It has been debated since the beginning of science. Whether who you are is seated in the mind or the soul. In fact, the debate gets muddled really quickly as philosophers discuss. If perhaps the mind is in the soul, or the adverse perhaps idea of the soul is part of the mind without any doubt, whichever interpretation you tend to lean towards, the physical squishy bioelectrical brain is an essential part of the picture and
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You are listening to Shaping Fire, and I'm your host, Shang Los. My guest today is Cannabinoid researcher state and laws. State and laws is an accredited health and wellness professional with an expertise in nutrition. And over 10 years in practice, he earned a degree in health sciences and is presently a cannabinoid researcher earning a PhD of medical science in the School of Biomedicine at the University of Adelaide Australia.
Staton has served as the graduate research assistant for several grant research projects in Hawaii, and is currently a teaching assistant at the University of Adelaide Health and Medical Sciences.
His research interests center on the nutraceutical properties of medical cannabis, and particularly he has been published five times regarding the neutral protective bioactivity of cannabis, prevalent terpenes, and its implication for the entourage effects of medical cannabis, full spectrum formulations, and potential use in dementia care.
Staton is also the owner and founder of the nutrition Company, sprouting Soul, which advocates a holistic approach to wellness, predicated on ease and simplicity. Staten leads nutrition and yoga workshops on topics including detoxification, ketosis, and the art and science of living foods dedicated to a lifestyle of wellness.
Staten Nest taught over 6,000 yoga classes in the U S A and Australia, and served as a lead facilitator for numerous yoga teacher trainings and masterclasses during the first set. Today we will understand what neurogenesis consists of and which cannabinoids encourage and support the creation of new brain cells. In the second set, we will learn about neuroprotection and how cannabinoids help us keep the brain
cells we already have alive and functioning. And during the third set, we will focus specifically on cannabis supplementation, including dosing protocols for folks interested in health and longevity, as well as cannabis patients experiencing Alzheimer's disease and dementia. Welcome to Shaping Fire, Satan. I'm grateful to be here. Really. Glad to have you. So let's get right into it. You know, when we say that cannabidiol causes neurogenesis, what exactly do we mean by neurogenesis.
That C b D promotes the creation of new brain cells? And is it, is it all types of brain cells or is it only particular varieties of brain cells that cannabidiol can, uh, cause to be produced? Well, I think we need to explain what neurogenesis is. Mm-hmm. and then break down how c b D plays a role in this process. Please. Alright, so if we're gonna break neurogenesis down into four different, I guess you could call them stages, and we're just fig we're, you know, we're figuring this out.
It wasn't until 1965 that we found in the denate gyrus of the hippocampus that neurogenesis actually occurs. So we've been doing a lot since then to figure out how C B D can play a role.
And look, we're still figuring out, but if we were to begin to address your question, where these cells multiply or begin to split is in the proliferation phase, and that this might be a stretch, and I'm gonna try to make an analogy with cannabis, because this takes a similar amount of time for a cell, a neural stem cell to multiply and then become a neuronal cell.
So in the proliferation stage where these newborn neuro stem cells and the hippocampus begin to multiply, we could compare this to the flowering tops of the cannabis plant. And these neural stem cells could be the seeds inside this flowering top, and they begin to multiply in about two weeks. Then this integration stage takes place, and that's after say, the seeds transverse to the ground. And these neuronal stem cells migrate to certain areas within the brain.
They begin to d differentiate and start to spread out their axons and dendrites forming these neuronal like projections and becoming more specialized as a neuron oligodendrocyte or astri. So that's sort of the phase where they change their specific function in the neurogenesis, uh, process.
And that's very similar to say like a cannabis seed sprouting in the ground, forming its roots, and also beginning to project its fan like leaves up towards the, the sunlight to receive photosynthesis and also
nutrition from the soil. And then as these neural cells differentiate, they actually start to receive communication from other neuronal cells, uh, and stabilize and begin attempting to establish functional connections such as receiving neurotransmitter signals, as well as trophic support, which is the feeding and nutrition, and also pro survival factors, which we'll talk a little bit about throughout this conversation, such as blood to Thrive, neuro OIC factor, neuro growth factor,
and a couple other chemicals that float around and sort of support this, uh, maturation process. And it ends up, in the best case scenario, about six to eight weeks, which you might be able to educate me a little bit more on, which is in my, uh, understanding is about the same amount of time it takes a seed to turn into a cannabis plant. Does that make any sense? Oh. It's six to eight weeks for flowering. Probably another four if you include veg,
but yeah, we're with you. And, and since we're talking about timeframe, I'm really surprised that there are, like, we're looking at this neurogenesis, um, timeline on a scale of weeks. The facts, the fact that this, um, this, this, you know, this brain stem cell gets created and then it takes time to, um, you know, split and mature and migrate and then become the type of cell
it's gonna be. In my mind, you know, when, when I see, um, uh, you know, illustrations on, on, you know, TV or the internet, all this stuff happens like really fast, right? The thing just moves and goes, and it happens. The fact that anything in the brain might take, you know, two to four weeks to develop and get to where it's going, that seems like a glacier pace to me for the brain. But, you know, uh, I, I'm a, I'm a novice at, at understanding, um, neuroscience, right?
So it would make sense that I would have some incorrect expectations. I mean, but the, the multiplication phase, you know, from my research, I can say that it happens quite quickly. We're all see cells double or triple within two to three days in the lab. Um, and that's probably the most tangible thing that I can say as far as being able to see it happen mm-hmm. , um, in real time versus reading about it. So yeah, it's, uh, I think we're all learning about the exact timeline of this.
I can imagine as a research scientist that when you're in the lab and you're visibly watching these neuronal stem cells, um, splitting over these two or three days, that it's a kind of exciting, and b maybe even makes you feel like you're having like kid like, oh, these are my babies, you know, these are my, you know, I'm, I'm growing these for research and I gotta take care of 'em and make sure
they're fed correctly and everything. I would think that, that you would have a lot of, um, like, uh, care emotions for them. I don't know, maybe I'm anthropomorphizing too much, but I think I would care. Yeah, I would say so. I'm sort of, my life is sort of dictated by them. Uh, I don't really have a schedule. My schedule's based off of the cell growth and, um, and also if I decide to differentiate them, that's another 48 hours with certain chemicals. So yeah, they.
Uh, the fact that they run your life may is making them sound more like kids. . Yeah, . All right. So lemme get you back into your timeline. So, so we, we've under, we've understood what happens, you know, regularly. So, um, I think where you were going next was, um, what adding, uh, cannabidiol C b D to this interaction does to, uh, encourage it probably. Yeah. So we'll talk first about the indirect way and then the direct way.
So the indirect way that C B D can help in the proliferation phase and the multiplication phase is by increasing anandamide, which is the bliss molecule that is an endogenous cannabinoid. And it does this by sort of blocking fa or fatty acid amide hydroxylase, which is an end enzyme that breaks down the Hyde and anandamide has the ability to bind to the CB one and the CB two receptor, which has been shown to promote cell proliferation. Mm-hmm.
So that's in the first phase. So I would say that C B D, you know, has its way to sort of tone up the endocannabinoid system to promote the first stage of neurogenesis.
And then C B D can influence cell proliferation directly by binding to the transient placenta, potential Vanilla Lloyd type one, or let's just call these things T rrp V one receptor, and the five HT one A receptor, which is the serotonin receptor, which is demonstrated to help, you know, the cell proliferation is also also blood derived nootropic factor, which, uh, C B D can also promote, not only helps with cell proliferation, but also with the activation, uh,
the differentiation and also helping the dendra complexity, which would form into the maturation phases as well as synaptic formation and plasticity of these newborn neurons. So through these T R P V one receptors, the five HT one A receptors and the blood derived nootropic sort of promotion, it has different stages of, uh, helping the neurogenesis process. That was a great explanation.
I really enjoy having hardcore research scientists who are in the lab all the time on the show because, you know, the fine mechanics and, and we're we're really interested in that and, and not, well, we're. Trying to figure it out. Yeah. It's really complicated. . Well, yeah, I mean, we all know that the science is active, right? But it's, it's, it's a lot different than talking to, um, a lay person who will give you the story of how it happens, like,
like when patients talk to me, right? Like, like I, I might be able to describe those three things happening, but I'm not gonna have the mastery of the language like you have that I think just makes us all feel like a bit more confident that,
that we're learning the good stuff, right? So, so I appreciate that. So, so as far as thinking about those, those those three, um, those three ways that, that cannabidiol supports neurogenesis, um, is it, is it a fair model to think that what, what happens when we take C B D is we are essentially like turning up the governor on the engine a little bit because your brain will naturally do these three processes, but when you add C B D, it makes the whole process happen, um,
with more gusto and, and so like, maybe, maybe quicker and more. Yeah, that's a, a good way to look at it. I was gonna explain it. Uh, as a, if you, if you play guitar, so you're like tuning your guitar, um, while the chords of each of the guitar or while a strings of each guitar acts, you're on a different note when you tune them correctly and you play that note, that sound travels with more precision and actually has a chord or a,
a tone. And so I would say that C B D helps with the overall, uh, tone of neurogenesis. Ah, so by your description, what then, one of the things that CB does is increase the efficiency of this whole thing. Yep. Got it. Because all these things are happening regardless of with C B D in or outta the body by putting it in, like you said, to rev up the engine, it's actually like turning up the, the volume slightly through a coordination of events. I get it.
So ev everybody is where they need to be when the performance starts and everybody's got all the resources they need. So the whole manufacturing team is just efficient and ready to go. Yep. Got it. So, um, you know, when we talk about neurogenesis in the, um, cannabis world, um, we're, we're usually exclusively talking about C B D because that's what most
people are familiar with as a cannabinoid that causes neurogenesis. Um, but I know that we're continuing of course to expand our research to other novel cannabinoids. Um, are we familiar with any other cannabinoids that cause neurogenesis in addition to C B D yet?
Yeah, I would go with, uh, delta nine, T H C as the other, um, Major phytocannabinoid that has been recognized as a promoter of neurogenesis in alignment with its function like anandamide and its ability to have an affinity to that CCB one, CCB two receptor, which along with that brain derived nootropic factor is what causes that first stage of neurogenesis.
And in a wrap model, I think it was around 1.5 milligrams a kilo, which they called, uh, somewhat lower dose acute and chronically administered to a certain amount of time, it did show that it enhanced neurogenesis cognitive function and performance. And so if we looked at the sort of function of delta nine T H c,
I'd maybe extend that. Maybe it's a bit of a stretch to delta eight, 'cause it does have some binding ability to CB one and CB two and maybe even C B N, which even has a lesser degree of binding ability to those two receptors.
Hmm. So when we're, when we're looking at the other, um, uh, significant neurogenesis agent in, in D nine T H C, um, is it essentially, um, helping neurogenesis in the same three areas of process as the C B D or is it mostly just at the first step since both C B D and D nine T H C are acting on the anandamide, which, which helps that first step is, is T H C helping all the way in the, all the way down the line in those three different timeframes like C, b, D does?
Or is it really mostly just there at the beginning? Uh, it's a good question. I would have to look into, you know, how much Delta nine plays a role in differentiation and integration mm-hmm. as well as the maturation of the brain cell. And I think that could get into to the, some of that controversial application of, uh, T H C and timeframes in life. Mm-hmm. . But my guess would be, yes, it does play a role in the development of the brain cell.
Interesting. All right. So, um, let's, let's switch sides of the equation here. So, so up to this point we've been talking about the, the, you know, the C B D and T H C helping, uh, and, and, and making this neurogenesis process more efficient and more robust. Um, these, these, these neuronal, um, stem cells that split, split split and then they mature and then they migrate to where they're going to
become the kind of cell they're, they're going to become. Um, can these neuronal stem cells, um, turn into any sort of cell in the brain, or are they only particular flavors? When you mean particular cell of the brain, they can become a neuronal cell, an oligodendrocyte or an astrocyte from my understanding, and to a certain degree, different areas of the brain. Uh, I think it was, we just recently saw how this, this kind of occur in the hypothalamus, the raum, the substantial negra.
And I think we're finding maybe some more areas of the brain where this does occur. Alright. On that is a good answer. And I, and I'm also going to change my question a little bit to get at something a little different, which is, um, what if I were to change the question and say, are there any brain cells that cannot be replaced by this neurogenesis that we described. Like areas of the brain that this.
Cannot not happen? Yeah, that might, yeah. The idea, the, what I'm, what I'm trying to get to is that it, it, it, you know, neurogenesis is great and if it can replace all the parts in of our brain, that's even cooler. But if there are some parts of our brain that, that just can never benefit from neurogenesis, I'd be curious to know what it is. Yeah, that's a good question. And I can't answer that specifically, but I have hope that the answer is yes.
Okay. Fair enough. Fair enough. And you know, and, and this is what happens when we do an interview on the edge of, of the science, we know, right? So we're, we're probably gonna run into some stuff like that.
Mm-hmm. . Okay. So if, if we're clear now that, uh, C b D and T H C can help along the neurogenesis, and, and we know that neurogenesis can, uh, replace an entire variety of, uh, of, of different types of, of, of brain cells, um, uh, I wanna look at a potential, um, other limiting factors that could slow down this neurogenesis since kind of the point of today is what is neurogenesis and how can we, you know, encourage it?
Right? So, so, um, are there other inputs and, and there might be too many dimension, I'm open to this, but, but are there other inputs that need to be present, um, uh, that, um, if not present is going to reduce the ability of cannabidiol and T H C to do this, um, increase of efficiency and increase in robustness of this
process? And, and, and what I imagine you might say is, oh, it needs this particular, um, brain chemical five H T P. And so, you know, we encourage people to take supplements to also encourage neurogenesis along with the C B D and T H C. I think the easiest way to answer that would be health. Oh, right. On whole food diet, . But. But, uh, get exercise, let's, uh,
break health down into three categories. We'll start with oxygen, which, you know, we, we gotta have that you hold your breath and you eventually, no brain cells will be doing much anymore. . Uh, next thing we need is hydration or H two O or, you know, water and, uh, nutrients. And so more specifically, when we sort of say, okay, well we can get air and water, we sort of take that a little bit for granted, hopefully it's both clean air and water and we get into nutrients.
I would say probably the number one would be long chain fatty acids, particularly omega threes play a, a pretty good role in, uh, some of these processes that promote neurogenesis. The second one would be polyphenols, uh, more specifically flavonoids. And then the third would be a healthy microbiome. And we, we can get into those three if you'd like. And what supplements may be, would be best if that wasn't part of your whole food diet approach.
Right. On. Let's hold on, uh, on that, that next protocol question and like, what and how much to take for the third set. 'cause I've got that. Yep. I got that sitting down there to talk about. So, alright. So, um, so assuming all these components are in place, um, do we know about a dosage threshold for, uh, C B D to cause neurogenesis, essentially, how much do we need to take for this process to be improved at all?
Oh. Well, I think most of our research that could get around a dosage comes from either in vitro, which means cellular or in vivo, which is basically rat models. And if I was to condense everything I've read up to this point, it would be around three to 10 milligrams per kilogram. And that becomes pretty hard to translate in a human due to the bioavailability and, uh, as well as where we're at with understanding how it even interacts different inside the human versus other, uh, creatures.
Um, me meaning that, um, you can make this guesstimate based on the lab science, but, but you just doing like a quick scale up based on your experience, you're saying upfront that it would be hard to defend this number 'cause we don't really know yet. Correct. Okay, got it. But. CB D'S a a relatively safe molecule, so it's therapeutic range is probably gonna be best, uh, gauge at what condition you might be trying to use it
for. Um, and I think the idea of using it for neurogenesis is really unexplored, especially in humans. So we, we have to, you know, traverse slowly with that recommendation. Yeah, I, I, I understand that. I mean, that's one of the reasons why I, I, it took so long me, for me to find you and hunt you down in Australia. Right. There's just not a lot of people who are doing this particular work that you're
working on, um, around cannabinoids and neurogenesis. Um, you know, uh, uh, I'm, I'm gonna ask you a quick math question just because you play with these numbers all the time. Um, but you know, the three to 10 milligrams per kilogram a day, you know, the very rough guesstimate that you gave, do you have an idea of how many milligrams a day that is for, say, somebody who's 150 pounds? We don't do metric here, so I haven't gone back and forth between, you.
Know. Yeah, I think that's around about 70 kilos. So you say that upper threshold times 10, 700 milligrams a day. Cool. Thank you. Appreciate. You doing that. Uh, lower threshold, uh, let's just say you weigh more and make the numbers easier. Say you weigh a hundred kilos and three milligram dosage would be on the lower
end around 300, uh three. No, no. Got, I think a recent study just came out that synthesized all the literature that they've done in human studies and said the safe dose is around 60 to a hundred milligrams per day. So, uh. 60 To a hundred milligrams per day when we were talking about 300 to 700. Yeah. That's more the therapeutic range. I see, I see. Yeah. So we talk a lot here on shaping fire about the compare and contrast
between, um, isolates and whole plant medicine. And, you know, anybody who listens to the show knows that, uh, I'm no, I'm no stranger to be pushing whole plant medicine versus isolates. While, while definitely also understanding that isolates have their place. For example, if you need a novel cannabinoid and it makes sense for you to spike your, your cannabis oil because you're, you need a cannabinoid that's very hard for you to get or to grow or something
like that. Um, like, like many of us did in the early days before we had access to C B D plants, but we could get C b D isolate from Europe. Um, and, and I, and I also know that most of these studies are using isolates because the studies, um, you know, are, they're, they're looking to set up future pharmacology and they want the isolates so that they can, you know, reproduce their results.
And also it is just, you know, a lot easier and, and less, um, I don't know, sloppy to work with isolates than it is trying to deal with, you know, a a direct whole plant resin. All of that said, we also know that the, you know, we're big believers in the entourage effect and the fact that having, you know, groups of various cannabinoids together, they, they, they act synergistically with each other, um, so that everybody can do their job better.
So all this just sets up this question. Um, do you think that you would get, um, a, a a better play from your C B D if you're, um, taking it in a whole plant cannabis oil, you know, commonly known to as like an R S O or something? Or, uh, do you find there's, or, or from your research, would you expect there's not gonna be any difference between the isolate and the whole plant? Or perhaps even it's, it's favoring the isolate, which will make me cry, but I'll believe you.
I mean, that's a, that's a big question. Mm-hmm. , but we'll go with, uh, let's just look at C B D as a molecule first. So we could call that an isolate or C B D and what we've learned on a molecular functional level has mostly to do with the isolate. So if we were to say that's, you know, the, the backbone and we were to go whole plant, uh, that it, we'd maybe have to look at extraction methods and what is in that, uh, whole plant extract.
But let's say that whole plant extract could be broken down into, uh, C B D, maybe some small, small amounts of other cannabinoids terpenes, which could be, you know, quite a few mm. Some can fla in. 15 Something, and then you have your canna flavin on top of that. And each of those has a little bit of a role in therapeutic, uh, targets. So I would, you know, I'm a, I'm a whole plant,
um, promoter as well. I would think you would get, uh, some sort of synergistic effect from a whole plant extract, and then we can get into maybe the bioavailability that it would enhance, uh, because terpenes do play a role in, you know, enhancing the bioavailability of, uh, cannabinoids.
That's interesting. So, so, um, we would think that the, the, the, the whole resin preparation, um, would just, you know, join with our body systems at a, at an easier and less frictionous rate than a straight isolate would. I think so. Mm-hmm. ,
I think our body would be able to handle it more intelligently. 'cause that's, if we were to look at the, you know, the, maybe the potential of 10,000 years of co-evolution with the plant and the fact that we could have been using this plant for that long, then our body would have more of an intelligence with it as a whole plant extract than an isolate. Right on. So, um, we. Have seen like an observationally in patients with severe epilepsy.
There have been notable improvements with far lower doses of C B D extract than purified C B D. So there is a little bit of, uh, clinical research around that, um, but not yet with neurogenesis. Right. On. Great. Thank you. Um, alright, one more question before we go to break and, and, and this one is kind of a corollary question,
but doesn't really stem from the last one. So, so we've been talking about this neurogenesis process that we like to, uh, you know, turn up the volume on by taking C B D and and T H C. And so everything is happening more robustly and, um, um, I was gonna say aggressively, that's probably not the right word, but robustly, um, I'm assuming that there are some either, um, um, resources the brain may need or damage that may have occurred to the brain that is impeding neurogenesis that not even
adding cannabidiol can overcome. And so what I'm specifically looking for are any suggestions you might have of, of, um, you know, pre-existing damage to the brain that might block C B D from doing its job because that, that brain issue is actually shutting down the, the neurogenesis in ways that the C B D cannot overcome.
Yeah. I think that's when we start getting into, or this leads into, uh, Alzheimer's disease, you know, once you get beyond that point of dendra and uh, axonal breakage, there isn't much of a chance that anything's gonna save that neuronal cell. And if we look that as a collective hole or a neuronal circuitry, uh, connection line, and if a certain amount of it gets broken down, then you know, the chances of recovery are gonna be pretty minimal to that circuit.
Uh, so getting on board sooner rather than later would make c b D more beneficial. Right on. Now, um, I know your specialty is more in Alzheimer's,
which we talking about at more length later. Um, but the, the other disease that I'm often talking to patients about that involves neurogenesis is Parkinson's. And, um, you know, I've, I've I've been told by scientists, you know, just, you know, standing at conferences and stuff that, that one of the reasons why C B D helps Parkinson's patients is because it causes neurogenesis. Because a good deal of the impact from Parkinson's is because they are losing
their dopamine excreting neurons. And, and, uh, that's a one-way trip if there's not neurogenesis. And so C B D is causing more of these, um, these brain cells to come into existence, which, um, kind of like holds the line on the Parkinson's to hold it from, from getting worse. A do you have any point of reference on this to speak to it? And, and, and b, does, uh, is that process potentially similar like to the one that we just described, um, around, um, Alzheimer's?
Yeah. If we were looking at, um, a level of dopa meic neurons in their ability to produce dopamine, which I just kind of recently learned, about 80% of Parkinson's is, or is due to the lack of dopamine and due to the lack of the dopamine producing neurons. So if we could create more of these neurons, technically we could create more dopamine and effectively treat Parkinson's disease. And Parkinson's disease also has a protein very similar to Alzheimer's disease.
So Alzheimer's disease, the main pathological hallmark is amyloid beta. And in Parkinson's it's alpha-synuclein. And C B D has shown or demonstrated in preclinical research that it stops the aggregation, not completely, but it will help augment some of the aggregation of these two proteins that create quite a toxic environment, extracellularly, which affects their function and eventually creates cell death or, you know mm-hmm. .
Uh. The no longer functioning neurons which connect to each other and create a communication line throughout the brain. Wow, that's really interesting. Alright, cool. Well, thank you for that statement. Um, let's go ahead and take our first of two short breaks and we'll be right back. You are listening to Shaping Fire, and my guest today is Phytocannabinoid researcher state and laws Fish poop. Brand fertilizer is an all natural fish poop concentrate with nothing added.
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Email hotspot@shapingfire.com to find out more. Welcome back. You are listening to Shaping Fire. I am your host Shang Los, and my guest today is Phytocannabinoid Researcher State and Laws. So during the first set, we, we brought ourselves to an understanding of what neurogenesis is and how c b, d and T H c and to a lesser degree, some other cannabinoids, we think, um, encourage and, uh, cause neurogenesis to be, uh,
more robust. Now, here in set two, we're gonna start talking about not how to, uh, make these new, um, brain cells. We're gonna talk about how to protect the ones we've got. So, um, so staton, you know, let's move on from neurogenesis. Which components of cannabis resin can be considered neuroprotectants, and can you give us a general definition of what that means?
Yep. So if we get back to that ability to protect a neuronal cell from, um, cell death or from Misfunctioning, there are many different constituents or chemicals inside the cannabis plant that could be made into a cannabis resin that will protect neuronal cells from things like the inflammatory response and, uh, free radicals such as reactive oxygen species. So they can either act as an anti-inflammatory compound or an antioxidant to protect neuronal cells.
That actually, when you, when put that, when put that way, you know, the fact that they are components of cannabis resin that decrease inflammation and free radicals. That's a lot of different stuff actually. Yeah. So that's, uh, that's the, the characterization of one compound and its ability to do multiple things in different systems or places in the body.
So, so whereas when it comes to neurogenesis, looking at the variety of all the components of the resin, you know, it's, it's primarily C B D, certainly some amount, T h c, maybe a bit a few others. But when we talk about neuroprotection, um, cannabis resins, it's just essentially a soup of, of good things that actually protect our brain in various ways.
Um. Yeah, I mean, if we start with the 545 identified compounds and we break that into 140 terpenes, 104 cannabinoids, 26 flavonoids, 20 steroids, and a whole bunch of lignin still being still OIDs and who the hell knows what else we're finding inside this in the next 20 years. Uh, and then we're mapping out their, uh, potential to be neuroprotective, uh, through all the different mechanisms.
It gets really complex really quickly. But as a, a blob, uh, cannabis resin, I think we, we've got a few, few things we can discuss. Um, it seems to me like this would be very, uh, since there are so many, uh, participants in neuroprotection, I would think that it would be hard to research them because you gotta tease 'em apart and they're all working together in very high numbers and symbiotically.
Yeah. Yeah. Um, alright, so, so when I asked you, you know, what are they protecting us from, essentially the, the first two you mentioned was inflammation and, and free radicals. Is that just like a huge bucket that, that holds just about everything or are there a couple others that you could
check off for us? Uh. Well, we can, maybe if you want to talk a little bit about the mechanisms, but if we were to look into diseases and what type of proteins might be causing these inflammatory responses and free radicals, we could look at, uh, for Alzheimer's disease, amyloid, beta and tau, which are two proteins that are forming to create inflammation and free radicals on the inside the cell, and also inflammation outside the cell and how C B D can play a role
in reducing inflammation and also, uh, helping with the maybe even endogenous ability, so the cell's ability to, uh, deal with these free radicals. Mm-hmm. , um, these, um, the, the, the, ah, I don't like putting all, I don't like putting like Alzheimer's and dementia all in the, in the same basket, and I don't, I don't like to generalize them,
so I guess I'll just stick with Alzheimer's. Um, um, do we understand, um, the functioning at this point of, of Alzheimer's in the brain where we are able to get down to the specific mechanisms that, um, uh, of, of cannabis neuroprotection that's working? You kind of, you gave me a little, a little bait there with the mechanism and, and honestly, if, if you can make it, um, understandable to some degree to a lay person, I'd like you to go through that.
Yeah. So if we looked at a protein in the brain that forms naturally, amyloid beta is a naturally forming protein. It, it, it's just part of everybody. Everybody's got some of that floating around in the brain. What happens is it begins to aggregate and when it aggregate, it sort of clumps together and forms a plaque. And when too many of these plaques build up inside the brain, they begin to form inflammation. They also begin to irritate the cells and they form reactive oxygen species
lipid peroxidation. Now, one mechanism that, uh, C B D and some of the other terpenes can do is actually to stop the aggregation of this protein. Therefore, it will reduce the cascade of negative effects from this protein by just becoming an anti atory agent. Therefore, protecting the cells from cell death, either from an inflammatory cascade of chemicals or from an overproduction of reactive oxygen species, it all leads to cell death. All right. Um, I've got two kind of corollary questions.
The first corollary question is, um, if, if inflammation is, um, trying to inhibit, um, neurogenesis and by using cannabis, we're decreasing the inflammation and, and helping the neurogenesis, you know, I talk with so many patients that have got all these different inflammatory diseases from, you know, autoimmune and rheumatoid arthritis and, you know, just like, you know, just, just like there's the whole list of these inflammatory diseases that are so
common in our modern world. Uh, um, will this body inflammation also be likely presenting in the brain? And, and, you know, the, the rheumatoid arthritis patient with all this body inflammation and all their joints is probably also having a difficult time, uh, with neurogenesis, but that's just not the part that's usually talked about in their disease.
Yeah, it's a really complex one. Uh, yeah, I would say that if there are targets inside certain cell families or on the cell, inside cell families that are the same similar targets in the brain cells, then we could say like one target that c bds pretty good at, uh, activating is the P P A R gamma uh, receptor, which once it's hit, it sort of blocks this cascade to pro-inflammatory molecules such as, you know, like the tumor necrosis factor alpha, the interleukin one,
and then all these other cytokine released, which, you know, this does, it is fueled by amyloid beta, but there are other factors that go on in different sort of areas of the body where this could be a target for C B D to reduce this inflammation. Um, you know, for a lot of lay folks, um, you know, neuroprotection and neuroplasticity, uh, for a lot of folks are like synonymous and they kind of use them
interchangeably. Um, uh, how much truth is there to that and, and if they're not the same thing, which I'm assuming they're not, um, would you explain what neuroplasticity is? I can give it my best attempt with saying neuroplasticity is the ability for the brain to communicate in a simple way. Mm-hmm. . So it's like, uh, uh, this communication that we're using right now on the phone, if it gets real staticky, then it's not very plastic. We're not making connections,
we're not communicating. But if it's clear, then we're having some good neuroplasticity, which would involve function, would involve, uh, communication. It would also involve being able to, you know, 'cause even cells can sort of change their shape to allow them to communicate better, which might even fall in the form of resilience or neuroplasticity.
So I'd say it's function, communication and adaption to different things that we learn or, you know, I guess we're still trying to map that one out, but if the cell is healthy, it's gonna function better, therefore ob more plastic or neuro neuroplastic. Using layman's terms.
I can see how cannabidiol would add to neuroplasticity since we often think of C B D as a signaling molecule, and if at the heart of neuroplasticity is community communication and the ability to communicate, you know, throughout the cells, it would seem that adding more C B D, um, would be able to, you know, encourage, uh, more and more rapid communication between the different,
um, you know, neurons. Yeah. Yeah. And one, uh, molecule in particular that I find interesting with CBDs abilities is to enhance acetylcholine, which is sort of like the master communicator between, you know, neurons and there's a particular enzyme acetyl colter raise
that breaks down acetylcholine. And, um, if we can block acetyl colter raise to a certain extent, we can enhance the ability of acetylcholine in its communication between cell and cell, which is actually some of the ad therapeutics drugs that are out there. Do so, and from that functional standpoint, C B D does in enhance the communication or the neuroplasticity between the cells.
So if, if we're wanting to use cannabinoids to increase our neuroplasticity, can you give me a couple of examples of, of things that either a, things that we might do that might decrease the neuroplasticity, or if you wanna keep it on the molecular level, the, the kinds of things that can inhibit our neuroplasticity? Uh, well,
there's lots of toxins that will get in there and block the communication. I, I think if you overdue t h c, it can somewhat crowd the communication line or just, you know, stop it wanting to function altogether, uh, which has its benefit and, and some degree. Uh, but if we wanted to enhance the communication, then we gotta make these cells functional and as healthy as possible. So there's a lot of factors that go into how to enhance this communication.
So it sounds like we're talking about like, you know, um, you know, everything en environmental toxins, um, you know, probably a lot of different types of pharmaceuticals, um, alcohol, um, you know, huffing, acetone, you know, there's probably lots, all all of these things probably ha uh,
would impact neuroplasticity in different ways. So that we're kind of, we're kind of back to the place where we were when first set we're, where we're talking about, you know, good living helps all of this stuff we're talking about. For sure. Mm-hmm. . All right. So, um, let's, let's now focus on the impacts of a brain, um, without neurogenesis, which will kind of set us up for the third set, talking about, um, um, you know,
some of these ways that, that we can help patients. So, um, I've always just assumed that, um, decreasing neurogenesis is generally a part of aging, and based on what we just said, if we're doing more things that age us, like, you know, smoking tobacco and drinking and, and you know, poor sleep and all these things that, that, um, these will all impede neurogenesis, um, over time. Um, is, is, is that true or is, is there a particular mechanism at the heart of it that I'm missing?
No, that in general, I'm going to agree with you that just aging itself will promote the degeneration of, uh, neuronal cells and inhibit the ability for neurogenesis to occur. But if we looked at, say, a toxin, like even alcohol, CBDs comes in there and we've seen that it can, one, reduce your cravings to take it, and two can also protect, uh, the liver from inflammation and even brain cells from oxidative stress.
Uh, so, you know, to some extent there is some things we can't avoid, but if CVDs coming around and, you know, showing us that, hey, this can show some neuroprotection alongside of a neurotoxin, then, uh, we've, we have a, at least some defense, uh, that we can use outside of just, you know, lifestyle. Right on. Great. Well, I don't think we need to, um, to, to bang on the eat hold foods, get exercise live, well drum anymore.
Um, I think we're pretty much set. So, so dear listener, um, stay with us. We're gonna take our, uh, second short break, but when we come back on, uh, for set three, we're gonna talk, uh, specifically, um, about Alzheimer's and dementia and also longevity. So if, uh, if you, you know, if you're presently pretty healthy, but you just wanna stay that way, um, uh,
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Shaping Fire. Instagram has follow-up posts to shaping fire episodes, growing and processing best practices, product trials, and of course, gorgeous flower photos. The Shang Lo Instagram follows My travels on cannabis garden tours, my successes and failures in my own garden, insights and best practices from personal grows everywhere and always gorgeous flower photos on both profiles.
The emphasis is on sharing what I've learned in a way that you can replicate it in your own garden, your own hash lab, or for your own canna Apathic health. So I encourage you to follow at Shaping Fire and at Shang los and join our online community on Instagram. Welcome back. You are listening to Shaping Fire. I am your host Shang Los, and my guest today is Phyto Cannabinoid Researcher State and Laws.
So here we are in the big third set. So Staton, you know, at the end of last set we were talking about how aging and, you know, depending on how fast we're aging, because of how much we're riding our body, hard and abusing it, you know, all of those things will decrease our neurogenesis and, uh, C b, D and t H C and some other cannabinoids can help support neurogenesis.
But, um, you know, there's only so much can be done if, if, you know, we're our body is aging right, either on its own or because we've been living hard. So would you explain a bit about, um, uh, you know, how this lack of neurogenesis, um, well, actually before we go to that, I want to ask a, a definitional question. You know, so, so often people are, they'll say something and then they'll just say, Alzheimer's disease and dementia. Like, like they'll group them together,
but they won't put them in the same bucket. So if you could, would you just give us a brief understanding of what's different between Alzheimer's and dementia? Because as a lay person, they kind of sound the same to me, but people always talk about them separately. So I'm guessing there's a difference that I just don't know. Yeah. So dementia can be categorized into different forms, but Alzheimer's disease is the most common form of dementia.
So if you were to say dementia is where these protein aggregates start to form and cause memory loss or body dysfunction and how it operates as it progresses, then it might form into a specific type of disease from dementia called Alzheimer's disease. Alzheimer's disease is kind of the end of the road of a form of dementia. It's the most common form. Mm-hmm. .
So, um, we talked a little bit about the mechanics, uh, last, uh, set about, you know, precursors to dementia and then Alzheimer's and you know, how it, how it progresses. Um, uh, and, and now you're talking about, you know, the d the different, um, uh, symptoms of the ailments, you know, um, um, uh, forgetting things and um, uh, uh, the changing relationship with one's body.
Can you just pick one or two of those and, um, and explain to us the mechanics of what's going on with Alzheimer's to cause the symptoms? So, so moving from what causes Alzheimer's two, what does Alzheimer's cause? Okay, well, I'll go with just the big definition and filter it down to what it, what happens mm-hmm. .
So if we have these natural amyloid beta proteins in the brain and they form aggregates, then at the same sort of time inside the cell are these neuro ular tangles, which consists of the hyper phospholate tau protein. Now this is partnered, uh, this deteriorate deleterious pro part process is partnered with reactive oxygen species, reactive nitrogen species, which is your oxidative stress, mitochondria damage, uh, redu that's inside the cell, outside the cell.
Reduction of acetylcholine levels, which we're talking about plays a role in the neuroplasticity or the communication. Then these networks begin to lose their connections. So misplaced networks among neurons inside the hippocampus, we've seen that the, it actually shrinks and we get this chronic neuroinflammation causing memory loss and cognitive impairment. Eventually, we can't even, you know, take care of ourselves in the end.
Um, this idea of misplaced networks, um, that's a really, um, that's a very efficient phrase because it really does describe what I experience when interacting with, um, Alzheimer's patients. Um, and also there's something about that phrase that captures some of the sadness of it too. Yeah, it's, uh, it can, you know, really take you down a road that affects you and your family members.
So, alright, so, so this brings us to a place where we know neurogenesis and neuroprotection are essential for our brain to function properly over the long term. And when it slows down with age, it leaves us open to debilitate debilitating brain issues. And we also know from first set that the cannabis compound, that the cannabis components, um, can support neurogenesis and neuroprotection. So,
so obviously we've made the case like take some cannabis, right? So, so, um, so I'm gonna ask you about, um, some cannabis protocols that you think that might make sense for someone who, who still has brain health and wants to keep it. And then, and then I'll kind of reapproach the question again for somebody who's already experiencing, um, you know, problems. So, so I guess this first one, let's, let's throw this kind of in the,
in the longevity, uh, bucket. Um, I've been doing a lot of thinking about cannabinoids as a, as a longevity tool and, and it really seems to work. So, so, so let's say that like, you know, even though we know that everybody's got something wrong with them, um, well, let's say that we're talking about a person who's generally brain healthy and they're not, they're not experiencing dementia or Alzheimer's at this point, but, but they don't, they don't want to, right? And, and, or, or,
or maybe they're like me. And, and some of that stuff runs in the family, right? So I wanna, I wanna bio protect against it in advance. So, so what would you see as, um, a, a, a dosing protocol for somebody who is thinking more about, um, uh, longevity and, um, and, and, you know, long-term health, um, before something a brain disease has has shown up? Um, I guess we've gotta always throw that disclaimer, alert out, yes. This is not medical. See your medical doctor.
Mm-hmm. Or, uh, and make sure you see your phys physician before taking a substance that is new to your body. So, well, thank you for that's put that you beat me to it. Sat out on the table. That's usually my job. You got it. Thank you. . Um, and are we talking all cannabinoids or just c b D?
Um, well, um, I would like to hear what your, your blend would be if you're gonna, if you, you know, maybe you're gonna tell me that, um, you know, a a 20 to one of a, of a certain potency taken every day or twice a day, um, you know, at this point, um, you have got all of this various information already preexisting in your head. And so if, if you were to put together a best practice for a cannabinoid supplement to preserve, uh, brain health, what would it look like?
I would probably start with just c B D personally. Mm-hmm. , uh, if you'd never used cannabis, you're like, I've heard cannabis, uh, is gonna help my brain as I age now, I mean, even we go back 20 years from now, that was the, you know, talking, you know, the, the Devil's Tobacco mm-hmm. . And, uh, now we're looking at it as a way to preserve our brain. So let's start with C B D because it's probably the safest.
And I would almost have to say that if we're going to even ask this question, then we'd probably be concerned around the age of 30 to 40 if we're, if we're still healthy, you know, this is around about 65 is when dementia like symptoms usually present themselves. So we're beyond that adolescent phase where T H C is gonna be as harmful as what we've experienced. And so we're in that phase where either C B D or T H
C could be helpful. So I would say starting with C B D, 'cause it can start to maybe help anandamide do its, uh, do its thing with the CB one and CB two receptors, plus there's some other benefits that come along with C B D. Now, if C B D is not effective and you slowly increment your dose and you're, you know, taking a plus a hundred milligrams a day and still not seeing anything, then I would start adding T H C and, and like you're saying,
maybe starting at that 20 milligrams of C B D to one milligram of T H C, and maybe we start, then we go 20 to five, 20 milligrams of C B D to five milligrams of T H C or maybe even go 50 C B D to five T H C. But I would slowly increment, especially T H C is, and even more specifically if you have an underlying psychiatric condition with T H C, because it is quite psychoactive. And then finding that that right milligram dosage and, you know, uh, uh,
T H C has its own unique benefits all in its own right. Uh, with helping the brain in many different facets outside of what we've mapped out pharmacologically, I believe. So start slow, see which one works best for you, and generally having a higher amount of C B D to T H C.
Right on. That's great. And, and you know, if, if, if you're at home listening to this and you're thinking about putting together, you know, a protocol of your own and, you know, maybe you are fortunate enough to be in, in a location where you can, you know, grow your, you know, high C B D, very low T H c, um, you know, plant some kind of high C B D hemp plant or something and make your own R S o,
um, that, that's very fortunate. And, and don't be shy about, um, you know, spiking it with C B D isolate because, you know, you can get really high quality C B D isolate out there right now. You know, you gotta shop around, you know, fi you know, find, find somebody who, who stands by their cleanliness and their tests, you know, like, like a future compounds or somebody. And, um, and then, and then don't be shy to spike with that to get up to the,
the C B D numbers that you're looking for. Um, because for, for most folks growing your own high C B D hemp plants and processing it all, um, is just not going to provide you with, you know, a hundred milligrams of C B D A day plus T H c. It's, you know, you know, if you've got a big farm like, you know, may maybe, maybe you're that much of a baller, but for most people, that's not the case.
And um, and you know, I used to talk trash about this approach, but, you know, I think that part of what's important is that we all remain active learners, right? And, and while I would love there to be, um, so much, you know, c b D resin available to everyone at cheap prices that, that we could only use that well, you know, when it comes to our health, um, you know, sometimes, sometimes we have to do it, um, in the way that works. Um,
not, not the way that we necessarily want it to be. So, so anyway, um, I just share that because I had to turn a corner about using isolate for some applications and, and, um, it wouldn't surprise me if some of you were the same way. So, so there's that. Alright, so, um, so, so now that we've got this, so thank you for this protocol. This was, this was a,
this was exactly the level of specificity that I was looking for staton. So, so let's talk about a, um, a, a a different protocol because now, and, and who knows, it might be, it might end up being the same protocol for you, but, but now we're talking about somebody who is an Alzheimer's patient and you know, they've, they've already been talking to their family that they wanted to try this and their family is in support of it, I hope, and everybody's working together.
Um, would you make any changes to this protocol to somebody who's already experiencing symptoms, who's already on this path? Not really. Mm-hmm. , um, 'cause we just don't know how they're gonna respond to either compound C B D or T H C or the plethora of other phytochemicals in this
extract. But, you know, if, if one's extremely irritable, then you know, a faster acting lower dosage in what you can get your hands on, um, approach could be T h C, uh, I mean, because it's, it's a tricky question to address this with so many different countries, laws states and, uh, financial burdens that getting a hold of these compounds will,
will do for that particular patient. So, I mean, it's easy to recommend if, if you're in a state that it's highly available, but it's even more difficult to recommend when one can't even afford the medication, especially when you're saying, oh, you know, you might, you need to be taking around a hundred milligrams of C B D to get any sort of effect from it when, you know, like here in Australia, the average milligram is about 10 cents,
so you're looking at a hundred dollars a day for a medication that might work. Versus if you can get your hands on, you know, a hundred milligrams A T H C and divide that between 10 days, you might be getting more, uh, therapeutic targets ticked by a less expensive, Uh, protocol. So once again, con consult your medical doctor first, and depending on where you live, it, it,
it could somewhat dictate this protocol. So start slow CCB d's a little bit safer, but you might work better with T H C, especially in later stages of Alzheimer's disease. Right on. So, um, what will our goal be, um, when the patient or, uh, is taking the, the protocol, um, with, with neurogenesis? Are we, are we just trying to like, hold the line or is it possible that we can improve the patient?
Um, because, uh, I believe that the, the case is, is that when we, when we lose, um, neuron producing, when, when, when our, when our neurogenesis flags and slows, um, it's, it's, it's harder to create new cells that do this. And so what we're just trying to do is, is hold the line on our ability to produce to cause neurogenesis where it is and just decrease the, the sliding of it.
Um, is that a, is that a correct understanding where, where, when we're supporting neurogenesis, we're just gonna be supporting where we're not, where we're at, we're not necessarily going to be improving it in such a way where, um, you know, we could pull somebody back from the grips of Alzheimer's, for example?
Yeah. Uh, if I've always got hope that no matter who you are out there, you're going to have the ability to create more brain cells in the right environment, let's just say through your lifestyle and through maybe some, uh, supplements that includes cannabinoids in the word supplements to
your protocol. Now, if you've got enough, uh, neurons that are functioning correctly in your goal here is to preserve these neurons, we're looking at, you know, there's some potential for these cannabinoids to help these neurons from being affected by whether it is reactive oxygen species, these cytokine storms from inflammation, uh, and also from acetyl colter raise from breaking down acetylcholine.
So with these exogenous cannabinoids, they might help with our endogenous OIDs such as C B D and anandamide, or T H C might go in there and help stimulate some more, uh, proliferation of these brain cells, and they might protect the ones that we already have and the functioning or the
neuroplasticity of these brain cells. So yes, there's a lot of potential here for this to help on a cellular level, and then also on a behavior level of why these, uh, symptoms of, let's just say Alzheimer's disease could be modified by these chemicals. Right on. I follow that. Okay. So let's, let's take, um, a step back one more time, uh, as we're wrapping up here. Um, so,
so we've, we've talked about neurogenesis and neuro protections. We, we understand how they work, we understand how our ability to do that ourselves worsens with age and how we can support that system by using, um,
by using cannabinoids. Excellent. And, and we've, we've looked at the applications for, you know, just regular folks who wanna take it as at, as a supplement and the very similar protocol for folks who are actually, um, showing the impacts of the lack of neurogenesis in things like Alzheimer's and dementia. So, so with all of that, you know, I, I've not really seen it called this, but for me, that sounds like we're describing C B D as a nootropic. Do you consider c b D be to be a new tropic?
Yeah. If it can improve cognitive function, then it would be, uh, I guess fitting underneath the umbrella of a new tropic. Yeah. That's, that's the way I see it too. And, and so far I haven't seen it marketed that way, but, um, it's, it's interesting 'cause like nootropics are like super hip for the, you know, the longevity folks and, and C B D is hip with a different group of people, but I haven't seen anybody like kind of cross market to both groups and call it
a nootropic. So, um, what I'd like to, to end the episode with, uh, Satan is that I know that, uh, you are, um, you know, you are a research scientist and you are looking at the specifics of neurogenesis, but I also know that, um, you know, you are a whole food advocate and you are a healer and, and you know, you teach, uh, yoga and, and so you're kind of a, you know, a holistically minded researcher who's, you know, doing this, this balance between holistic mindset and,
you know, western medicine, which is gotta be a very interesting balancing act for you. Um, but, um, because you think about this all the time, um, I'd just like to like kind of hand you the mic and have you kind of take us out of, um, you know, what advice would you give to a human who wants to keep their brain, um, functioning as far into life as they can with all the benefits of neurogenesis and neuroprotection.
Would you just describe some of the, you know, lifestyle attributes that this person may want to consider beyond simply taking a C a A A C B D and potentially t h c protocol as we've described? So, are we addressing just the general person that's after mine longevity? Are we addressing the Alzheimer's patient? I, I would say just a regular person. Um, somebody, somebody who's not, uh, uh,
you know, not experiencing Alzheimer's yet. Um, just, just somebody who wants to, you know, keep their brain healthy. This is a general brain health question. Okay, well, we'll break it down with, uh, the necessities again. So we gotta have oxygen, water, and nutrients. So oxygen with, uh, breathing, we all can learn to breathe better. That's the truth. How we breathe. You can get into the anatomy, but simply, if there was one word I would say to use and to learn would be UJA breathing,
and that's a yoga concept. I can get into that if you'd like, but basically it's, it's a way to take air in and outta the body with more efficiency. Maybe just spell it. 'cause we, we won't go into it today, but people might wanna look it up. I think it's u uh, . Sorry, I didn't mean to. Do that to you. U j Yeah, it's funny. U double j a y i. Great.
Uh, second. So what goes with yoga course is posture, uh, learning how to lengthen the spine, keep it straight, which supports the blood flow or the nutrients into and out of the brain, which the next one would be understanding a little bit about the lymphatic system and helping the clearance of too much of these aggregate proteins
throughout life. So it's also making sure your body, let's just call it clean and it, uh, is functioning to deliver nutrients, but also to remove or detoxify, uh, these potential proteins in the brain that are gonna mess you up, which is what some of the, you know, ad drugs recently come out to do, is actually to remove the proteins. So we've got, uh, breath, good clean water, um, and which considers, you know, some electrolytes if it came from a really clean natural source to make cellular
hydrated have good posture. And then we get into, you know, doing our best to not expose ourselves to too many toxins. So trying to live in a natural place, trying to get outside. And if we looked at what can stimulate neurogenesis, I think probably one of the biggest ones is exercise. And, uh, you know, exercise produces more of that brain deprived nootropic factor. It also creates more endogenous cannabinoids. So those two combined together is what helps the cells proliferate.
Then we can kind of get into that neuroprotection side with, uh, some of the protocols of our supplements that will help protect us. So when we get into nutrients, I'd probably be looking at, uh, your meg omega threes, like E three live, which is a, it's, um, uh, an algae that's quite high in D h a and e p a, which is known to support brain function. I look at making sure the diet is actually extremely high in plant secondary metabolites, which those include a big pool of the polyphenols.
And if we looked at those specifically, it would be the flavonoids and even maybe look at getting the microbiome up as far as the good bacteria. So making sure you take some form of a probiotic on a regular basis, whether it's through sauerkraut and the diet, or whether it's through, you know, active. Yogurt or something. Yeah, something like that. And maintaining that with lots of fiber.
So you got your pre, which is your fiber, you got your pro, which is your bacteria, and you combine those two together and you get these postbiotics. So having a healthy microbiome, these molecule or not molecules, these bacteria in your gut will chew up fiber and basically create these postbiotics,
which are nutrients that they create that are good for the brain as well. Like, for example, a lot of these flavonoids or polyphenols that we consume don't actually get into the body till they hit the, the gut bacteria,
and then they get turned into things that are gonna be good for us. So, uh, and then, you know, being positive about life, I think cop probably could be the number one thing to have a bit of a passion for whatever you're doing in life, whether it's doing the, the laundry or the dishes, just, you know, being positive through the whole process, having a will to live will ultimately expand your lifespan.
So keeping yourself healthy and feeling as good as possible definitely helps with that will to live.
Excellent. I think that's a great list. And, and I gotta admit, some of it isn't, you know, like the exercise, um, isn't too surprising, but to, um, to see it put together in such a elegant package with explanations about why, um, I, I always, I always find it easier to do the healthy choice when I understand why I'm doing it instead of just like feeling like I'm not allowed to have something anymore, which, um, doesn't usually work super great for me, , but, um, but, but,
but getting inspiration to go towards something I do want, like long-term brain health, especially since I've already had a brain injury, I don't really have anything to, you know, I don't have much left to lose, you know, I need to, I need to protect what I've got. So, so anyway, um, state you, you've just been like absolutely delightful.
I appreciate your ability to translate, um, a lot of this, you know, hardcore bench science that you do, um, you know, at the university, uh, to translate it into lay language so that, um, you know, you can bring some of, um, you know, some of our lay people along with the citizen scientists, along with, you know, the caregivers and the doctors who listen to show you kind of like provide, um, in, in information in a way that, that we get to bring everybody along and,
um, you know, that's not a skill that everybody's got. So, um, I appreciate that skill in you and, um, your good heart and your, your wanting to, um, you know, uh, be here and, and help. And also your willingness, like you're, you're doing this interview in the future, you know, since you're in Australia, you're actually doing this interview tomorrow while I'm, I'm having this interview tonight, so I, I appreciate a little bit of time travel as well.
So thank you so much for being here on Shaping Fire. Well, it's been a pleasure and I hope all the listeners out there, uh, benefit from everything that's been discussed over the past 90 minutes, and we keep, uh, transversing into the future to help each other understand, you know, how natural plants and behavior and lifestyle modifications can all benefit no matter what stage of, uh, life that we're at.
Excellent. Thank you so much. So dear listener, if you want to get in contact with state and laws, there is one way to do it and you can reach him, uh, through his LinkedIn profile. Now, be realistic about the time. It might take him to get back with you because he is actively, you know, working at the university and he's in the lab every day. He's not like other folks who are sitting at their computer all day or have PR
departments to get back with you. You know, if, if, if you, if you have a question, if you want to connect or, or, or especially if you have an opportunity for him, um, you can, uh, reach out to him, um, through his LinkedIn. I also wanna, uh, uh, plug two other episodes because if you like this idea of, of longevity and, uh, nootropics, uh, you probably also want to check out, uh, the last episode of shaping Fire number 1 0 8 on Longevity and the
Endocannabinoid System with Hunter Land. Um, we talk a lot about keeping your endocannabinoid, uh, system functioning over the arc of your life and things that you can do to keep your endocannabinoid system functioning over time. Um, and then also, uh, shaping Fire, episode 36, which goes all the way back, like three or four years ago now. Um, and that is with the Fantastic Robert Litman. And this is an episode on,
on Breathing, on cannabis and Breathing. And I gotta say, I think it's one of my favorite shaping fire episodes because of the uniqueness and usefulness of the information. He talks about, you know, how we breathe the common mistakes people make in breathing, um, how breathing in, um, uh, combusted smoke and vaporizing, you know, how that functions. And, um, and, and, uh, here he, he offers some, uh, exercises to, uh, improve your breathing as well. It's, it's a very, uh,
delightful episode. And that's Shaping Fire, episode 36. You can find more episodes of the Shaping Fire Podcast and subscribe to the show@shapingfire.com and wherever you get your podcasts. If you enjoyed the show, we'd really appreciate it if you would leave a positive review of the podcast. Wherever you download your view will help others find the show so they can enjoy
it too. On the Shaping Fire website, you can also subscribe to the newsletter for insights into the latest cannabis news exclusive videos and giveaways on the Shaping Fire website. You also find transcripts of today's podcast as well. Be sure to follow on Instagram. For all original content not found on the podcast that's at Shaping Fire and at shang los on Instagram, be sure to check out the Shaping Fire YouTube channel for exclusive interviews, farm tours, and cannabis lectures.
Does your company wanna reach our national audience of cannabis enthusiasts? Email hotspot@shapingfire.com to find out how. Thanks for listening to Shaping Fire. I've been your host, Shang Los.