[Music] Welcome everybody to another episode of Dr. Martin Dr. Mike's medical podcast. I am your host Dr. Mike Tadarvich. Thank you, thank you, thank you. And. Crowds, the crowd's still here. They're still here, I decided, well, look, I paid. We've got them for half a day, so. And I'm joined by my co-host, Dr. Matthew Barton. Yeah, I know. I'd laugh at him too. If you're watching this on our YouTube channel, which you can, you can look and laugh at Matt as well. Otherwise, you just have to laugh at his horrible, horrible voice. I am and Matt together, senior lecturers of bio sciences, which is anatomy physiology, pathophysiology and pharmacology, to health science students. We help them understand how the human body works by going through various human body issues. Well, that's true, but systems and structures and things like that. And some of our best or most. Well, best received episodes are those that cover the entire. System. Body. But before we begin, I just want to ask how are you? You good? Yes, I'm well, thank you. What's new? Um. Well, you know that I had a daughter. Yep. That's all news, man. She's seven weeks. No cares anymore. Yeah, okay. Sorry. That's it then. Wow, that's really all. Boring. Is she well? Is she good? She's well. Healthy? Plump. Plump. Good. They want to be plump. Yep, so she's gone through a couple of sizes already of clothing and nappies. Good, I know. Good, I know. That's good. It's all good. Wonderful. More busy. I'm definitely more busy. It needs your time up, I'm sure. Yeah, I know. So. But no complaints. Good. Good and. Just one word, care. Yeah, well, um. What about you? Yeah, okay, thanks for asking. Yeah, it's just, um. But you really think, guys, stop it. Get out of here. Mike, god. Um. You're really fishing for that, weren't you? I'd look, I sometimes I just need to be, um. Uh. Just how I am. I'm well. Well, I generally do that, but, you know, Aaron and half later, still going. Yeah, I do talk a lot. Uh, and I do talk a lot about me. And, you know, just how good and amazing and. Anyway, I'm fine. Nothing new, but I tell you what I was doing. I was thinking about. I was playing a video game the other day. I was showing my daughter one of the old video games that he used to play. And I was. Sonic and Hedgehog. Uh. No, uh, Monkey Island. Did you ever play Monkey Island? No, none of this. LucasArts game. They made a number of them. They're brilliant. But I was talking to her about SimCity. Did you ever play SimCity? Yeah. All right. So, I was thinking about SimCity. And. I loved, you know, you basically. You've got the mayor, which is like this deity figure. It's the overarching figure that controls the whole thing. And underneath the mayor, you've got the governments that can be controlled. You know, so you've got things like. These various organizations like Town Planning that can help produce more and bigger cities. You've got the developers that can help grow the city. You know, make buildings and various constructions. You've got the energy power plant that delivers the energy to the various houses and buildings. You've got the individuals and the companies that deliver the resources to the power plants and things like that. And you've got like the emergency services, police department, fire brigade, ambulance service, right? And I was talking about how I used to play this game. And my aim was to just build it bigger and bigger. My trouble is. Yeah, make it as large as possible. So I would basically put everything on steroids, right? So I would make the town plan is create more cities. I would make the developers create bigger buildings. And how did you like prevent natural disasters? Well, there you go. So this is the problem. I invested so much in just building and amping everything up that it just failed. Because I couldn't make it sustainable. Ultimately, the mayor became corrupted with power. That's you. And decided to. I am the mayor to continually just amp everything up. And I failed. I failed. And my daughter said, well, that's unsurprising because in my eyes, you're also a failure. And I said, that's not a hybrid. You're five. She's only five. That's right. But yeah, I mean, so you played some city you said? Yeah, I played it. I wouldn't say it's the frequency that it sounds like you had. Well, it was so far away. It was a day for seven years. I just used to get attacked by the. What was it? Not a Godzilla, the other thing. There was a big reptile that used to come in. Oh, yeah. Flattened my city. Well, that's. That only happened to you. It didn't happen to any other player. Oh, yeah. Yeah. It was. Okay. That's what the game developers did. It's just for you, specifically. So. Yeah. But I didn't do all those. I didn't go to the degree that you sounds like you went to. I just built and didn't do it very successfully. But. Yeah. I am thinking that you're using this game as an analogy for today's. Would I. Topic. Would I be that smart? Would I be that wily to be able to do that? So, am I correct by assuming that? You are correct. So today's analogy I'm using. Well, you got a city. I do. Which I guess is the body, the human body. Okay. And a whole lot of things have to be well regulated for the body, in this case, the city, to function effectively. Okay. And if you don't have all these things in balance, quite deleterious outcomes. Okay. Like buildings fall on a part. Fluds. What else could happen? Not Godzilla. But. What would that be? It could be an infection. It could be a fungal or bacterial or viral infection coming in rampaging the city. But yes, I was using this as an analogy or euphemism for. The endocrine system. I and I have intentionally said putting things on steroids, Matthew. Yes, I got that. Because it's just. But I didn't think I should bring it in because then it might. It lose its. You know. Whatever. Whatever. Yes. The point was that the endocrine system, just like SimCity, has to be this nice harmonious balance. If you want to build something up, it's going to cost something and there's going to be repercussions of that. And so you don't want to continuously build a building as high as physically possible, because it's not going to hold. It's going to be problems. And the same happens if you want to start to just reproduce as many cities as possible. Or if you want to start pumping out as much electricity as you possibly can, there's going to be downstream and upstream effects. And that is just like the endocrine system. There are upstream downstream effects for everything that happens. And it has to be this dynamic, homeostatic balance that occurs. And today we're going to talk about the endocrine system and highlight the various structures and functions. And hopefully be able to demonstrate to everybody the major hormones, major glands, and how they maintain balance. Yes. You good with that? Yes. So we'll start with some fundamentals and basics first and then we'll go into the specifics of the glands. Do you know what the etymology of endocrine is? To cry. Sorry? To cry. Crying. I thought it was cell crying. Cell crying doesn't end domain within. Possibly within crying. I think what it's referring to is structures that can release chemicals for itself. Okay. So hormones, which are the major chemicals released by endocrine tissue, are released into the local environment, but also the systemic environment. And so it's basically like these glands are crying. They're releasing these chemicals because they don't release them into ducts. And I'm not talking about quack, quack, which I wish I had a drop right now to be able to press. But I'm referring to DUCTS. So if a structure releases a chemical into a duct, that's like a. Like a. Like a. A slibrary duct or a sweet gland or the pancreas. Yeah. Perfect. That is exocrine, not endocrine. But in this case, endocrine is releasing it out into the open. So it can jump into various, let's just say, the bloodstream, the lymphatic system, and carry it to either local or distant areas of the body to have its effect. Yep. All right. Let's jump back to the beginning. What do you want to start with? Well, I think firstly we just say that it's a communication system in the body. Yeah. Because the body is made up of trillions of cells and they are distant away from each other. So to communicate until something a long way away to do something requires some degree of communication. Isn't the nervous system. Yeah, we did a nervous system last week or four or nine. Yeah. That was a form of communication. But that's a very fast form of communication and a very localized form of communication using electricity and direct. Yeah. So I think that's the major difference is right. But the nervous system and the endocrine system, yes, they're both communication networks. They're both there to tell structures.
to do things, but the nervous system is a lot faster. It's direct and it's short acting. Yeah, on and off. Yeah, and very localised. As you say that. I didn't. I just said direct. So then if we focus now on the endocrine system, which is a system of crying for someone, there are a couple of fundamentals to bear in mind for all this system, regardless of how we break it down. So the first fundamental is the it's made up of glands or tissues that will do the excretion, the crying, the crying. Now the tear is hormones, which are just basically chemical messages. Yeah, so students will ask me things like, what's the difference between a hormone and a neurotransmitter? And the answer is, well nothing, nothing really. They're basically the same. It's just about the tissue that releases it and where it's released onto, yeah, into. Yeah, exactly right. So that then goes to the fundamental three, which is just a needs a target organ or a target tissue. Right. And so I guess with those three fundamentals in mind, what are the three? Yeah, gland or tissue that will do the excretion, the hormone itself. What's the second one? The hormone itself. You've got three fingers already up. So first one, the first one I go, I go, gland and tissues. Okay, but that's one. That's one. All right. Allmone, which is the messenger. Yep. And then the target tissue. So it needs a target. Okay, so they're the three things it needs. That's right. And a hormone and a target tissue. Right. Now with that said, I guess, I once, well, I guess you could say somewhat historically, but I think the endocrine system as in the systems of the body was a fairly recent system to be discovered. So you mean like out of the cardiovascular system, respiratory system, it was more recent. Yeah, I think pretty much the turn of the 20th century was where significant advancements in the endocrine system was discovered. Well, I think one of the reasons why is because if it's very easy to have a look at the cardiovascular system, it's all connected. Digestive system, it's all connected, respiratory all connected. The endocrine system isn't connected. Right? Like the only connection between them is probably the cardiovascular system, blood supply, but that is not in itself part of the endocrine system. So that's probably one of the reasons why. And I probably understand enough chemistry wasn't fully accomplished at that point and possibly microbiology. Yeah, I guess microbiology in terms of seeing well into small cells and knowing what the cells are doing. Yeah. But you know, an example, and this was a debate recently on Twitter. What should what should be the name of the pituitary gland? Right. And now, my understanding of the etymology of the pituitary gland means to produce mucus or something like that. Yeah. Now that would have been assumed probably centuries ago that when it was looked at, it did secrete a fluid that was probably mucusly like. But they wouldn't have known it wasn't snott. Yeah. They wouldn't have known chemically what was coming out of it. Right? So it's kind of right, but they just didn't know what that mucus was. Yes. Right? Yes. So they probably had an idea that there were these things like, you know, the pancreas, the adrenal glands. I'm sure they'd definitely were discovered. Yeah. But what they truly did was a bit unknown. A bit unknown. And it wasn't until they started to experiment with these glands like shop them up and swallow them or something or inject them into animals to see what they actually did. And you know, that's where you get to discover insulin or adrenaline is or thyroid hormones just by going, "Here's something weird. We don't know. Let's just crush it and inject it into a dog or a rat and see what happens to the. Oh, pull it out. Like, you know, let's pull out the the parathol or gland and see what happens to the dog. It can't regulate it's calcium well and it gets weird bones. They used to do a lot in dogs and cats, didn't they? Pretty horrendous. But not anymore. It's probably a good thing, I think. So, but following that. Yeah. So with the endocrine system, because I guess at least when I started it, it was these discrete organs, right? So hypothalamus, pituratory, adrenal glands, thyroid, pancreas even. But more and more now, we're discovering that it's beyond just glands. Tissues can do it that aren't necessarily considered an endocrine gland. Yeah. So, you know, like the pancreas, which is a bit debatable. But that's probably more exocrine than endocrine. The gonads, you know, that's probably more for producing sperm or eggs than producing hormones, but they can do it. And then you have smaller amounts of tissue that does completely opposite functions like kidney. Right. So the kidney, as we know, it's function is more to filter blood. But it can also produce chemicals that can be pushed out into the body or maybe just local to the kidney that will have endocrine-like effects. Yeah. I think we could we're pretty safe in saying that probably most tissues of the body would, by definition, secrete a hormone or a number of hormones. And it would secrete it potentially just very locally to act upon itself or to act upon something within its close vicinity or even release something to jump into the bloodstream and act quite distally or far away. And in actual fact, they're the three major ways that- Well, it's actually four, but it get- Oh, okay. Okay. So if a tissue releases a hormone that allows for it to act upon itself, we call that autocrine, right? If it releases a hormone to act upon its local environment, it's called paracron. And then if it releases it into the bloodstream to act distantly- Because blood goes everywhere. What do we call that? Endocrine. Endocrine. But what's this fourth one? I think it's intra-crime, which is- It doesn't even release it. It's just within its own cell. So it's not even released. It's just made and then it acts upon an internal receptor. And I guess a lot of- Give an example of that. I was meant to do that. See, it's just- Yeah, that's fair. That's fair. That's fair. But that's more of a modern addition. There are. But that could be just all the internal signaling, which is interesting because once we talk about- But how can it be termed a hormone if by definition a hormone must- is a chemical that must be released into the environment? Otherwise, it's just a chemical mess- And an intracellular chemical messenger. So I say to those people- Okay. I could have, you know, potentially not explained it well, but inter- inter-crime- Potentially. Is the term. All right. So we've got Bauticron at least Paracron and Endocrine. So some examples. Yep. Let's say an example of Paracron would be, let's say, during inflammation, you have cell injury and you would have a certain- not- You'd have certain cells that are located in tissue that is likely to be injured with anything from the outside world. You know, this could be a microorganism. Yep. It could be from mechanical trauma. It could be temperature changes. It could be pH changes. And then you could have some cells that are within your outer tissue, like your skin or maybe your cast membrane, that when they pick up this stimulus, they release chemicals, which then act on the local environment. And that's why you have local inflammation. And so an example here could be histamine. Right. And so histamine being released by basophiles or mast cells have a quite profound impact on blood vessels in that local region. So is histamine termed at hormone? Well, it's a chemical messenger. So this is again where we start to get- The boundaries- the definition boundaries are a little bit blurred. Because an example of auto-crime is interleukin-2 being released by the T cells. T cells. Right. And so it can be released and act upon itself. Whilst it's signaling to another immune cell to activate it. Yeah. So it's kind of like, hey, B cell, I found something dodgy. I want to communicate with you to tell you that there's something here that I want you to make antibodies for. Yeah. While I'm also going to tell myself to just make more of me- That's right. So I can release more of me- Yeah. So I can start cloning myself. Yeah. Because it's important that I'm as a T helper cell. I'm going to regulate this immune response. That's right. And I mean, it's all in the name interleukin between white cells. So the interleukins are the chemical mediators between the T and B cells. And also between T and T cells and B and B cells. And endocrine could be a whole- Insulin gets released. And that's a good one because insulin gets put into the blood and in theory should go everywhere because it's important to allow glucose to enter certain tissue. Yeah.
bring the blood sugar levels down. The question we need to ask ourselves now is, what can trigger or stimulate an endocrine tissue to release this hormone, right, or a hormone? And so there's, we spoke about three major ways that the hormones can work, auto, parat and endocrine. But there's also three different types of stimulus or stimuli that can trigger an endocrine tissue or gland to release a hormone. So the first one could be neural. So in neural stimulation, so you could have a nervous innovation, a neuron that basically speaks to a endocrine tissue and says, hey, release the hormone. Got an example of this? Yep, the innermost part of the adrenal gland, called the medulla. So this has a cluster of cells that will release catacombs. So adrenaline, I guess adrenaline. Is it Nordrheinland as well? Yep. OK. So this nerve will go there from the sympathetic nervous system and it will speak to this cluster of cells when you are having a profound sympathetic fight and flight response. And that tells those cluster of cells in the deep part of your adrenal gland to pump out adrenaline into your blood. So you got a neuron coming from the spinal cord speaking directly to your adrenal gland. And it says, hey, adrenal gland, release adrenaline, release into the bloodstream, and let's have this whole body fight a flight response. Which is interesting because typically, when we do this last podcast, but when we do the sympathetic nervous system, we actually both parasympathetic and sympathetic, they usually broken into two neurons, right? Yeah. And so sometimes when you study the sympathetic, this is always the outlier. Right. So this is the only one. So when you say two neurons, just for the listener, if they haven't listened to that episode, let's just say the fight-of-flight system going from the spinal cord to whatever organ it wants to affect to have a fight-of-flight response. Let's say the heart, it's only two neurons. So it goes from the spinal cord to the sympathetic chain, which then speaks to the second neuron-- Which is usually a long one. --and that long second neuron goes to the organ to have a defect-- such as the heart. And that seems to be this global dogma, universal dogma for sympathetic and parasympathetic. They're both two neuron chains. But not in this case with the adrenal gland. So this one was always considered the outlier. So when I was in my undergrad, and I was studying the sympathetic parasympathetic nervous system, you'll be told, here's the anatomy. Here's the two neuron pathway that you need to learn. And but there's always one exception. And that's the adrenal gland. It only has one neuron going to it. So it's a pre-ganglonic neuron. Just that first one. But then when you learn a bit of embryology, you realize that the medulla is just the post-ganglonic neuron. So that whole cluster of adrenal medulla cells are just neurons. Really? And so they're just releasing again the neurotransmitter, which normally would just go onto the organ. Of course. But in this case, it goes into the blood. Isn't that amazing? Yeah. Love it. So it goes back to what you're saying about the neurotransmitter now becoming a hormone. Exactly. So that's the neural stimulation. You've also got hormonal stimulation where a gland can release a hormone that travels to another gland to tell it to release a hormone. And there's a lot of examples of this. But the first thing I want to say is that the first gland that releases the hormone, usually the name of that hormone ends in the suffix, tropic. OK. And that term "tropic" really refers to the fact that this is a hormone that's going to travel to another gland to tell it to release another hormone. So as a listener or a student or a learner, when you see or hear that word "tropic" on the end of any hormone word, go, oh, that means this hormone is going to go to another tissue to tell it to release another hormone. And so examples of this can include the hypothalamus. It releases a bunch of hormones to talk to the anterior lobe of the pituitary gland, like gonadotropin. So gonadotropin, that travels from the hypothalamus to the anterior pituitary to release the gonadotropins. So you're going to get a tropin releasing hormone from the hypothalamus. And it goes to the anterior pituitary to release the gonadotropins, which are more hormones that go to more glands to release more hormones. Right? So anyway, that's the hormone. Now the last one, it depends on the textbook. Is it a funny one? Yeah, it's called humoral, but-- You didn't get that. Oh, I get it. Funny one. Sorry. That was-- [APPLAUSE] Why is it? There we go. Yeah. But it deserves both. No, they're not laughing because it was funny. So the humoral, like you said, it's an odd one, because many current textbooks don't really refer to as humoral, because it's referring back to the old term, the humors of the body, which is based in pseudocytes and not in science. The humors are-- They don't have to-- To the Greeks. Tell that today, ancient Greeks. I would. I don't know how, but I'll say to them. It's about having nutrients. Pretty much it's nutrients inside the blood stream. And these nutrients are the stimulatory signals to tell a gland to release a hormone. So a great example of this is glucose. Glucose in the blood stream goes to the pancreas, triggers the beta cells to release insulin. And now that insulin can go to the various tissues and have its effect to help bring that glucose into certain cells of the body. And that is the humoral response. So there's three-- Neural, hormonal, and humeral. Three different stimuli. And so the humoral is basically just the concentration of a molecule, really, right? Yeah, yeah. So that will impact. And so if you're-- I think mostly, most of the time, it's a nutrient. And then it's feeding back on its own self. So if that goes in the opposite direction, then it will then usually shut off. And this kind of goes to the regulation of these. So you said how they're secreted. Yeah. But also we need to regulate them to not overrelease. Yeah. And so usually the two ways that we do this would be a negative feedback loop or a positive feedback loop. That's important. That's how we maintain that balance. And so most of the hormones that we're going to be speaking about today is in negative feedback. So that means, again, we'll use insulin as an example. No, is that the best example? Well, it is kind of humorally. Yeah. How about the example I like to use because it makes sense to people is when people take anabolic steroids. And let's just say people are taking testosterone, right? And so if they take exogenous testosterone from a needle and inject it into them, if they're taking so much testosterone, that it goes super-- Yeah. --for physiological levels, so above normal levels, because of the negative feedback, if your testosterone levels in the body go up, that's going to negatively feed back on the tissues that make your endogenous testosterone. And like your gonads, for example. So you take a needle, filled with testosterone, inject it, your gonads go, oh, I've got heaps of testosterone here. I don't need to make any negative feedback it switches off. But because your testes need to make that testosterone and part of their function for growth and development is to create testosterone, sometimes the testes in themselves can change their size. Yes. Right? They can shrink a little bit because those cells that make the testosterone can atrophy. Yeah. Right? And so-- And then also the negative feedback. But also the releasing hormones as well that are going to the particular regions of the-- so from, let's say, the hypothalamus-perchurchic limit normally would oversee testosterone release. They would also go, why are we so-- why is this testosterone so high? Yeah. I better turn off. That's right, because when you really think about it, it's not just at that place where that testosterone's released. That testosterone will act upon all the precursor or upstream regulators and will affect them. So that's why when you affect one hormone through a drug or intervention, it generally will affect a multitude of other things. Yeah. Because the hormones in the endocrine system are a cascading system where it has a domino-like effect, except both upstream and downstream. All right. Before we jump into the specifics, I think we need to talk about the fact that some hormones-- if you, again, categorize hormones now by what they're made up of-- the chemical structure. Yeah. Some are going to be made up of individual amino acids, or single amino acid-- You like tyrosine. Like tyrosine. Some are going to be made up of multiple amino acids. So peptides and polypeptides or proteins, usually between three to 200 amino acids. And then you've got the steroid hormones, which are made up of cholesterol. Yeah. And if you have a look at the aim
means for example, so the A means basically the hormones made up of tyrosine. The amino, so tyrosine isn't amino acid. And tyrosine is the basis to create the catacolomines, which is dopamine, nor adrenaline and adrenaline, which can also, also hormones. Yeah. Then you're a trend that is also hormones. Also the thyroid ones as well. Yes. So three people. Yeah. Okay. So thyroid hormones are made up of tyrosine as well, but they're iodized. Yes. So that's the A means. They've got a half life in the body once they're released of about two to three minutes. So what that means is the hormone after two to three minutes is 50% as effective as it was when it was first released. So very short acting, right? Except the thyroid hormone. When we talk about the A means the thyroid hormone has a half life of between half a day and seven days. Right. So for whatever reason, it could be because it's iodized, it could be because T4 is sort of like a stored version of thyroid hormone. It has a longer lasting half life. If you look at the point also isn't the T3, T4 carried on a caramolical as well with that impact the way it's maybe degraded. Yeah. I'm not sure, but I know most tissues have receptors for them and can many of the tissues can actually in a way store them themselves. The polypeptides. So this is between three to 200 amino acids. This includes things like insulin, glucagon, adrenocorticootropic hormone, even like gonadotropins, like luteinizing hormone, follicle stimulating hormone. They're all polypeptides. So multiple chains. Their half life is between four to 40 minutes in the body. So again, not super long. And some of them have carbohydrates attached to them, some of the polypeptides. So for example, the luteinizing hormone, follicle stimulating hormone. This is what we're called the gonadotropins. So these are the hormones that have their effect in the sex cells or the gonads of the males and females. They have carbohydrates attached to them. And that changes the way that they bind to receptors, but also changes the way that they're targeted for degradation. And then finally, the steroid hormones. And the protein hormones together have the half life of between four to 170 minutes. So they tend to last the longest outside of the thyroid hormones. The steroid hormones are made up of cholesterol. And this mainly happens in the cortex and the gonads. Right. And there's two major categories of steroid hormones. So you've got the corticosteroids. So they're the ones made in the cortex of the adrenal gland. And you've got the sex steroids, which basically is like the androgens, the estrogens and progesterone. So they're also made, so they're both made in the sex organs, but also in the adrenal cortex, right? Yes, androgens. Yes, absolutely. Now, we'll talk about the specifics of the corticosteroids when we get to the adrenal gland. I think the other thing just to mention is by their nature, then the way that they would interact on the target cell is going to be slightly different. So with the amino acids and the proteins, because they are polar, charged, they can't get through the membrane. So remember, if it's large or charged, it can't get into the cell freely. So when they come to the cell membrane, let's just say insulin comes to a muscle cell or a fat cell, they can't just barge their way through the cell membrane to tell the cell internally what to do. So the protein or the amino acid hormones need to have a receptor on the outside of the cell. And so these can be linked to other things. So sometimes they're linked to an ion channel, so that could be like a ligand-gated ion channel. They could be coupled to a G protein or sometimes to enzymes. So I think using insulin still as an example, I think that's a tyrosine kinase, which is it phosphorylates a whole lot of things internally, which I think correct me from here. I think that then just either creates or just sends glute transporters to the top of the membrane to allow glucose to come in. Is that basically right? Yeah, it's at the surface. Whereas, do you have anything to add for the. No, no, that's fine. That's fine. Yes, so those amine-based and peptide-based and protein polypeptide-based, they have their receptors on the surface. What about the steroids? So they're in nature because they are acted on surface receptors. I still talk about the. Just really quickly. Yeah, we're going to then have a fairly quick response in response to the hormone binding to it. Yes. So when you now come to the steroid hormones, because they are fat soluble, like you said cholesterol, they don't need to have a receipt on the outside, because they can just squeeze their way through the membrane. Lipid soluble, lipid soluble. So then they come into the cytoplasm, and many of them will then encounter a receptor or some binding protein that they will jump onto, which then will take them like a spaceship into the nucleus, which then affects gene expression. Yeah, it finds what's called a promoter usually on the DNA and allows for it to either activate and transcribe more genes that can turn into proteins and have downstream effects. Or it can inhibit depending on what it is. Yeah. And I think a good example for that one would be our Dosterone. Yeah. So our Dosterone is produced in the adrenal cortex. It's a steroid based. It's from cholesterol. And so when it leaves the adrenal cortex, it will travel to the kidneys, I think primarily to the distal convoluted tubule, go into those cells that align in the tubule, and changes the gene expression. And makes more sodium potassium pumps. Yeah. And so that then changes the way that those cells handle salt, or should I just say sodium and potassium. Yeah. And that then allows more reabsorption of salt back into the water, back into the blood. Yeah. And therefore more water goes with it. And that's pretty much the function of our Dosterone is to hold on to salt and hold on to water. In the body, don't let it pee out. Don't pee out sodium, don't pee out water. I'm dehydrated, my blood volumes low, bring it back into the body, and that's how it works. All right. So we've covered that. Now I think we can get into the guts of it. And we can start talking about the, if we talk about my simsidian allergy, we can, we've got to start talking about the mayor. We've got to talk about, Mayor Grimby. We've got to talk about, I did not. So we're going to talk about the mayor and the mayor in this case is the deity overriding figure that controls the whole city. And in this case, it's the hypothalamus. Right. Matt, quickly, very quickly, where is the hypothalamus? All right. So in the brain, that's how you can say it. All right. No, no. Is there another way that you'd like to describe it? Well, the region, I guess you put it in, is a dyncephalon. Yeah, that helps everyone. I'm just trying to think the quickest way to get there. Probably with an ice pick. Three of those. There you go. That's actually how you do it. Okay. Corpus closer. The top. What's the knee, the genu? Right. You can't describe it by using more technical complex terms. Basically, it is, if you take the brain, under the brain towards the front, you've got the hypothalamus. It is a little outpocketing, little projection that you'll see. And it's a tiny little innocuous looking structure. But blow the thalamus, which are the eggs of the brain. Yeah, that helps people as well. So the hypothalamus, its job is the mayor. It is the master regulator of the endocrine system. So, all right. The hypothalamus has a projection underneath it called the pituitary gland. Now, the pituitary gland actually has two lobes associated with it. Very interestingly, these lobes have different embryological origins. Very quickly, the anterior lobe, also known as the adenohypophysis, which means gland under the hypothalamus. It originated not from the brain. It originated from the ectoderm, from the roof of the mouth. What's the name of the pouch? So, the pathogies. So, the pathogies' pouch are at development. So, basically, it came from non-neural tissue and projected up to attach to the hypothalamus. Correct. The posterior lobe of the pituitary gland is a projection of the hypothalamus. So, it's neural tissue. And the reason why we're highlighting this is because the way that the hypothalamus speaks to these two aspects of the pituitary gland is different. So, for the posterior, which is simply an extension of itself, it's just got neurons that connect to it. Basically, just neuro transmitters. That's right. For the anterior, because it had to connect to itself, it has a bloodstream that connects the two. So, if we start with the. do you want to start with the anterior posterior? We'll go posterior because there's only two hormones in there. So, because the hypothalamus connects to the posterior pituitary through neurons, they, the posterior pituitary, also known as the neurohypophysis, it doesn't produce its own hormones. The hypothalamus produces it for them, transports them down those neurons, down the axon, down the axon, and says, "Hey, we're going to have a lot of fun."
posterior pituitary store these for me, I'll tell you when it's time to release them. So just vesicles of neurotransmitters sitting at the end terminal and instead of going into another neuron or another structure, it then just gets put into a blood vessel which goes to the whole body. Yeah, but it needs to be stimulated to be released in the posterior. And so it's still the hypothalamus, the the the the mayer that tells it when it needs to release it. Two hormones are oxytocin and antidiuretic hormone. Yeah. Or vasopressin. In the US vasopressin. Because we don't call it vasopressin here in in in Australia, Australia land. Right. So start with oxytocin. So oxytocin is sounds like a washing detergent. But you too, you'd put into like to get stains out. Yeah. On how good oxytocin would be getting stains out. All right. Let's let's. So when my wife was pregnant, oh, sorry, no pregnant with a developed embryo after about 41 weeks. Right. A fetus. Well, my daughter had about 41 weeks. It was time. 41. Yeah. It was I would you. Yeah. Well, cooked. So we had to go into the hospital and my wife needed to become induced. Oh, okay. So they do a couple of things. So first you can sort of like tickle. Stretching. Stretching sweep, which basically irritates the cervix. Right. Yeah. You can put some prostate glands on there, which we know from previous podcasts, prostate glands, do a whole bunch of stuff, but they can irritate the area. And that's sometimes why they recommend intercourse. Yes. Because semen has prostate glands in it. So the prostate gland produces Prostar glandans. And yes, that's semen could potentially irritate the cervix and say, it's hard. It's a little submarine's bastion into the cervix. That's right. And anyway, so we tried that. The prostate gland gel, the prostate gland gel. Keep it, be gene. Yes. It didn't work. So my wife went on an oxytocin drip. And so this highlights quite nicely some of the functions of oxytocin. Oxytocin can tell the uterus to contract. She fell in love with you again. All right. So oxytocin, she needs to fall in love with me in the first place. Oxytocin has people recognize if having two main roles. The main role that you ask someone down the street, hey, what's oxytocin? Do they go, oh, it's the love molecule. Which is true. Well, in a way, it's true. It is a relationship or bonding molecule. It's not about just positive relationships. Oxytocin can solidify negative relationships as well. In humans, yes. Yes. But I think animals is much more bonding. Probably right. Yeah. Can I just add a story here? Okay. My dad, he grew up in a sheep farm in New Zealand. Okay. Did he fall in love? No. No. Anyway, he would say that when it is lamined season, which I think is the end of winter, right? I think, anyway, it doesn't really matter. Occasionally, what would happen? Mothers. Some of them came out and they had his eyes. Mothers would die in the birthing process. Oh, no. Well, that came off the back of what I said. I'm trying to forget that. It doesn't matter. So basically, what happened was there were sometimes lambs that didn't have a mother. Okay. And so what they would do, as in the mother gave birth to the lamb and then passed away for whatever reason. Yeah. Okay. And so there would be lambs that needed caring. Right. And so what they could do is a couple of things. They could either get all the afterbirth and rub it all over the lamb. And then from another mother who's given birth and that smell. Oh, you take the afterbirth of another infant. Yeah. That mother gave birth to and put it on this quote unquote foreign infant. Correct. And then the mother would smell it and think it's its own. Yeah. Right. Or sometimes also what would happen is if a mother has rejected her own lamb. Yeah. What they would do is if there had been a lamb that had died, they would kind of put the coat on the sort of that it's always skin it. And they put that on there and then the smell would allow the mother to accept the lamb and not project it. Wow. But I think in more recent times they are just using oxytocin. So if they have done experiments again, I think mice and rats where if they were just to artificially inject the mothers with higher amounts of oxytocin, they would start nest in and then they would accept offspring that aren't there. Right. Okay. So it definitely is a bonding. But I think that is possibly reversed in humans and that's what I think you'll get into. Yeah. So there have been studies that have shown that oxytocin will be released in relatively higher amounts when you've got people solidifying negative relationships with others. So sort of having negative thoughts, negative connotations, really solidifying somebody's hatred for somebody else. In the bonding relationship with a mother and a child, and that makes sense because oxytocin is released during that birthing process and continues to be released during that process as well. Because oxytocin, one of its major roles is smooth muscle contraction. And this smooth muscle can include the uterus to help push the child out during labor, and also contraction of the muscle of the mammary tissue to help milk ejection to get milk out when the baby is suckling. So if the baby suckles. That's a letdown reflex. Oh. Okay. No, you're letting the baby. So when the baby is suckling at the nipple that stimulates to the hypothalamus, neurologically, the hypothalamus will stimulate through that neural innovation, the posterior toteric gland, to release oxytocin, and that contracts the muscle tissue surrounding the milk. The milk is ejected, and simultaneously the release of that oxytocin at the time of breastfeeding solidifies your relationship with the infant. So it's this two-fold effect. And I guess in both in these examples that you provided, they would be positive feedback. And so where if you remove the stimulus, I think the better one to illustrate this is the birth and process. So the head of the baby is pushed on the cervix, which is causing a stretch in stimuli, which neurologically goes back up to the hypothalamus and tells the hypothalamus we need small oxytocin down here to push the baby out, and this keeps reinforcing and reinforcing and reinforcing until there's no more stimulus. And that's hopefully the head's gone. Yeah. But the baby needs to be very, very particular with the terms you use, Matt. Yes. Until there's no stimulus of the head stretching the cervix. And I'll add one story to add on to yours. When my wife's been in her last, in our last baby, she had quite a significant bleed. And so baby was fine, but placenta wasn't detaching completely. And so she lost over a liter. And so the emergency kind of obstetrician came in and they put oxytocin on the drip plus another drug on that short what it was. And the obstetrician literally was just pushing her uterus from through the abdomen as hard as they could because that would again be stimulating neurologically to release more oxytocin. And that would then tighten everything up. And stop the bleeding. Wow. Amazing. I think they do a similar thing with the prolapse uterus. Okay. So let's move on from oxytocin. The other hormone is from the, that's released from the posterior pituitary is ADH, which is anti-diuretic hormone or synonym's vasopresin. So anti-meaning opposing diuretic means to release excessive water or just to release water hormone. So it's stopping the release of water from the body. And obviously the kidneys are the primary organ that help filter the blood and release that water from the body. So this is where ADH acts. The question is why would you want to hold onto water? And I think it's a pretty simple reason is due to times of dehydration or low blood volume levels. Yeah, or high osmolarity. A good point. So if you've got a lot of things dissolved in your blood, that is an indication that you might be dehydrated. Yeah. Because if you think about it, if you've got a bucket filled with salt, right? And so if you drink salty water like it. No, no, no, no, let me do this analogy first. If you got a bucket filled with salt and you would only take, so a bucket with a liter of water with, let's just say kilogram of salt in it. If you were to take half a liter of just the water out, you are going to have a higher concentration of that solute in the water, right? You haven't actually changed the number of those solutes, those salt particles.
but you've changed the water and you've changed the concentration. So the body thinks that if you've got a higher concentration of things dissolved in it, that you're dehydrated. But that may not be the reason. You may not be dehydrated. You may have just had too many chips, for example. And that's going to tell you, "Ooh, I need more water to dilute this out." So the ADHD is released from the posterior pituitary and it goes to the kidneys. And I remember the kidneys feel to blood. This filtrate travels through these convoluted tubes, specifically they're called convoluted tubes. And we pull 99% of whatever it filters back into the body. And then we'll pay out around about two liters per day of water, solutes, wastes, and so forth. ADHD will travel to the distal convoluted tube bill and the collecting ducts. Collecting ducts. So the very end of it, and it inserts these little pores, called aquaporins, these little proteins that allow for water to just be pulled back out. Because they're just instructed just to bring up the cytoplasm up to the. Yeah, okay. Yeah, I think, yes, that's right. And then the water will go from the tube bills back into the body and you don't pay it out. And that's that role of ADHD, right? Anything you'd like to add there? Or just issues that could go wrong with the ADHD is in two ways. So either too much ADHD is released or not a love. Not a love, you're back on oxytocin. Not enough. So these two conditions would be, if you're producing too much ADHD, that would be syndrome of inappropriate ADHD. Yep. So that could be from head injuries or brain surgery or something. And that causes a hypersacretion of ADHD. So too much holding onto water. Yep. And then those osmilarity fluctuations. Yeah, and you could have a lot of neurological effects if your ions are not in the right concentration. And then the opposite one is a form of diabetes, but it's diabetes and cipitors, which means. Don't know. Watery? Something like that. The amount of times that we've. Because malitis is this. It's honey. Yes. Diabetes means like to pass or to siphon in cipitors, I'm thinking is clear or. Yeah, it doesn't matter. But essentially in this case, because you're not producing any ADHD, tasteless. Tasteless. That makes sense. Yeah, yeah. Because diabetes malitis means taste sweet. Diabetes in cipitors means it has no taste. So it's saying, oh, it's not a glucose thing. It's not a pancreas thing. It's because diabetes was originally defined by the fact that the person with it passed a lot of. Polyurea. Yeah, passed a lot of urine. And so this is also passing a lot of urine, so they called it diabetes, but it's totally separate origin. It's got nothing to do with glucose, nothing to do with insulin, nothing to do with the pancreas. Correct. Yeah. And so in these individuals, you could be passing up to 20 litres of urinal day. Oh, and so they have obviously dehydration issues. Absolutely. All right. Okay. Now let's talk about the anterior pituitary. This is, like I said, also known as the adenohypophysus. It does produce its own hormones and stores it, but still waits for the hypothalamus to tell it to release those hormones. But because we said that there's a bloodstream called the hypofacil portal system that sits between the hypothalamus and the anterior pituitary, it means the hypothalamus needs to release its own hormones to travel through that bloodstream to stimulate the anterior pituitary. So this is a hormonal stimulus with the posterior pituitary. That's a neural stimulus, right? We spoke about those because we're very good at preparing you to understand what we're talking about. Hopefully. All right. So there are six hormones that are stored and released by the anterior pituitary. Oh, actually. Okay. How is your analogy here now? Yeah. Well, I'm going to bring this in. Maybe later. All right. Maybe later. So we'll get there in a sec. The anterior pituitary has six hormones. Let's talk about those hormones first. You've got a adrenal corticotropic hormone, horrible name, but it actually tells you exactly where it does. So adrenal gland corticot, cortex of the adrenal gland. Tropic to grow. Well, it does simulate to tell that to do something. Next gland to release its hormone hormone. So it's going to the adrenal gland, the cortex specifically to tell it to release a hormone and it can stimulate the release of a number of hormones. But let's talk about that when we get to the adrenal gland. So that's ACTH, adrenal corticotropic hormone. Number one, number two, growth hormone. Yeah. Growth stuff. I think this one's also called somatotropin. Yep. Yep. Which just means body growth. Body growth. Right. The third one. And again, this is no particular order. This is the gonadotropins. And there's actually two here. So this would be three and four, which is lutinizing hormone and follicle stimulating hormone. And they're both named after what they do in the female reproductive system. But they're equally important in the male reproductive system as well. Yes. So there's four. The fifth is going to be prolactin, which stimulates lactation. So this is the production of milk, not to let down, not the ejection. That's what oxytocin does, but the production. And then the sixth one is thyroid, the thyroid stimulating hormone that goes to the thyroid to stimulate it to be released. Now the hypothalamus must release hormones to stimulate each of these. We're not going to go through those because I don't think there's much point, but each one of those hormones released from the anterior pituitary has an equivalent stimulatory hormone from the hypothalamus. So for example, except two, which ones? Well, they're inhibitory rather than stimulating. Okay. Let's do the stimulatory one. Or releasing, or like, yeah, you can go stimulating. That's fine. Okay. So the hypothalamus will release, get out of tropin, releasing hormone. That goes down to the anterior pituitary stimulates luteinizing hormone and follicle stimulating hormone to be released. The hypothalamus will release growth hormone, releasing hormone, inhibiting hormone. Growth hormone inhibiting hormone. That's right. And it inhibits the release of growth hormone. Correct. And then you'll just produce growth hormone. Okay. So what about when the hypothalamus releases dopamine to go for prolactin? Is that inhibitory for prolactin? Yes. Yes. Right. So don't mean inhibits the release of prolactin. So again, without the hypothalamus signal, prolactin will continually be released. Correct. Right. That's important. I wonder what that, okay. We'll get back to there in a second. We've got the, now what triggers, we've got adrenal corticotrophic. Or just corticotrophic. That's it. Corticotrophic. That stimulates the release of ACTH. Adrenal corticotrophic hormone. What am I missing here? Thyroid. Thyroid. And this is thyroid trope. No, thyroid stimulates the release in hormone. Yes. We always bugger this up. Thyroid. Releasing hormone. Thyroid trope and releasing hormone. Okay. Yes. And that stimulates the release of thyroid trope and also known as thyroid stimulating hormone. That's right. I think confused people any further. That's why I didn't want to go through it. But now we've got those six hormones from the anterior pituitary. Which one do you want to start with? Well, start with the growth hormone. All right. All right. Growth hormone, because I think it's pretty simple. Growth hormone is released from the anterior pituitary gland and its job is to grow stuff. Right. So one, so basically what it does is growth hormone will stimulate the release of something called insulin like growth factor one. Right. So insulin like growth factor one basically promotes cell growth, proliferation and differentiation of tissues of the body. Primarily for children and adolescents. Yes. So very important in development, early development. But also for adults as well, mobilizes the breakdown of triglycerides in adipose tissues. So you release energy, quote unquote, energy into the bloodstream to be used for growth and development. It reduces glucose uptake into those adipose sites because it doesn't want to store energy there. So it says, hey, don't jump into fat cells. But it does say, hey, jump into muscle cells because I need, we need this energy to grow muscles. And so also protein formation, right? Yep. Stimulates protein synthesis as well within the muscle tissue. And also stimulates osteoblasts and collagen synthesizing factors, which both are connective tissue. So stimulates the growth of connective tissue, bone and other types of connective tissue. So really important in that growth and development. If you have too much growth hormone, just so this would be going to the energy of sim city. Yep. This would be the building developers of the town. Yeah. So these are those, that business that is basically just building the crap load of big buildings. If you build, just buildings. If you build too big, things are going to not be able to hold. So who was in history? Who was the tallest man to live? Was it still Robert Wodl? Yeah, there we go. Yeah. So as an example, so he had a tumor, which I guess was not releasing the inhibitor, but inhibiting hormone, which then meant growth hormone was left uninhibited. But he could have potentially also had it in the anterior pituitary, which still didn't release. That's true, yes. Yes, growth hormone. Which is what I think you had. I think you're right. Yep, I think you're right. So he's producing a huge amount of growth hormone.
And so because he is in childhood, the big difference here is that all his growth plates in his long bones are open. Yes. And so that means they just keep long, lengthening. Yes, so basically his body grew significantly, but evenly. So he just looked like a giant person. Correct. But this happens as an adult. So just some, I think this is off my head. Yeah. As an eight-year-old, he was tall and his dad. Yeah. As a 12-year-old, he was six foot seven. Right. And then I think at the point of him dying, which wasn't that old, I think he was in his 20s or something. Yes. I think he just hit 30. Yeah. He was almost nine foot. Wow. Did you know there's a person in history, and I wish I could remember the names for the listener. The only person in history to both be defined medically as having dwarfism and also having drug antism. So when this person was younger, they had something that inhibited growth hormone being released. I think it was a tumor, that inhibited growth hormone being released. And they were something like four foot up until they were like 18, 19, 20. And then the tumor flipped in a way and pumped out a bunch of growth hormone and then grew to be like seven and a half eight foot. Oh, really? Yeah. Amazing, right? So it was the only person to have been both on either ends of the spectrum. Wow. So growth hormone, obviously very important for that growth and development. And obviously both ends of the spectrum, if you don't have enough under growth too much. Yeah. But I do think dwarfism is slightly different, I think that's. Yes. I was just going to say is genetic, right? But I think it's also there's a connected tissue difference at the growth plate, which just kind of closes it prematurely, opposed to a growth hormone issue. Yeah. Now going to the other thing that could happen with growth hormone would be if you've already reached puberty, and it will not puberty, but you've kind of passed the point that the growth plates have closed and then you were to add growth hormone excessively into your body. Right. The long bones don't have the ability to lengthen anymore because the long bones are closed. And so what happens is the growth hormone, if you're looking at the bone side of things, it will only allow growth at the tips of the bones. And this is what the term actually means agro-meachly. Agro means, or acro, like a chromium. The tip. The chromium is a tip you shoulder, but the tips, so the tips your bones will grow. And so this is where these individuals get really big hands and jaws, protruding jaw. Yeah. Like eyebrow ridges, I think they're maybe they're forehead. And so they develop it that way. So this, if this goes back to your city analogy, this would be kind of inappropriate development that is kind of not just tall, but the building structures grow outwards, which then make it quite dangerous. Yeah. Exactly. So I want to hyper-pituitarism, because I believe what this individual had, both hypode in the early stages and then hyper in the later stages, leading to undergrowth hormone and overgrowth hormone. Do you listen to, if you can find out this person's name and correct me if I've got the medical conditions wrong, that would be awesome. All right. So that's growth hormone. What we've got now is let's do acTH, adrenal corticotropic hormone. This hormone is released and travels to the adrenal glands, specifically the cortex, which is the out a few millimeters of the adrenal gland and stimulates the release of cortisol and aldosterone. Mostly cortisol, mostly cortisol. Yeah, because aldosterone release, because this is the interesting part. So when you go to the cortex of the adrenal gland, the precursor for all these three hormones, which are going to be our dosterone, cortisol, cortisol and the androgens, they're all cholesterol based. Okay. Okay. Now, it almost works in a way that cholesterol kind of comes into the top and like a percolator, as the cholesterol is getting modified, it's kind of filtering through the cortex and going deeper. Right. Right. As they're kind of getting modified, they leave out of the cortex at different points. And so whatever's left is there that's for availability to make the next one in a way. And so the cortisol, sorry, the cholesterol gets modified kind of into precursors of progesterone. Right. Okay. And then that can be modified by a number of other enzymes into our dosterone. And then that progesterone or similar precursors to it can then filter through. And then that can be modified off into cortisol. Then we did an episode of steroids, right? And then it goes into these kind of early phase of an androgen testosterone like and it can be modified into testosterone or estrogen. Yes. But this will probably not normally just happen regardless of hormone stimulation. But then if you stimulate it with ACTH, then you're bumping up the process to go more down the line of cortisol. Right. And if you stimulate the adrenal cortex with endotensin 2, then you're bumping out more adolosterone. Right. So let's just say now we are in a state of stress, right? Firefly. Something's happened. I'm scared. I'm stressed. I've got a deadline at work. I need to get it done. I've got that feeling, that stressed feeling. This feeling of stress is intrinsically linked to the amygdala, is linked to various areas of the brain that can speak to the hypothalamus, triggering ultimately the release of adrenal corticotropic hormone, which travels to the bloodstream to the adrenal gland, stimulating the release of cortisol. Everyone has heard that cortisol is our stress hormone. Now what this means is and I don't know if we do an episode on court. We didn't episode on stress and cortisol. Anyway, remember the fact that cortisol, this is important for people to understand. Cortisol doesn't make you stressed. Cortisol is released as a result from your stress. Well, it's released throughout the day. That's right. So it's going to end all. Diurnal. Diurnal. It's released early in the morning and then in kind of pulses, but I think the greatest pulse or pulsatile release is early morning to prepare you for the day because you need more energy, you need more glucose utilization and release and so forth. All right. So let's talk about what cortisol does. Because like I said, cortisol is released because not because it wants to make you stressed, but it wants you to be in the best position physiologically to respond to the stress. So that's how you should be thinking about it. But in my mind, I say cortisol helps our body deal with the stress in the immediate moment, but also helps future-proof the body for future stress. And the reason why I say that is because a couple of things that happen is this. It stimulates the muscles to undergo glycogenolysis, which is breaking down glycogen into glucose, so the muscle can use the glucose to do stuff. That's important because if you're stressed, you need to be able to do things, get work done, run away, whatever it may be. It also goes to the liver and tells the liver to do the opposite, not break things down, but store the glucose as glycogen. And it wants to store the glucose as glycogen for future reasons, right? To future-proof it so that it's there. It also goes to fat tissue, tells it to break the fat down into lipolysis. Yeah, lipolysis and breaks the fatty acids down so they can jump into the bloodstream again, so we can use it for energy. And so, depending on the tissue and its function, it depends on what it does. It goes to, well, speaks, interacts with the immune system, tells some aspects of the immune system to ramp up, other ones to bump down. Again, it's saying we don't need to waste time and energy on the immune system right now, but so for example, what it can do is say, hey, you don't need time to go in inflammatory responses. It's a very energy, a highly energy costing, let's save that, let's push that down and we'll put our energy elsewhere, right? And so that's how you should think about cortisol. And also bone, so it changes the model and the bone. Yeah, presumably to liberate calcium ions. Yes, because we need calcium for muscle contraction. And also neuron firing. And also the way it kind of freaks your late homeostasis in the skin, particularly kind of repairing the connective tissue aspect of it. So that could potentially thin the skin off if it's around for too long. And that's the other thing, is that just like with the sim city analogy, you don't want to amplify anything more than you need to. So cortisol, people think it's a negative thing or a bad thing because some of us always feel stressed. Therefore, the cortisol release for too long can actually significantly modulate the immune system to the point that we can get sick. It can significantly impact our bones and we can actually get more brittle bones. It can significantly impact the way that we deal and handle
glucose and you could possibly alter your insulin sensitivity and get metabolic disease and so forth. So, this is the reason why it's not because insulin's doing anything wrong. It's a great, it is such a wonderful hormone and is required, but it's required to help us deal with stress in the moment. And that's important. And that's because of ACTH. So now we're just going to take a very quick break and we'll be back in a moment. So welcome back. We've spoken about ACTH, adrenal corticotropic hormone, the fact that it's released from the anterior pituitary gland in response to the hypothalamus stimulating it and the fact that it travels via the bloodstream to the adrenal gland, specifically the cortex, to stimulate the release of cortisol. And we spoke about the effects of cortisol. But there are other important functions of ACTH that I think our dear listener needs to be aware of Maddie, but also the adrenal gland has a number of other hormones that it releases that we should probably touch upon. So firstly, I want to say that ACTH is actually produced interestingly from this sort of pro hormone. And this is called pro-opio melanocortin. Or pomp. Pomp. Or pomp. Pomp. Yeah. Pro-opio melanocortin. Interestingly, it's basically a molecule that gets chopped up to produce a peptide. Big peptide, right? Big peptide. Chopped up produces ACTH. It also gets chopped up to produce something called MSH, specifically alpha MSH. And that's melanocytes stimulating hormone. And its job is to stimulate melanocytes. What do melanocytes do? They provide the. The one that doesn't know is. Molecular subsets. Well, I do have them, but they're just not very efficient. They don't have these hormone at all then. That's right. They stimulate these melanocytes to produce pigment in this pig. Molecular sunscreen, Michael. You could call it a molecular sunscreen. I call it an umbrella for the cell and melanin. And that's what MSH does. MSH being made from the same pro hormone that ACTH is, tells us something. Because ACTH can, because it's such a similar chemical, bind to the same receptors that MSH binds to on the melanocytes to stimulate it. Now, generally, it's a very poor stimulator of the melanocytes, ACTH. But in high quantities, it can stimulate the melanocytes to produce all this pigment and can result in hyperpigmentation. So in cases of too much ACTH being released, you can get hyperpigmentation. Now, do you know any conditions where ACTH is released at high quantities? Yeah. I guess the two well-known ones would be cushions and addocents. Cushings and addocents. So these are conditions, diseases, disorders associated with increased ACTH. Yep. So in addocents, which. Can you tell it addocents? You made a male quimbee joke earlier on. And now, because male quimbee was his character, he's based off JFK. Right. And JFK had addocents. Yeah, yeah. So I was going to say the common clinical scenario or study used for addocents is JFK. Right. And I think he had like a bronzy colored skin. He did. Hard to tell, because all the footage is black and white. But yes. Okay. So with him, so with addocents, essentially what the issue is adrenal insufficiency. Right. And so what's in there is. Not adrenal fatigue. No. Which doesn't exist. Okay. Just to make sure. Because. Do you just mean like it gets worn out or something? Yeah. There is a condition that people, which again doesn't exist, that people call adrenal fatigue, where they go, "Oh, I'm so tired. I've got lethargy. My hormones aren't working properly." Okay. So stressed all the time that my adrenal gland is just so tired and fatigued, it doesn't release the hormones it needs to. That doesn't exist. You can have adrenal insufficiency, where there's an actual, what you're going to talk about, which is a pathology, which something has happened structurally or functionally to stop from working properly. Well, maybe even arthrogenically. So if you. What does that mean? That drugs. Well, usually healthcare driven. Yeah. In this case, if you had been on longstanding steroids for a long periods of time, that your adrenal gland may become downregulated. Yeah. Because you've. And then this goes back to feedback loops. In this case, this is the hormonal feedback loop. So if you've got a lot of cortisol in your blood because you're taking prednisone or other things similar, then the feedback loops would be into negative inhibities. That's right. Because the body's thinking why I have such a high amount. Yeah, it's not fatigued. It's not tired. And so if you were to go off quickly, then you would have a. Read that. would be fatigued. It would just be insufficient. Yeah. That's right. Okay, so let's just get back to this. You said, "Jafe Kaye had atticence, which is too much ACTH." Oh, the issue there is. Because at the adrenal gland, there's an insufficiency. So it's just not release in cortisol. So you're saying that ACTH is probably being released in a normal ish amount to begin with. Yeah. But when it goes to the adrenal gland, it's almost like the adrenal gland's not responsive to it. Correct. So as we know with the feedback loops, if there's no cortisol to feedback negatively to the hypothalamus all-petritic gland, therefore it's going. We need some more, obviously. Right. It just keeps ramping it up. And so high ACTH. So it's not a problem at the pituitary or hypothalamus. It's a problem with not picking it up properly. So in atticence, they don't have enough cortisol. And so you're going to see downstream effects of not having enough cortisol, I assume. Yeah. That potentially be. Well, I guess if you just go to what cortisol does and we spoke, it has the metabolic effects. So it would. What's the term? Not utilized, but release from various locations of the body for glucose to be available. Yep. Immune function, vascular function, other things in the kind of stress response. And so if you'd not. and then possibly the earlier stages of how cortisol is made is outdosterone. And so you're going to have similar. because if you've got an insufficiency of those two hormones cortisol and outdosterone, which ACTH can stimulate both, can't it? Well, also cortisol. Yeah, mostly cortisol, because outdosterone, which we'll get to, is more driven, releases more driven by angiotensin II. But because the ACTH would drive the cortisol, which then drives the precursor, it would still feedback on outdosterone release. And so presumably a person with addocents would have issues with both the cortisol, not being high enough and also outdosterone. So that would be fluid balance. Yeah, so they can have hypotension, right? Somebody. So basically, you can say that addocents is a hypocortisolism, right? Yeah. But don't have enough cortisol. And like you said, cortisol is important for mobilizing the glucose into the bloodstream for us to use for energy. So if that's not happening, then you may be fatigued. Yeah. And also going with cortisol, which we spoke about that kind of sensitizes the body to the catacolamines. So. Good point. for the fight and flight. Not to say that you want to be in a fight and flight response, but it just makes it more sensitive too, so keeping your heart, right, blood pressure, all that kind of things responsive to those hormones. Yeah. That would be an issue as well. And so because that ACTH, so again, low cortisol, this affects in addocents is going to be low cortisol. Again, weakness. You're going to have dysregulation of your blood pressure. You're going to have dysregulation of your immune system. And sugars. They're going to be off all that type of stuff. But we were talking about ACTH because it's now elevated because of the negative feedback. You can get hyperpigmentation, right? Now, the other disorder associated with elevated ACTH is cushing's. Yeah. So now this is not by the same process, but this is actually probably from a tumor in the pituitary gland. And. So this is directly stimulating ACTH from being released. So it's not a negative feedback issue. It's just hypersecretary. Right. And so then because the adrenal gland will be responding to it, unlike addocents, now you are also pumping out. Sorry. Now you are pumping out a huge amounts of cortisol and now you get in an effect of hypercortisollemia. Yeah. So you can have primary cushing's, which is the tumor at the pituitary. Or you can have is it secondary when the adrenal gland? So that's a good point. So these definitions come based on which is cushing which. Yeah. So primary endocrine disorders is at the organ level of the secretion of the hormone. Okay. So to be a cortisol here. So to be a primary endocrine disease for cortisol, it has to have hypersecretion at the adrenal gland. Gotcha. Okay. But if it's going to be a secondary, then it's at the. To a trofen release point. So that would be ACTH. Gotcha. So whereas if it's tertiary, it's at the hypothalamus. Okay. So to clarify, for people who think the way I think, which is more slowly, you might look at. both cushings and addisins, or let's say addisins and cushings, as both having elevated ACTH, and that can be true. But the end product is cortisol, ultimately, and some aldosterone, but let's just focus on cortisol. Because in addisins, the problem is ACTH isn't stimulating the adrenal gland. All the adrenal glands are just problematic. So you got adrenal insufficiency. You've got low cortisol output. Correct. Low cortisol leads to more ACTH being produced, but it's not a problem with the ACTH release. When you look at cushings, you're going to have a problem with either too much ACTH being released due to a pituitary tumor, or you're going to have too much cortisol being released due to an adrenal tumor. Because the problem here in cushings is too much cortisol, you've got hypercortisolism, which is the opposite of addisins, which is hypode. Now, because the problem is cortisol, ultimately, if the tumors at the cortisol producing tissue, that's primary. Yep. But it can also be a high post-accreting one as well, which would be addisins. Which would be addisins, yeah? So addisins take the technique. It's technically a primary, yeah. Yep. If it's a hyporeleasing, yeah. And then we go back, because you confused me, then we go back to the pituitary gland, and if the tumor is there to release more ACTH, then it's going to be a secondary. And if it's a group of phalmus, even higher up, it's a tertiary. Yep. All right. And so cushings would be a secondary? Yes. Generally, right? Because it's at the pituitary level. Most commonly, yeah. All right. El Dostro. Because El Dostro and is also a hormone released from the adrenal gland, right? And ACTH can stimulate it, particularly at normal physiological levels, not really, but at super physiological levels, ACTH can definitely stimulate the release of El Dostro. And I just wonder, I don't know the answer to this, but this is just me working back from first principles. As we spoke about earlier, the adrenal cortex is just like a percolating coffee machine. If you're kind of sucking out the coffee at a lower level, you still need to bring more in at the top. Yep. And so therefore, you're going to, by default, produce. And which did you say was produced first, the cortisol? No, the. The El Dostro. Okay. So if you're really stimulating the cortisol, by default, you're also going to be producing El Dostro. Because they're similar molecules. Yeah. No, it's a great point. And so I think that is definitely what's going to be happening in this case. So when you've got too much ACTH being released, El Dostro is released. But. Let's just talk about. But also just a tumor in the adrenal gland in the cortex. Yes. But before we go into disease disorder, to release all this El Dostro. El Dostro is released under normal physiological conditions in response to alterations in blood pressure, blood volume. And so El Dostro is truly there as a way to maintain our fluid balance. And so if, at the end of the day, the way I think about it and the way I talk about it with my students, is that your blood volume is intrinsically linked to your blood pressure. And your blood pressure must be maintained at around about 120 systolic over 80 diastolic. And this is, you know, the nice, good, roundabout, perfect pressure to be able to deliver enough blood to the tissues of our body to feed it so that we survive. That's why we need a pressure because it's the pushing force to say, "Here you go, organs. Here's your oxygen. Here's your glucose. Here's your gases." But the thing is that if your blood pressure drops and your tissues don't get perfused, well, there's a bit of buffering capacity. Your blood pressure can drop lower and it can still get that stuff. But the problem is at your kidneys. Because if your blood pressure drops to 80 systolic, then you're not going to be filtering as much blood. And you need to filter the blood to get rid of all the metabolic waste of the blood products. And that's important because very quickly, if you're not filtering enough blood, those products accumulate, you get sick very quick. So your kidneys are probably very sensitive early on to changes in blood volume and changes in blood pressure. So they have evolved mechanisms to control blood pressure and blood volume. And so blood volume blood pressure drops. Your kidneys release renin. It undergoes a renin angiotensin-odostrone system. We've done a whole podcast on that. Ultimately, it releases something called angiotensin-2. And angiotensin-2 is the trigger to stimulate aldostrone release from the adrenal gland. So that's telling us that primarily, aldostrone doesn't get released. Unlike all the other hormones we've spoken about today from the hypothalamus impotuitary, it's mainly a kidney controlled response. Angiotensin-2. It releases aldostrone, travels to back to the kidneys, specifically those nephrons that do the filtration that will decide how much fluid and waste and products and particulates and solutes it wants to hold on to or throw back into the body. And just tell it to throw more salt or sodium back into the blood. And wherever salt goes, water follows. And that's always thinking about that. When you eat a lot of salty chips, you get thirsty. If you take a lot of the salt and throw it from one cell or tissue or compartment to another, water is going to follow. That's the same thing. So if we throw the salt or sodium back into the blood and not peer it out, then we don't peer the water out because it follows the salt back into the body. Does that make sense? It does. And so you can have too much aldostrone being produced. So what would that then tell you? What do you think would be the issue here? Yeah, would just be high blood pressure. Essentially right. Blood volume goes up too high. And you can obviously get a dimmer. Yeah, yeah, yeah. Additional salt. That's right. Retention. Yeah. And obviously the opposite would be dehydration associated effects. You just peer out way too much fluid. And that's aldostrone. We would be interested to see the comparison between a hypo aldostrinaria versus like a emia in the blood versus diabetic insipidus. Yeah. Like which one is more powerful and right because what you're saying is ADH. Because we know that if you do a similar role to aldostrone. Yeah. The only difference between the two is ADH is just making water carriers. Yeah. Whereas aldostrone is making pumps. Pumps. Yeah. And so I think aldostrone would have a bigger effect on electrolyte management because it's not just taking more sodium back into the body and water follows. It's also excreting more potassium. Yeah. So you can become hypochalemic. That would be a problem. Oh yeah. Because we need potassium at appropriate levels in the body. Body is very sensitive to potassium changes. And potassium is required for neurons to function, for muscles to contract, for a whole range of things. And that's where some people who are on diuretics, if they are losing too much potassium, they may have to shift to a potassium spirit. What's a diuretic? Diuretic is just a peon drug. Sorry? A drug that makes you pee a lot. Why would you take that? Or a demer? Or in some cases, high blood pressure. Right. There'll be other indications, but there are two common reasons for why you take a diuretic. So the thought is, if your blood pressure is really high, well, we know blood pressure like we stated before is really closely linked to blood volume. Let's just pay out more water and drop out blood volume and our blood pressure will drop. Correct. So let's do that by giving tablets that make you pee more. Yeah. But one of the side of the pieces is you pay out too much potassium with it. So that would be like loop diuretics, such as furus, myotheraides, they will result in potassium loss. So you can take potassium sparing, did you say? Potassium sparing diuretics, which would work in a different part of the nephron and hold on to the potassium. And therefore you're not losing potassium, but you still pee and stuff out like spirulactone. Yes. Okay. Wonderful. All right. So that is aldostrone. You mentioned it earlier. I just want to finish off the adrenal gland with its name. Add renal. Mm-hmm. So I think that's more Greek, isn't it? Yeah. Add is Greek for on. Renal is kidney. Whereas I think the Latin would be epinephron. Epinephros. Yeah. So epineaning around or near to nephros being kidney. Hence why adrenaline is produced from the kidneys and epinephron is also produced from the kidneys and they're synonymous. It's just that in Australia where we say things correctly, we say adrenaline and in the US, which is interesting. We've got those funny accents in the US, don't they? Howdy, parotoner. We're joking. We're joking. We're joking. In the US, we love the US and we love our US listeners and tell us where you're from. Actually, send us an email if you're from the US and you listen to us and you enjoy what we, the content that we put out, tell us where in the US where you're from and Matt and I will try best to do that accent. Boston. Hey, get out of here. You're, you're man. Was that all right? Anyway, what he says, forget about it. Is that the, that's New York? I think it's New York. I'm walking here. Yeah, that's a funny video, that one. Yeah. Oh, yeah, you showed me that. Anyway, we don't know. Are you saying before that? I'm going to step back. Oh, yeah, it's something. A drain all, a drain all, a drain all, a drain all gland. It's interesting that.
Yes, in the States they'll say epinephrine. Yeah. But then when the receptor, what's the receptor chord? Adrenergic. Yeah. Not epinephoric. Yeah. Yeah, you're right. See, full short. Yeah, it does. Full short, doesn't it, guys? Time to change. Time to change. Great. And the metric system. All right. So, so the reason why I wanted to say that wasn't just to talk about neurodrenaline, sorry, adrenaline and epinephrine. But obviously Matt spoke about earlier the fact that it's produced and released from this gland because the adrenal gland is simply a modified what? Oh, the adrenalin medulla is. Yes. But that's where neurodrenaline and epinephrine is produced. It's just modified pre post ganglionic neuron. Yeah. The cluster of neurons. That's right. And the reason why we brought it up again is because I just wanted to make the statement that. When you are in a phytop flight response, okay, so I'm going for a walk in the park. So it's 10 o'clock at night. Don't know why I'm walking at that time. And then next minute somebody jumps out of the bush with a knife and holds it to my neck. I am obviously plunges it into your neck or holds it to my neck, you know? And they say, oh, you get out of here. Give me your money. And I say, which one do you want? Forget about it. Forget about it. Okay, do you want my money or not? Give me your money. Forget about it. So I will get frowned and by all of it. And what's going to happen is my hypothalamus, which is the master regulator of the endocrine system will release ACTH. Well, we'll trigger the release of ACTH from the anterior pituitary, which the ACTH will travel via the bloodstream to the adrenal gland, stimulate the release of cortisol and mobilize. But I will say, wait, wait, wait. Let me just finish this because you love interrupting before I even finish any sentence. Mobilize the glucose into the bloodstream, play around with heart rate, play around with the immune system. It's basically trying to make sure the environment's as best as possible to deal with that situation and prepare it for the future. But the hypothalamus will also stimulate the sympathetic neurons or sympathetic outflow from the spinal cord that go directly to the adrenal gland, specifically the medulla and stimulate it to release adrenaline into the bloodstream. And the thing about that is once adrenaline in the bloodstream, it goes everywhere and it will bind to all adorinergic receptors and you have a system-wide phytopflight response. That's important to say because you can't really have a localized phytopflight response. You can't just say, I'm scared and I can, and only my pupils are dilated or I'm scared and only my airways are dilated or I'm scared it's only my heart rate that's gone out. It all happens. And that's because your system's flooded with adrenaline. All right. What did you want to say, Matt? Well, I was going to say this. If this was the case, let's say you weren't to also bring in the sympathetic neuro system and you just did the cortisol release. Yes. By the time you were spotted to that hormonal influx to the situation that you get in and mugged, by the time it causes an effect, you'll be dead and a bloated corpse. Yes. Because really, cortisol is- Bloated corpse. So chuck me in the river after the after-restaurant, okay? That's right. Yep. So my point here is, cortisol. You thought about this. Cortisol is a steroid and the way it responses, response is via gene expression. All right. And so this is going to take probably a few days to really get to the point of response to do all these things. And so in a way, the cortisol is probably more a medium term stress opposed to a very high acute stress. Yes. So we spoke at the very beginning of this podcast that both the nervous system and the endocrine system, a communication networks, one's fast, nervous system, one's a bit slower. And while both the sympathetic response and the result of cortisol are both there to communicate with the body for times of stress, it's the sympathetic nervous innovation that is allowing you to deal with the situation in the moment. Yeah. And it's the cortisol, like we said earlier, that's helping you basically prepare for the next one. Yes. Or to prepare for the next day. Oh, it's an extended one. Yes. That's right. So it's going over days. Yes. It's trying to maintain, because when you have a final flight response in the moment, your body gets kicked out of homeostasis. Yeah. A whole bunch of things are happening that is not to the benefit of the body, individual long term, so the benefit in that moment. So the cortisol is there to help sort of bring it back and maintain homeostasis throughout that time of stress. Correct. That's what, and so it's sole purpose, shouldn't say sole purpose because it's biology, but it's major purpose is for me talking about cortisol is let's keep this body as best within the homeostatic range as possible during this time of stress. Now, if that lasts too long, then it becomes detrimental. Yeah. Because as we spoke about, it has immune modulating effects, bone modulating effects, all these other effects that then would be harmful if you keep it going for longer periods. Exactly right. Exactly right. And now we've spoken about, did you want to talk any more about the adrenal gland? Obviously it releases angriagens. These are important, which is still cortex, but we can bring these back in once we do the genetic troughs. Yeah. So the angriagens is basically referring to the fact that they. The Andrew. They play a role in creating Andrew. No. But in a way, they play a role in various sex associated characteristics. So an example here would be, many people think, say in the female sex, that it's purely just estrogen. Yes. And myelosis purely testosterone. But partly for these adrogens in the cortex, at least for the female sort of things, there is testosterone being released. Absolutely. And that would result in some of the second sexual characteristics like hair, pubic hair, underarm hair, and they even suggest libido, sex libido. And because these angriagens are steroid hormones, they play. Their effect is within the cell transcribing DNA, turning genes on, turning genes off. Many can have what's called anabolic effects, growth like effects. So people thought, so probably most commonly within the community, people think, "Oh, testosterone is an anabolic steroid." It makes your muscles grow big and strong. That's why body builders take it to get big and strong. Okay. Truth there. Estrogen is also an anabolic steroid. But it's anabolic in the sense that it helps the growth and development of the endometrium to prepare the lining of the uterus for egg implantation. Yeah, I'm breast tissue. I'm breast tissue. But estrogen is a stimulatory growth associated steroid, right? It's anabolic. It's a fig growth. Caterbolic means to break down, right? Anabolic means to. Cortisol will be a catabolic. Yeah. But let's talk about some of these hormones when we get to the gonadotropins. I think it's time to talk about the thyroid. Okay. All right. So importantly, we're still talking about the anterior lobe of the pituitary gland. And we spoke about the fact that it releases six hormones. And the third hormone, which we've spoken about, adrenal corticotropic hormone, which we've spoken about. Do we talk about any others? Now we're up to. I think we still do pre-allectin. Yep. And thyroid stimulating. And gonadotropins. Okay. Cool. So now let's talk about thyroid stimulating hormone. The hypothalamus will release a hormone, thyroid trope, called thyroid trope and releasing hormone. Travels down that blood supply the epopophysyl portal system down to the anterior pituitary, stimulates the release from the anterior pituitary of TSH, which is thyroid stimulating hormone. That travels via the bloodstream to the thyroid and stimulates the thyroid to ultimately produce thyroid hormones plural. Yes. So what are the two thyroid hormones, man? I'm not going to pronounce them. Okay. I will. But T3, T4. All right. T3 is triiodothyronine and T4 is thyroxene. That's easy. And importantly, people need to know that thyroid hormone is made from the amino acid tyrosine. But even though that's the case, it still needs to be, once it's made, it needs to be transported with a transporter protein. Thyroid's a real weird one because one, it's an amino acid-based hormone, but it acts more like a steroid-based hormone in regards to its intracellular and plays a role in transcription, but also it needs a carrier molecule in the bloodstream. And amino acids don't because they're polar. Yeah. They can float in the plasma of the bloodstream and steroids can't because they're lipids, so they need a carrier like albumin. And that just why you're stating that. Yep. The cortisol and probably udosterone is the exact opposite. In the sense they're more steroid-like. Yeah. So they're hydrophobic. Right. However, they are hydrophilic enough to be transported in the blood without a carrier. There you go. your thigh beacon now.
that they can cross the cell membrane to get into the nucleus. It's a biology cool, but also tricky because it's not black and white. Alright, so thyroid. The thyroid is this butterfly shaped gland sits right at the front of the trickier sort of hugs it. Not very big, not very heavy, but pretty important. It is like a shield. Yeah, it looks like a shield, right? Is that etymologically what thyroid means? I don't know what thyroid means. It doesn't matter. So, I said it's made from the amino acid tyrosine, but also is made from iodine, which is an important element from the periodic table, an important element that exists within salt, the environment well. So, iodine is often in many plant, what, it's in the soil. In soil. Right? And then the plants grow in the soil that contains iodine, and then contains the iodine in the plants. The animals eat the plants, and then the animals contain the iodine, and we eat both the animals and the plants, and we get iodine. However, there are some places and spots within the world where there's not much iodine in the soil, and therefore not much iodine in the plants and the animal material, which means our body is deficient of iodine. Once iodine gets in the body, it becomes iodide, and the iodide is in the bloodstream, and the thyroid pulls that iodide out of the bloodstream, and snaps it together with tyrosine to produce thyroid hormone, or hormones. But here's a really cool and interesting point. If you look at the. Thyroid tissue, there's thyroid cells, which we call follicles, and these follicles, they take the tyrosine, they take the iodide, and they push it into this little pool, which sort of sits in the. And when I say "pull like a swimming pool," that the thyroid has called colloid. So colloid is like a jelly like. Think of it as the water in the swimming pool, right? So this colloid helps to pull the tyrosine and iodide, and bring it together to form thyroid hormone. But I want you to think about this. There are some places that don't have enough iodine, and think about negative feedback. So you've got the tyrosine, because that's an amino acid we can get very easily. No problem. But then the body goes, "Hey, I've got the tyrosine, I've got the colloid, I don't have the iodine, therefore I'm not making thyroid hormone, I'm deficient of thyroid hormone, this feeds back to the hypothalamus, and goes, "Oh, better produce more thyroid trope and releasing hormone, which travels to the anterior pituitary, which goes, "Oh, better produce more thyroid stimulating hormone, which goes back to the thyroid, and it tells it to make more colloid, pulling in more tyrosine, but still isn't pulling in any iodide, because it's not available." So what ends up happening is over time, this negative feedback system, bulks up all this colloid. You build up all this colloid fluid inside your thyroid, and your thyroid gland swells up, and you get this enormous protrusion in your neck called a. -Goiter. -Goiter, that's right. You don't really see goiters anymore, why? Because we. what's the word, doesn't matter. We just put iodine into the salt. -It's now iodized. -Idized salt. Yeah, that's right. So if you see iodized table salt, it's there to help your thyroid. -Yeah. -It's important. -You need that. -Which is different to the salt you use, the pink Himalayan salt, which I still tell you not to buy. -Radioactive. -Radioactive. There are radioactive elements in that salt. -There are. -But there's probably radioactive elements in men. -Bananas. -That's true. We'll talk about radiation. -Yeah. -All radioactivity. -Oh, yeah. -You just quickly mentioned then if you were to be in locations where nuclear bombs went off or nuclear meltdowns, why you may be instructed to take potassium iodide. Because the iodine is one of the very first to be affected radioactively. -Right. -Yep. And if that's the case, and you're using that iodine to make thyroid hormone, and then that thyroid hormone travels in your bloodstream to basically all the tissues that thyroid hormone has receptors in nearly every tissue of the body. And then you've got now radioactive thyroid hormone traveling through the system. -Oh, it's the main reason. -Well, the main reason is that that's the thyroid gland itself. -I just thought either knock that out or you got cancer of your thyroid. -Yes, which is what happens. So what they tell you to do is take potassium iodide tablets. -And it just gives you supplies. -Fresh. And therefore, the thyroid gland doesn't need any more iodide that's obtained radioactively elsewhere. -Exactly right. So if you go to watch, I think Oppenheimer, which will be coming out soon, but I think also what was the TV show made about? -Chinobyl. -Chinobyl. They talk about that as well. -Because it's just a lot of. -That's a good TV show. -There was a good show. -It's full-on. -Yeah, it is full-on. But you know what? And I know this is a bit of a digression. But we need more nuclear plants as alternatives for fossil fuel. -Does this take a long time to make? -Not really. -Well. -To build. -My readings suggest. -You mean to build the entire. -Yeah, ten years. -Yeah, well, it's definitely a cleaner energy, but there's pros and cons obviously for it. -I think one of the issues that people have is they can fight nuclear power plants with nuclear weapons. -That's true. -And then not even close to being the same thing. It's just simply the term nuclear is referring to very small. And so when you look at nuclear weapons, they take very simple atoms and elements from the periodic table, like hydrogen and helium, and they either try to split them or fuse them. Generally, they can't fuse them, because that's what the sun does, and it needs a huge reactor to do that. So they try and split them. And when you split them, you release huge amounts of energy, hence what the Oppenheimer movie is going to be about, is trying to split the hydrogen atom. And theoretically, Einstein, who played a role here, he did the calculations about the. He's basically the one that wrote the paper that said, "Hey, you know what? If you were to split a hydrogen atom, this is the amount of energy that theoretically could be released." The thing is that the theoretical energy release from it is so enormous that they could not tell if they were going to release the full amount of energy from splitting the atom or only a part of the energy, hence why during Oppenheimer, when they did the very first atom bomb explosion, they did. -It wasn't in the deserts of Arizona or something. -In the U.S. -Yeah, I think Nevada. -U.S. -U.S. -They did not know how big the explosion would be because the physics said it could potentially be big enough to destroy the country or it would only be big enough to destroy that local. They didn't know how much it was going to be released. That enormous explosion that came from doing that, and I could be wrong, and I love someone to correct me. So I'm just working off the back of my mind. I think that was like 1% of the possible energy that could have been released. -Isn't that the problem with it? Because there's still so much energy. -You're complaining. -That's the radiation that's still present with you. -Yes, that's right. So because you get radioactive decay of particles over time. Now, this is not what happens when you use nuclear power for energy. It's a different process. And in actual fact, and I know this is a huge digression, but if you compare it to fossil fuels, tens of thousands of people die every year, arguably hundreds of thousands of people die every year due to fossil fuels, whether it's directly because of work conditions and location, but also because of the pollutants that exist. -Oh, you just have pollution, right? Millions people die per year just on the air pollution. -Exactly. From fossil fuels. Nuclear energy is clean. People who work in these nuclear power plants aren't exposed to excessive amounts of radiation. Water can hold nuclear energy. Water is very good at containing radioactivity. So as soon as you put something radioactive in a big container of water, basically, if you're sitting. You could be a few meters away from a nuclear rod and you won't get any radioactive exposure. Because it's really good to. As soon as you take it out, sure. So it's just about trying to maintain these big structures to get as much fuel. And the amount of fuel we pull out isn't not much. Like by the time we exhaust a fuel rod, still over 99% of its energy available in the rod, hence why they have to bury it deep within concrete and it's going to sit there for millions of years and people might go, "Oh, this is a problem. We'll go radioactivity. We're going to hit a point where we'll be able to probably dig them up and safely use them again to get the rest of the energy from it." Huge digression. Everyone's probably turned off now. But I think it's important because people are scared. They go, "What about meltdowns? What about, you know, the again, Chernobyl?" Well, I guess an interesting consideration now, currently with the war in Ukraine, is that it can be possibly weaponized that a aggressor could threaten to bomber.
You could a power point, power up and have the ramifications of fall out like a bomb. Yes, that's true. That's true. But I think, you know, if you're living in a world where there is safety and assurances that there's not going to be another country that's going to blow you up. But we're difficult in these daynades. Yeah, very true. But a few people die from this. Even with those meltdowns, there are a few people died in Chernobyl. A few people died in Japan. Anyway, huge digression will probably get letters about all this. We don't need them. All right. Firerode. So inside that follicle, where it's producing the colloid and releasing the colloid and then the colloid is pulling the tyros in and the iodide, it makes T3 and T4. Now ultimately, it makes T4 is what it makes, first of all. That's the first thing it makes. Now, T4 is thyroxene. That's what it releases into the bloodstream. And that's what travels to the tissues. It's T4 is like a pro-hormone. Right. Doesn't really do anything. That's being remade into T3, right? Yes. And it's at the tissue that T3 has all its functions. And we said earlier, basically every tissue of the body has a receptor for thyroid hormone. That's how important thyroid hormone is. So you know, it has receptors at bone to influence bone growth and bone breakdown. It's got receptors at the cardiovascular system at adipose tissue. You know, all over the place. That's why thyroid disorders. So we're named. So one of the classic functions that we're all told that thyroid hormone regulates is the basal metabolic rate. Yes. Can you just explain what that means? Yes. So it's basically referring to the way that you. And is this in all cells or just the most energy, hungry, producing cells? We're not producing cells, but just cells that are very energy, hungry. Okay. What thyroid hormone does is it has receptors at adipose tissue and it can play an important role at this adipose tissue with mobilizing the tissue. So mobilizing the fat, releasing the stored nutrients into the bloodstream, but also can play a role in the way that it's broken down and the way that it's stored as well. So and it depends on the tissue. But for example, if you've got. and this is just one example, if you've got a lot of thyroid hormone, it stimulates lipolosis, which is the breakdown of fatty tissue at adipose tissue, which means that people who have too much thyroid hormone probably be weight loss. Yeah, have weight loss. Hypo, it inhibits lipolosis. So even if you need that fatty tissue for energy, it won't let you access it and it stimulates the storage of fat. Even if you need that fat for energy, hence what it's doing is altering your available fuel sources and altering your metabolic capacity. That's why it says that. But it's not just the adipose. It also plays around with glucose as well, but also plays around with all the tissues of the body that need to grow and develop like bone and muscle as well in addition to that adipose. So it's actually extremely tricky to figure out the right amount, right quantity and the right effect that thyroid hormone can have on the body when it comes to metabolism. Hence why people who have issues with their thyroid and thyroid hormone, they can go from one day having problems with sweating, nervousness, palpitations to the next day, lethargy, extremely subject to the cold, feel the cold. So it fluctuates. But broadly speaking, if it was to oversimplify, you could say that hyper thyroidism, too much thyroid hormone, resulting in an overactive metabolic system and hypod. In conjunction with a kind of a stress system as well. Yes. And hypod. And again, it's because thyroid stimulates, that thyroid hormone has receptors everywhere to stimulate and that hypod is an underactive metabolic system. Now that's a gross over exaggeration, but that is broadly what it does. So again, if you have a hypod, increase lipolusys, palpitations, tachycardia, weight loss, nervousness, if you have hypod, decrease lipolusys, tardness, cold intolerance, decrease appetite. So generally speaking, you might find weight loss in the hyper and weight gain in the hypod. And it's also the distribution of the adipose tissue as well. It will break down adipose tissue in certain regions of the body and spare others. Right. So you might find that the weight or the fat accumulates in some areas, but disappears in others. So it's a really tricky, hard to sort of understand and balance hormone. But it's T3 and T4. It's the T3 that is the active hormone. Okay. Anything else you want to say about thyroid? No, I think we obviously need to do a whole episode on it. Which I'm not sure we have. Have we done that? I don't think we have, but we need to. Okay. It's pretty important. So that's the thyroid. What do we left with? Prolactin and the genotaute opens. Okay. So prolactin, as the name would suggest, is promoting lactation. Right. And so this particular hormone, what's the feedback loops again going back up to the. So you were saying earlier that it is a negative, it needs to be inhibited from the hypothalamus. Yeah. Right. And I think, was it dopamine or one of those? Dopamine generally is considered an inhibitor? Yeah. So without the inhibition, prolactin is just freely released. Yeah. All right. There are other things that will feedback to it to increase the secretion, obviously. But without that inhibitor, in fact, which is, as you said, dopamine, it would be kind of left to be on its own to be amplified. And so where does prolactin act? Primarily, it would be considered at the breast tissue. And so what it mostly does is in the early phases of, let's say, pregnancy. So this would be before the baby is born. It would be lactogenic, right, which would be the development of the lobules and the. I mean, not the darks, because I think that's more estrogen progesterone. That quick. Duct. Right. I think we made that clear earlier. So that I think is considered the abiotic cells, which are the milk producing cells. And then. Not those in the lungs. Not those, but similar kind of arrangement, I guess. Right. The way they look. Yep. And then once the baby is born, it would be to maintain milk production. And I think that's. Gallic toe. Because Gallic. What is it? Gallic toes? Gallic toes. Yeah. Is milk sugar? Yep. Gallic toe poetic, which is. Oh. Producing the milk production whilst the baby is feeding. Not in the moment, but it's kind of a supply demand. Did you know a relationship? So when a baby's suckling, this results in inhibition of dopamine. And so if that's. Doppler means being inhibited, then prolactin is free to be released, hence the prolactation. Estrogen, particularly in really high quantities, which occurred during pregnancy, stimulates prolactin to be released. That would make sense. So at the end of the day, I think. And I think vice versa, prolactin increases the sensitivity of estrogen and progesterone in, say, the uterus and the developing fetus as well. Yeah. Exactly. Generally speaking, you can say that dopamine inhibits the release of prolactin and that estrogen stimulates the release of prolactin at high levels. Yep. And that there's various things that can be done to either stimulate or inhibit dopamine. Yeah. And that actually goes to the effects, the clinical. If you have situations where you have hyper-prolactemia. Yeah. And so one of them would be pharmacological agents like dopamine antagonists. Yes. I just come across a resource that says in terms of the main causes of high prolactin release is a way to remember this is the five Ps. Yep. So you can have physiological as one of the Ps and that would be breastfeeding. Right. Other things could be stress, like high acute stress. And I wonder if that. Because you've come across before where in starvation states where even men. In small quantities lactate. Right. And I wonder if that is from the same mechanism of high acute stress somehow physiologically inhibiting the dopamine. Yeah. And then releasing prolactin and small amounts of lactation from males. Right. Then you have pregnancy, which is. That's another P. Yep. The next P is pharmacological, which we just mentioned. That's dopamine antagonist. And you could have a tumor, so that would be a prolactoma. Right. And that would be a tumor in the anterior pituitic land. Yep. And the last one would be polycystic over in syndrome, which presumably produces high amounts of yeast, which then has some kind of feedback loop on prolactin release. Okay. So that's prolactin. A few other things, which are a bit of a tangent, but just of interest, it seems at least in humans prolactin is really just a hormone mostly centered around the. the milk production, but if you were to go into some other animals, it has other quite varied effects. So in birds, it helps with plumage, so feather production. Really? And I think it also nests in behaviour. Okay. So what determines the, particularly the female chicken, to then sit on the eggs for a period of time? Nests in. This is pro-lactin. Pro-lactin. Also. Even though they're not mammal, sorry, they're not mammals. Yeah, it's interesting because you think that pro-lactin would be mammal-specific. Yeah, I think, for my understanding, the closest crossover from a vertebrate into a mammal, because you kind of have the crossover of what is it, the. What's the egg laying? Monotrains. Monotrains. Yeah. But I think there are some birds that produce small amounts of epidermal secretions that are milk-like, that are somewhat like that, that have. But they're not monotrains. They're not their birds. Right. That the young chick feeds off, but it's purely immunogenic. Wow. So, my understanding is the mammary gland is just a modified sweat gland. Yeah. Right. Its first primary function is immunological. Okay. And its second function, which obviously mammals have been selected for, is nutritional. Huh. And so, because it's a epidermal driven kind of gland, it also has a role in. Like sweat, eye on regulation. Right. And so, in other animals like fish, it has osmotic. regulatory. regulation. Wow. Or fowl. There you go. Which makes sense, because if you wanted to produce milk, you have to shift a whole lot of ions around to make the fluid, right? Yeah. You need to bring calcium in, you need to bring fluids in and shift with types of carbohydrate. And that's just moving fluids into different compartments. I didn't realise that. See? So, for the first time, you've brought up something that's. Useful. Well, still don't think it's useful. Anyway, is that all about prolactin? Anything else you want? That's the main thing is okay. Okay. So, we now need to go and add a tropins. All right. So, the gonadotropins plural gonad, referring to the gonads, these are basically the tissues that hold our sex cells. That tropins tells you that these hormones go to these tissues to tell them to release more hormones. So, the anterior. Or hormones slash cells, max more sex cells. Yep. So, the gonadotropins, which are released by the anterior pituitary, is called follicle stimulating hormone and luteinising hormone. They both play a role in the male and female sexual reproductive systems, but then. We have to do the female reproductive system. That's one of our next podcasts. Correct. These hormones are named after what they do in the female reproductive system. So, it actually gives you a really. Once you understand what these terms mean, it tells you really well what they do and where they act. It tells you nothing about what they do in the male reproductive system. So, the males don't have follicles? No. Not the same way. And we don't have anything that luteinises, which means to make yellow. So. Okay. Let's first talk about the role that they play in the female reproductive system. And let's start with follicle stimulating hormone, because this tends to be the first hormone that's released. Can I. During the reproductive. Can I use an analogy here? Go for it. I hope it. Doesn't fall short. I hope it doesn't. But it kind of illustrates this point well with feedback loops. But this is going to stuff up your analogy of the city a bit. Oh, look, everyone's forgotten about that anyway. Okay. All right. So, let's say the. There is a father. Yep. Okay. And he has ten daughters. Okay. One second. I've got a cough. All right. So, he's got a father, ten daughters. Yep. Right. So, he gives them all pocket money, right, so they can survive on their own. Any sons? No sons. This is a female reproductive system. Okay. So, here you go. Here's your money. You'd look after yourself, but I'll give you the money. You just have to be independent. All right. And so, he's paying them every day. And so, slowly after over time, there is a difference between the ten daughters. You know, some are more independent than the others. Some are really just relying on just the money and don't do overly well on one. Some of them are much more proactive and doing better things with sure, with outcomes. To the point where maybe one or two start to earn their own money. Okay. Okay. So, in doing so, the father realizes that they're making their own money and goes, "You know what? You become independent." I'm like, "Give you any more money." Right. And stops paying them all. Okay. Now, as a result, pretty much only one is independent enough to survive. Okay. And the rest, what? Dive starvation. Oh my gosh. This is a terrible father. So, nine die. Whoa. One survives. Okay. Bad dad. One will continue to develop, develop and develop until she's ready to leave home. Okay. And the daddy goes, "Well, I'm pretty proud of this." So, who cares about that? Nine others that are now dying. That's right. What I'm going to do is I'm going to use this huge lump sum. Here you go. Now, get out of here. And how long will that lump sum last this? 14 days. Oh, you mean, how long does that lump sum or how long does that lump sum last? Well, it really depends on what happens next. Oh, okay. But he's basically saying, "Here's a water of cash. Get out of my house." Okay. And. And. Off with you. Okay. And then the daughter leaves and that's the end of it. Okay. So. So, that was pointless, wasn't it? So, the analogy here. Oh, it isn't an analogy. All right. The father was the Paturegic land. Oh, you're not the dad. I thought that this was me. Sorry, this was something that happened recently. I've got two daughters, but not ten. Well, you did have ten. So, the father's the Paturegic land. All right. Okay. And the money he's paying is a follicle stimulating hormone. All right. Okay. And the ten developing eggs of that cycle. Okay. All right. Now, from a cycle, usually only one will dominate. Are there usually ten eggs that do start with, even possibly more? Yep. Okay. And then what happens is one of them becomes more dominant and starts producing estrogen. Right. And that estrogen feeds back to the dad. And that's the money that they're making for ourselves. Feeds back to dad. Yeah. Dad's like, "Oh, look. Don't you do it. Make any more FSH for this point in time. I'm going to stop until about mid-cycle and then you get the LH surge. Yep. We probably also some FSH. And then that's the point of ovulation. So then the daughter leaves or the egg leaves out of the ovary into the floating tube. All right. And then that point onwards really depends if the egg gets fertilised or not. Okay. Look, not about an allergy. I'll do that. But then I'll quickly follow it with that. I'm happy with that. No, no, it was good. So, okay, let me then again try and reframe this in a way that makes sense to me. It's not upsetting and resulting calling docks. Exactly right. Exactly right. So we've got these two gonadotropins. These two hormones released from the anterior pituitary. Follicle stimulating hormone and luteinosing hormone. So follicle stimulating hormone, when it's released into the bloodstream, travels to the gonads of the females and stimulates the eggs that have been there since birth. Right. These primordial uricytes as they're called and basically says, okay, right now it's time to grow and develop. And like you said, a number of them will grow and develop, but only one will really push through into maturation. If you have more than you likely would have, you know, twins and so forth. The rest all atrophy and be reabsorbed back and reutilized in other ways. Right because they're broken down and we'll use the fatty acids and so forth to create other things. Yes. So that's what the follicle stimulating hormone does. Stimulates the follicle. So follicle is just, or follicular is just another word for the cells associated with the egg with the egg around the side of the, oh, oh, oh, oh, oh, oh, oh, that's right. So these are the cells that help produce the estrogen. Yep. So as soon as they get bigger and bigger and bigger, you produce more and more and more estrogen. As soon as it's at a point where the one of those eggs is big enough to have big enough follicles to produce enough estrogen, that negative feedback goes back to the brain and says, hey, or the pituitary says, don't worry about any more follicle stimulating hormone at this moment. Correct. Then that egg will ultimately within a couple of days after that be ovulated. So that means it needs to leave the ovary and be pushed out towards the finbre, the fingers of the. Blipping tube. Yes, the uterine tube. Yeah. But in order for ovulation to occur, we need the second hormone.
Lutinus. Usually, yeah. That's where the surge comes in, yeah. So, lutinizing hormone would then be released at about day 14, which is usually the ovulation day. And what it does is it sort of helps to weaken the wall of the ovary. And then that egg can be ovulated out of the, so remember, you've got those follicle cells that have been produced from the FSH that are surrounding the egg, surrounding the ursite, just maintaining it and looking after it. And there's other cells like thicker cells and so forth that are present there, which again, help them produce that estrogen. But at day 14, when the lutinizing hormone is produced, it basically says, away with you egg, pops it out. This is the daughter leaving home. And what's left of these remnants of cells, like the egg shell. Yeah, it's like an egg shell that's left over, which is yellow, which then turns yellow, right? Which is called the luteum, the corpus luteum, the yellow body. And hence why the lutinizing hormone means to make yellow. So it creates this yellow body. Now, as the egg gets taken in by the fingertips of the uterine tube and massages it into the uterine or phloepine tube, that egg will continue to move down the tube and hopefully meet up with some sperm if that's what's intended at this time. And that remaining body, that corpus luteum, that yellow body produces another hormone called progesterone. Progestation. And so what we've got is four hormones, really playing a role in this female reproductive cycle, where you've got follicle stimulating hormone to begin with, which then produces estrogen. And then you've got lutinizing hormone, which then produces progesterone. So one of the things I tell students is, think that FSH helps produce estrogen. And estrogen prepares the lining of the uterus for implantation. LH produces progesterone, which further prepares the uterus for implantation. You know, it's. And both of them also go back to the breast to start to make the breast, you know, ductal cells and so forth, starting to grow to prepare for the possibility of a baby coming. Yeah. And remember, estrogen goes back to the anterior pituitary and stimulates prolactin, further preparing milk production within the breast tissue. And so that's basically what what these hormones do. FSH and LH in the female reproductive system makes sense because they're named after what they do. But then when we start looking at the male reproductive system, which is a lot simpler, like us, like you at least. And poorly named. Yes. Correct. Like Matt. Michael's a good name, I think. Let's talk about what they do. So the way I think about this is remember I said FSH produces estrogen. LH produces progesterone. And together it prepares the uterus for the rest of the reproductive cycle. FSH and LH in the male does a similar thing. So basically FSH makes tadpoles. Well, well, wait a second. FSH stimulates cells in the testes called satoly cells. And these satoly cells produce something called angrogen binding protein. A B P. Angergens are. Is there another name we can use instead of satoly? Are they satoly? Satoly. Satoly. Satoly. Satoly. They release angergen binding protein. So it's just sitting there now in the testes. Not doing much. But LH when that's released, it stimulates the lady cells, which are called the interstitial cells. They release testosterone. So LH releases testosterone. Now testosterone is an angrogen. That's good because we just released angrogen binding protein from the FSH. So they bind together. And together testosterone and A B P stimulate the process of spermatogenesis. It stimulates these stem cells in the testes and says it's time to produce sperm. Not the right one. That'll do. That'll do. That one. That's the one. Should be pressing every time you make a joke. That's a sperm with a with a wheel wheels wheel chair. Oil in. So now we've got spermatogenesis. And it's pretty much that simple. So if you think about the testes and you think about the cells present, the sperm is made in the epididimus. No, they're mature in the epididimus. But they're made in the cells within the testes themselves. Seminephus tubules. Seminephus tubules. And if you think about the tubula as a hollow tube because it's called a tubula, the cells on the outside are where the stem cells are. And they produce these blackest head look like tadpoles. Well, not yet. They kind of just globular. Well, that's what I'm saying. As they move in towards the middle of the tube. That's right. They mature. And then they get once they get into the hollow tube, they've got a tail. They can swim towards the epididimus. They can mature there. And then they can be pushed through the vast efference or the, you know, and for ejaculation. So for those students who are sitting exams, for female reproductive system, FSH leads to estrogen. LH leads to progesterone. For male reproductive system, FSH leads to angiogen binding protein. LH leads to testosterone. Both of those systems together work to produce gamates, but also produce the hormones that will have, you know, changes in sex characteristics. Absolutely. There you go. And that is the, uh, gonadotropans. We missed one. Well, we did, that's all that's all the hormones associated with the mayor and the what the mayor and the what's the next level down from the mayor? Oh, sorry. Are you talking about with the analogy we use? Not a female horse, no. Yeah, what are you talking about? Back to your animal analogies. Yes. So the, the mayor and its various administrative parties that sit underneath that run the government. All of those are hypothalamus and protrusion surgery. But there are other hormones that aren't necessarily directly regulated or produced from the hypothalamus and protrusion. Yeah. And that's one of which is the parathyroid hormone. That's what I was going to mention. So behind, at the back of the thyroid, you have these four little P-shaped structures known as the parathyroid glands, four to eight. And sometimes they're not where you think they should be. Do you mean? Well, they're not always neatly positioned behind the gland. They could be positioned elsewhere. Like in my ear. In that. We're not so much there, but maybe in the superior medius diamond. Right. And part of the issue is if a surgeon wants to go in there to remove other tissue. Yeah. The surgeon could accidentally remove parathyroid. Okay. So why do we need a parathyroid gland? I think predominantly it's to do with the regulation of calcium. Okay. So parathyroid releases a hormone, which very simply is called parathyroid hormone. So that's nice. And it's paraming around. Yes. Around the thyroid gland or around the thyroid hormone. It gets stimulated to be released when your blood calcium levels are low. So it's released to try and maintain homeostasis. So to ultimately try and boost the blood calcium levels up. So to do this, it must act on a number of tissues because calcium is all over the place. So if you think about it, where is most of the calcium in your body stored? I think like 99% is in bone. Right. So that would be a great place for parathyroid hormone to act to try and release some calcium from the bone. Look, you got enough here. Give the blood sum. And the way it does it is it doesn't act directly on the bone, but has to stimulate certain cells called osteoclasts. Osteomining bone clast referring to its crushing capacity. It sort of eats away. It's actually like a modified macrophage, right? Yeah. So in your city analogy, this is the construction workers with jackassians. Yeah. Definitely. Swinging balls. That's right. On a crane, not and personally not me. So this osteoclast comes in and it starts to sort of eat away at the bone tissue and releases calcium into the bloodstream. They're by increasing blood calcium and rectifying the drop in blood calcium. But that's not all parathyroid hormone does, right? It can actually work synergistically with vitamin D, which is another hormone. So vitamin D is made from cholesterol. That's in our skin. And when UV light hits that cholesterol, it stimulates it to change chemically. Now, it undergoes a number of different changes where it changes in the skin and then changes in the liver, then changes in the kidney and ultimately produces the active form of vitamin D. And that vitamin D can work with parathyroid hormone to help things like increase the absorption of calcium from our intestinal tract can stop the kidneys from peeing out calcium calcium and holding on to it. It sort of just helps to and also plays around with phosphate as well. So blood calcium levels are intrinsically linked to phosphate levels and vitamin D plays around in actual fact, parathyroid and vitamin D can together alter both calcium and phosphate. But individually, they can't do both together. Yeah. Right. So they need to work together in order to play with both calcium and phosphate. But that's the function of the parathyroid. Now, interestingly, there was
another hormone that the thyroid gland produced that we didn't talk about, which also plays with blood calcium called calcium tonin. Okay, yeah. So the thyroid releases calcium tonin, which basically does the opposite of parathyroid hormone. So blood calcium levels are too high. It's going to say, hey, let's take some of this calcium out of the blood and put it into the bone, peat out or poop it out. Yeah. Simple. Yeah. And so, you know, when people do blood tests and they find that they may have elevated calcium or decreased calcium levels in the blood, outside of looking at, you know, do you get enough calcium intake or have you been taking too much calcium in? They could look at the parathyroid and thyroid hormones to see, hey, could it be an effect from these two glands? That's right. Yeah. And as I said, I think at the start of the podcast, you know, the way that these were discovered by, you know, the earlier science projects were to remove them out of animals to see what the effect would be. And, you know, like we said, dogs and rats and by doing so, by removing these glands, the result would be poor regulation of calcium and then bone deformities. Yeah. So, what about, there's a hormone released from the heart, atrial, maturatic peptide? Now we're going into it into, is that a hormone? It is right. Yeah. But even though it's a peptide, it can, it's a peptide hormone. But what, what were you saying? We're going into what? Territory where we could go on forever. I know. But I think we should bring this one up big simply because it does the opposite of ADHD. Well, I'll do a strong both really. Yeah. Well, it's countering high blood pressure and high pressure in the heart or in the atrium. Right. And then, natural retic is referring to sodium. So, since our Dostroin deals with sodium to try and increase it in the blood, to increase the water that follows and increase the blood volume and increase the blood pressure, the heart, if it's experiencing too much stretch because the blood volume or blood pressures too high, it will release this atrial, maturatic peptide, AMP, into the opposite. So, hey, look, just pay out more sodium. The water will follow and blood pressure will drop. Counteracting the ren and angiotensin and Dostroin system. But you're right. Were you going forever? Because nearly every tissue is going to release a hormone that will do something. We haven't even spoken about the hormones released from the gastrointestinal tract. I think the last one we should finish on is just the pancreas. Of course. Of course, this is a very important one. But even this one is considered when all these things we spoke about just now are glands. So, you could make an argument that these are tissue or organs that are pretty much focused on just endocrine function. Right. Right. So, the paturgy gland, for instance, is pretty much tissue or an organ, if you want to call it that, that's solely reliant for functions as releasing hormones into the blood. Okay. Whereas the hypothalamus, it has a whole lot of other functions outside endocrine. So it's probably a bit like the pancreas in the sense that it's a tissue that does endocrine stuff, but it also does a whole lot of other stuff as well. And so, and the heart, another good example where it's a heart function isn't as an indecrindable. But it can do some of these things. So when we look at the pancreas, the pancreas by far is an exocrine. Yeah. It's producing pancreatic enzymes to be secreted into the duodenum as its primary job. But it does have these small cluster of cells and they were developed, what shouldn't say developed, they were discovered by Paul Langahan, a German scientist. Is that why they call Langahan cells? Yeah. And so these are just eyelets, the little islands within the greater exocrine pancreas. Yeah. And so it's discovered, it releases this thing that has an effect on blood sugar levels. So and I think the first term used for this was eyelets, eyelets, eyelets, not insulin. So where did insulin come from? I think it was derived from that. Oh, okay. Yeah. Now, the reason why I like talking about the exocrine and endocrine function of the pancreas is because they work together. So when you ingest a delicious burger and you're breaking down those macronutrients, proteins, fats and carbs, by the time it hits the duodenum, the very first, so it goes through the esophagus into the stomach, from the stomach into the small intestines, that very first part of the duodenum has a direct connection with the pancreas, has a tube adduct. And as soon as these macronutrients hit the cells within the duodenum, so the proteins, and carbs, it stimulates the pancreas to release those enzymes, those pancreatic enzymes you were talking about. And these enzymes break down fats, proteins and carbohydrates. Now, ultimately, the enzymes at the pancreas releases that break these substances or or macronutrients down will produce the smallest subunit of these nutrients that can get absorbed into the bloodstream. And now that they're absorbed into the bloodstream, they can then directly stimulate the pancreas again to release the hormones. So if your blood glucose levels are high and even to a degree amino acids and fatty acids, they can stimulate the pancreas to release insulin. And the job of insulin is to go, "Oh, I've got all these nutrients available in my bloodstream, but they're locked away in the bloodstream and they need to be taken into certain tissues. So I'm the key to open the door to certain cells, like the adipose cells and muscle cells. And now these nutrients can be brought into these tissues to be stored or utilized." And that's the job of insulin. When these nutrient levels increase in the bloodstream, particularly almost profoundly glucose, insulin's released to drop the blood glucose levels down and bring those nutrients into muscle and fat. And we've spoken previously about the fact that insulin isn't required for many tissues of the body to bring the nutrients in, but it is for fat and muscle. Which is on bulk, the majority of volume, right? So if you just look at the. If for me, I'm mostly muscle, and for you, mostly adipose tissue. So if you look at the cell number, they're not that high, but in terms of volume in the body, they're quite significant. And so if you're not getting glucose into these two tissue types, then you're keeping a lot of sugar in your blood. And the problems with this twofold, one, those tissues don't get energy, get tired, get many issues because you're not producing ATP. You don't function. But the other is we know that glucose isn't really nice to the blood supply, right? Gluc. What I should say is glucose and blood vessels don't get along, particularly the smaller ones. And so if you've got elevated glucose. Oh, you may have a long period of time. A long period of time, that glucose can slightly change because of all the other substances that are present. And it changes in a way that's detrimental to blood vessels and damages often the smaller blood vessels. You know, those that feed the eyes, those that feed the extremities and so forth. And you can get diabetic neuropathies because it's damaging the blood vessels, but also damaging the nervous tissue that's present. So glucose can be quite detrimental over time if elevated and remaining in the bloodstream. And to the kidney. And to the kidney. To the three-fold glycosolation effects. So that's kind of like the sugar at the top of a donut. That's what happens to these cells. Blood vessels, nerves, kidneys develop a nephrapathy, retinopathy and neuropathy, which is quite devastating to these tissues. And the result is profound. But even in the short term, if you just were to drink, you know, a liqueur, I could even say later, okay, right, which has a lot of sugar. Sugar, it's a osmotic diuretic. So you'll be urinated for the next hour and a half. Yes. So if, yeah, it's not non-stop, but you know, but a lot will be coming out. Yeah. It's just called polyheteria. Your body is very good at managing and balancing two things. Sugar and salt. Right. And you can really put a lot of both of those two things into your body for a long period of time before you have the detrimental effects. Obviously, some people are going to be more sensitive than others in a multitude of ways. When it comes to sugar, one of the biggest side effects early on is simply just weight gain, simply because of an increase of calories that you bring into your body. And for salt, it, you may only just peed out, right? But over time, these things accumulate and it's just about homeostasis, managing and having a balance and so forth. So, yeah, in the short term, your blood glucose levels going through the roof isn't a problem. It's about how well is it managed over time and throughout periods? So for example, people have the constant blood glucose monitor on, which measures your constant blood glucose levels and your insulin release and how it can change. If you're not a diabetic, it's telling you nothing. Because of course your blood glucose levels are going to change. You drink a coke, you eat a meal, blood glucose levels go up, you release insulin, it goes down again. It's not about you trying to just maintain low levels of glucose or whatever it may be, right? Anyway, that's again, a bit of an aside. There's another hormone, the pancreas releases that does the opposite.
sort of insulin called glucagon and it's released when glucose is gone. I like that. So if your blood glucose levels are low, it's like, oh, okay, this is telling us we don't have any available energy in the bloodstream to deliver to the tissues. What can I do? I know I've stored some energy for later and the kidneys and the liver and the muscle. They have stored glucose energies in the form of glycogen fat and fat. Yes, and adipose tissue as well. The low blood glucose levels stimulate glycogen to be released into the bloodstream and that mobilizes the stored glucose to be released back into the bloodstream at least mostly by the liver, not as much by the kidneys and definitely not by the muscle because the muscle is selfish. It's stored glycogen stays there for itself. And that's the hormones of the pancreas. Oh, the pancreas. I thought you were going to say the whole system. Any others you wanted to touch upon? No, I think we've gone well over two hours. Do you have any emails? No. Okay, no emails at the moment. Feel free to send us an email if you want to ask us a question or if you want to say how awesome I am at what I do, you can send that to GU,
[email protected]. So that's GU biosciences. Probably need to change that email at gmail.com. You go to our website and I think maybe the website contact us is now working. Yeah, well, I'm going to emails from the website wonderful. So you can email us through the contact us on the website or you can contact us on social media or at least you can contact me on Instagram, Twitter, TikTok, Facebook. I mean everywhere else. Dr. Mark Tadek. The new one. Threads, I'm on threads now. How's that going? I like it. It's basically a non-toxic Twitter. Is it? There's no ads yet, but they will come soon. You don't have a search function, which is great and you don't have a recommended either. So it's basically a showing the people you follow in a chronological order and I don't think people know how to use it yet. People are trying to figure out what their voice is on that platform, but it's sort of nice because you're just sort of seeing what people are thinking and saying in a way with no sort of goal in mind per se. Instagram people are very much selling themselves visually. Yeah. On Twitter, people are selling all their trades. Yeah. Which is fine. I think Twitter has drastically changed in recent months. So I was listening to a professor at NYU, Scott Galloway, and he was talking about a busk, Elon Musk. He said, "You know, if Elon didn't buy Twitter and use it the way he did, he would be seen by most people around the world as one of the greatest human beings of our generation. But as soon as we saw the type of person he is on Twitter, and the types of things he's willing to say, I think there was already, I do mean if you never use Twitter full stop ever, not border, but just ever, even if you didn't use it. Both." Yeah. Because I kind of got the feeling that he was starting to gravitate that way in line before he bought it. What do you mean in what way? Controversial. Sure, but if you have a look at him in interviews, generally he seems to be relatively reasonable, thoughtful and so forth. But then you read the stuff he says on Twitter. It's intentionally provocative. That's what I mean. A little bit childish. But he was doing that before he bought it. That's what I'm pointing at. On Twitter. Yes, exactly. And if he just didn't jump on that platform, I think people would be like, "You know what? This guy has Tesla, SpaceX, PayPal, all these amazing things." And then jumps on Twitter, tries to jump into the space of the zuck. Mark Zuckerberg does it poorly. No one wants to advertise on there. He gets rid of, you know, 6,000 of his 8,000 employees, mostly for no apparent reason. Mostly all those guys jump to threads. I don't think so. I actually think that I think from what I heard that Musk is suing meta. Just for copying threads. Not just for copying, but also for taking their employees. But then thread. Well, threads, well, because you saw clauses, non-compete clauses. But I think threads stated that they don't have any x-employees of Twitter. I don't know what's going on there. But anyway, it's interesting. And I feel like I still like Twitter because I've got, you know, 60,000 followers on Twitter who appreciate the content I put out on Twitter. I've actually built a really nice community on Twitter. But there's a lot of toxic stuff on Twitter. But if you want to join me there, please feel free. But I have on threads. Again, it's @doctomiketodowicz@drmiketod. O-R-O-V-I-C. Please give us a five-star rating. This isn't me begging. This isn't me demanding. It's also recommend topics that's important. Yes. Send us emails. I think currently we're trying to work through all the systems as overviews. Yeah. So this will be a three hour endocrine podcast. But you know what, I think people okay, here's another thing. Send us an email and let us know. Do you prefer like do you mind if we do a three hour episode that covers everything? Or would you rather us break it up into an hour, you know, multiple hour long episodes? I mean, yeah. I like the system wide approach. I think with say the endocrine as an example, it's smart to do an overview. Yes. But then we could go in more depth in each individual gland or hormones. And we have and we will do we know what the next thing we should do? Well, then we can't really single out female reproductive system. But we should probably did we do mail? We did mail. Okay. So should we just do an overview of the reproductive system? And then obviously probably spend a bit more time focusing on the female. Sure. Things we got idea. Or maybe we do them separate since we've already done mail, we should do female. Okay. Yes. So like Matt said, send us suggestions. What do you want us to cover? What do you want us to do? Again, I know that a lot of people will listen to this because they're students and they're studying. So, you know, don't really send us an email saying, Hey, I'm a biochemistry student and I'm doing an assignment on a mutation in this very small niche gene. You do an episode on that. Remember, it needs to be broadly relevant to many people. Hence why we don't do super niche stuff. But diseases and disorders, yes, we still need to do certain neurodegenerative diseases. We need to do dementia. So Alzheimer's, we need to do Parkinson's. This new drug released. Yes. We need to do multiple sclerosis. So we need to do a range of neurodegenerative stuff. There's heaps heaps heaps heaps. I still want to do one on all the energy systems of the body. So phosphogen, glycolate anaerobic aerobic, talk about all that. We've sort of touched upon them in various episodes, but haven't focused heavily on them. We also do a lot of embryology ones. Anyway, I think it's time to, um, time to go. Is it sperm again? Listen, everyone, we do our short form eight is ends. We release two every week Monday and Wednesday. Again, provide us feedback if you enjoy those. Obviously, there's a lot of fun in these long form episodes, but feedback. We love feedback. We do this for free. We take it out of our positive feedback. Just like the end of the Consistency. That's right. Thank you, everybody. You have a wonderful day and we'll see you soon.
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