Homeostasis

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You have a not just talent, a face for radio, but a voice for something undisclosed. Homeostasis. I'm Dr. Mark Tadarvich. I'm joined by my co-host Dr. Matt Barton. And this is Dr. Max Medical podcast. If we were Beatles, you'd be Ringo. I would likely be John. Because I've watched that get back documentary. Have you watched that? I've watched the movie. So the movie was done on the back of this Docko that they filmed 50, 60 years ago. They took all this old footage and remastered it. The guy that did Lord of the Rings, Peter Jackson. Oh, really? He also did that World War One remake. Did you see that where he took all old footage from World War One and colorised it and made it HD? Wow. It's amazing. You've got to watch that. But the Beatles one is pretty cool. And it seems like John runs the whole show, John Lennon. Not John Lennon, sorry. Paul McCartney. Did I say I was John or Paul? You said John. Yeah. Paul, I'm Paul, definitely. You've fended a lot of people. Well, you're like Ringo. You just sit back and just go with it. Ringo didn't say, I think Ringo spoke three times in that whole documentary. Anyway, I was busy doing Thomas Stink engine. That's true. That's true with the fact controller. Today, we're talking about homeostasis. This is a very, very, very important topic for anybody doing health science, medicine, nursing, paramedicine, physio, whatever. If you're doing anatomy and physiology, homeostasis is probably the most important concept to understand. Do you agree, Matthew? He agrees, everyone. It's nodding his head. He may have said something else, but he agrees. And the reason why homeostasis is important is because homeostasis is what allows for us to maintain an internal stability or an internal stable environment while adjusting to changing external conditions. So our body is constantly trying to be swayed either externally or internally by different conditions and variables, changing temperature, for example, pressures, so forth, and the body needs to respond so it can survive. And if it doesn't, and if it doesn't, disease occurs. That's the amazing thing is that homeostasis being maintained is health, and if homeostasis cannot be maintained, it's disease. That's right, that's right. So I just defined homeostasis. Again, when an organism can maintain an internal stable environment while adjusting to changing external conditions, that is homeostasis. Homeo means similar, stasis means standing, similar standing. Okay, so how would that be different to if the word was homeo in the same, right? Yeah, homeo means same, stasis means standing, similar. That's right. So what that's indicating is that there is not one particular value that any function in the body needs to sit at. It's a range that it needs to sit within. So similar standing. So there's an upper limit and a lower limit for all the functions of the body. Could you do an example? Yeah, so temperature. So body temperature isn't just internal body temperature. It doesn't have to be 37 degrees flat otherwise you get sick, Celsius. That's quite cold in Fahrenheit. It can go a couple of degrees higher and a couple of degrees lower, and so there's a range. But if you go outside of this range, problems occur. That's right. And the same thing happens with oxygen saturation status, like glucose concentration, blood pressure, like literally pick any function of the body and there's going to be upper and lower margins. Limits. And the body must stick within it. And so what we're talking about today in homeostasis is how does the body stick within those limits? Okay. When something happens and it happens all the time to push it up, how does the body bring it down or if something happens to push it too low, what does the body do to bring it back up? So that's only one part of it though. There is, that's negative feedback on your stasis. Well, it goes in the opposite direction of the stimulus. Yes, but at the end of the day, regardless of whether it's positive or negative, it needs to go back within that happy, healthy balance. So there may be some short acute bouts or moments within homeostasis where it continues to push it outside of its normal functioning range. But ultimately, it's trying to get back to a particular state where it's protective or functioning correctly. And that may not sound right at the moment, but we'll talk about that when we come to it. But I wanted to start off, just talking about a little bit of the history of homeostasis or a historical perspective. We're not going to talk much about this, but I thought it was interesting that obviously the Greeks, Greek physicians, the Greek physician and philosopher, Elk Mayon of Croton, 500 BC, proposed what can probably be called a balance of opposites in regards to health. So he said he used a political analogy as the Greeks back then often did to define health and disease. So he said, "Health is the equality of rights of the functions." So wet, dry, hot, cold, bittersweet, and the rest. But single rule of either pair is deleterious. What is basically saying is that everything needs to be balanced out. Because their notion of health was probably the human's right. That's right. So if one was out of balance, then you'd get sick. Exactly. Try to oppose the other. So basically what he's saying is if you had too much heat, you're going to go into a manifestation of disease. So you need to balance that back out. Exactly. All the humans had to be in balance or something. So he was probably one of the first to start to insinuate that things need to be in a balance when it came to health. He obviously didn't understand to what degree and the mechanisms involved. But today, we do know. And when we look at the mechanisms behind homeostasis, depending on your textbook, it'll either state there's three fundamental mechanisms of homeostasis, or it will say there's five components, or it'll say there's six, three, five or six. - Okay. - We're just gonna talk about all of them, because they're all important, and it doesn't matter what number you attribute to them. But everything we're about to say is an important aspect of homeostasis. So to begin with, regardless of what we're talking about in regards to some physiological function, there's always gonna be a stimulus, which is either external or internal, which is the thing you're trying to regulate. - Yeah, that's right. The thing that's probably trying to push you out of range, so it could be temperature, it could be pressure. - So should we do a chemical? - Should we do two examples concurrent? Should we all do one example of a system you do another, opposed to, let's say, do a temperature, and then I'll go to another, which kind of just, we have that with both due temperature, but we do the opposing. - What do you mean? - I mean, I do cold. - The stimulus is, for you, the stimulus goes hot, and for me, the stimulus goes cold. - All right. - But regardless, again, the stimulus is the thing that's trying to push us out of our physiological limits. That's the stimulus, that's part one, that's gonna be the beginning. And like I said, it can be temperature, so thermal, chemical, mechanical, right? It can be a whole bunch of things. Regardless of what that stimulus is, you can't respond to it unless your body can pick it up. - Okay. - Right? So that thing that picks it up is a. - Oh, it's okay, we're starting. So. - It's a receptor, this is what I'm looking for, Matt. So I didn't ask for you to start to go on this massive diatribe about something else, it's a receptor. - Okay, so for our example today, we're gonna do temperature, Mike's gonna do hot, I'm gonna be doing cold. - Oh, so we're gonna get straight into it? - Yes. - I thought I was gonna define all the things first and then. - We'll do it along the way. - Okay. Okay, so the stimulus is temperature. - Right, happy with that? - Sure. - Yours is too hot, so the temperature's out the range of, we're gonna work in Celsius? - Yeah. - So 36, 2 to 37 ish? - Yep. - You're happy with that? You don't look confident. - Are you under the components first? - Yeah, I think so. - Yeah, because otherwise we're gonna pigeonhole what the control center is and what an effector is. - Okay, so forth. - So I think we should just define them first. - Alright, so the stimulus is the thing you're trying to control. That needs to be picked up by a receptor. - Yes. - And the receptors, depending on where the stimulus is located, you would probably want the receptor to be located in the region of the body that's most likely to pick that stimulus up most effectively. - Yeah, so it could be superficial or internal. - Yep. - The control center is the thing that makes sense of the whole, it's ultimately the computer of it all. - Yeah, but we haven't spoken about it yet. So once the stimulus is being picked up by the receptor, the receptor needs to transduce that signal and send it somewhere for a decision to be made. And so the receptor then sends it to, like Matt said, is the control center. And that control center, like you said, can be, anyway, it just needs to make a decision. - And it's a higher ordering function of it all. So based on how it computes that stimulus that's coming from the receptor. Now, we're gonna talk about the systems that do this, whether it's communication systems, if it's generally the nervous system, which is done through electrical activity or through the end of crime, which is usually chemical. Do we want to talk about that? - Nothing, that's enough. - Okay. - What I think that's a good way of doing is that those control centers are gonna be communication networks. And the two major ones, like you said, are nervous and endocrine. - So the control center is receiving a signal from the receptor that's telling it to do something. And so it's now computing this and going, all right, something is out of range that I'd prefer it not to be. For me to maintain health, I need to respond back to that kind of initial stimulus. So it will send an effector response, which again, could be a neurological effector response or a chemical hormonal effector response. So that then goes to an effector, which is, it makes it has an effect, a change. - Efector with an E, so we've got the stimulus, we've got the receptor, we've got the control center, then we've got the effector, and the effector is controlled by, like Matt said, the control center, and it elicits the change, it has the effect. And that effect is in whatever scenario you're referring to is trying to address the stimulus. So you can see it's this circle of life that's happening here. Now alluded to earlier that sometimes, most of the time in homeostasis, we try to negate or do the opposite of the stimulus, 'cause if it's too hot, then it wants to bring it down and make it cold, and if it's too cold, the effector wants to bring it up and make it hot again. But sometimes we want to exacerbate the stimulus for a particular outcome. But I think first, like Matt said, let's use an example and work our way through it of temperature, where Matt is very subject to the heat and I'm subject to the cold, this is quite true. And Matt and I go outside, he walks out into a nice Queensland summer, and I walk into a Tasmanian winter. And we are now exposed to the elements, to the external environment. - So the stimulus here is hot, mine's heat. So it's mine's a 38 degree Celsius day. - Yes, and mine is a two degree day, and it's cold, and therefore that temperature's trying to drop my internal body temperature from 37 to something below that, and the temperature's trying to raise Matt's from 37 above, something above that, and again, it's okay if he goes a little bit higher, or for me a little bit lower, but not too low, or not too high. - So that's a stimulus, so that's the first component done. We're happy with that. Now the receptor, for temperature, generally you would probably say is on the skin, or associated with the skin, because that's what's associated with the outside world. Okay, but saying that there is also internal thermoreceptors, that can also pick up temperature. But I think for this particular example, we'll just say the receptor is located on the skin. - Yeah. - Happy with that? - Yeah. - So my receptors on my skin pick up that higher temperature. So we have temperature receptors, which are heat and cold gates on our nerves, that would then stimulate. And we could artificially, just for a side tangent, you could artificially stimulate these through chili, capsules, and that makes the sensation of heat. So if you put a chili in your mouth, it makes it feel hot, but it's not really, it's just the capsules artificially open in those receptors, those temperature receptors. Or the other one is menthol. So these things like chewing gum, toothpaste, cigarettes, cigarettes, or menthol, menthols, menthols, anyway, it doesn't matter. That would give the sensation of cool menthols. There we go. - Sensation of cool. - Cool. - Cool. - Anyway, so that's the receptor. So that's gonna tell the receptor. Here's a stimulus. - Yeah. - What are you gonna do about it? - So the receptor transduces, it changes one mode into another mode. So here it's temperature. So this thermoreceptor changes a temperature stimulus into an electrical chemical stimulus, which can then be sent via nerves to the control center, which in this case, for temperature is gonna be where? - The hypothalamus of the brain, that's right. - So just as a point here, this is where you could get an additional component, and this is known as the afferent signal, yeah. And all that is, is the nerve that's. - Yeah, it's from the receptor to the control center. It's just the nerve that's bringing it to it. - Yes, the connection between. - So as Michael said earlier, sometimes it'll be only three. If you add this one, this is gonna end up making them five, six. So this neurological stimulus travels in our peripheral nerves to our spinal cord, up the spinal cord, to our brain, where we have in the diencephalon, the hypothalamus. And that's the control center for today. - Yeah, absolutely. - How about that? But as just a side point, the control center, and I don't wanna confuse people, but I just put this in for detail, the control center can also be a receptor for temperature, as well, but as an internal thermoreception. - Yeah, there's a lot of overlap where these receptors are. Sometimes the control center is located where the receptor is, which we can give you an example of that. - Exactly, so full. So now the control center, the hypothalamus has picked up a temperature change, or a signal regarding temperature. It's been sent from the receptor via the afferent nerve signal. And it goes, "Okay, what do I need to do?" So in mat scenario, it goes, "It's hot." - Well. - And internal control center is like the thermostat, right? There's a set, there's a base point. And just like the egg mixture. - Like the egg mixture. - Of your home, it knows that it needs to be sitting at a particular temperature range. And if the room gets too hot, the thermostat kicks in to try and job things down, and if it gets too cold, the thermostat kicks in to bring the temperature back up, 'cause it knows it needs to sit within a range. Hyperthalamus does the same thing. So regardless of what's happening with mat or myself, thermostat of the hypothalamus knows what to do and that's the control center. So it controls the outcome, it makes a decision. So for Matt, the decision is, I need to cool down. And for me, the decision is I need to heat up. And so this is where we diverge. This is where we become different in our example. Yeah. So up to this, up to this point, it kind of the same, right? Yeah. I mean, so so both have, both have effectors to make it simple. But the effect is different is what Matt's talking about where it diverges. So once let's just take Matt's one, for example, once hyperthelmas has gone, all right, it's too hot. I need to cool down. And it's decided what it needs to do. Just think about, well, what do you do when things are too hot to cool down? What's one of the, what's one of the first things you do? And Matt, what's one of the first things you do? Well, you could say, behaviorally, you've already done it. Let's talk physiologically. All right. Physologically, probably the first thing that happened to me is I, my skin, the blood vessels in my skin or just under my epidermis would start dilating. So the blood vessels will start to get bigger. So I would start to go red. Yeah. That was too late for you and went to the sun. What about sweat, Matt? Yeah. Then sweating would probably come shortly thereafter. Let's just stick to sweat at the moment. Okay. Keep it simple. So the brain goes, I'm going to sweat. Okay. So sweat glands on my epidermis would start to release the fluid. So that is the effect of the control center sends a signal to the effector. And this is called an efferent signal. So think of efferent with an A going to the effector with an A. So remember, we said that the stimulus stimulated the receptor, the receptor sent an afferent signal to the control center, the control center decided what to do sent an efferent signal to the effector. And in this case, because it was too hot, the effector was sweat glands in Matt's skin and it released sweat so that when a breeze came past through the process of convection, the sweat evaporates, taking the heat that has now just been pushed to the surface via his dilated blood vessels get taken away. And so now Matt is cooled down. Yeah. So the outcome was the opposite of the stimulus. So it negated it. So it's a cooling effect. So it's a negative feedback. For me, my control center says it's bloody cold out there. You need to heat up. What do you do when you're cold, Matt? Isn't that what your start jumps? Well, you just go and chop a tree or feed the goats or something. Yeah, that's right. Well, probably one of the first things would be you get goose bumps. Yeah. You'd start to go wide. And then if it's bad enough, you might start shivering. Shivering. Let's keep it simple again, do shivering, because it's just a simple outcome. So the effector is going to be our muscles. Yep. So the control center sends an efferent signal to the muscles and says, all right, time to contract, relax, contract, relax, contract, relax, contract, relax, which is shivering. Why do we do that when we're cold? Because when muscles contract and relax, they release heat and you warm up. And again, the outcome from the effector was the opposite of the stimulus. So we've just provided through temperature probably a very common example, two common examples of negative feedback. Yep. That's pretty good. Now, I just want to throw a really quick one in here. Just as a second one, because it's important for when we talk about a system not working. Yeah. So let's do blood sugar. Oh, okay. And this is a good one because it also confuses. But it's good because everyone's going to get confused. It just highlights where, in some cases, the distinction between the receptor, the control center, the effector. All right. Let's do it this way. I'm going to state each component. And you're going to tell me what the specific structure or thing is, right? So in this scenario, we always start with the stimulus. What's the stimulus in your scenario? Blood sugar. Okay. Is a high or low? Go high. Okay. So the stimulus is high quantities of sugar in the blood. So high blood sugar called hypoglycemia. It has to stimulate a receptor to have an effect. So what is the receptor? Where is it located? All of the above. Okay. The receptor is in your pancreas. Okay. And it is a beta cell. All right. So because blood glucose is internal, it has to be an internal receptor. And it is a cell on the pancreas, you said, called a beta cell. And it picks up high blood glucose. All right. It's now transduced, a high blood sugar stimulus into what sort of stimulus? It's going to move into a, well, this is a hard one because it's technically in the same cell. Okay. Great. So the receptor is located at the same place as the control center. So both are in the pancreas. So then it will, through an afferent signal of some sort, stimulate the control center of the pancreas. Yeah. It's kind of an internal stimulation. It's a, it's a, a little bit of a confusing example. Yeah. But it's a good one to, to, to learn. Absolutely. So basically what happens is the cell within the pancreas is one of the, the first regions to get this glucose from a meal. Okay. And let's just say you had a can of soft drink. You shouldn't because it's not good for you, but let's just say it because it has a lot of sugar in it. You drank it, it gets pulled, the sugar gets pulled across your gut wall, goes into your portal blood system and then, you know, it's going to live on the pancreas. Now, the cells in your pancreas, the beta cells, pick up the glucose and the glucose goes into the cell, which makes the cell really energized. Yes. Lots of ATP. And as a result, this is now going to control center. That high energized cell now is what is basically going to activate the control center to do the effect. Yeah. The cell is both the receptor and the control center because the cell and so the afferent signal, right, that gets sent is this, and this is where it gets tricky, is still an electrical chemical signal, like it does with sending a signal from your skin to your brain via your neurons. It's just that the, the same cell depolarizes. That's right. Yeah. That's a good example. Right. So as soon as the glucose goes in, that cell depolarizes due to ionic charge changes. And a big one is potassium. Yeah. That's right. And then what that does is it causes the release of insulin from that same cell. So that control center now releases insulin, which is going to be the efferent response. Yeah. Okay. But it's a chemical response. That's right. So now the beta cells from your pancreas just start dumping insulin into the blood. Yeah. So off it goes into the portal system. Yeah. And this is the afferent signal is insulin traveling through the bloodstream. Yeah. So now it's going to go to regions of the body that is sensitive to insulin, which is that chemical. So the first stop, and I'm not necessarily saying it has to work in this order, but the first stop this insulin is going to go to is the liver. Okay. So the liver is getting insulin from the portal system. Okay. And at the same time, it's receiving a lot of glucose from the meal you just haven't. Right. And so the, the liver says, well, that's a lot of glucose. And I've got insulin here. You know what? I might stall this for later. So it says, I'm going to stall the glucose, snap them all together and make a product called glycogen. That's right. Okay. So the effect here is glucose intake into the tissue and storage. Yeah. And then by sucking all that glucose in from the portal blood into the liver, that means blood sugar will slowly start dropping, which is perfect because the effect negates the stimulus. So negative feedback. Now, the other thing is because it's now going systemically. So now there is insulin in your whole blood with glucose from the meal. Any other cell that is receptive or sensitive to insulin. And what are some of those cells? Muscle cells, kidney cells. Okay. Fat, fat cells. And so now they're going to, because the insulin opens the doors for the glucose, not only glucose can't get inside a cell, but as soon as insulin binds to it, the cell doors open, glucose goes into these cells. So it's clear to muscle can use glucose for either contraction or it can store glucose for its own glycogen or fat will just store it as fat. Okay. But in any case, all these examples will start pulling glucose out of the blood and that's going to slowly drop glucose levels. So the great thing about this example is obviously temperatures are nice clear cut simple example, which everyone should start with to understand the different components of homeostasis. But I like this example because it still incorporates every single component, but in a different way. Yeah, that's right. So people need to realize that regardless of what mechanism of homeostasis, those components are still there in one way or another. And you know, just like with temperature where we did hot cold, Matt just did high blood glucose. But low blood glucose is a similar thing. When the blood glucose levels are too low, it gets picked up by cells in the pancreas. So that's the receptor called an alpha cell, which is also the control cell. - Yep, just next door to the beta cells. - That's right, and releases not insulin but glucagon, and then that does the same thing, jumps into the bloodstream, which is the efferent signal, travels to cells, like the liver, and tells it to mobilize the stored glycogen into glucose to release into the bloodstream for blood glucose levels to go up, and that's the effect. So again, you've still got all the components of the homestatic mechanism present. But what we've only spoken about thus far, Matthew, is negative feedback, where the effect negates, or does the opposite of the stimulus, goes to high, brings it down, goes to low, brings it up. But there's also something called positive feedback, which is not as common as negative feedback, but it uses the exact same mechanisms. So all, you know, stimulus, receptor, afferent signal, control center, efferent signal, effect are, but the effect, the outcome, actually exacerbates, stimulates, amplifies, other synonyms of the stimulus. So I think the best example of this is labor. - Yep. - So should we start talking about that? - Sure. - All right. - Let's just say, so what's the ultimate outcome that wants to be achieved here before we say anything? - Well, still wants to normalize homeostasis. So the stimulus is still going to be something pushing homeostasis out of range. And at the end of the day, it needs to get back into the healthy range, but it does it by the circuitous sort of route, by exacerbating it, to try and overcome something first, to get there. - So I guess the point here is, the example that Mark's going to give in terms of labor. What the body's trying to achieve here is to get the baby out of the uterus, okay? Now, the stimulus, unlike the negative feedback, the result is opposing the stimulus. But for this one, it actually amplifies the stimulus until the whole system turns off. - Yeah, so let's give the example so it makes sense now. - Okay, so the baby's in the uterus. - Yep. - It's engaged, heads down and it's starting to push against the neck of the uterus, which we call the cervix. Okay, so let's say, the uterus starts to contract somewhere, so we're slowly going into the start-- - Let's not do that yet. - The start of the first contraction. - All right, all right, all right, all right. So just waves, small, infrequent waves of contractions are going into the uterus. Now, when this is happening, it's pushing the baby down onto the cervix, okay? Now, that's going to, so the stimulus is pressure on the cervix, should I say. The receptor is in the wall of the cervix. So it's just pressure receptors, stretch receptors in the cervix. Now, the afferent response is a neurological response that's going to go back into the spinal cord all the way up to the brain. Again, we go to the hypothalamus, but a different region to the temperature, but still in the hypothalamus. The hypothalamus picks up this afferent response that basically just says the cervix is getting pushed on. So it says, okay, I think I know what's going on here. There's a baby wanting to get out. So what I'll do is I'll tell the uterus to contract more. So I'll release a particular hormone called oxytocin, and that goes into the blood. So that goes everywhere in the body, but for this particular case, the effecter is the uterus. And when the uterus picks up this oxytocin, it's basically oxytocin is kind of a smooth muscle contractor. And so what that will do is tell the uterus to contract more. And so if the uterus contracts more, it puts more stimulus on the cervix, which stretches the receptor more, sends more afferent signals to the control center, which says the baby's still there, I really need to get it out. I'll send any more oxytocin, and this keeps amplifying, amplifying. And this is why the waves of contraction increase, more forcefully, shorter time periods, and it's pushing and pushing and pushing and pushing. Is there anything more to add? - No, that's there, that's perfect. And until baby's out, and then there's no more cervical stretch, so there's no more stimulus. And so the stimulus is gone. - Yeah, and so now the stimulus is all done. And then completes. - Done. - So as you can see, what we're trying to allude to before going through the example was that the effect of exacerbating, amplifying the stimulus, the final and result actually resulted in homeostasis being regulated, going back to normal. Because the only way out of this situation was getting bubb out. There's nothing else the control center could do to stop the cervical stretching, right? That was the stimulus. And so they go, well, they gotta get this baby out. And another example of this positive, so that's called positive feedback. Another example of this is blood clotting. And so if you have a cut in a blood vessel, it obviously makes sense of the body wants to seal it up, clot it up. Now, if a blood vessel is cut, that's the stimulus. Receptors are going to be picking this up. But what ends up actually happening is it's, again, this is another different scenario in which, when a blood vessel is damaged, it exposes certain connective tissue within the vessel, which platelets that are going past all the time, stick to. And as soon as a platelet sticks to that, it releases chemicals to call on more platelets. 'Cause it goes, hey, guys, this thing is cut open, we need to clot it up. And those chemicals released stimulate more platelets to come in, to bind, to release more chemicals, to stimulate more platelets to come in, to bind, to release more chemicals. And so forth, until there's no more room for platelets to bind because it's all clotted up, there's no more cuts so the stimulus is gone. Now, the argument or the question could be, what's the receptor, what's the control center, and what's the effector. But again, you can have these as all in one. So the stimulus being the cut, the damage, the platelet is acting as both the receptor and the control center, releasing the chemical to have the effect. So it's sort of all in one. But still, all those components are there. And it's still positive feedback, because homeostasis at the end of the day needs to be maintained. And homeostasis was to bring things back into the normal range. So there's a cut, well, there's damage, it needs to be healed and needs to be fixed, otherwise disease occurs. And so, that's what happens. Because, and so, there's many examples of negative feedback, not too many more examples of positive feedback. But. Well, the other one, also in the context of mums and bubs would be breastfeeding. Exactly. And so that's still oxytocin. Very similar to the first one with oxytocin, but the different receptor here is going to be receptors in the breast. What is the stimulus? Well, it's suckling from the baby. So, the stimulus being mechanical stretch or movement within those particular receptors in the breast, sending a neurological signal, again, to the hypothalamus. Oxytocin is the release, so it's a chemical release, so it's a hormone and the effect. And what do we say oxytocin does? It's a smooth muscle contractor. So, oxytocin in terms of breastfeeding is milk letdown. It's not milk production, that's prolactin, but milk letdown. So, it kind of contracts the ducts to push the milk out into the nipple and out into the baby's mouth. So, and once baby is satisfied with all that milk, no more suckling, no more stimulus, no more oxytocin, and then it's all done. Now, because this is done more frequently than the birth, what actually happens is a kind of reinforcement for the mother. And so, the mother will start to, I guess, behaviorally see this system being used constantly. And usually, what goes with a stimulus, as I said, is the suckling, but what other things can go around the same time of that is the baby crying, because the baby crying, usually in those early days is crying because I'm hungry. So, usually shortly after the cry will be the suckling. And so, many mothers will report that, as soon as the baby starts crying, they get milk letdown almost straight away, because they're reinforcement. Yeah, yeah, yeah. So, that's not necessarily homestasis, but it's a behavioral. It's just showing you how that reinforcement occurs because it's happened so many times. And also, if we're digressing, that oxytocin release, because it can track smooth muscle, obviously, mothers who are breastfeeding have likely just given birth, it helps contract the uterus and bring it back to a. Yeah, yeah, yeah. That was prior to giving birth. So, it sort of helps bring things back into its right location. Yeah, it's a good point. So, look, I think there's not too much, not too much more to say about homeostasis. Well, there's one thing I just wanted to add, and that's more in terms of when it doesn't work so well. And I think if we can jump back quickly to the blood sugar example, remember the. Oh, a good point, yeah, yeah. So, the example we can. was the beta cell, okay? And we know that it disease, yeah, I'll call it disease, that causes a dysfunction in the way the blood sugar is regulated. And this is collectively known as diabetes. Now we know there's at least three types. There's probably even more now, upwards of about five, but for today we'll just say two, okay? So diabetes refer into a excessive amount of urine being passed. That's what the word means, essentially. But what is actually happening is those beta cells that we spoke about aren't working as efficiently as they should do. So we'll stop the diabetes, you're talking about. So if we go type one, type one is essentially kind of an auto immune disease, which kills off beta cells. And so this is happening generally in younger childhood, but slowly over time, the beta cells are dying over time until they get to about 80% died off. Now, you don't have enough beta cells to do that regulation that we spoke of. So what happens is you're having enough insulin being released as the effector. So that means sugar will remain high. And so you get all the side effects of having sugar too high for too long, as well as your cells not getting fed with enough glucose. So that's essentially type one diabetes. So importantly here, what Matt highlighted is that a disruption in any of the components of homeostasis can cause disease. So in this case, in type one, if the beta cell doesn't produce insulin, that's the control center not working. So you got the control center's damaged here. So the beta cell still works as a receptor because it's still picking up the high glucose levels. They're still depolarizing. It just can't produce the insulin. So it's not working as a control center, but type two diabetes. That's different, right? Yeah. So type two is probably a mixture of a few things because type two, more and more, they're saying there's a genetic basis to it that you that you inherit, but a big part of it would have come from a long-standing environmental change impact over time. So certain things like obesity, diet, have an effect in the way that insulin's efficiency works in the body. So pretty much over time, the amount of insulin might be okay, but the receptors that respond to it become kind of desensitized to it. And so it's a less efficient as a system. And so slowly what happens is the system doesn't respond as efficiently as it should. And it goes back to the control center and says, "Hey, we need more insulin." And you keep bumping up insulin and insulin. So you can actually, in early stages of type two diabetes, you can actually get hyperinsulemia until the pancreas kind of gets exhausted with it. And then you kind of drop off and don't produce enough. But the summary of it is still you get hyperglycemia, which is not enough, or sorry, too much sugar in your blood for extended periods of time. And at the same time, you're not getting the sugar into your cells. So you get dysfunction in certain cells from running out of energy. So in that example, in type two, it's making the insulin. So there's no problem with the control center. It's just that the effector, the effectors who respond to the insulin are no longer responding to it. So it's an effector issue. So again, it just highlights that and that again results in disease state. But Matt also nicely highlighted that just because the effector doesn't work doesn't mean again, the body doesn't try to continue to maintain homeostasis. So for example, when that blood glucose goes up, it stimulates that whole process. Insulins even been made and it's been released. It's just the effectors aren't responding. The body doesn't really know that. All it knows is that blood glucose levels are continuing to rise. So it continues to feed through homeostasis. So more and more insulin gets pumped out and released. But blood glucose continues to rise and so forth. And this is actually a nice example of what happens in many disease cases when there's some issue with one aspect of the components of homeostasis. Is that homeostasis continues to try to be maintained and continues to ramp through and is probably one of the reasons why you get some of the ill effects of certain hormonal-based diseases. So for example, in thyroid disease, if somebody. So thyroid hormones are really important for metabolism growth and development, right? They're made from the thyroid, which is sitting at the front of the trickier. Now you need iodine to make thyroid hormone. If you don't have iodine, your body doesn't make thyroid hormone or at least not functional thyroid hormone. So the body goes, hey, I don't have enough thyroid hormone. There's the stimulus, low circulating thyroid hormone. So it stimulates this whole homeostatic mechanism to produce thyroid hormone to negative feedback, right? Bump it back up again. But without the iodine, the thyroid hormone that it produces is just like it's what we call colloid. It's just a fluid that accumulates and it's not functional. So thyroid hormone relays, remains low circulating in the system and the whole thing continues to stimulate. And what happens is people tend to get all this colloid fluid being produced in the thyroid and they get this massive thyroid gland called hyperthyroidism in the sense that a goiter. And so one of the issues here is there's a breakdown in homeostasis. One of the components isn't working. And it continues to try and push through to maintain homeostasis. But the end result was a disease or disorder, which is a goiter or a hyperthyroidism or hyperthyroiditis or whatever it may be. So that's just again, and you can pick any single example, any example at all. And you can probably identify all of these components and find a disease. And this is what students should be doing is that when they start looking at disease states, try and identify what the cause of the disease is and what component of homeostasis it's affecting. And then you'll sort of see how things flow on from there. And that's a really nice way of looking at disease states. What else did you want to chat about? I think we covered pretty much the main crux of this concept. The main take on point from me at least, the mat may have something to add is that homeostasis is an organism trying to maintain an internal stability while adjusting to changing external conditions. And it happens with every single function of the body. There's a number of components of homeostasis, a mat and I outlined six of them, the stimulus, the receptor, the afferent signal, the control center, the efferent signal, and the effector. Now, the effect of the effector can be to do the opposite of the stimulus, which is negative feedback. Or it can exacerbate the stimulus up until a point where everything gets off. And that's positive feedback. And anytime there's a disruption in the components of homeostasis, a disease state can occur. And that's it. It's homeostasis in my eyes. And that really feeds on well, because homeostasis is usually a concept you'll learn in AMP, anatomy physiology, and then when you build on it, usually you're going to say a second-year subject of pathophysiology, which is a study of diseases. As Mike said, a lot of the diseases that you learn is really a disruption or a derangement of homeostasis. So, when you are learning your diseases, if you can always go back to this principle, it'll make your understanding of the disease, but then the diagnosis and the treatment of it much more simple, because you can critically think it, rather than just wrote, wrote, learned components that are really meaningless. All disease treatments, every single one tries to reestablish homeostasis. That's their aim. That's the aim of all disease treatments is to reestablish. Obviously, some disease treatments are symptomatic, but if you want to be curative to remove the root cause of it. That's right. Well, we're done. We're done with homeostasis for the rest of our lives. If you want to contact us, you can. You can do it on social media. Mainly me, because Matt doesn't do those sort of things. He just tends to his goats and moses yarn. But you can contact him. A lot of work to do. A lot of work to do. So much so that he can't do any social media. That was smart enough. I could use the goats to do social media. No, to cut a long way down the moat. It's a post on Instagram. There we go. At Dr. Mark Tadorvich on Instagram, at DR, M-I-K-E-T-O-D-O-R-O-V-I-C. I don't know. I've got such a long name. That's also me on Twitter, and you can find me on TikTok as well, and Facebook and wherever else. You can email us topics, suggestions, comments, whatever it may be. We get them all the time. Thank you to everyone that has emailed us. I'm sorry if I haven't got back to you. It's busy, crazy times, preparing for the semester. G-U [email protected]. Otherwise, you can send me an email, Dr. Mark [email protected]. Give us five-star rating on Spotify and iTunes. Leave a comment saying how amazing we are so that other people can see how great and useful and helpful we are if you are a student studying. Let us know. Tell us what you're doing. We love to hear from you and leave some comments and best of luck. I agree. Good luck. 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