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cover of The KJM Podcast raw audio 19
The KJM Podcast raw audio 19

The KJM Podcast raw audio 19

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The speaker is introducing a new segment on their podcast where they will have solo episodes. They plan to discuss various topics, starting with a book on neuroscience and the effects of exercise and diet on the brain. They also mention a paper on distracted driving and another paper on Alzheimer's disease and stress. They describe their reading style as "weaving," where they read a page, research related topics online, and then return to the book. They talk about a study on the effects of exercise on students' reading comprehension in a school district, which showed significant improvement. They highlight the importance of incorporating physical exercise into the curriculum. Hello everyone. Welcome back to the Tom Maxwell podcast. Today is the beginning of a new segment on the show, which is going to be solo episodes featuring just me. On the regular podcast, I interview various guests such as psychologists or teachers or cultural leaders and we talk about various topics on the show. But for this segment, it would just be me and the camera and I would try to be myself and be as informative and entertaining as possible. I have a guide, but I doubt that I will use it. But on this first, not the first episode of the podcast, but the first solo episode, I decided that we'll do different topics or I'll have like a set topic so we know what we're getting ourselves into. So I won't yap too much. So we'll just get into it. Today we're going over three things. Number one is this great book that I read that was a gift by someone, Spark by John J. Rady. This is a really great book. It dives into neuroscience and how exercise and diet plays a huge effect on the brain. We're going to get into this, review it and talk about some of the things I agree with, some of the things that I have questions about and why I encourage you all to read it. That's the first thing we're getting into. Second thing is a paper on distracted driving. This is something that I'm reading in my university now because I'm pursuing a bachelor's in psychology and then applying to medical school to get into an MD, PhD program in neuroscience. And this is a paper that we had to read. This, hopefully I'm talking in this right. I'm just getting a, wow, that wasn't supposed to happen. I'll cut this part out. Okay. We had technical difficulties. Sorry about that. This is a paper on distracted driving. So this is a study showing how multitasking behind the wheel plays an extraordinary effect on our cognitive skills, not our skills on driving. And it just pointed out very different aspects of how our cognition divided attention can impair our performance behind the wheel and certain measures that we can do to prevent that. So I thought that was very important. And then the last, what we're going over is this paper on Alzheimer's through the lens of stress. It's called the Research Progress on the Etiology and Pathogenesis of Alzheimer's Disease from the Perspective of Chronic Stress. This is a paper that I read last year on Alzheimer's and this is what I plan on doing when I plan on applying to my MD, PhD program in neuroscience. I want to do a focus on neurodegenerative diseases and do Alzheimer's disease because something I'm just interested in. And I read that paper last year and from the lens of stress. So it was very important. So I'm going to tie how stress and elevated cortisol levels deal with our exercise and how that affects our cognitive ability. So I figured that this is all kind of together at one point. So without further ado, we're going to jump into Spark. This was a book that my girlfriend's brother gave me for Christmas and I almost read the whole entire thing on the ride home because I was that interested in it. So to dive into this, Spark by Dr. John J. Rady, Rady, I hope I'm not butchering his last name. Dr. John J. Rady is a psychiatrist, an associate clinical professor of psychiatry at Harvard School of Medicine. He practices privately in Cambridge, Massachusetts. Spark is a revolutionary new science of exercise in the brain and it dives into many different things other than just exercise. It talks about stress, talks about anxiety, major depressive disorder, and he really breaks down and he really goes into detail about how exercise plays a huge impact on our cognitive abilities and how we can help alleviate some of these illnesses that we see going around, these mood disorders going around, how we can naturally ameliorate them through just regular diet and exercise. And he goes over a very important case study that happened in the late 90s, which I'll go over soon. So that's a little background of Spark. I usually don't read books cover to cover because I get the gist of the book. I'll read a little, I have a weird, I actually have a theory. I don't think I've ever said this publicly. I have a theory of reading. It's called weaving. I don't know if that's ever a thing, but I'll read because I think of reading, if you think about reading, reading a page cover to cover, that's not how I think about reading. A good book, you never finish a good book. So I will read a page. Let's say if I'm reading a book on Spark, I'll read a page on these certain things here, these neurotransmitters that are activated when you're engaging in a high-intensity interval training or whatever. And then pretend I don't know what a HIIT workout is. So I'll say, hmm, so these levels are activated when I'm doing a HIIT workout. What is a HIIT workout? So then I'll put the book down, and then I will go to Google, and then I will Google, what is a HIIT workout? And then I'll look at the HIIT workouts, oh, this is when you're doing this and that, and you get your elevated blood pressure, and then this, and then this helps lower your what levels, and then we've seen these studies. And then I'll say, hmm, that sounds like an interesting study. So then I'll leave that Google page, then go read the study, and then circle my way back to the original text. And maybe that's not the most effective way of reading, but for someone who's me, like, your brain is kind of, I don't have attention deficit hyperactivity disorder or anything, but if your brain is all over the place, like me, I like to weave and see if I can direct my way back to the original text. I do that when I'm reading the Bible as well. It's very interesting when you're doing that reading the Bible. But anyway, we're gonna get back to the book. So this is a very interesting book, and I wrote a little bit of notes. Spark is a best-selling investigation to the effects of health, diet, and exercise on the brain, written by, like we just said, John J. Rady, including regular exercise in the curriculum. He goes over this remarkable study called Naperville School District, started in one school in Naperville, and then the curriculum began to spread, and more and more gym teachers were hearing about this, how they were incorporating gym or physical exercise into the curriculum, and then it began to spread and turn to an entire movement throughout the Naperville district. So without further ado, we're going to get into that. So what was the, so we're going on page, let's see here, I'm going to try to find my exact page on this, but I know I'm not going to find it. But anyway, so the Naperville was a teacher, you know, he was, uh, they had like their school, whatever, this particular school was in a lower kind of funded, not as, uh, not really up there, like kind of district, and this school, and the teacher was, I forgot his name at the moment, teacher was like, you know what, how are we going to, you know, get the test grades are not looking good, the, uh, everything was kind of just like, kind of murky, and then they had this idea, you know, what if we, what if we incorporate or make up it mandatory, that's called the zero factor movement, I think it was called the, uh, let's see. I'm going to cut this part out. Ta-da-da-da-da, welcome to the revolution. I'm going to miss it. So it became this big movement, and we're going to read a few sections from this, from the book, if I can find my place. The kids in zero hour hardy volunteers from a group of fresh freshmen required to take a literacy class to bring the reading comprehension up to par, workout at a higher intensity than Central's other PE students. They're required to stay between 80 and 90 percent of the maximum heart rate. What we're really doing is trying to, trying to get them prepared to learn through rigorous exercise, says Duncan. Mr. Duncan was, uh, the supervisor, um, at the time. How do they feel about being Mr. Duncan's guinea pigs? I guess it's okay, says Michelle. Besides getting up early and being all sweaty and gross, I'm more awake during the day, I mean, I was cranky all the time. Beyond improving her mood, it will turn out. Michelle is also doing much better with her reading, and so are zero hour classmates. At the end of the semester, they'll show a 17 percent improvement in reading and comprehension, compared with a 10.7 percent improvement among the other literacy students who opted to sleep in and take standard physical education. So one of the things that Duncan realized was, and it's very smart that he was able to focus on, focus early on, was the impact of the gyms and the physical education movement at that time. So he realized that, you know, there was a lot of kids who were, when you're going to a regular gym class or when you're working out, period, there's a lot of resting moments. There's a lot of moments when you're waiting for, you know, if you're playing baseball outside, you're waiting to get to the bat. If you're doing something like running, you know, you're kind of waiting there to, you know, get the time for the person running behind you. If you guys are like doing like shooting drills or whatever, there's like, depending on the size of the class, there's like 30 students. There's other students that are kind of just waiting around while the other people are going. They realized this early on and they adopted the zero, I forget what it was called, the zero hour. So the zero hour was what we just went over, keeping their heart rate at 80 to 90 percent. And the movement behind this was to prepare the students so they were able to read and be more effective in school. And this, you know, this study, I mean, it just started in this one school and then it spread throughout the whole Naperville school district. And what made it, you know, so interesting to me was kind of being like an exercise guy myself, knowing the relationship between keeping someone's cognitive ability going, jogging at the moment, literally, and then how that affects their, and then it had a positive effect of it had a 17 percent increase in reading and literacy. And that's just amazing, just seeing the relationship between your cognitive skills and your regular exercise and how that has a direct effect on how the kids were performing in school, performing in in-school settings, tightly, highly controlled settings. So imagine how better the impacts would be in a regular day life. And just to get a little, not sidetracked here, but just when we're thinking about, you know, the brain or we're thinking about exercise, you know, what is really going on when we're exercising or when we're doing resistance training or when we're actually reading? What is going on? So when we're exercising, it's, so the brain needs oxygen no matter what. If your brain doesn't have oxygen, well, that's how, in fact, 99 percent of deaths, you know, people say atherosclerosis or the number one cause of death, number one cause of death is, you know, cancer. The biggest cause, this is what everyone dies from, no matter if you're a burn victim, if you're a wounded, if you got shot, if you got blew up in like a, in the war or something, everyone dies of apoxia. That's lack of oxygen to the brain. So the brain needs oxygen in order to survive. I mean, it's an instant death. That's why when, I mean, not to get too dark, when people hang themselves, they disconnect a particular nerve, a particular muscle in the neck that separates the, I think it's in the spinal, I think it's in the brain stem. It separates that nerve so then oxygen can no longer get to the brain and it's one of the quickest and most less painful ways to die. So the brain needs oxygen in order to function properly and well, you definitely see this and we'll get into later on the Alzheimer's paper. If you don't move, if you don't use it, you lose it and early onset Alzheimer's and people who are in dementia as a whole, dementia is the umbrella term for, you know, you put Alzheimer's in the Lewy body dementia, vascular dementia, all dementia is the umbrella term that what's, that gives birth to all the other subsidiaries underneath and when you don't participate in regular activity, in regular exercise, you are putting yourself at risk for early onset Alzheimer's and this is actually clinically proven. Fifty percent of, you get a regular exercise and just regular dieting puts you a 50 percent less chance of having an onset of Alzheimer's disease. That's been clinically proven and that is an amazing, that's an amazing stat to know because you, I can literally stave off a deadly, I mean a life-changing, life-threatening disease, a progressively worsening disease. I can stave that off just by getting regular exercise and diet for a few hours per week. That's an amazing thing that we know now and, you know, why not take advantage of that? So back to the Naperville study, I thought that that was very important because just to show like just the effects of exercise and diet, you know, I was, you know, in the gym and exercising and dieting for a while and it wasn't until I started getting into Brazilian Jiu-Jitsu and the reason why Jiu-Jitsu was such an effective exercise for me is because it was consistent and I started eating besides the dieting but it was consistent. You know, if you go to the gym, you can kind of, you know, you kind of choose what you want to do, you can choose the rate, you can kind of choose the terrain you're on, you know, you're kind of really in control but when you really sit down and you join a Jiu-Jitsu gym and you're part of a team and you're really into it, you know, you're really not, you have a coach, like you're really not in control of what you're doing really. So, I mean, the regulus rolling on the mat for two and a half hours, doing kickboxing, sparring in the ring, this is, I mean, just doing that four, five days a week. Now, obviously, that's an extreme example but it wasn't until I started doing that that really got me into shape. I was over 200 pounds just a little over a year ago and just within that year of kickboxing and doing Jiu-Jitsu, I shed at least over 30 pounds. I'm in the best shape of my life right now. Not to mention how that's played an effect on my cognitive skills. You know, I went back to school, I mean, I started reading higher level papers now. It's just, there's no negative, that there's no downside to regular exercise and dieting and reading more and, you know, doing things to improve your life. There's no downside to that. So, that was the SPARK book and I just wanted to go over a little things and little parts in there because that was really interesting to me. Now, there was a second part in SPARK, you know, we're not done with SPARK yet. We're going to go to the part when Dr. Rady started talking about anxiety. So, we're going to skip to page five. I'm going to read a section of that and start talking about anxiety. Anxiety is, sorry for doing that in the microphone. Anxiety is a natural reaction to a threat that happens at a certain point in the stress response. When the sympathetic nervous system and the hypothalamic pituitary adrenal axis, HPA axis, I know it's a very long, very long word, shift into high gear. When you're facing upcoming speech or brewing confrontation with your boss, anxiety sharpens your attention so you can meet the challenge. The physical symptoms range from feeling tense, jittery, a short breath, to experiencing a racing heart, sweating, and in the case of full-blown panic attacks, severe chest pains. Emotionally, what you fear, what you feel is fear. If you're in a plane that suddenly drops several hundred feet, you and everyone else on board will be edgy and acutely concerned. Are we going to make it? The nervous system stays alert for a while, hypersensitive to any further turbulence. That's normal. But if you worry when there's no real threat to the point where you can't function normally, that's an anxiety disorder. The symptoms crowd your consciousness. Your brain loses perspective, and you can't think straight. Clinical anxiety affects about 40 million Americans, or 18% of the population. In any given year, it can manifest in a number of ways. They include generalized anxiety disorder, panic disorder, specific phobias, and social anxiety disorder. They all share the physical symptoms of severe stress response, as well as similar dysfunctions in the brain, namely a cognitive misinterpretation of the situation. The common denominator is a rational dread. The differences are mostly a matter of context. Now, this part really, uh, interested me when he was talking about anxiety, and I'll go back to Brazilian jiu-jitsu. So, I've been doing it for a little over a year and a half now, and I would say one of the biggest things that jiu-jitsu has played a part for me as, for me, is dealing with stress and anxiety in situations where stress and anxiety are actually permitted, or actually needed. So, when you're on the ground getting choked by this super strong dude, and you're inexperienced, and he has you in a rear naked choke, and you don't know what to do, the normal response in that situation is to obviously get the hell out. You know, our amygdala fires, so the amygdala, the hypothalamus, and the premotor cortex are all involved with the limbic system. So, they all work together to turn on when something, when you're in that fight or flight situation, your sympathetic nervous system, it fires off when we're in those situations. If we're, um, if we're in like a tight space and we're closing in, we get caught in like a trash compactor or whatever, you know, when we talk about we get super strength, like, it's not a metaphor. Like, you actually get stronger. You actually begin to sense things out. Your sympathetic nervous system actually tunes things out. You're able to focus more because your brain is producing more norepinephrine and epinephrine. Epinephrine and norepinephrine are catecholamines, so they are essential neurotransmitters that occur in the brain when you need to focus, and it sends adrenaline throughout the brain, and it helps increases your heart rate. It helps your pupils become dilated. You can actually see more. You're literally in the moment, and you have superman strength, and it's neurologically proven that that happens in life or death situations. So, when you're on the mat, and, you know, someone's choking you, and you're almost, you know, you're getting your oxygen cut off, this is triggering all, I mean, your brain is like going into super hyperdrive. When you're new, you know, you're producing extra norepinephrine, more epinephrine. Your body is just in total amygdala mode right now, so you're trying to flail. You're trying to, you know, go around, trying to get out. You're trying to grab his hand. You're trying to squeeze out, like, because you don't know what to do, and this is not necessarily a bad thing, but the thing about the brain is, is the, you want to be efficient with your energy. You want to be efficient with your stress. You want to be efficient with your focus, and this is where we start getting into other mood disorders, like attention deficit hyperactivity disorder. When, because you'll see when people have ADHD, they don't have a problem focusing. They have a problem knowing what to focus on. They don't have a problem, you know, having their attention is there. Their will, their drive to do something, hence the hyperactivity, their attention is there. They are inefficient with their ability to attenuate their attention to things, because they don't know what to attend to, so a lot of that is a behavioral problem, and I will, and I'm not a doctor or anything, so I would get a tax for that, but selective serotonin reuptake inhibitors can help with that. Antidepressants could help with that. NSAIDs, non-steroidal antidepressants could help with that. Stimulants could help with that. Psychomotor stimulants can help with that, but to engage in a pharmaceutical treatment for ADHD without the behavioral therapy, without the behavioral techniques is a waste of time, because you will see that, and I know this, because I have people in my life that have this, and my sister was diagnosed with it as well. They have the ability to pay attention to something. They just don't know what, they don't have the ability to use that resource wisely, and the ability to not use that resource wisely then affects their situation, and now their situation is now telling them that they need to make a wise decision, so now in that situation, now I'm not, now, so we're going back to the amygdala, the hypothalamus, pituitary gland, or the hypothalamic pituitary adrenal axis, now I'm producing more cortisol, because my body is telling me I need to make a decision, I need to make a decision, so now this is going out through the brain, now this signal is being sent to the thalamus, the thalamus is now going out to my limbic system, now it's telling me I need to make a decision, or now I don't know what to do, I made a bad decision for my last one because I'm producing too much cortisol, so now I made a bad decision, now the outside phenomena is now telling me that I need to make a decision, and now I need to make a worse decision, I'm making a worse decision, and then later on, do you see the loop that's going on here? Now I'm making worse and worse decisions, because the initial problem was that I didn't know which one to pick, I didn't have, I didn't pick the right problem, there are multiple different effects, and multiple things are affecting the decisions we make, so it's not a 100% determined thing, like, oh I can just take this pill, and then now I'm gonna, I'm gonna turn into Nostradamus, but that's not how, that's not necessarily how it goes, it is a behavioral problem knowing, okay, so when I get in this situation, what sort of techniques can I do so that I can make a better decision, and that's going to obviously take you a time to slow down, you're going to be, you're going to need to be in a more relaxed state in order to make that decision, and that's where the SSRIs come in, so the normal, so let's, we can probably get into that, so the normal way of, you know, how we make decisions, or how we do something, and if you're looking at this on like a, a neuroanatomy level, you know, we, so we, it starts at the, the fibers, the, the cerebral fibers, so our neurons are, you know, playing around, and they're, they're talking to each other, and, you know, there's dopaminergic neurons, there's serotonergic neurons, there's a gabinergic neurons, and they're all talking, and, you know, conversating, sending back and forth their chemicals and electricity in the brain so that we can do things, so one comes down, and let's say these two dopaminergic neurons are interacting with each other, and let's say, you know, this one, you know, this one clamps on this one, and then now it's sending this serotonin down, so it's starting in the soma, we're looking at the picture of a neuron, it's coming from the soma of the cell body, then it's going down the axonal terminal, down the myelinated sheath, it's getting across the nose of Ranvier, then it comes out through the synaptic bulbs, and then now it's here in the middle space, so now the serotonin is going, coming through the cell body, down the axon, out the synapses, and now it's coming on to this one. For people who are listening to the audio, I'm trying to visually explain this, so now there's serotonin in between this little gap here between neurons. Now, in normal cases, all the serotonin doesn't go from one neuron to the next, so this process is called reuptake, so the neuron will take back all the serotonin that the other neuron didn't use. It's kind of like if, you know, you were running out of sugar, you're trying to make a cake or something, and you ran out of sugar, and you went to next door, and you said, do you have any sugar? And they said, oh yeah, how much do you need? I'll just need, you know, a half cup. You know, they're not gonna, are they gonna come bring, or come give you the entire thing of sugar? No, because I didn't need all that, so the neurons, our brain works the same exact way, because it's efficient. I'm not going to give you my whole entire package of sugar if you didn't need it, so it gives you just the amount that you need, so that, and it takes it back up, so it goes back up through the axon, it goes back up to the cell, to the cell body, and then the protein becomes synthesized, and it turns into more, then it just goes down, so it's a continuing process. That's in the normal, that's in the normal situation. Now, if you're taking something like SSRIs, if you're taking like a scitillopram or something else, what the selective serotonin reuptake inhibitors do, they do what the name suggests, so they act as serotonin receptors, so when you take one, if you take one orally, so serotonin, norepinephrine, epinephrine, these catecholamines, they can cross the bloodline barrier. Now, dopamine can't, so if you see this in patients like, sorry, I've hit the mic, people like who have Parkinson's disease or Huntington's Korea, they have to take substances like levodopa. Now, levodopa is the precursor to dopamine, but dopamine can't cross the bloodline barrier, then it starts competing with the, starts competing with the precursor of the dopamine, so they take more things like carbidopa, and we'll get into that some later episodes, but neurotransmitters, catecholamines like serotonin or whatever, they can cross the bloodline barrier, so when you take something like an SSRI, what it does is, so normal neuron activity, serotonin goes down, other neuron takes what it needs, then the excess serotonin goes back up through the axon. When you take something like SSRIs, it blocks that process of reuptake, reuptake inhibition. If I inhibit you from doing something, that means I'm preventing you from doing it, so now this cell body is producing the serotonin. When we do something out in the world, or we obtain a certain thing, serotonin is the, it's not the feel-good short-term hormone, this is the dealing with the bodily function, how my sense of self, looking at it from a psychological perspective. So now the serotonin is going down the axon, now it's in this little gap here, now what the serotonin does is it pauses that, it blocks that neuron from taking that excess serotonin back up, so now your neurons are able to obtain more of that serotonin, more of that, so now you're doing more with less, because initially you had to do all this, and you had to, you had to think about all this stuff, and then you had to do things harder, you have to do things faster, so that you could get that level of serotonergic satiation that you were looking for. What SSRIs does, it allows you to do less, and to get more of that satiation, which inevitably slows you down, so then once now you're in this slow down spot, now I can make the behavioral, the habitual decisions, which is the dopaminergic function in the substantia nigra, now I can make the habitual decisions. Maybe I shouldn't do that, maybe I should do this, let's talk this out. So this is like the whole roadmap with ADHD and anxiety, and how all this stuff plays together, and regular exercise and diet helps facilitate this cognitive function, helps you slow down, helps you think, doing regular participating in things like jiu-jitsu. Jiu-jitsu is not for everyone, I understand that, but it's something that has definitely helped me in those situations, because before when I was on the mat getting choked, my amygdala was firing off, I was producing excess cortisol, which is preventing me from thinking. John J. Raddy goes on and talks about how the hypothalamus is involved with depression, and how it becomes generalized, literally, into generalized anxiety disorder. So the heightened level of cortisol, this is involved with the limbic system, it works with the hypothalamus to help you, so the hypothalamus is helping you, it's spatial recognition, knowing where you are, it's kind of like a temporal parietal function, helping you know what is actually going on, it sits below the thalamus. So the thalamus is sending out sensory information to the cortex and to the other parts of the brain, the hypothalamus sitting down is controlling things like your thirst, and your hunger, and where it is, and what's going on right now. So I'm talking about the HPA axis, I'll say HPA for now just to keep things simple. Now, when you're actually stressed out, you are burning out your hypothalamus. So now, so to go back here, talking about memory, and using memory, and a working memory, our hippocampus, our hypothalamus, all these things are helping us, you know, remember cholinergic neurons are helping us with bodily functions and learning. When we burn out our hypothalamus, when we burn out the hippocampus, what we're doing is we're sending, we're sending, we're sending negative signals to the, to the thalamus back up to the cerebral cortices, saying that this is a sense of danger, this is something that I, so I need more cortisol to calm these levels. Now, this is something bad because when you get into general, generalized anxiety disorder, that's because there is a, there is no specific phenomena that is occurring that is commensurate with the amount of stress that you're in. So, for instance, and when you're getting diagnosed with general anxiety disorder, they actually take out, this has been the DSM-IV, I believe it's in the DSM-V as well, so they exclude public speaking because who isn't, because that's, that's a too general situation to be stressed out in. So, they take out public speaking, so that, that, because so if you're scared to talk in front of 10,000 people, you don't have generalized anxiety disorder, you're just a normal person. In fact, you probably would have something wrong with you if you weren't scared out of your mind to speak in front of that many people. So, for instance, if you're at Walmart and you're talking to a cashier, you're just buying your stuff, then out of nowhere your heart starts racing and you can't even think straight and you're sweating and you're hyperventilating and you feel like you're about to pass out your light head and you can't remember where you are, you don't know what your name is, you forgot how old you are, that is not good. That means something's wrong. That's because you're giving bad signals to your hypothalamus, it's not understanding what is going on, it's becoming generalized. It generalizes, that's where the G is, in generalizing anxiety disorder, it's becoming, it's taking stress and it's generalizing it, so it can no longer pick up or adapt to actual phenomena that's occurring. It can't adapt to things that are actually putting you in danger, so it's triggering, everything becomes a stimulus of everything. If you're looking at it from a cognitive psychology standpoint, this is called combinatorial explosion. This is a term that John Verbeke had a great conversation with him. I can't have one podcast without telling people that I talked to John Verbeke. Combinatorial explosion, everything matters, everything's coming into it at once and I don't know how to synthesize and think through and think clearly through everything else, everything's coming at me at once and this is triggering my cortisol, this is triggering my stress and it's sending back to my hypothalamus, it's sending negative signals back to the thalamus, up to the cortices and now it's becoming a negative feedback loop to now that my heart is racing, now that my heart is racing, now I'm producing more epinephrine, now I'm producing less norepinephrine, now I can't focus and now this is just going, going, going, going, going. So when you get to that point, it's not good and there's a lot of things, there's a lot of free things, well not free, but there's a lot of easy and natural remedies that we can do to help prevent ourselves getting to that point, which is something that John pointed out in the book. Spark is regular exercise, regular eating right. I'm not a nutritionist, I don't really know that much about nutrition, but as far as exercising, having them at a healthy exercising diet is super, super important and just like the kids in Naperville, increasing their reading literacy by 17 percent, it's just incredible and John talks about all this in the book, Spark, and I said I was going to do 35 minutes on Spark and we're over three minutes, so that was Spark, great book, I highly recommend you read it. He goes into more about anxiety, depression, he talks about, I mean everything, hormones, he goes into neurotransmitters, he's a great psychiatrist, I'm an aspiring neuropsychiatrist myself, I highly recommend you get this book because it's very important. Okay, that was good, we're actually making good time now. We're going to switch gears and talk about the next topic, which is distracted driving. Now, for those who are maybe unaware, I just started going back to school in January. I'm a student at University of Maryland Global Campus, they're not affiliated with the University of Maryland at all, but it's kind of like an online thing. Psych major, I plan on applying to a MD, PhD program, so I'm kind of on like a pre-med track right now. I'm a pre-med student applying to the MD, PhD neuroscience program at the University of Maryland School of Medicine, where I'm trying to do my dissertation on Alzheimer's and possible treatments, and then I want to do my residency in psychiatry, so that's the pipe dream there. In the psych class, this was a paper that we had to read on distracted driving, and you know, it wasn't like a remarkable paper, but I thought it was interesting and important, and it had made some really good points, some cognitive psychology points. We tend to think that driving is a motor task, or I say kind of like we think it's something that we actually have to do, but really it's something that we're really not even thinking of itself. You know, we're driving, we're doing a break, we can't consciously do all that at once, so the thing about driving in a period is that that you're not thinking while you're doing it, so the fact that your limbic system is now on autopilot, any other distractions by definition are going to impair your ability to balance these two things, and this paper dives into that phenomena. So this paper is called The Passenger and Cell Phone Conversations in Simulated Driving. The results indicate the passenger conversations differ from cell phone conversations because the surrounding traffic not only becomes a topic of conversation, helping driver and passenger to share a situation or awareness, but the driving condition also has a direct influence on the complexity of the conversation, thereby mitigating the potential negative effects of a conversation on driving. Now this was very cool because the way they set up the experiment, so they had different groups drive a simulated driving thing, a simulated driving machine, and they wanted to know how having conversations with other people via in the vehicle with them or somewhere else in the world, how that had an effect on the driver. And in one group, they had the other participants, they had in-vehicle conversations, and in the other group, the other people were having conversations somewhere else. And what they found is that conversations that occur inside the vehicle, both of the passengers shared a common goal. They called this grounding. One of the linguistic psychologists called this phenomena grounding. So you have a passenger and a driver, they're both attenuating to the common goal. They both share the same fatality. They both share the same psychological fatality, because they know if I distract the driver too much, not only is he going to swerve off the road, I'm going to go with him. So they share that shared level of fatality, of mortality. How many times am I going to say that? The conversations, and also while having the conversations, there was a specific conversation that was called something that was made to generate an intense conversation. They were talking about something that happened in the past. But the conversations that occurred outside the vehicle, those by almost 50% caused more distraction behind the wheel, because the person on the other end of the phone had no idea that the person was driving. They had no idea what was going on. So their level of speech, their speech pattern, the things they were bringing up, they weren't talking about the road, the person was just blabbing, blabbing, blabbing on the wheel, flabbing on the phone while the person was trying to focus their attention on the person on the phone while looking on the road. This phenomena is called the cocktail phenomena. So this is where we're dividing our attention between someone talking in our ear, which is what this experiment was done in person, versus someone speaking in the other ear. And they actually did experiments about this, and actually they started to, they asked the contestants, you know, what do the people say, and they actually started to blend in. So they took a bit of the story of the people from the right ear, and they took a bit of the story for the people talking in the left ear, and they made one story out of both because they were trying to listen to both conversations at once, called the cocktail phenomena. So I thought that was really cool. But in this study, however, the data was quite remarkable. So I'm just going to read a few highlighted things I highlighted in this. More evidence was presented recently by Strayer and Drews, 2007, demonstrating reduction in the amplitude of the P300 as a result of a cell phone conversation in response to the onset of breaking lights of a car that had to be followed. The P300 component of event-related brain potentials is sensitive to the attention that's allocated to a task. So this part of the study was super interesting, and I actually included that in one of my classwork assignments. So they found that when someone's speaking behind the wheel, they're actually producing less event-related potentials. Now I'm not going to get too deep into the neuroscience of that, but basically they said they found that the neurons are producing less excitatory effects. So if you see a breaking light, that should indicate to stop. Now you're not going to consciously think that, but that should indicate you to stop. So in order to stop, I first have to see that that image has to be caught in the retina, that has to go to the occipital lobe, and then that has to send messages back out to the foot, and then that foot has to go back up to the premotor cortex, then I can hit on the brakes. That all happens subconsciously, by the way. So in order to do that, I have to have a lot of excitatory potentials going on in order to produce that limbic function of hitting on the brake. Now what they've seen was having conversations on the phone dramatically reduced the level of excitatory potentials going on in the brain. So you're working with less. So it doesn't mean that you can't hit on the brake, it just means that it dramatically reduced your reaction time to hitting the brake. And that on the surface, it's like, well, it doesn't seem that drastic that, you know, it just limited your reaction time just a little bit, but when you're talking about instances on the road, you know, that's someone's life. All you need is one second off and then the person's dead. So I find that very interesting. One is simply that an in-vehicle passenger responds to demands of the driving context by reducing demand for the conversation task. That is, by changing the production rate, the modulation hypothesis. So this is really cool. So when both people were driving in a simulation, the person, the passenger, the people who had a passenger in the vehicle with them, they made efforts to slow their speech patterns, to talk less, to reference the road. The people who had passengers in the vehicle mentioned the road by, I think it was almost 40 or 46% more than passengers who were having had conversations outside the vehicle. When both people are in the vehicle, they both made references to the road. And that was really cool because that just shows, like we said earlier, that kind of rounding phenomena, how both people are kind of sharing a common goal and how that can help not, totally not distract someone behind the wheel. But every now and again, you know, referencing, oh, bro, that was a red light. I mean, I do that all the time. I'm driving in a car with my friend, you know, he's on the phone and I'm just in the passenger seat and he's on the phone and the green, the light is green. I'm like, uh, it's green. He was like, oh, shoot. And then, then he goes. So just, you know, just knowing that, it was just really cool. We're going to get to the, the figures now. So the navigation task. Now you can't see this because this is just audio, but the number of participants is exceeding. So you can see this figure, people who had passengers performed, outperformed the people who were on the cell phone almost by 50%. And the order of a single and dual task conditions were counterbalanced on the assignment to cell phone and in-person conversation was randomized. After familiarization, one participant of the DIAB was randomly selected to drive the vehicle. The other, based on experimental conditions, was either the passenger or talking on the cell phone to the driver from a different location. You can get some more of these figures here. Means and standard deviations of lane keeping, driving speed and distance of both experimental conditions, single and dual tasks. So the mean distance of the single task drivers had a mean, kept the mean distance of 72.3. I think that's feet. I'm not sure. Meters, 72.3 meters. They kept that as, as a mean with a standard deviation of 27.4. They had other data on this part, like lane keeping, the mean speed, but those data were kind of insignificant. The most significant of the dual task. So this is when someone was driving and they were on the phone, they kept a mean distance of 85.3 meters. So that's not a lot, that's not bad, but keep in mind that if you were at 85.3 meters behind someone else, that means that you are drastically slowing your speed, pissing people off behind you. And so that, that data point was extremely significant because that just shows you just how unaware you are when you're dividing your attention on the road. And of course this, uh, this study wasn't like an alone study. It was given in, uh, with another video of this, uh, a girl who was not, she wasn't distracted driving at all. She was actually hit by someone who was texting on their phone. And this woman happened to be with, uh, she was with her parents in the car and the girl who was texting while driving, she hit the other people, killed both of her parents, but the girl survived, but she has permanent brain damage and she can never do any of the activities that she wanted to again. So, um, aside from the cool, uh, science stuff behind this paper, um, just, just make you think about, you know, what we're actually doing and, you know, this is the best decision I should be doing right now. Uh, what can, what kind of things can I do to, to, uh, practice, have safer, better habits. And, uh, I tie all this in with the anxiety and the ADHD and, um, the diet and exercise that ties us all in because when you get, when you really get down, so this is like the philosophy part coming out, things really tie down to our behaviors and our ethics and what we value. You know, if I value that life in front of me, you know, why am I not taking the necessary precautions to help save it? You know, if I value this person, am I supposed to value this person? Why am I talking to them, to them this way? Why am I acting this way towards them? And, um, these questions are not, they're not easy to answer, but it all goes back to the behavior to what we value the most. And we can talk about neurotransmitters all day long. We can talk about, we can talk about all these fancy diagnosis, diagnoses all day long. When it comes down to at the end of the day is what do you value? Do you value time? Okay. If you value time, why aren't you acting like it? If you value space, do you value boundaries? Do you value other people's values? Do you value yourself? If you do, why aren't you taking the necessary steps to help get better? Why, if you value your life, why are you putting junk food in your body? As I say, I have a bag of Skittles on the desk. If you value yourself, why aren't you, why aren't you contributing in regular diet and exercise? So not saying that every single thing. Now, obviously a cancer patient didn't do anything wrong to get that. I mean, in most cases, now we're not talking about lung cancer or anything, but in most cases, you know, someone didn't, they didn't bring the plague of, of pancreatic cancer on themselves. They didn't do that. So those people are obviously excluded from this, but at some point, you know, you're not going to have a, that's not a moral debate. How about at some point, you're going to have to ask yourself, what do I value in how is me not understanding or not accepting what I value? How is that playing an effect out in the real world? What can I do to help ameliorate some of my suffering so I can suffer less? So I can have less agony. So I can have less anxiety. What can I, okay, what is in my peripheral right now? Not reaching out for the outlandish decisions, for the outlandish solutions. What can I take part of right now? Can I start walking once a day? Can I eat one less gram of sugar a day? It's called collaborative empiricism. Start small. What can I do right now to help improve my life for the better? It comes down to behavior, and I'm getting kind of pissed because a lot of people like to focus on the most outlandish solutions to the most simplest problems. Like you don't have to, you don't have to get a six-pack in the next two weeks. You don't have to lose 50 pounds in the next month. Why can't you just take the small steps and eat better or take one less cookie out of the cookie jar? Or why can't you jog an extra 10 minutes? Stop making it impossible. I think sometimes people like making the solutions impossible so they can stay in the same ridiculous, mediocre state that they're in. I mean, I was over 200 pounds at one point. Making excuses. I was saying, this is the way I am. Oh, I could have said this is how I am. Oh, this is how I was born. Oh, I had this. My family was like this. Oh, well, that just runs in my family. I can't do anything about it. Oh, well, my family has high blood pressure. Oh, well, they all have diabetes. They all had type 2. I could have said that. But no, I took charge of it and I did what I could. And I broke that curse. People like to live in this hyper-deterministic lifestyle. Oh, well, I had x variables so that's why I'm this. But then simultaneously require you to treat them as if that's not plaguing their existence. Oh, well, I had this problem, but on top of that, you're going to have to understand when I do this because I had that problem. Well, I don't know what to tell you. I tried to offer a solution, but you insist on using this problem you have as a crutch so you can continue being mediocre all your life. That's not my problem. It's a behavioral problem. It's a moral problem. Going off on a tangent here on the First Solo podcast. So that was the distracted driving portion. Sorry to end on such a dark note. So now we're going to go into the last portion, which is what I'm kind of basing my future career on, which is the study of Alzheimer's. So I joined a Alzheimer's prevention non-profit the other day. I'm planning on doing the bike ride in Philly. I don't know how long I'm going to do, but I'm going to do the bike marathon sometime in Philly in May. So I'm looking forward to that. I'm trying to conduct research with them to see whatever I can get my hands on. So I plan, and I'm also planning on doing this in graduate school. So we're going to go over the research progress in etiology and pathogenesis of Alzheimer's disease from the perspective of chronic stress. This is paper done by Yung Shi Liu, Hafei Zhao, Wang Li, Hanwang Kui, and Guidong Wang. I don't know if I put their names right. Pretty sure I didn't. Now, getting to, this is like the bread and butter of what I've kind of been working on for like almost half a year now. So what is Alzheimer's disease? What is it? It is a progressively neurodegenerative disease that occurs in the failing of the cholinergic neurons in the brain that result in a neuronal death. And the cholinergic neurons are responsible for memory and function. And over a long period of time, those neurons begin to die. And that leads to neuronal death. And neuronal death means you are no longer remembering how to do anything like your name or anything. And it is a terrible disease that scientists and doctors are doing everything to try to find treatments and prevention for. So there's many different aspects you can go down in Alzheimer's disease. For instance, one of the big ones is the presence of the amyloid beta. So amyloid beta are the amyloid precursor proteins. So these are proteins that are present in the brain and are also present with, and so when you do autopsies, there are some brains that are found with huge portions of the presence of amyloid precursor proteins, but no onset of Alzheimer's. So it's not 100% determined how the impact of amyloid precursor proteins have on the onset of Alzheimer's, because people have died with the heightened levels of amyloid and didn't have anything wrong with them, no sign of dementia at all, or cognitive impairment, to even say the least. But one of the known factors are the presence of the amyloid beta. So what this does is, so normal amyloid beta, they work at the cell, they help cell functions, the functions of amyloid are kind of ambiguous, but the normal folding of the amyloid protein is they approach the fold in two, and then that helps the proteins become synthesized, and then so on and so forth. But something happens when the amyloid proteins become misfolded. They then fold into three. So that misfolding of the amyloid protein in the brain, this makes that amyloid susceptible to aggregating amyloid beta, beta amyloids. Beta amyloids are these little mini misfolded parts of the amyloid that begin to accumulate in the misfolding of the amyloid. And then the misfolding of this creates the amyloid beta, and then these clump together, these amyloid clumps, and these clumps block the normal conversations between neurons, and that leads to neuronal death, and neuronal death specifically in the cholinergic neurons. The cholinergic neurons can then no longer produce acetylcholine. So acetylcholine is a neurotransmitter that helps with functions in memory, in bodily functions, and when they don't produce acetylcholine, then acetylcholine and dopamine levels are kind of always like this, and you'll see really low dopamine levels in people with Parkinson's disease because the striatum is not producing any dopamine. So amyloid is one of the three horsemen in the onset of Alzheimer's disease. The next is the hyperphosphorylation of tau proteins. Now tau proteins help with cell structure. They help with cell growth, help carrying different microorganisms throughout the cell. They have their normal utility, but for some reason, when tau proteins become hyperphosphorylated, so hyperphosphorylated, that's because they get a phosphate group, so that means they get one hydrogen with four oxygen atoms. So when that tau protein becomes hyperphosphorylated and becomes susceptible to the helical, I forgot the name of this, paired helical filaments, I was going to remember it. When these tau proteins become hyperphosphorylated, they begin to get entangled up. These are called tau tangles. This is like Alzheimer's 101. So hyperphosphorylation of the tau proteins become, they lead to the tanglements of the tau tangles, and when these tau proteins become tangled, that then leads to neuronal death, and then neuronal death, and so forth, loss of the collagen neurons, and then that eventually progresses down, and then when it gets down to the hippocampus, down to the subcortical subcortices of the brain, that's when Alzheimer's then progresses to its final stage, and then that's when it becomes untreatable then. So there's the hyperphosphorylation of tau proteins, there's the aggregate of amyloid beta, and now that's just to name a few. So the particular thing about this study was they looked at it through the lens of stress. So our brain and our gut is called the gut-brain axis, the gut-brain axis. So our gut is constantly communicating with our brain, and it's sending signals back up to the brain. So our microbiome are these little, we have like millions of organisms that are living within the gut, and when certain microbiomes become, when those levels become, it's called dysbiosis. This was mentioned in the study. Dysbiosis is when there's an inordinate level of microbiome occurring, and so this is sending negative signals through the gut-brain axis. It's sending negative stress signals, higher cortisol levels, back up to the brain, and that increase of signals being sent up to the brain is actually was proven to induce, and especially with rats, to induce a form of dementia, a form of Alzheimer's. So we can see here, I'm going to put up the I'm going to put this up so everyone can see it. So the microbiota gut-brain axis. So the vagus nerve signaling, so the hypothalamus, pituitary, and adrenals, we talked about the HPA axis earlier. So in the gut, we have the intestinal dysbiosis. So the the neuroendocrine regulation's bioactive molecules. So these are let me see so so here we go. So we're looking at the, right now, we're looking at the microbiota gut-brain axis. The microbiota gut-brain axis is working with the HPA axis, the hypothalamus, pituitary, adrenal gland axis that we talked about earlier, the HPA. So heightened levels of stress, and this figure five we're looking at, increase the permeability, I can't pronounce this word, the permeability of the gut. So heightened levels of stress are increasing the permeability of the gut. Alterations in the biodiversity in the composition of the gut microbiota. That is signaling the stress, the vagus nerve signaling in particular. So the stress is then sending that to the hypothalamus, the pituitary gland, and then the adrenal gland. The increase of the permeability in the blood-brain barrier is then sending those signals to the metabolic, is then creating the metabolic effects in the gut. And then that's going down, and then that's found to increase beta amyloids, tau proteins, oxidative stress, neuroinflammation, and synapse degeneration. And the aggregation of beta amyloids that we know, tau proteins, oxidative stress, neuroinflammation, synapse degeneration, are all linked to Alzheimer's disease. And this is all induced by stress. And they actually use many different rat models, rat testing, yeah, testing rats with the, if I can find where this one rat model was. So the presenilin-1 and presenilin-2. So these are two gene mutations that they put on rats or mice in the lab so they can test how they have the onset of Alzheimer's disease. So the presenilin-1 gene and the presenilin-2 gene were used in these studies on this one table. So and this one table isolated rats were housed in cages measuring 38 by 22 by 20 centimeters, while group rats were maintaining cages measuring 48 by 30 by 20. In this cage, tau proteins were spiked in spatial memory deficit just by being in this cage. Another incident, isolated rats were housed for five weeks. So these rats were in this little cage for five weeks. Within the five weeks of being in the cage, this is the spatial, causing the spatial stress. Within the five weeks, they actually were able to detect the difference in the size of the cage. So they were able to detect the difference in the size of the cage. So they were able to detect the difference in spatial stress. Within the five weeks, beta amyloid and tau proteins increased, spatial learning and memory decreased. You can also have the noise-induced stress. So they emitted the intermittent 3,000 hertz frequency sound of 90 decibels for one second in intervals of 15 seconds during the entire day. This is with the C57BL gene mutation mice. And just by playing those 90 decibels, inducing the noise-related stress, learning and memory performance in the mice decreased. So this is called chronic noise stress. It has been linked to the pathogenesis of Alzheimer's disease. So just wrapping up this study, sorry for getting, I didn't want to get too deep into that, but this is very interesting how stress just not makes us more susceptible to having heightened levels of cortisol, heightened levels of cortisol, but leaving us susceptible to making bad decisions, having onset of attention deficit hyperactivity disorder. There is one study, I will go over this maybe on another episode. They did a study on children with it. And kids who reported who had attention deficit hyperactivity disorder, there was underlying illnesses that were underneath of that. And many of them had anxiety and depression or made them susceptible to anxiety and depression. Many of them had, I believe the correct term was judgmental mothers. And that was a very, very eerie study that I read. The correlation of judgmental mothers to the amount of children that grew up to have the onset of ADHD was incredible. So judgmental mothers, anxiety and depression equals ADHD. And I'll go over that study perhaps in the next couple of weeks. But the onset of Alzheimer's, and there's also genetic ones that we didn't go over, like the APOE, the epileptic protein E2. It's a gene that has been proven to fight against Alzheimer's. But the big one is the APOE E4, epileptic protein Epsilon 4 gene. That mutation increases your likelihood of having onset, the likelihood of onset of Alzheimer's disease by six times. So if you get the APOE E4 from both of your parents, there was actually a study that Peter Retia, physician of St. John's Hospital, he recorded this in his book, Outlive. If you get the APOE E4 gene from both of your parents, your likelihood of developing Alzheimer's disease increases by almost 12 times if you have both of those genes. And there's many other gene variants that make you susceptible to Alzheimer's disease, but the APOE E4 in particular was the biggie. But the APOE E2 actually prevented you from getting it. APOE E3 was found to not have any effects. So in closing, stress, anxiety, all these things, what do they mean? There are certain things that we can do that can prevent us from having increased stress, that can prevent us from being susceptible to dementia and potentially having Alzheimer's disease. There are certain things that we can prevent us from making better decisions. It is by exercise. That is the whole entire purpose of this episode. Exercise. People who exercise and have a regular exercise and diet not only stay away from anxiety and depression and a plethora of other mood disorders that we didn't even talk about, but they stave off neurodegenerative diseases like Alzheimer's, dementia. I can't stress it enough how important exercise and diet has been for me, how it's been for my memory, for my cognitive abilities. If you do not take precautions now to make the decision now, I'm going to eat better. I'm going to get out and run. Not walk. I'm going to run. I'm going to jog. A brisk jog has been proven to be better than a walk. I'm going to go out for a brisk jog, 20 minutes, three times a week. You make that decision now. Make the decision now so that you can prevent the onset of these ailments, so you can not have to worry about it. You know, the worst thing that I think about is being on my deathbed or getting a phone call from a doctor saying, you know, you have this disease, or you have this cancer, or you have this type of sclerosis. And it's like, the news doesn't scare me. Because, you know, there's a billion factors that could have played into that. What scares the hell out of me is knowing what I could have done to prevent it. Knowing what I could have done. The easy, simple things I could have done. That's what scares the hell out of me. I don't know what scares you, but what scares me is the possibility that I could have, the precautions I could have taken. That I was being so foolish and so stupid that I overlooked them and I thought that I was invincible towards them. Get it now. Get the help you need now. Get the meds you need now. Get the help you need now. Before it's too late. So, I thank you guys for watching this. I wrapped it up in an hour. I was all over the place, but that's how I am. That's why you subscribe to me. And thank you for your time. This is episode 9, 19. First solo episode. It went pretty well. I hope I didn't confuse anyone. I know I, of course, the parts I gotta take out. But that was it. So, I thank you all for listening and thank you for your time.