Ep10 - Optimizing the Mind with Daniel Schmachtenberger of Neurohacker Collective

Neurohacker, systems scientist, and philosopher Daniel Schmachtenberger discusses the questions at the heart of modern science which will allow us to unlock the secrets of the most complex instrument in the known universe: the human brain, and offers avenues to begin quantifying and hacking it.

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Daniel Schmachtenberger, a neurohacker, systems scientist, and philosopher, explores the fundamental inquiries within modern science that hold the key to unraveling the mysteries of the human brain, the most intricate instrument in the known universe. He provides insights into ways to initiate the quantification and optimization of this complex organ.

The podcast with Daniel Schmachtenberger covers:

-Optimizing human brain function through neurohacking.
-Quantum mechanics and its impact on brain function.
-Consciousness and the nature of reality.
-Neurohacking and biohacking challenges and growth edges.
-Analyzing brain data with limited information.
-Aging, disease, and complex causation.
-Aging, stem cells, and neural development.
-Neuroscience, neurofeedback, and complex systems.
-Nootropics, risk-benefit ratio, and optimization.
-Nootropics and cognitive enhancement.
-Neurohacking and brain optimization with Daniel Spectrin Berger.

Speaker 1 0:07
Welcome to another episode of headfirst with Dr. Hill. Today’s guest is Daniel shmack Limberger, who is a co founder and r&d Director of the neuro hacker collective, which sounds kind of exciting. So Dan is going to tell us all kinds of cool things today and dig into his history a little bit and some of the projects he’s working on. So welcome to the show tonight. Daniel.

Unknown Speaker 0:27
Thanks for having me. It’s fun to be here with you.

Speaker 1 0:29
Yeah, happy to have you. So first of all, what is this collective of neuro hackers you are assembling? It sounds like a, you know, sort of pie in the sky big project where your head you’re aiming for a lot of world changing goals. But can you unpack a little bit for us what your your approach here.

Speaker 2 0:48
So by neuro hacking, we mean anything that can optimize the mind brain interface and the function thereof. So this is cognitive and psycho motional and health and well being. And so we could roughly define it as well being optimization. But even larger than that, we think of it as sovereignty, optimization, people’s capacity to make good choices, right to be adaptive, which is a function of intelligence, of agency of sentience, all together. And there’s, obviously, kind of human software, right psychology, and there’s human hardware physiology involved. And we know that the software hardware divide in humans is a plastic one, right? It’s continuously intersecting each other. And so, you know, your work with neurofeedback is neuro hacking. The other people you’ve had on the show, discussing meditation, etc, is all in that space. So we’re interested in all categories of technologies that can meaningfully increase the homeostatic capacity dynamics, as you’d like to call them, of the human neuro regulatory system, and thereby increase people’s capacity for complex thinking, emotional resilience, etc. And the reason why Collective is anyone that is doing meaningful work here, we want to figure out how we can participate at a research level and, you know, information, product level, etc. So like us talking here together is, is awesome shaped co sharing information in the space?

Speaker 1 2:18
That’s great. So you say, sovereignty, it’s an interesting way to way to frame that agency. What do you mean by I mean, what what kinds of things are bottlenecks to human agency that appear to be a mere? affected by things we can do to the brain? Like what how can we affect agency and tractable ways? What are you saying what are you exploring?

Speaker 2 2:43
So by agency here, we mean, the the actuator capacity of a complex system, the ability to act on and in the world, okay? sentience is kind of roughly related to our sent our sensory input capacity, intelligence to our information processing of that sensory input, so that those exist in a closed loop, take in information about the world, which is internal and external sensing, process it to inform choice, make choice, get that about that choice, recursively, up regulate. And so on the agency side on the capacity to act, obviously, that requires the capacity to have good information and information processing. So there’s good choice in forming it right and also requires impulse control. Yeah, and can actually have executive function and all that they know come to bear, it also requires the on the kind of choice making side of it requires the capacity to think through things using different frameworks, right, critical thinking frameworks, systemic thinking frameworks, lateral thinking, etc. But also on the agency side. Emotional resilience is a key factor so that as one is working with things and difficulties come, they can process that physiologically and psychologically in ways that empower them to continue to learn rather than get shut down. And so when we look at the physiology of that, we know a lot about how dopamine about how adrenal hormones about how you know many different aspects of neuro chemistry and physiology are involved in one sense of drive one sense of reward dynamics that can predispose dysfunctional or more functional patterns of human behavior, increased sense of capacity, psychologically, physiologically, etc.

Speaker 1 4:26
So again, we’re back to this somewhat soft division between the software in the hardware. So on the hardware side things as you said, like impulsivity or executive function, I think you obliquely refer to working memory essentially, which is, from my perspective, the biggest bottleneck in human performance, and one that appears to be the least responsive to change. But also ways of thinking about emotional regulation and decision making criteria. I’m much more familiar with the physiology side, you know, The biohacking idea is the brain not the mind largely, what are you seeing as some interesting ways that we can get into cognitive change?

Speaker 2 5:12
So the the psychological brain mind question, right is at the core of the philosophy of neuroscience, the philosophy of mind the philosophy of science itself, right? Because the brain mind gets into the brain physics and the question of what is consciousness? What is physics? How do they interact? Is there bi directional causation? beyond the scope of what we’re probably going to dive into here, but it’s definitely at the core of what’s informing the work we do.

Speaker 2 5:42
How in any model of philosophy of mind, however, we addressed this, it’s clear that what’s happening physiologically is affecting one’s subjective experience. And what’s happening in one’s subjective experiences is being mirrored honor, you know, affecting the physiology side. And so we can obviously, modify brain chemistry the whole field of psychiatry is focused on this right psycho neuro pharmacology and not just pharmacology, but neuro tech in general Sure, sure to affect cognitive and psychological predispositions and capacities. We can also do practices that are involving one’s direction of their own attention and subjective experience, whether we’re talking about cognitive behavioral therapies, right, CBT, DBT, other psychotherapeutic processes, or even what we call more kind of mindfulness processes of proprioception, and paying attention to various sensations in the body parts of the body and watch the changes, as I’m sure you’ve done a lot of on physiology, EEG processes, and then watch the capacity for neuroplastic changes in the connectome with enough time and input in there. So it’s not only that the division between hardware and software is soft, it’s, they are both co evolving

Speaker 1 6:59
all the time, and interdependent and changing each other as you alluded to, yeah, yeah, I mean, I have to say I’m a I’m a reductionist in the space a little bit. So for me, the mind is simply the part of the brain that we are aware of and experiencing. And I kind of don’t go below that I have somewhat of a Buddhist perspective where I don’t really believe in consciousness. I believe in moments of consciousness, but not the overarching. I like if the brain falls over. From my perspective, that’s it, there’s, there’s there is no mind outside of the corporeal boundary of the skull, so to speak, even though I know that there are non local phenomena that we’re observing now in the brain. And I’m sure you are deeper into this idea of begin the physics affecting consciousness. I’ve just saw paper last week, that showed that water has some strange kind of non local, I hate to use this word, but quantum tunneling in microtubules, apparently, under some conditions, it appears like water molecules have a superposition and can be in more than one place at once inside of cells. This is getting very quickly out of the realm of anything we fully understand. But do you think that we are getting to a place where we’re starting to run up against the you know, the the edge of Wonder said science and we’re off in the quantum weeds? Or is there something here that we’re making actual progress in in actionable understanding of the brain? Both.

Speaker 2 8:37
So quantum mechanics brings us to the limit of understandability not just what we currently understand, but the upper limits on epistemology, it’s measurability, even Yeah, and even beyond measurability, the upper limits on ontology, right. Eisenberg’s theorem doesn’t just say, we can’t know what it is because of measurement issues, it says it, it depends on which interpretation of quantum mechanics but standard model interpretation, its fundamental nature is not yet defined independent of an observation dynamic, that observation that subject object interaction or CO defining at the level of quantum particles. It’s a very philosophically weird thing for us to think about, using the intuition that we have from traditional larger particle physics. Yeah. Now, we have historically kind of written that off is just super weird phenomena that happens only below atoms and then cancels itself out at the level of atoms. And so we don’t have to worry about it. The topic of quantum amplification, are there quantum phenomena that didn’t affect the behavior of things at a Mesoscopic

Speaker 1 9:41
level at a Newtonian physics level or right. So

Speaker 2 9:45
this is, you know, the work of Stuart Kaufman, the work of other people at Santa Fe Institute of complexity science, the work of people like Stuart Hameroff have really shown quite clearly that quantum amplification does happen, which means Now that the non deterministic, right a causal phenomena at a quantum level are affecting macroscopic behavior at the level of brains that still follows probability distributions, but not determinism. And so this is this is a very interesting, right very important topic and the whole topic of microtubules microtubules in neurons and specific and superposition dynamics and quantum information processing is one of the like, kind of interesting cutting edges in the field. The work of Stuart Hameroff and Roger Penrose kind of open that space up. And the work of Dr. Honor bond, there’s a few people kind of working in that space and is only scratching the surface of what we can claim to know well, but there’s already application happening and things like transcranial ultrasound that were based on the philosophy from there that seemed to be having positive results. So super interesting field.

Speaker 1 10:54
Interesting. That’s, that’s wonderful. Thanks for unpacking that just to touch force.

Speaker 2 10:58
I would say one more thing about the the Buddhist perspective, the kind of John Searle idea of that the the mind is what the brain does. This is one interpretation of Buddhism, right? There’s different schools of very different interpretations here. Obviously, the foundational idea of what’s real in Buddhism coming from Vedanta, was that consciousness is what we actually have a stronger sense of knowability on than physics. Right? Sure, sure. And so their model was, well, I know that I’m experiencing something, there’s an experiencer here, I don’t know that what I’m experiencing is what I think it is, but in an almost kind of Descartes like way, there is some witness that is witnessing changing phenomena, that is premise facial real, right? So their model was the was reductionist in the opposite direction, right? Right. Rather than that consciousness is an emergent property of physics, which is where physicalism and science is gone, they saw the rest of universe as either not real or an emergent property of consciousness. And that, that kind of idealism physicalism divide is right at the heart of what we’re figuring out when we’re studying consciousness via objective methods and brain science.

Speaker 1 12:16
But correct me if I’m wrong, but you know, old school, you know, early poly Buddhists wouldn’t consider consciousness a phenomena outside of momentary experience mean, I Nietzsche, impermanence, the nature of reality is transient. So even consciousness, the I always fall back to the metaphor, the classic metaphor Ship of Theseus, you know, a thought experiment, here’s a model ship, if I replaced one plank, is it the same ship? habit to habit? Three? At what point is this capital I self? The same if every seven or eight years, all the molecules, my body are completely different and have been replaced? You know, this is where it fundamentally breaks down for me personally, in terms of consciousness. But would the you know the Vedantic approach say that there is a cohesive sense of consciousness? Or is it an emergent property of just you know, having a meatsuit. So

Speaker 2 13:15
Sanskrit has a lot more words that have a lot more specificity in their definition than just consciousness, self awareness, and they’re actually very key distinctions in their philosophic system. Okay. And again, there are different interpretations and in these systems, but the Buddhists traditionally say that the foundation of reality is neither self nor non self, because that distinction doesn’t exist at that level, the rational distinction of the concept of self other than self is more superficial than the foundation of reality, right? It’s, it’s ontologically, less primary, okay, so the idea that it’s non self, or the idea that itself are inadequate, so what we think of as self itself, other than self division, right? They talk about a foundational oneness beyond division, it would be neither of those concepts, right? Not self nor non self. That’s different than the traditional way that is spoken about in Vedanta, which is that at the foundation of all of it, there is consciousness with a capital C, that is, that is different than self, right? That can, which is basically if you think about it, almost in terms of a unified field of physics, as a field of potentiality for dynamics to occur, quantum foam to emerge from etc, that there is reference happening, but it’s referenced within the only thing there is, so there’s self reference and that the foundation of what we think of as self referentiality happens at the level of unified field. Interesting. Now, I’m not saying this is what I think but this is some of the kinds of interpretations there I will say there are real people blooms with most of the models of physicalism. There are real problems with these models. And this is why these are unsolved, famous problems in philosophy and even see like, you’ll see a couple physicalists like the classic debate that Sam Harris and Dan Dennett had After Sam wrote his book on freewill was that Dan fundamentally said, consciousness isn’t real, right? He’s a radical limit to this. It’s an illusion, but freewill is real. And Sam said, consciousness is fundamentally real, an emergent property of brain but freewill is, okay, this is a core disagreement on the most foundational concepts of existential ism of what actually is, both being physicalists and having the same kind of critical thinking background and bring on a lot of other things. So it’s part of why these have been so hard as they’re beyond our current tools of knowing more epistemic logic tools. When we do science. We are studying third person things. That Sure, sure, yeah. So when we try and study consciousness, which is first person by looking at the third person CT correlates, we’re actually doing a category mistake by assuming that they’re the same thing. Also, when we assume causation, when we get to the level of things that are for sure, via Bell’s theorem, a causal, our intuitions get off, right. And so these are fascinating and tricky areas, what we can say at the level of what’s probably useful for people right now, is that we can do things with our own subjective experience of self. So what we focus on what we put our attention, and the meaning we give to things that has a real effect on brain and physiology. And we can do things to our physiology that are not obviously utilizing our subjectivity that will affect our subjectivity. And there can be recursive effects between subjective and objective that can either depending on how you do them have the potential of being virtuous cycles in more adaptive evolutionary directions or vicious cycles. And so learning how to use both the conscious direction of our thought, awareness attention, and what we do with our physiology in mutually reinforcing adaptive ways is I think what we’re interested in here.

Speaker 1 17:11
Wow, it’s quite heady stuff. No pun intended. So he’s doing it’s like a philosophy. Guy here. Do you have a philosophy background? Yeah. Yeah. Tell us about that. What is your what is your journey been there?

Speaker 2 17:26
So I was homeschooled growing up, okay. And all the sciences and all the philosophic traditions were what I was fascinated by. And so our particular homeschool didn’t have curriculum. So I just got to study what I wanted. And that was interdisciplinary science, system science and the various philosophic traditions because the, the, the impulse to study science was the impulse to understand the nature of reality we live in sure better yeah. Which is a philosophic impulse, right. Science is a method of knowing that correlates to a particular philosophic system, right philosophic system usually have logical positivism, or the idea that reality exists, objectively objective stuff is real, we can measure it get the same results. So science is a subset of philosophy, it’s a particularly useful, meaningful one. It doesn’t happen to be an exhaustive one of all. Yeah. And so I fortunately got to study many different Eastern traditions and Western traditions and my early and then deeply in my kind of method of understanding any new discipline is, I like to start by going to the edge of what the hard problems that are not understood and your beliefs may be unsolvable. And then understand the range of opinions on that and why and then go back and understand the core axioms of the field in light of recognizing where they might actually have limits. Oh, alright, so

Speaker 1 18:46
let’s go with that perspective with this lens into you. What are the hard problems you bump up against and enjoy bump bumping up against in the biohacker? Neuro hacker world? What are the what are the growth edges? I mean, I see people acquiring tools and technologies and ways of modifying their physiology and their minds constantly and I provide some of those tools. A lot of the time we’re operating in space, we really don’t fully understand, you know, what we’re doing it’s there’s somewhere between art and science. And I’m sure half the things that biohackers do are completely irrelevant. And a certain percentage is probably working counter to what they actually want to do. What do you find the hard problems are in neuro hacking or bio hacking?

Speaker 2 19:35
So neuro hacking, bio hacking, and what the hard problems are in medicine and we kind of looking at that as medicine moving from dysfunction to function, neuro hacking, biohacking, generally thinking of it as trying to enhance function beyond previous baseline. We think of that as one gradient. Some of the hard problems that are not like philosophically hard problems and terms of maybe unsolvable ality or epistemic limits, but like the holy grails of the space. Yeah, one of them has to do with complexity. Okay. And so when we’re trying to look at what’s going on for an individual person say we’re trying to look at addressing anxiety for someone is their anxiety, primarily fizzy, agentic, or psychogenic. And what causes in each of those, if we just look at physio, genic physiologic causes, we see a whole good body of work on the ability for microbial imbalances in the gut to cause anxiety, anxiety predispositions, because of decreasing the total amount of GABA produced in the gut or serotonin produced from God or inflammation on the enteric nervous system or whatever. So if someone went traveling, the third world got a parasite microbiome got off has never restabilized afterwards. That could be a tier one cause of anxiety that no amount of nootropics or CBT or DBT. Sure, yeah. Or if they had minor head trauma, where the CAT scan or the MRI didn’t show anything, but maybe a QE G would, or maybe a SPECT scan wouldn’t exist, you know, functional pleasure hadn’t shown off how we’re going to address that, that might require neurofeedback, that might require neurogenic chemistry, right? That’s going to be totally different. Again, if they were exposed to mold or other forms of excitotoxin, jour, that can cause anxiety. So there can be genetic predispositions there, and then you can, we can continue to populate, there can be methylation disorders, right, there’s 1000s of different things. And then the confluence of those things, right. And then if we’re looking at the psychogenic side of it, we’re seeing someone who had anxiety since childhood because of kind of attachment, early childhood attachment stuff with parents versus only after a very acute trauma, PTSD, like trauma. Sure. They’re, they’re different psychologically, they’re different neurologically. And there are different best practices and therapies to address all these things. And for one particular person’s anxiety, we might be looking at some confluence of some number of these factors, right, where there was a causal cascade, and then that person with anxiety maybe also has a sleep issue or not, or maybe also has some autoimmunity or so as we’re trying to help them, are we how do we factor all that? Certainly complexity and personalization. Now,

Speaker 1 22:32
is this possible? I mean, I work with brains every day and I am humbled every day by how little I actually understand. And my strategy for dealing with that is you know, Maslow to man with a hammer every problem is a nail my my hammer, is Neurofeedback and meditation, and to some extent nootropics. But I view the brain as a regulatory machine. And and when I do a cue EEG and see something off and it matches symptoms, it’s you know, it’s a little bit more skilled than being a mechanic perhaps, but it’s not, it’s not approached that to the let me go return when tweak this and see what happens. I would I mean, I’m working on integrating lots of different information systems so that I can, you know, do visualization, do big data, do a better sense of what’s happening. But even that will have a fraction of the hype of the degree of things you’re talking about. Is it a solvable problem? Can we actually bring in personalized medicine? If you will, personalized psychology track data this way? I mean, is this being done? Can we do it, I think we’re getting enough information about the the individual data points, you can do a methylation analysis, you can do a theta beta ratio, you can do you know, a blood flow, imaging or something. But these measurement tools are limited by the tool space that they are using, and IQ eg gives me one thing, because me less than half the EEG only the dipoles that are at right angles to the skull. And it’s a 10,000 foot view population average of average the EEG across several minutes. So you’re missing states completely only emphasizing traits. And this you know, 30 or 40 big features in the Q EEG that I look at. And then I operate on in terms of intervening. But it’s, I default back to that, because I can’t do everything because I can’t hold everything in my mind. And I can’t ask everyone all the right questions to tease out what might be going on. Because I just don’t understand the brain fully. I mean, as you say, probably none of us do. Why are we getting to the place where we’re gonna be able to aggregate and analyze and extract meaning from this complexity? Or is the complexity kind of obscure our ability to know what’s real and know what’s important?

Speaker 2 24:47
Yeah, I do believe we are starting in the next few years having an exponential

Unknown Speaker 24:52
curve. So this is a Kurtzweil in predicting here.

Speaker 2 24:55
sorts in a different direction than that Much of what we hear about what is gonna happen with brains from Singularity, okay? As you said, we can’t hold it, you can’t hold it on your brain, that’s true. Total amount of information exceeds our conscious processing by a lot.

Speaker 1 25:15
Because of working memory limits, mostly right? Yeah, there’s a storage limit in the brain as far as we can tell. But

Speaker 2 25:20
there is a working memory limit for your ability to consciously try to make sense of not just how many different metrics, but the relationships between those metrics are real relationships. So say we start looking at the genome. Most things aren’t affected by by snips right by one snip, there’s very few things that are mostly we’re looking at dynamics combinatorial dynamics across 10s, or hundreds of 1000

Speaker 1 25:45
downstream effects, essentially. Right. And but that’s, that’s a lot

Speaker 2 25:49
when you look at, you know, 3 billion base pairs. Yeah. And then we have to deal with the fact that that doesn’t tell us which ones are actually coding, right, we have to look at the epigenome for that, which is not something we do well, right now. So we actually have to look at the transcriptome or exome proteome, which is all stuff that is emerging but hard. And that’s

Speaker 1 26:10
just the human genes, which is not actually the majority of the genes we carry around are actually aren’t ours aren’t human. Right. So

Speaker 2 26:18
if you think about it this way, right, when you’re saying the brain has regulatory system, it’s a top down regulatory system, right? The bottom up regulatory system is the code layer, the genomics, the microbiome mix of ironic, right, they are creating a distributed bottom up regulation of individual cell function, right and protein coding? Sure, sure. That bottom up regulatory capacity is what led to the evolution of top down regulatory capacities that get to control larger groups of cells and tissues working together in coordination, the feedback relationships between the bottom up and the top down regulatory systems and all the dynamics in between is where we’re, what I think we’re starting to do is map the human as a cybernetic organism, okay, right, as a regulatory organism, apply complex adaptive systems science and kind of systems modeling, to understanding that better and it is, what in computer science is called a NP complete issue. It’s it’s an uncomputable issue, okay, there’s an uncomputable amount of information. So we’re not just going to brute force, big data and machine learning and figure it all out.

Speaker 1 27:20
Well, it’s a chaotic system, we have, we do not have infinite precision. Therefore, any model that steps into time, far at all diverges from the chaotic system. And

Speaker 2 27:33
so yes, it’s chaotic, meaning. There’s some fundamental unpredictability, there are measurement limits. And then there’s, there is uncomputable complexity. And so what that means is, rather than just depend on brute force computation, we have to understand the dynamics of causation and a complex system better so we can compute the things that actually seem like they would make sense to me. That’s the modeling part. I think the modeling part is key. And that’s it, neuro hacker, what we’re really focused on is taking models like cybernetics, right? Like complex adaptive systems science, like information theory, and putting what we understand from human biology and medicine into those more complex models to understand dynamics, better, right, complex dynamics, and getting to the place where we can start to aggregate tremendous amounts of data there. And data that is, has progressively better sensitivity and specificity. And then be able to process that data where, you know, right now, for the most part, when we look at a biometric, we look at someone’s hemoglobin or their vitamin D or whatever. We’re looking at it in relationship to a reference range. Sure. But when we look at someone’s, someone has a kind of dynamic homeostasis, right? I actually really liked your word homeo. Dynamics, it’s a better word because the stasis is nonsense, as you mentioned. Sorry,

Speaker 1 28:54
I yeah, I knee jerk response when I hear the word homeostasis. Sure. Life is not stasis, we have

Speaker 2 29:01
these homeo dynamics. And then thriving health has to do with the homeo dynamic capacity and resilience across all of those homeo dynamic axes, right? Ageing is decreased homeo dynamic capacity across some of the axes.

Speaker 1 29:17
And does that mean decreased range of variability, essentially,

Speaker 2 29:21
decrease capacity to have a stressor, right, something’s the train to create deviation from homeostasis, and the ability to stay within the homeo dynamic range. So then, if which which means less resilience, so

Speaker 1 29:36
to be concrete, things like insulin or cortisol refers to insulin rises when you consume sugar, right, when you know that it’s a signaling molecule cells suck up the glucose, insulin goes back down. If you chronically preserved the insulin system to the top of its range. Eventually it stops veering,

Speaker 2 29:55
and we call that type two diabetes. And on the way there that kind of syndrome Max dynamics where fasting insulin levels raise, you get insulin resistance at the level of cells now, you take sugar in your blood sugar is going to go further out of balance for longer, causing more effect on other systems that are affected by blood sugar. So more than pathophysiology. So we’re defining here. Aging is not disease because disease, we’d actually say is the deviation from homeostatic range or homeo, dynamic range where some metric actually goes out of effective range, and then you get a pathophysiologic cascade, right? So aging is not that it’s the increased susceptibility for that. So it’s increased susceptibility for disease because someone could have all of their markers within homeostatic state range, but more sensitive to them being able to go out of range from whatever stressors,

Speaker 1 30:48
so they’re, they’re less able to sit in the, in the in the healthy basin of the phase space, so to speak. Right. Okay. All right. And

Speaker 2 30:55
so what we’re interested in here is, how do we, where someone already has disease dynamics going on? How do we identify specifically what cause deviation from homeostasis? On which dynamics? What was the causal cascade that happened? And how do we specifically reverse it? Like we mentioned with the anxiety? Are we? Are we chelating neurotoxins, or are we fixing the gut brain access, or those are very different things. So it requires specific addressing of what the causal cascade was. So this

Speaker 1 31:25
is not like, let’s say, go back to insulin, the insulin insensitivity that cells experience after high levels of insulin, that’s not the disease itself. That is the failure of the dynamic range, correct. And then call these diseases, things like diabetes and Alzheimer’s and other things because of the failure.

Speaker 2 31:44
Now, there are some people who get type two diabetes who did not consume too much carbohydrates relative to what they burn, but they are deficient in Chromium or vanadium, that are necessary to actually have insulin process. It’s at receptors. So there are other dynamics that can go on, which is why we actually have to understand what are what is the entire causal phase space of what can cause an imbalance all the things that could be involved. And this is what we’ve sucked at at medicine so far, is dealing with complex causation. Yeah, acute causation. Straightforward, right? So injury, pretty straightforward. And so we’re going to be able to address that in a clearer way. But where the causation is either delayed in time, right, so something happened, and it led to a slow deviation from homeo dynamics over the course of years or decades. It’s hard to assess what it was, yeah, yeah. Where it’s multifactorial, there’s many different things going on. And where it’s a combination of some multifactorial said, it’s different for different people. So I don’t think MS is a disease, I think it is. And I don’t think Alzheimer’s is a disease or anxiety, I think they are conditions where some cluster of symptoms and biomarkers come together where we call it that. But the actual causal etiology going into it can be radically different from one person to the next. So whenever the syndrome,

Speaker 1 33:00
less of a disease, a cluster of symptoms that may have multiple causal features interesting. I saw a study out of UCLA couple weeks ago, that suggests Alzheimer’s insulin insensitivity, if you will, can be reduced simply through behavioral mechanisms to a bunch of people off of all the meds off of anything and instead of doing a specific intervention, they said, Let’s do lifestyle things. And did you know paleo diets and exercise and lo and behold, symptomatic Alzheimer’s individuals showed recovery of some function. This is fairly magical things. There was a study out a couple of weeks ago showing that even in people with type two and type one diabetes, who have no beta islet cells, essentially anymore in their pancreas producing insulin, short period of fasting, if it was 12 or 24 hours, a very short period, seems to cause a re differentiation of non beta islet cells into beta islet cells to produce insulin, right? That flies in the face of what we thought of in the disease model of diabetes, where it’s either auto immune or it’s toxic from the sugar essentially, that kills in some production cells. Once they’re gone, they’re gone. That does not appear to be accurate. Is this the kind of thing that you’re you’re doing the same thing

Speaker 2 34:15
with the idea that we don’t produce new neurons, right? That was an old idea. And we realized neurogenesis happens, and it can be up regulated. Okay.

Speaker 1 34:21
And that was only in three places. And now it’s pretty much everywhere we look in the brain, we’re finding new pluripotent stem cells, so

Speaker 2 34:27
and so can we increase pluripotent stem cell production and their differentiation throughout the connectome? And can we increase neural protection and synaptogenesis? And yeah, like we’re learning a lot about how that works. Any when you have a system that generated itself, it was a self generating system, the idea that it just could not generate those tissues that had originally generated again, doesn’t make them there’s obviously capacity to do it. And then the capacity decreases or turns off for some reasons. Those than likely are modulated will do who turn on again? So sure, when we think about life extension, how do we increase progenitor stem cells? How do we increase the rate of purging senescence structures? How do we protect cells from senescence, these are all things that happen already. Sure, they can start happening at suboptimal levels for a lot of reasons. We can support them happening at optimal levels, and maybe even beyond previous genetic optimality. Right,

Speaker 1 35:30
just to give us discrete example, is I’m a gerontologist teach courses on Aging, there’s a term in aging called antagonistic pleiotropy. The idea that a mechanism that is healthy at one point in life is harmful. Another point in life and the telomeres, you know, the shortening, end caps that prevent replication forever, when you’re young, prevents cancer from running away with your cells, when you’re old, keeps fibroblasts and your collagen from clean themselves up, and they become homes for a pro cancer environment, basically. So it’s this kind of thing, where identifying where the natural arc of development may not be optimal for long term performance and turning these things back on and controlling it. I mean, from the point of view of telomeres, you know, for a long time, that was the first the holy grail in anti senescence. Now we realize if we could give everyone a pill to lengthen telomeres, you know, ridiculously it would probably just cause huge amounts of cancer. So we can’t simply reach in and turn one thing on, I mean, this is something I struggle with in neurofeedback, it’s not reaching in and dialing up and down different neurotransmitters or different brainwave ratios. When I perturb a system, the system reorganizes. And I’m never quite sure how it’s going to reorganize. And this is a little frustrating sometimes.

Speaker 2 36:46
So if we think of it as increasing system resilience, right? homeo dynamic capacity, because it is a self organizing system. And the complexity is well beyond what we’re going to understand in a momentary view, right? We’re never going to factor all of the dynamics happening probably even in one cell. But we can understand the dynamics that are involved in its some of the key ones and its own regulatory dynamics and how we can increase its regulatory capacity. And so, in general, do we see things like redox signaling decreasing and efficiency in cells? Yes, yeah. So this is why all the nicotinamide riboside stuff has been so exciting. If you can upregulate the NAD plus NADH ratio, there’s a lot of cool things that happen. Do we see ATP decreasing inside of cells? Yes. Do all the things that cells do need those chemicals? Sure. So if we can support mitochondria biogenesis, if we can support ATP production efficiency and Krebs Cycle upregulation? Yep. If we can support protection of the mitochondria, so they don’t become senescent. Right? These are key things that what exactly is that going to do? Well, it’s going to help the complex dynamics of everything that the cells are doing happened better. And so I think those are one of the key things. So, you know, we were saying earlier, there are specific sources of pathology, right causes of deviation from homeostasis, that we want to identify specifically in reverse pathogens, toxins, deficiencies, etc, then there are general system dynamics, that support system resilience, and we want to support those, even though the effects of that are going to be general, increase wellbeing across systems. So EEG regulation is going to produce, you know, how much is it going to affect a particular gastrointestinal sure dynamic? Well, it depends on what all the causal dynamics are. Yeah, it should move it in the right direction, to the degree that it’s creating better sympathetic, parasympathetic, you know, ratio dynamics, etc. Yeah. So we want to, in general, support the homeostatic processes that are fundamental, and get better at diagnosing individual sources of pathology and reversing them. This is great.

Speaker 1 38:59
I mean, this actually ties into how I often frame Neurofeedback for people and they say, oh, I want to do this. And I’ll say, Well, we’re probably going to give you more resources and all the regulatory domains of sleep stress and attention. And what that means is resilience. And we can probably reach in and do more specific things for you. But let’s see what happens first, when we bring the resilience way up and get you sleep in like a rocket well, and being creative and flexible. Let’s do that for the first few weeks. And then we can go in and try to target the thing you think you care about, right? And usually the thing that they really want to work on sorts itself out along the way towards just silting everything that

Speaker 2 39:34
the complexity of the interconnectedness of everything is, again why specialties have failed at complex illnesses. But it’s also so fascinating because, you know, we can look at a structural issue, right, like a postural issue or osteoarthritis that’s causing continuous inflammation within the inflammatory molecules, right cytokines can cross the blood brain barrier caused neural insulin Asian damage to neural circuits, also where the continuous pain dynamic is causing sympathetic feedback into the brain, which then is going to cause effects on all the things the brain is regulating from some perspective, right? And what needed fixed was a structural issue in a knee. Right? Right. And or mold in the environment or a runaway process of, of dysfunctional information processing in the brain from a particular psychologic meaning making pattern, right? So Can Can structural issues in joints or psychological patterns of focus and meaning making or things going on in the gut or affect any other system in the body? Yes, this is what’s fascinating. That’s why trained to separate neurology and Gastroenterology and oncology. Yeah, and so now it’s how do we synthesize what we understand about the parts to understand what happens for whole systems and what happens across systems?

Speaker 1 40:56
So now you’re doing this at the neuro hacker collective with this idea of bringing in different aggregate data types and modeling and trying to figure out what is the meaningful inflection points for these models where you know, where’s change happening? That’s very, you know, high level, and those are the kinds of projects that frustrate PhD students for, you know, 2030 years. Yeah. I think it’s great. I’m, you know, incredibly noble pursuit to enter those big questions. I also know you guys are doing something a little bit more. Okay. Here’s some things we can actually do. There’s a product you’ve produced called qualia, which is in the tropics, is that is it and then tropic space? Okay. Do you consider it an tropic? Or is it more than that? Is that a good frame for it? Or is that too limiting?

Speaker 2 41:39
I think that’s a fine frame is you know, that term no tropic is a little bit loosely defined in terms of how it’s

Unknown Speaker 41:44
generally Yeah. How do you define it?

Speaker 2 41:47
Well, I would, I would, in general, start by making the distinctions between brain nutrient nootropic and smart drug, which are commonly used kind of in relationship to each other, it’s worth distinguishing. So brain nutrient means something that you’d normally get from a dietary source that’s critical to some part of neurologic function that can often be at sub optimal levels, precursors, like tyrosine, all your amino acids, fatty acids, vitamins, minerals that are part of neurodynamics. And when we talk about medical deficiency, we’re talking about the level at which acute pathologies happening below that level. There’s a pretty huge range between medical deficiency and optimality. Right? And so we can call that subclinical deficiency or sub optimality. And so there’s heaps of brain nutrients that depending upon what kind of tests we do we see in sub optimal levels all the time, right, okay, Vitamin D is a

Speaker 1 42:41
pop. Sure, yeah. Even in Southern California, even in Southern California.

Speaker 2 42:45
And, and because it’s not at a level for you know, rickets. Right, someone has a, you know, 30, vitamin D, traditional medical process hasn’t addressed that, but when we, you know, have deeper insight about where optimality occurs, it’s a far way away, which is why vitamin D supplementation is meaningful, same would be true with Omega three or tyrosine, or etc. So brain nutrients that are either hard to source adequately in diet, or where modern lifestyle has used them faster. So if we’re talking about highly or stress lives, where B vitamins are gonna process faster, whatever those are

Speaker 1 43:23
meaningful, or wherever you’re going, and you’re eating anything has B vitamins in it.

Speaker 2 43:27
So diet, you know, any kind of dietary limitations or things to address nootropics starting with, you know, defining Piracetam as a field is some chemical that can increase some aspect of cognitive function beyond baseline without meaningfully negative side effects. Thank

Speaker 1 43:44
you for including that last piece, the the original definition, essentially, I, this is one of the axes I love to grind. You know, I’m all over the nootropic forums and things and I can’t tell you the number of times I have to resist reaching through the computer and throttling some kid who thinks that Modafinil is minute tropic, nothing with their feet with a significant side effect should be considered and I’m guessing you have the same perspective I do if your performance is already relatively good. Why would you risk side effects for small incremental improvements, Supra baseline improvements if trying to remedy a deficit than okay, maybe you need to risk some things to get a problem sorted out. But I don’t understand the incredible marketing and consumer push to seek for all of these drugs and compounds that had some have very, very significant side effects on the off chance that they’re gonna be, you know, designed for your sort of neuro chemistry and give you that little boost. I don’t understand the the philosophy if you will, behind that, that this idea that you can, you can reach for something that might not be unilaterally good, just in case it might, you know, that’s that seems very non nootropic to me, so to speak.

Speaker 2 44:57
So the topic of the risk benefit ratio is core to Western medicine. And it’s partly why we only have a disease model, and we don’t have an optimization model is because in the disease model, there is risk to not treating the thing, right? Pain problem. So some risk of a treatment seems warranted, sure, to make sure that the risk makes sense to a possible benefit if people are already generally healthy. And this is also why longevity research hasn’t, you know, had a lot of support until recently, or any kind of optimization, which has been left to biohackers. is how much risk can we justify for how much benefit beyond baseline? Right? It’s actually a really deep question. And it’s a question that should be answered individually within a range that is reasonable for the field as a whole to pursue. Now, I think bodybuilding and steroids is a classic example of this. Okay, so can people perform in fundamentally increased ways with anabolic steroids that they couldn’t otherwise?

Unknown Speaker 46:06
Obviously, right, you know, otherwise, you wouldn’t ban them and sports

Speaker 2 46:09
is. And you know, we’re the people who are really pioneering this risking their health, and if many of them experienced the downsides of that already, totally. Yeah. And for them, at least knowing that quite clearly for many of them, it was worth it, because that’s what they wanted to do, right? Like the same reason anyone would do anything that was not a smart longevity decision for what they do. And then the field of steroids itself evolved from a lot of that experimentation to where the, you know, the some of the SARMS today have, compared to the early anabolics have radically more benefit for much less risk, partly evolved by kind of the citizen science happening in that space that just for ethical reasons, couldn’t happen in formal reassure. Sure. So it’s a very interesting topic, right. And it is a place where citizen science is always going to be advancing the front edge. And I would say, all of the Psychonauts working with deep psychedelics are in the same place. And so one of the things we really like is for people who are for whatever reason inclined to do their own research, give them better quantified self tools, and learn from that if it’s outside of what we can do formal research on and then, you know, be able to take the form of research

Unknown Speaker 47:21
from crowdsourcing at a very big level, essentially,

Speaker 2 47:24
that’s great now with regard to what the appropriate risk benefit dynamics are. So you mentioned Modafinil and take it further methamphetamine definitely increases certain cognitive capacities, and it kills the flu virus. It has a number of positive medical potential. Yeah. And it has very real side effects. And so if someone is in a combat situation, and they need to stay awake a little bit longer, meth might make sense, right? Part of how those drugs were developed. Yeah. For general use for your midterms, you know, it’s not a good idea. Now, if we look at how much off label Adderall and Modafinil and Red Bull and whatever right, happens for those purposes, this was one of the main reasons we decided to make qualia was not only are the downregulation and side effects, pretty significant of most of those, but even the positives are fairly narrow. Right? So if you have, if you use a presynaptic, dopamine agonist, right, like Adderall, you will get increased focus, but you might actually get simultaneously decreased working memory. And we’ve seen studies, which is not the kind of total intelligence that we’re interested in, as well as, you know, anxiety, irritability, depersonalization, all of those other dynamics. And then of course, because it’s an external override of an internal regulatory system downregulation independence. Yep. And so what we’re really interested in and what I’m sure you’ve been interested in, in the space was, can we understanding the system more completely and nowhere near total completely, but more completely, right? We’re not just trying to do a single molecule intervention, can we have a much more comprehensive set of positive effects rather than a narrow set without the negative effects in real time and without down regulation, so that when someone gets off of them, they’re not experiencing addiction come down, but if anything experiencing long term upregulation of the capacity of their system, so that’s obviously that’s the design principle with which we approach the whole space quality and all the products and development so

Speaker 1 49:39
far is your first product then yeah, what’s in it? I haven’t dug into the ingredients at this point. So

Speaker 2 49:45
brain nutrients and nootropics okay. And so as you know, when people start in the nootropic space, usually they dive into acetylcholine for sure, sure. And so RAS attempts and some choline donors like you The Foundation for memory augmentation, sensory nerve motor nerve, you know, cute etc. So, but which Rasul Tangie us are going to have a bunch of other differential effects and uracil, phenol prasadam are very different creatures. Oh yeah. And also are we going to address the ability for the acetylcholine wants to produce to get across the synapse? Are we looking at acetylcholine esterase inhibitors? Are we making sure that the acetyl groups aren’t rate limiting for the choline that’s there that people aren’t getting over cholinergic we look in different choline donors, central phenoxy is going to act on the central nervous system more than Alpha GPC on the peripheral nervous system. If we look at the conversion of europeen to citicoline, to fossil titled choline, Alpha GPC, acetylcholine, you’re also going to get different peak plasma times when acetylcholine kicks in. So if you want to be able to have less of a spike and more of a continuous process, you might put a number of those so we focused on like with acetylcholine, we were looking at what is the whole acetylcholine regulatory process? And how can we address any of the rate limiting factors and make sure that we’re we’re acting on peripheral nerves where we’re acting on central nervous system differentially more is what we want to be doing that the kind of pharmacodynamics and kinetics of should not just where it’s acting, but how long it’s operating for those curves are things that we really look at how much acetylcholine we’re producing it so that you’ve also got not just acetyl donors, which is why people love altcar. Right, and seal quarantine. And one of the reasons in addition to what quarantine does in the Krebs cycle is B five is often a rate limiting factor for the synthesis, the acetyl, eighth edition of choline. So, you know, what are the right ratios of those things together? And then how much acetylcholine support for how much NMDA upregulation and then where do you get rate limiting effects in terms of the total cellular energy to process more acetylcholine? And then all of that just acetylcholine? Yeah, then we look at glutamate, and typically, it’s pretty common that RAS at times have AMPA keen like properties, you know,

Speaker 1 52:11
certainly any rest stem does and Noopept which, you know, I always get confused Noopept seems to have Raisa Tim like properties but not be a Raisa to him. I mean, I look at the structure and doesn’t have a protein ring. That’s correct. So

Speaker 2 52:28
it’s called rest at him like an advocate like okay upregulating acetylcholine uptake, and the NMDA complex and up regulating glutamate uptake at the AMPA complex, but it is actually not structurally either of them, okay. But it’s very interesting. It’s a precursor to cyclopropyl glycine, it is neuroprotective, it’s anti excited, it anti excitotoxic because of the way that it brings excessive glutamate outside of the synapse. So it’s a very interesting molecule

Unknown Speaker 52:57
A new pepsin quality as well. Great. Now,

Speaker 2 53:00
there are plenty of things that we would have in qualia if there was different regulatory dynamics. Okay. But, you know, so we’re working within both the general well tolerated space, the effective space the and the legal space. Sure. Yeah. People microdosing LSD, or psilocybin has a lot of neat effects. We can’t touch that right, right, right. Not yet. Not yet. So actually that space of the appropriate legal categorization of medicines is it space that we have worked in and intention more because it’s important so

Speaker 1 53:38
more political legal and regulatory? Not at the physiology but at the body politic.

Speaker 2 53:46
Exactly. Interesting. So when you look at acetaminophen being over the counter as a you know, Legacy thing and the toxicity of it compared to pot having been illegal for and still illegal in so many places for so long, it’s just nonsense. Right? Right. And we can look at the whole history of why those nonsense decisions were made but they’re not just nonsense they’re really bad for people. Yeah, because pot doesn’t cause liver damage and acetaminophen does and but it addresses the same pain dynamics that people using

Speaker 1 54:17
Yeah, but you can put acetaminophen it with opiates and that prevents people from taking all the opiates and overdosing in theory that’s that’s that’s course the the Tylenol three Vikon and kind of approaches to bind acetaminophen to of what to say it’s gonna kill you if you take too much. Don’t take too much.

Speaker 2 54:33
And so then people take too much and get liver damage. Right. Right.

Speaker 1 54:37
So sounds like a good idea but maybe it didn’t it didn’t wasn’t well thought out. Right. So it’s been heavy stuff. Daniel, thank you so much for sharing a bit of your wisdom where can people find out more about you? What other projects do you have going on? How can they dig into the the Daniel this that we have here in front of us a little more if they have had their interest sparked

Speaker 2 54:59
was Are as the topics we’re talking about here neuro hacking complex neuro hacker.com A good place to go check it out and great publishing more information there. And I want to say that the work that you are doing in Neurofeedback in the fact that you’re scaling it with quality control and with the systems that allow that to happen. That’s one of the areas that if you hadn’t done it, we would have eventually got into because it’s critical, and we think it is one of the really, most meaningful neuro hacks that has the least the least damage possible, really small downsides. And if done well, yeah, yeah, yeah, it’s true, super high reward possibility. So I’m excited to look at if there’s a way we can partner and support what you’re doing. I’m

Speaker 1 55:40
sure there is we’re we’re both in Southern California. So we should at the very least try to work them great. So can they follow Can folks all you on Twitter, Instagram, LinkedIn, what’s the what’s the if they want to, you know, follow you and here’s the drop wisdom and see all the things you do? What’s the best way to do that? Facebook is probably best Facebook. All right, great. So today’s guest has been Daniel spectrin Berger of the neuro hacker collective. We’ve packed more into this hour than I think most most shows we’ve had, I’m gonna have to go back and listen to myself and look up a few terms, which is great. So I rarely have to stretch myself that way. I really appreciate it. So folks, it has been another show of headfirst to Dr. Hill, take care of your brains, and we’ll see you next week.


Daniel Schmachtenberger

– Global Strategist Systems & Data Science
– Social science & Memetics

Daniel Schmachtenberger is a member of the Neurohacker Collective and founder of the Emergence Project. His areas of expertise include evolutionary philosophy and strategist. processes capable of organizing and supporting a distributed and and continually updating, comprehensive critical path management system for Humanity’s total evolution.

He has worked to repurpose and synthesize relevant state-of-the-art systems for information management, complexity processing, mathematical forecasting, and other data science tools into an integrated set of functions capable of global resource allocation planning and strategy. His goal is the shortest path to a fundamentally redesigned world-system that makes possible and supports the highest quality of life for all life, now and ongoingly. Specifically, his focus is on the development of new systems of economics and governance that intrinsically incentivize life-enhancing behaviors at all levels of agency, supporting distributed and spontaneous problem solving and conscious participation in our global evolution.