctor network,
1:35:03
they have access to the Prodrome scan technology.
1:35:05
The bioscan we have in part of our perpetual health group here.
1:35:09
So Dr. Goodenowe, Perpetual Health is more of our advanced
1:35:12
~ programming for individuals.
1:35:15
And that looks at a larger portfolio of biomarkers.
1:35:19
And it's designed to look at what systems are functioning versus others
1:35:23
and tells us where do we need to support biochemical systems.
1:35:27
Right? Mitochondrial, peroxazone,
1:35:29
methyltransferase, muscles, and so on and so forth.
1:35:31
And then the nutritional program is tailored to that pro protocol.
1:35:36
There's there's a base nutrition that we all need.
1:35:38
That's that's where the the the blood testing is using
1:35:42
our advanced mass spectrometry,
1:35:44
the ion cyclotron technology measures all these molecules that
1:35:46
you can't get measured anywhere else.
1:35:48
So that's where that part is. And then the MRI,
1:35:51
neuro MRI, is it actual MRI imaging.
1:35:54
So you go in, you put your head in the MRI,
1:35:56
and
1:35:57
We tune the MRI to look at multiple sequences of the brain.
1:36:00
We look at volumes, cortical thickness,
1:36:03
we look at white mac white matter microstructure,
1:36:05
we look at blood flow, we look at cardiovascular reactivity,
1:36:09
we look at ~ the vasculature of the brain with the you know
1:36:14
~ susceptible susceptibility weighted imaging.
1:36:16
We look at the biochemistry of the brain using magnetic resonance spectroscopy.
1:36:20
~ we look at the wiring of the brain using the ~ diffusion tensor.
1:36:27
imaging we get the all the the wiring map of the brain.
1:36:30
We look at functional MRI, so we look at how the brain is functionally connected
1:36:34
to the regions and we look at how the brain is how the brain
1:36:37
is physically connected and how the brain is firing in sequence with each other.
1:36:41
So we have a very comprehensive picture of the human brain.
1:36:43
~ And that that's what we use to measure the restoration of the brain and
1:36:49
and me and then ultimately long term maintenance of you know keeping the brain
1:36:55
in a healthy
1:36:56
state indefinitely. These both are amazing for getting up baseline information
1:36:57
Yeah. And these both are amazing for getting a baseline information,
1:37:02
but also to see how you're progressing,
1:37:03
but also just see how you're progressing if you're progressing and what else
1:37:04
if you are progressing and what else you need to work on.
1:37:07
But you also have trained a network of pro-drome professionals
1:37:07
you need to work on. But you also have trained the network
1:37:09
of pro joint professionals and elite practitioners around this work
1:37:10
and elite practitioners around this work and this testing.
1:37:13
and this testing. What does that training cover and why was it important
1:37:14
So what does that training cover and why was it important for you
1:37:18
to build the practitioner community that understands the testing,
1:37:18
for you to build a practitioner community that understands the testing
1:37:21
but also the lipid biology and the clinical reasoning behind it?
1:37:22
but also the limit biology and the clinical reasoning
1:37:26
behind
1:37:27
So we're fundamentally building a parallel healthcare system.
1:37:30
Okay, one that's based on the restoration of health versus the treatment of disease.
1:37:36
And in order to do that, we need to have our own manufacturing facilities,
1:37:39
which we do, our own laboratory testing facilities.
1:37:42
But we also need a distribution of trained practitioners who understand health,
1:37:47
not just disease. And the practic the Prodrome Practitioner Network is
1:37:51
a network of individuals that are that are trained in plasmalogens
1:37:55
and lipid science.
1:37:56
And all and and more there's different levels of training that
1:37:59
the different protom doctors will have access to.
1:38:02
And then the goal then is we have this large clinical study that we've
1:38:06
now been approved to to to start working on.
1:38:09
When we look at people that are part of a comprehensive wellness program
1:38:12
and we can track how certain programs reduce and restore,
1:38:17
reduce disease incidence and restore health,
1:38:20
then those protocols and programs can then be incorporated.
1:38:24
And distributed through doctor networks as we go forward in this.
1:38:27
And then the Musha Vitality Project is designed to look at at
1:38:30
a whole community level how we can start doing this.
1:38:32
So this this these systems all work in in sequence with each other.
1:38:37
And of course, the Prodrome doctors are are professionals in their own right.
1:38:42
They're gonna they're gonna have areas of expertise.
1:38:43
Like they might be experts in Lyme and mold,
1:38:46
and they could be exercise experts in in in sports medicine and so on and so forth.
1:38:50
Cardiology, cordi cardiology.
1:38:53
you know, oncology. And so we're not trying to we're we're
1:38:57
we support their expertise,
1:39:00
right? And so that's where the protom network has we they can
1:39:04
add this lipid chemistry and biochemistry into their existing knowledge base
1:39:10
and improve their current ~ patient outcomes.
1:39:14
The perpetual health group we've is our own group of of of network that we're
1:39:19
building that focuses really on these core systems that
1:39:22
that we work on, which is our area of expertise,
1:39:25
which is really biochemical engineering,
1:39:27
and this kind of additional ~ supportive technologies that can that can do that.
1:39:32
So it's a big tent. We need lots of people with lots of experience doing lots
1:39:36
of different things. And we learn from everybody.
1:39:39
And then we have all of, you know,
1:39:40
our work is all self-directed research.
1:39:42
We really, we want to interact with the client in a manner that they teach
1:39:47
us as much as we teach them as it goes forward.
1:39:50
Amazing. No, that's wonderful.
1:39:52
So now the question is where does this all go if the research continues
1:39:53
Wonderful. So now the question is where does this go if the research continues
1:39:56
to move the way you hope it will?
1:39:57
to move the way you hope it will?
1:39:58
And you spoke a little bit about your FDA process right now.
1:39:59
And you spoke a little bit about your FTA ~ process right now.
1:40:03
So you found it Goodenowe dietary therapeutics to move your plasmalogen precursor
1:40:04
So you found it good enough dietary therapeutics to move your plasmalogen precursor
1:40:07
work through an FDA regulated development pathway.
1:40:08
work to an FTA regulated development pathway.
1:40:11
And you have publicly discussed,
1:40:11
And you have publicly discussed,
1:40:13
including at the beginning of this episode,
1:40:13
including at the beginning of this episode,
1:40:15
the phase two B program.
1:40:15
the phase two program,
1:40:17
Where does that program stand now as far as timelines?
1:40:18
where does that program stand now as far as timeline?
1:40:20
So you talked
1:40:21
about it, I would love to know a little bit what timelines we're looking at.
1:40:22
We talked about it. I would love to know a little bit what looking at
1:40:24
We're all impatient here. And if it succeeds,
1:40:25
for all your patients here. And if it succeeds,
1:40:27
how could that change the way plasmalogen precursors are used within mainstream
1:40:28
how could that change the way cosmological healthcare?
1:40:32
healthcare?
1:40:34
Correct. So problem with current dietary supplements is that you can't patent them
1:40:40
as a general rule, right? And so there so an acetylcysteine
1:40:44
or your acetylcarnitine and all the people that do
1:40:48
functional health, they look at these supplements and say these
1:40:50
are very powerful supplements,
1:40:51
right? They do certain very important things.
1:40:53
But there's no label on it. You can't say,
1:40:56
hey, take an acetylcysteine for the reduction of complications from
1:41:02
~ a stroke, for example. So there's no label.
1:41:05
Like there's no there's no disease label on those things.
1:41:08
And and rightfully so, because no one has actually done the clinical trial research
1:41:14
and taking
1:41:15
An an acetylcysteine molecule and actually getting FDA approval of N acetylcysteine.
1:41:19
The reason why they don't do that is because if someone does all that work
1:41:22
for multiple millions of dollars,
1:41:24
then you can just go buy an acetylcysteine from anybody,
1:41:26
Yeah. Exactly.
1:41:26
right? And so who's going
1:41:28
to put that money in to get this FDA label on it when they can't protect that
1:41:33
product? And that's why
1:41:34
IP. Yeah.
1:41:35
none of these dietary supplements have an actual FDA validated label
1:41:40
for the treatment of X, right?
1:41:41
And so and that's a that's a that's a problem.
1:41:45
in it just just in a credibility perspective.
1:41:48
So I created Doc Dr. Goodenowe's Dietary Therapeutics to do that.
1:41:51
Okay. It's basically plasmalogen precursors,
1:41:55
which are not patentable, but we're going to start doing some of that
1:41:57
~ FDA validation just so that it can be in the traditional way validated.
1:42:02
Right.
1:42:03
there because the plasmalogen precursors just by themselves do have
1:42:08
~ you know pharmacological benefit.
1:42:11
Okay. We do believe like in an Alzheimer's or Parkinson's
1:42:14
Like we'll see benefits in a manner that would normally be done through
1:42:20
a clinical trial process. Now in our
1:42:22
Right.
1:42:22
protocols, we don't provide just plasmalogens.
1:42:25
We we do other things. Like what if I'm gonna start restoring plasmalogens,
1:42:29
I'm still gonna fix your mitochondria and your methyl transfer system
1:42:32
and your and so on and so forth.
1:42:33
So I'm not going to do that. So I think it's important for us to,
1:42:37
as we build the credibility of a biochemical approach to health,
1:42:43
that we
1:42:45
do both. We do the protocol side,
1:42:47
which is the epidemiological tracking,
1:42:48
but we also go into the traditional system because there's certain certain molecules
1:42:52
that should be used ~ in a traditional clinical setting to become standard
1:42:57
of care in certain aspects. And ~ that's what that company's been des
1:43:01
is designed to actually do that work.
1:43:03
And we're we'll start with dementia and aut and autism are the two
1:43:07
~ issues that we'll go after in the new year.
1:43:12
And so we're just in we're in the
1:43:14
We're we're building the facilities in Canada right now and we're getting ready
1:43:19
for some you know, we d some pre-IND work and we hope to have
1:43:24
the clinical trial starting by,
1:43:26
you know, next year.
1:43:28
Next year. Okay. That's the timeline.
1:43:30
And how long do you think it would take?
1:43:31
Yeah. And how long do you think it would take?
1:43:32
~ basically, what's the the plan?
1:43:33
~ it's hard to tell. It would
1:43:34
be a couple years. It won't take that long because we've done so much work
1:43:36
in advance, but you're still looking at two to three years probably before
1:43:40
Two to three years. Okay. Yeah,
1:43:41
you actually get an actual ~ new drug application.
1:43:43
that's that's feasible. Okay.
1:43:44
If we follow
1:43:45
the drug approval process of Aricept,
1:43:47
for example, how Aricept was approved for Alzheimer's disease using ADAS-Cog,
1:43:51
a couple a couple phase two B studies,
1:43:54
it can be done in a reasonable period of time.
1:43:55
Because, you know, anecdotally and in our in our patient popul
1:43:59
in our client populations.
1:44:01
we see pretty significant improvements.
1:44:03
So if we do if we actually do a a full randomized placebo control trial,
1:44:08
~ it's the likelihood of of of success is very high.
1:44:13
'Cause we've already we've already s seen it.
1:44:15
You already know. Exactly.
1:44:16
You've already done it. Okay, wonderful.
1:44:18
So before I ask you my very last question,
1:44:18
Wonderful. So before I ask you my very last question,
1:44:20
I'd love to make sure that people know where they can keep learning from you.
1:44:21
I'd love to make sure that people know where they can keep learning from you,
1:44:25
Where can people find you and follow your research,
1:44:25
where can people find you and follow your research,
1:44:28
educational work, which is a lot.
1:44:28
educational work, which is a lot.
1:44:30
There's a lot going on there. And we'll put all that in the show notes.
1:44:31
There's a lot going on there. I'm gonna put all that in the
1:44:33
show notes. Right. So there's three areas that you can find me.
1:44:36
So the educational content at drgoodenowe.com So drgoodenowe.com that's where
1:44:42
a lot of educational components like web webinars ~ will be found.
1:44:46
So that's my
1:44:48
global kind of outreach. Then you have drgperpetualhealth.com,
1:44:53
so DRGperpetual Health.com.
1:44:57
That's where we ~ offer the Brain and Body Assessment Center and our MRIs
1:45:03
and our ~ bioscan and our BioNutrix technologies directly to consumers.
1:45:09
Okay, that's that's basically us being this advanced practitioner.
1:45:14
And then if you are a practitioner,
1:45:16
okay, and interested in
1:45:18
you know, learning how to use plasmalogen in your practice,
1:45:21
then you go to prodrome dot com.
1:45:23
And at ProDrome, that's where we support doctors and practitioners by ~ teaching,
1:45:28
you know, giving them access to advanced blood testing and access
1:45:31
to the supplements ~ that they can then incorporate into their practices.
1:45:35
So those three those those are the three areas that you can go ~ interact with us.
1:45:42
Yeah. So Dr. Goodenowe, always ask every guest the same final question.
1:45:43
Dr. Gunau always ask everybody the same final question.
1:45:45
I would love to frame yours around your work and ~ that you've spent your career on.
1:45:46
I would love to frame yours around your work and that you spent your career on.
1:45:50
So if you had that magic wand,
1:45:51
So if you had that magic font already,
1:45:52
although you might already have it,
1:45:53
you might already have it. And every family affected by autism
1:45:54
I have a feeling. And every family affected by autism and every person thinking
1:45:57
and every person thinking about longevity and health plan had access
1:45:58
about longevity and health span had access to plasmalogen precursors,
1:46:01
to plasmalogen and pre-cursors,
1:46:03
hopefully in a few years, and the ability to understand this biology earlier,
1:46:03
hopefully three years. And the value need to understand this biology career,
1:46:07
what would you hope changes?
1:46:08
what would you hope changes?
1:46:12
Yeah, so my personal passion is to make this type
1:46:17
of simple metabolic intervention standard of care in our in our world.
1:46:22
Okay. And so in Moose Jaw and in other,
1:46:25
once we once we ~ learn how to work at an entire community level,
1:46:32
okay, I want to see the incidence of autism basically being eliminated
1:46:38
or down to the level of rare diseases,
1:46:40
okay.
1:46:41
Should be a rare disease event.
1:46:42
So if we if we can get the incidence of autism down to one in a hundred thousand,
1:46:46
for example, and and that's where it should be.
1:46:48
It should be in that range of,
1:46:50
you know, un undetermined genetic diseases,
1:46:55
basically, is one area. So that it should that would be my magic wand
1:46:58
and improve maternal health and early childhood development health in that process.
1:47:03
So we I think that's one major area.
1:47:05
And then my other magic wand would be at the other end of the spectrum.
1:47:10
which is in the elderly population,
1:47:12
is re-engaging the elderly population,
1:47:15
improving mental health and physical health in the elderly so we can reduce
1:47:19
the the healthcare burden. Okay,
1:47:22
like the the healthcare burden that we have with our elderly is high,
1:47:25
and we I want I think I want to improve that.
1:47:29
I also want to improve the intergenerational transfer of knowledge.
1:47:32
I think we're losing a lot. Like we need to engage our elderly community with
1:47:38
the world.
1:47:39
Okay, we don't want to lose the knowledge that they have gained,
1:47:41
we want to find purpose, ~ and find better ways of keeping them engaged
1:47:46
in the workforce. and because we need to figure that out.
1:47:50
~ if we start restoring the health of our elderly,
1:47:53
then we need to, you know, find ways of of incorp of keeping them in our workforce.
1:48:00
In our workforce, generational wisdom.
1:48:01
intergener generational wisdom in local knowledge.
1:48:03
I love that and knowledge. That's wonderful.
1:48:05
That's wonderful. Well, Dr. Goodnow,
1:48:06
Well, Dr. Goodenowe thank you so so much for this conversation.
1:48:08
thank you so so much for this conversation.
1:48:10
I really wanted to have it for a long time and I think I know this will give
1:48:11
I really wanted to have it for a long time and I think I know this will give
1:48:14
families a completely different way to think about brain biology across a lifetime.
1:48:15
families a completely different way to think about brain biology across a
1:48:19
lifetime. Well thank you Nadia.
1:48:21
It's been a pleasure. Well everything we discussed today including Dr.
1:48:23
Well, everything we discussed today,
1:48:25
including Dr. Dr. Goodenowe's work and the research we referenced,
1:48:26
Dr. Goodnow's work and the research we referenced will be in the show notes.
1:48:28
will be in the show notes. I'm Nadia Elkhatib.
1:48:30
I'm Nadia El Kati.
1:48:30
And if this
1:48:31
episode gave you a new way to think about the brain,
1:48:31
And if this episode gave you a way to think about the brain,
1:48:34
share it with someone else. And I will see you next week.
1:48:35
share it with someone else and I will see you next week.