Regards, Devon Johnson
On Tue, Apr 14, 2026 at 8:51 PM Devon Johnson
Speaker 1 0:00
Alcohol metabolism, a lot, a lot that goes on. None of it's good.
Unknown 0:07
So when you drink alcohol, it's absorbed into your blood.
Speaker 2 0:15
So that is that, that little myth that you always heard, make sure you eat something if you drink right? That's true, because the less you have in the stomach, the faster it leads the stomach through the stomach lining and enters into the blood. And when it's in the blood is when you start feeling all the effects of it, right? But here's the deal, the second someone consumes alcohol, your body wants to get rid of it, right? It's it's toxic. It's poison. I enjoy a cocktail every now and then, but it's poison, and immediately your body starts to eliminate it, right? So when it gets absorbed into the blood, immediately you start having an increased production of hydrochloric acid in the stomach, so you start becoming acidic, right? And that the stomach doesn't like acid. That at that hydrochloric acid really starts to irritate the lining of the stomach, and that's what makes people start to feel sick. If that hydrochloric acid increases too much or too fast, you start buying right? It's what kind of leads to your hangover your body starts to become so you guys all had a and z too, right when you learned about renal physiology and acid base balance. Right? By the way, renal physiology was my least favorite in grad school. I had to take, I had to take specific phys classes like cardio Fizz, muscle Fizz, renal, bids, Gi, phys at the med school, and renal was my least favorite. So you start to have an imbalance of your acid your base, right? So if you start vomiting, you might start having it come out the other way, right? Because your acid starts dropping and your base starts increasing, and vice versa. Your body's trying to get itself back into acid base balance. Okay? So once that alcohol is consumed and it's absorbed into the blood, it very rapidly wants to get distributed to other tissues in the body. Tissues absorb alcohol at different rates. Muscle absorbs it pretty fast. So it leaves the blood and enters the muscle pretty fast. Adipose tissue absorbs it much slower. So if you have more body fat, the alcohol remains in your blood longer, right? If you have more muscle mass, you're able to drink more, right? Here's the bottom line, the more muscle mass someone has, they can tolerate more drinks before they become intoxicated, the higher percent body fat someone has, they're going to be intoxicated on fewer drinks. That's why, typically women can't drink as much as men, because typically, I'm going to exclude myself from this fact, typically women have higher percentage of body fat than men, right? So men are able to drink more alcohol before they start healing the effects of it. Okay, now we're going to talk about how does the body metabolize it? So these first two steps, they have to happen before you can metabolize it. You got to consume it, and it has to get absorbed into the bloodstream. Once it's in the blood, once it's once you drink it, once it gets absorbed in the blood, it starts to get metabolized. So these are the three steps. So now it's all about metabolism. Okay? These are the three steps of alcohol metabolism, or sometimes it's called alcohol processing. The first is the alcohol gets converted to acetyl aldehyde, alcohol to acetyl aldehyde. The second step is acetyl aldehyde to acetate or acetic acid, and then finally, that acetic acid gets converted into carbon dioxide, water and fatty acids. So energy here means fatty acids. Okay, I'm going to do it again. So all this takes place in the liver. All alcohol metabolism takes place in the liver, your poor liver, which is why people who are chronic alcoholics have the very high risk of getting cirrhosis of the liver, because their liver is so stressed.
Speaker 2 5:00
So the liver produces these two enzymes that help in these metabolic steps of processing the alcohol. So in that first step of alcohol to acetyl aldehyde, it's just alcohol dehydrogenase that catalyzes that reaction. And in that first step, you have an NAD that gets reduced to NADH, alcohol to acetaldehyde by alcohol dehydrogenase. And there's an NAD that gets reduced to NADH. And then where would that NADH want to go? It's going to want to go to the electron transport chain in the liver. Everybody, we don't stay in the liver, right? The second step of acetyl adehyde to acetic acid, the enzyme that catalyzes that reaction is acetaldehyde dehydrogenase, right? And then the last step is just the acidic acid to water, fatty acids, carbon dioxide, okay, so the fatty acids when they're digested. So you probably learned in nutrition that one gram of alcohol is equal to seven calories, right? That's from fatty acids. Okay, so that, that little myth of you're gonna get a beer
Speaker 1 6:32
back. Okay, questions on this, Josh, did I answer your question? Anybody else?
Speaker 2 6:38
Okay, so now it's just, what are the acute effects? This is how I wrote this down, to help you kind of figure it out.
Unknown 6:49
There's acute effects. What's acute mean?
Speaker 2 6:54
Sudden, right? Yeah, there's acute effects. Then there's this transition of attacks from acute to chronic, and then there's chronic effects. So we're going to start with the acute effects of alcohol metabolism. The first thing is there, this, is this, is this, is it? Man, there is a cellular imbalance in that NADH to NAD ratio. Okay. So this, these three steps that I just went through. These take place in the cytosol of the liver, okay, but where does the electron transport chain live? In the mitochondria? So that NADH, this first step where the NAD got reduced to NADH, that NADH is going to want to get into the mitochondria, to go into the electron transport chain, because if it doesn't, it needs to get oxidized back to NAD, right? So that NAD can come back to the cytosol and get reduced again, right? We all remember that from glycolyte, okay? And it's going to take that NADH is going to take one of the shuttles, mallet, acetate, glycerol phosphate, in order to get from the cytosol into the mitochondria of the liver, right? We don't need to worry about which one it takes. Who cares? Okay? You're also with me. Here's the problem. In order for that NADH to get on one of those shuttles, and that shuttle to take it into the mitochondria, it relies on the fact that that liver, the liver cell, function is going to be 100% and it's not, and it's not with alcohol metabolism. Okay, so I'm just going to read this the way it is. The shuttle relies on liver cell function, which in turn is affected by the rate of the citric acid cycle in the liver mitochondria. Problem is there's impairment in the citric acid cycle. The citric acid cycle is going to be impaired. I'll tell you which enzyme specifically on the next slide. I think the other thing is this step in glycolysis, glycerol aldehyde three, phosphate dehydrogenase. This step right here, step six, right is also inhibited. So energy production all around is going to be impaired. So that means that all that NADH that got made in this step is not going to be able to get oxidized back to NAD. Okay, everybody's
Unknown 9:42
still going still good, all right?
Speaker 2 9:47
So what's going to happen, right? We can't really use the citric acid cycle, right? We can't get the NADH into the mitochondria to go through oxidative phosphorylation. Your body can't use can't make energy thoracic. So what is it going to try and do? What's it going to
Speaker 2 10:11
use anaerobic glycolysis? Right? It's going to shift gears and use anaerobic glycolysis so you're going to have more pyruvate going through that lactate fermentation, and this pyruvate getting converted to lactate, so now you got more 80 as well. Right? Alcohol is just the biggest sitting mess. There's also impaired gluconeogenesis in the liver. Who remembers? Remember, that's called the Corey cycle. So this lactate is not going to be able to convert it back to pyruvate to make new glucose. So that Corey cycle is going to be inhibited. Now we have glucose
Unknown 10:59
problems too, right?
Speaker 2 11:02
So the final results from this are possible lactic acidosis and possible hypoglycemia. Okay, so let's talk about the hypoglycemia. The reason for this is, remember, I said the second we take that first sip, body's like poison. Get it out of me. So the body is always and forever. Amen, going to prefer processing that alcohol over production of glucose. Okay, get rid of the bad guy, glucose. I'll deal with you later, right? So it could cause hypoglycemia. So one of the reasons would be, like we just said, we've got decreased liver glucose output. So in the liver, glycogenolysis, which is going to tell me what glycogen analysis means,
Unknown 12:09
the breakdown of stored glycogen. Oh, it's right there.
Speaker 2 12:14
So a significant amount of alcohol can completely stop glycogenolysis in the liver completely shut it down, so you're not going to break down any stored glycogen to make glucose. And the reason is, heavy alcohol metabolism kind of decreases the sensitivity of the beta receptors, so epinephrine can't buy and remember, you need epinephrine to bind in order to break down stored glycogen, right, in order to activate that glycogen phosphorylase. It's not going to happen. Not going to happen. So that's one way we could have low glucose. The other is what I said on the previous slide. We're going to have inhibited quarry cycle right inhibit gluconeogenesis, because we can't get that lactate to get converted back.
Speaker 2 13:13
You also have remember that step six, that glyceraldehyde phosphate dehydrogenase, step in glycolysis, is impaired. That's everywhere. That's happening everywhere in the body, with alcohol, muscle, liver, brain. Okay, so there's less glucose to enter into cells. So we got a cellular imbalance of NADH and NAD. We've got a possible hypoglycemia situation. So now here's how alcohol inhibits the citric acid cycle. So you've got that decreased pyruvate concentration because we can't use aerobic glycolysis. We're using anaerobic glycolysis, and the lactate can't get converted back to pyruvate, okay, so we're not able to convert acetyl CoA in that pyruvate. We can't in the pyruvate dehydrogenase complex. We don't have pyruvate getting converted to acetyl CoA because we can't make the pyruvate. Okay, so that's step one that affects the citric acid cycle. You've got no acetyl CoA through glucose. These two rate limiting steps of the citric acid cycle are inhibited, citrate synthase and ISOC isocitrate dehydrogenase. They're going to be inhibited with alcohol metabolism. So that's going to remember they're two of the three great limiting enzymes. So that's going to slow down the whole thing, the whole citric acid cycle. And then the third thing is, there's less oxaloacetate that's going to be made, because this enzyme, malate dehydrogenase, is this step right here that makes more oxaloacetate. This enzyme is inhibited. So you've got major inhibition of this entire citric acid cycle. You've got it here because pyruvate, we don't have pyruvate, so it can't get converted to acetyl CoA. Then you've got citrate synthase inhibited. You've got isocitrate dehydrogenase inhibited, and you've got malate dehydrogenase inhibited. So there's like four places that are like saying, No way
Unknown 15:31
you are you are not operating.
Speaker 2 15:37
So now let me tell you how quickly this happens. Blue are males, orange are females. Here's age differences, 18 to 40. That's you guys, right. 41, to 65 over 65 the number of drinks, the number of drinks that you would need to consume to inhibit the citric acid cycle and increase the production of Oxy
Unknown 16:07
that's not a lot, right,
Speaker 2 16:14
right? I don't think that's a lot. So it has this is acute like this happens really quickly. You start to have energy production in area. This still happened,
Speaker 2 16:36
because there is a little bit like happened, because there is a little bit of alcohol. So alcohol, so one drink. This is based off what is considered one drink. Anybody remember what that is? 12 ounce right? 12 ounce glass of wine, three ounce shot, no.
Speaker 1 17:01
12 ounce fear, right, right, and a three ounce shot, that's what that's basically,
Unknown 17:16
right? So, yeah,
Speaker 2 17:20
I'm sorry. Go ahead. Go ahead, vary with the size of muscle. Yeah, right, so the more so hold on, no, okay,
Unknown 17:34
this is the number of drinks,
Speaker 2 17:38
the absorption rate of how quickly the alcohol moves from the blood into a tissue. Is slower with more muscle, okay, but it'll eventually get there, right? This is like the number of drinks that are going to just inhibit energy production.
Unknown 17:56
Anybody else questions?
Speaker 2 18:01
All right, so that's the acute effects. I'm going to summarize them again at the end. But those are the acute effects. Why does the age matter? Specifically,
Unknown 18:14
anybody want to take a stab at that? Because people who are at
Unknown 18:19
a younger age, exactly amen, amen.
Speaker 2 18:24
You guys, your metabolism is like skyrocket this right now, right when we talk about peptides like mine, has slowed down significantly, right? Like it's it's crazy how you and you can feel that you can sense that changing right from like what it was, what my metabolic rate was when I was thinking, and I was thinking in my 30s and early 40s, and was still insanely fast, and how much we'll talk about peptides, The Secret longevity of all that. Okay, so you're good, all right. So now let's talk about that transition from acute to prime. One thing happens, so the NADH that gets produced in that first step can't be oxidized in the mitochondria because it requires oxidative phosphorylation, and oxidative phosphorylation requires oxygen, right? We don't have enough oxygen to accept all that NADH because liver cells are hiding it all up. Okay? The liver cells have to take up more oxygen than normal in order to process the alcohol. So we don't have enough oxygen to operate oxidative phosphorylation to remember, remember the liver is like, get this poison out of here. Nothing else matters right now. Okay, so alcohol consumption can result in pretty significant hypoxia, low oxygen state in the liver cells, liver cells. So that's what happens in the transition of acute to chronic. So now,
Unknown 20:18
now we're in the chronic effects.
Speaker 2 20:22
So once hypoxia has set in, you are now in a chronic state of alcohol metabolism. So the first thing that happens is the electron transport chain is blocked. When that happens, remember, in the electron transport chain. Protons get pumped out into the inner membrane space, and they float around up top. And eventually they enter into complex five, the ATP synthase, who remembers how many we need to make? One? XP, three. Great. Okay, they're stuck with alcohol, the chronic effects of alcohol metabolism, the protons, hydrogen atoms, protons, are stuck. They can't they can't do anything. So we've already said the body tries anaerobic glycolysis, right? Can't use oxidative phosphorylation, right? Can't use aerobic glycolysis. So the body shifts, because once you're once, once you can't use anaerobic glycolysis anymore. Which body to try and do? It's going to use fast. Glycolysis is going to start accelerating. You're going to start breaking down more storage triglycerides into free fatty acids. Those free fatty acids are going to go where?
Speaker 2 21:58
Yeah, how do you get there? Which shows carnitine. Thank you. Those fatty acids are going to join carnitine. Carnitine is going to take them into the mitochondria. They're going to go through beta oxidation. The bottom line is, you guys, increased glycolysis, increased beta oxidation. What's the end product of beta oxidation? Acetyl CoA. The acetyl CoA is going to want to want to go where citric acid cycle. But what's happening? There? Nothing, right? So what's that? What's that acetyl CoA gonna do? It's gonna do two things. Some of it is going to become ketones. Some of it is going to become fats again, right? So the bottom line is, you're going to have increased lipogenesis and increased formation of this ketone, beta hydroxybutyrate. So when we talk, when I taught ketones at the end of the lipid metabolism unit, we talked about this ketone, mostly because we were talking about diabetic ketoacidosis, right? But in alcohol, I remember saying when we talk about alcohol, we're gonna talk about a different one, right? In alcohol, it's beta hydroxybutyrate, so some of that acetyl CoA will become this, and that is going to increase the risk of ketoacidosis. It's more acid. It's an acid disaster alcohol metabolism, right? Because the reason why you have a risk of ketoacidosis is you're going to make more ketones, but the body can't clear them out fast enough. I can't get rid of them fast enough, right? There's also dehydration from alcohol that will impair the blood flow to the key. So remember, kidneys help get rid of ketones. Liver and kidneys help to get rid of ketones. Well, the liver is pretty busy, right? So the ketones are going to try and go to the liver to get clear but there's dehydration that can occur from alcohol, and whenever you're dehydrated, you impair blood flow to the kidneys. And if blood flow isn't going into the kidneys, what did we say about the GFR? Glomerular filtration rate goes down, so the kidneys can't filter things out of it as quickly. So that's why the risk of ketoacidosis goes up. Some of that acetyl CoA will go to make new triglycerides, right? So the reduced rate of the citric acid cycle causes the fatty acids to turn back into a triglyceride. And because that glycerol three phosphate dehydrogenation, Step Six of glycolysis, is kind of free, because it can't do its job in glycolysis, it's like, hey, use me as a glycerol backbone. Come on, free fatty acids attached to me, and
Unknown 25:03
we'll make a new triglyceride, and we'll store it right?
Speaker 2 25:08
So we're going to make more fats, we're going to store more fats, and we're going to make more ketones, and we can't get rid of them. So because that glycerol, three phosphate is available. If we make more fats, that's what leads to fatty liver syndrome. That's what increases someone's risk of getting cirrhosis of the liver and getting high cholesterol levels. Too much fats in the blood, too much free floating fatty acid triglycerides in the blood, right will raise the LDLs in your cholesterol. So this is why sometimes chronic drinkers can be overweight or
Unknown 25:57
they're skinny,
Speaker 2 25:59
but they've got a stomach, right? They've got a stomach. The stomach is from two parts. It's from this, right? It's from the lipogenesis. But when the liver starts to become disease, person gets something called ascites. You ever heard
Unknown 26:28
of that? Oh, god.
Speaker 2 26:35
Remarkers, ascites of the liver is fuel it fluid accumulation in the abdomen,
Unknown 26:44
first sign of a chronic trigger.
Speaker 2 26:47
Their body shape starts to change, and they start getting this belly that's ascites. Okay? Questions, because that's the whole story, and now I was just going to review them for you. Yes, so through the lipogenesis part, so it's because a few fatty acids can be used if they find glycerol. The glycerol is available, right? Because it can't do its job in glycolysis. So it's available for fatty acids to attach to it so we can make more triglycerides. Yeah.
Speaker 2 27:28
Okay, so if we review a cube, there's a cellular imbalance in the NADH NAD. Make that that NAD gets reduced to NADH in that first step of alcohol metabolism it wants to get into the mitochondria, taking one of those shuttles, but it can't, right? But it can't get in there because there's impairment of the citric acid cycle. There's low oxygen in the liver because the liver cells are hogging it up. So you've got impaired citric acid cycle. You've got these two enzymes, citrate synthase, isocitrate dehydrogenase are inhibited. This step in glycolysis is also inhibited. The pyruvate gets converted to lactate, because now we're using anaerobic glycolysis, so you've got more lactate production. Remember, that's called lactate fermentation, and you have a possible risk of lactic acidosis. Also, there's the possibility of hypoglycemia, because we've got decreased glycolysis, we've got decreased glycogenolysis, we've got decreased glucogenesis, right? Just decreased glucose production. There's also less oxaloacetate available because that malate dehydrogenase enzyme, that last step in the citric acid cycle that makes more oxaloacetate, is inhibited. So that's all the acute effects, and that's all the stuff that happens on my bar chart according to your age and gender, how many drinks you would have to consume for all this to start happening.
Unknown 29:14
So for me, it's three. You should be should remember the number.
Unknown 29:20
Now, I just thought maybe that would be interesting
Speaker 2 29:29
to know the transition from acute to chronic is just the liver cells are hogging the oxygen, right? So the person starts to become hypoxic, the liver starts to become hypoxic. The liver starts to become hypoxic. Chronic effects are when the hypoxia has set in. Right now, the liver just just can't really do anything, right? You've got electron transport chain is reduced. Protons are blocked. They're stuck up in the inner membrane space. So your body's got to shift to a crazy increase in lipolysis and be oxidation, because it's got a body's always going to try to keep you alive, right? So it's going to shift to the next thing that's this. It's going to make more acetyl CoA. It can make lots of Acetyl CoA, but because the citric acid cycle is not working, that acetyl CoA can't go there. It's going to go in two places, right? It's going to either get converted those fatty acids are going to get converted to ketones, right? Or we're going to make new triglycerides. We're going to have increased lipogenesis. And the more ketones, increases the risk of ketoacidosis, because the ketone is beta hydroxybutyrate,
Speaker 1 0:00
Here's your big outpour of epinephrine. We're gonna have more of that. It's going to elevate the activity of a dental recycling. Increase the activity of cyclic AMP. You're going to have more phosphorylation of sensitive lipase. You're going to start breaking down a lot of store triglycerides have more free fatty acids that join carnitine, go into the mitochondria, go for beta oxidation, make acetyl CoA, right? Same thing with glycogenolysis. You got more epinephrine output. It's going to increase the activity of a dental and cyclase. It's going to increase cyclic AMP. You can have more phosphorylation of glycogen phosphorylase. You're going to start cleaning off those glucose units on that stored glycogen, till you get it down to G, 6p and it just goes straight through glycolysis, right?
Unknown 0:49
So, big metabolic benefits.
Speaker 1 0:52
Now you think you get those mindbog benefits more from a big coffee or from like caffeine tablets
Unknown 1:01
you got to drink. A lot of
Speaker 1 1:05
coffee, but a naive or novice caffeine drinker would have those benefits sooner than somebody who drinks a lot of caffeine, your tolerance is limiting those metabolic effects at some point. This is another reason why anybody drink those pre workout drinks. So caffeine is in them, taurine is in them, right? So that's that. That's what helps you, like, have the energy for the workout, is caffeine and taurine that's in them. So said this. This is a beta two receptor agonist, the beta agonist. So caffeine could help. Could be impossible asthma treatment, right? So, faith, you have asthma, do you drink any caffeine? Never, I see no, I'm drinking when you can. When you have drank, it and you feel like you breathe better anybody else? Well, it could be. It could absolutely be, because it's opening up the vessels in your lungs, right bronchi in your lungs. So it's, it's, it is a drug. Caffeine is considered a drug, and it's very similar to something called theophenoline. And theophynoline is a prescription bronchodilator drug for asthma, and it has many of the same properties, so caffeine can help people who have breathing difficulties who snore at night. I mean, it's kind of like a catch 22 you snore at night, but you take caffeine. Does that keep you up, right? So, but it does all right. So, ergogenically. Ergogenic means
Unknown 2:59
what it helps athletic
Speaker 1 3:01
performance, increases performance. Ergolitic means increases performance. So who would use caffeine as an ergo gene gate? Well, not everybody, but a lot
Speaker 2 3:16
anything that doesn't, yeah, I said any sport that doesn't have to do with like precision. So, like,
Speaker 1 3:21
yeah, yeah. I mean, a lot of athletes will use caffeine, right? I mean, think about this. How many of you like, Okay, so my Red Bull guy, you could almost say that was an ergogenic he took, he drank six Red Bulls to increase his performance of study, right? So there's a lot of people that will use caffeine for focus and attention and alertness and energy right now. Who? What athletes would this would be herbalitic. Yeah, right. All the ones that might want a beta blocker might not want this because of the jittery This is the central nervous system stimulant
Speaker 3 4:03
for sports like basketball, right? It's like a combination of different things like focus, yeah, and eye coordination. Would it
Speaker 1 4:12
be that depends on the person? That depends on how sensitive they are to caffeine, right? So if it's somebody that's really sensitive to it, it's going to be more ergolitic for them. And the other thing you have to think about, though, as far as an athlete, that diuretic effect, right? So think about a runner. Okay, let's all just be real for a second. Let's just think about a cup of coffee, right? Some of the most disgusting bathrooms in the world are the bathrooms in a coffee house. Okay? So I know personally, somebody who was running a marathon, and she consumed caffeine that morning, and it kind of ran right through her, and she was a good marathon. Good marathon runners are going to win. They're not going to stop using the Porta Potty. Okay, so it happened she ran, she finished the race. Disgusting, but it is what it is, right? So you have to be careful of the diuretic effect with athletes, though, not just like that story, but just the cramping that the diuretic effect could cause, right? Yeah, are you saying like she likes Cuban herself? Because one. Try the other one. Yeah. She did well, though. Hey, what I said? Okay, one athletes are good athletes. Little mental Kathy like you trained for months for something. You're not going to let something like that, right? I mean, okay, so here's all. I mean, I don't even think we need this slide, right? We can, we can talk about what the Herbalife effects could be, right? So impairs fine motor task. So here I have some sports that probably would not want to take caffeine, unless it was somebody who consumes so much caffeine that they don't have any effects from it, then it wouldn't bother them for that sport, right? Okay, so I think we kind of so here's the other thing with caffeine, it can cause some GI difference, besides the bathroom issue, there could be like stomach cramps, a little nausea that's involved with caffeine consumption.
Unknown 6:39
Let's talk about withdrawal.
Speaker 1 6:46
Talk to me about your caffeine consumption. Yeah, let's be real. Tell us. Tell us how much it is, anywhere from like 300 to 500 milligrams a day. Probably Okay, so times more. Did you ever not get that much in in a day? For a while, it's been a long time, okay, but when you didn't, how'd you feel? Constantly, groggy,
Unknown 7:15
groggy. Anything else,
Speaker 1 7:19
headache, I guess, easy. Crazy headache, crazy headache, right? So here's what happens with the withdrawal caffeine is a vasoconstrictor. Okay, let's get a little jump on cardiovascular for the fall. When a vessel constricts, does blood flow go down or up down? So when you have caffeine, Jack here is all cracked out on caffeine right now, his vessels are constricted, so his blood flow is is a little less, okay. It's inhibiting adenosine. Adenosine is a vasodilator, okay, so when he doesn't get the caffeine, his vessels dilate normally, that constriction is removed. So his vessels dial, I'm not saying they like dilate more than ever. They're just dilating normally because the caffeine hasn't been consumed, so the constriction has been removed. So what happens when a blood vessel dilates, blood flow goes up. So he doesn't get his caffeine, his vessels dilate normally, it increases blood flow, headache, pressure and volume have a direct relationship. So when you've got dilation, you've got increased volume, which means increased pressure. So a headache is the number one thing caffeine users report when they try and get off the caffeine, and as soon as they get like, if they can't take it anymore, they get a cup of coffee. Boom, headache long, right? So that's why it's hard for them to come off caffeine. Years and years and years ago, we went to a conference with some students. We stayed overnight. And this one student, Courtney, she was a runner, Exercise Science student, the most massive caffeine drinker I've ever seen in my life, caffeine, right? She dated the Red Bull guy, and the Red Bull guy actually worked at Starbucks, so she could get all these free like ventas, right? Like, I never saw her without coffee. Well, that morning we were leaving, she didn't have time. She was running late. Didn't grab her coffee. She is laying in the back of the van in a fetal position, screaming that she's having a brain hemorrhage, right? And I just looked at the other fat I go pull in the restaurant and let her get a cup of coffee, and then she'll shut up for the rest, right? So we let her go in, she got her coffee, and then she was fine, right? But it was, this is what was happening, right? So adenosine is the first thing. If you're trying to withdraw the inhibition of it has been removed, the blood vessels are dilating like normal, and you've got an increased blood flow. That's causing a headache. The other thing is, you're not going to have as much epinephrine output, right? Reduced catecholamine activity. So that's why Jack says, I feel groggy, you feel tired, you feel fatigued, because you don't have as much epi in your bloodstream, right? So you're not making as much ATP. Lipolysis isn't as accelerated like a geologist is. You're not making as much ATP, right? Then there's something called serotonin syndrome. Has anybody ever heard of this?
Unknown 10:41
You know what it is? Just heard of it.
Speaker 1 10:44
So what gene is stopped, serotonin levels go down, serotonin left. Serotonin is kind of like what helps with your mood, right? So people get irritable, right? Cranky, they have a hard time concentrating, hard time focusing, and that's because there's a big drop in serotonin when caffeine is not consumed, when it's been regularly consumed, right? So you got three things that happen. 123, that's known as the crash, right? All, it's not like, Oh, this one happened to me that no, all of them are happening. All of them are happening simultaneously. And that's why it's really hard for people who get addicted to caffeine to get off of it.
Speaker 1 11:40
So what about hypoglycemia, low blood sugar. So we all know what symptoms of hypoglycemia are, right? You might feel nauseous, you feel sweaty, you feel dizzy, light headed, shaky, right? Because the amount of glucose in your blood is going down. So caffeine, because it's such a powerful central nervous system, stimulant can mimic a lot of these same effects as hypoglycemia, and this is what we see and remember. So caffeine increases epinephrine, but there's also an increased glucose uptake with epinephrine and with exercise. Remember, we said exercise, so let me ask you this. We know that insulin is what comes out and moves glucose out of the blood through the glute four into the muscle, right? But when you exercise, does the concentration of insulin go up or down, down? But when you exercise, you're having muscle contraction, right? What causes the muscle contraction? Calcium? Calcium mimics insulin, so that calcium can make more glute, four transporters come out more glucose moves. Even though insulin isn't increasing, the calcium is making the glucose move out of the blood. So you've got the caffeine, which is doing it, and the exercise, which is this is what happens with those pre workouts, right? I see so many times people that within the first like 20 minutes of their workout feel like they're either going to puke or pass out, right? And that's because of this. That's because the blood glucose levels drop so quickly from the combination of the two things I took pre workout one time, I didn't I drank half of it, and that happened me, I was like, Yeah, I'm done with this was like the most unproductive workout in my life. So that's something you need to be really, really cautious of when you're working with people. Because everybody I get asked all the time. My 85 year old father asked me two weeks he still goes to the gym. What can I take for energy?
Unknown 13:50
They have these pre workouts. Please don't take
Speaker 1 13:53
I said, just have a little bit of coffee or something. Just don't spend your money. Don't do that. I don't need you to pass it out in the middle of the gym when I'm two hours away, but this is something that's really common. People are always looking for, what can I take for energy before my workout? Right? And this can happen really easily, okay? NCAA and Olympic Committee, caffeine is considered a restricted substance. It's not banned, but it's restricted. But here's his statement from the Olympic committee, any physiological substance taken in abnormal quantities with the intention of artificially and unfairly increasing performance should be construed as doping. So they don't test for it. But I guess if there's suspicion they could test you. I don't really know how they do it, but that's the statement that Olympic Committee has with all substances that could potentially be used as an autogenic aid. So guidelines try to avoid routine use of caffeine. It builds tolerance. Be careful with the abrupt like, if somebody you know or yourself wants to decrease the amount of caffeine you consume, do it slowly. Don't do a cold turkey stop because that you're going to have that crash. It's going to be horrible, right? Oh, my God, we got
Speaker 3 15:22
go for it. Just so, so, alright, so during the school year, I might drink a cup of coffee a day. During the summer, since I'm in
Speaker 4 15:29
school, I don't really drink coffee. How long would it take for you to stop
Speaker 1 15:35
so you drink like one cup of coffee a day. How big is the one
Unknown 15:40
the large enzyme might be 20 ounces.
Speaker 1 15:42
Okay, so you drink a 20 ounce a day. Do you feel like when you start that, you get a little bit you feel a little symptomatic, but then, like, within a week, that goes away. I never noticed it. So what was your original question? How long
Speaker 4 15:55
would it take if I were to get withdrawal symptoms? How long did that time period before the symptoms kind of fade?
Unknown 16:01
Or within a week, to get that, to get a headache. I do get a headache.
Speaker 5 16:06
Yeah. So I normally run, run with the caffeine. But like, this morning, I ran a fast, festive and like, it's just like, like, I noticed like, it was mainly like, honestly, I wasn't the like, actual, like, fasting, but like, the like way, like, having like, like, without caffeine effects is just insane. I'm just
Speaker 1 16:31
like, so that. So those of you who are saying, No, I don't feel any effects, try going without it. I know. Like, if you, if you, you drink it, and then go work out, do what Tommy did, and you're gonna realize, Oh, I do rely on that caffeine, because when I don't have it, I have a really crappy workout, right?
Speaker 5 16:49
Yeah, honestly, wasn't even bad. It was just, like, a lot worse than feel, feel feel
Unknown 16:57
bad, but like the like
Unknown 16:58
performance drop, yes, yeah. Any other questions?
Unknown 17:04
Sam's thinking, Could it be possible that like, recorded, like, caffeine, can be, like,
Speaker 2 17:15
banned in the country? I mean, because, like, it's pretty let's eat. It's really easy for I think he addicted?
Speaker 1 17:25
Yeah, I don't see it ever getting banned, but it's a decent question.
Speaker 4 17:32
You go back to the slide where the Olympic Committee was like, giving their statement on it.
Speaker 3 17:38
So you were saying that, like, if there was, like, suspicion, if they're using it? Yeah, I don't know.
Speaker 1 17:45
I'm just maybe I don't know. I mean, honestly, I just think this is such a everyday, common substance. How could they police this? Yes, what I'm saying, right? Unless it was the fastest, way for it to hit you would be IV, right? So if they suspect an athlete was taking IV caffeine, and honestly, like a professional athlete, if they're going to rely on caffeine as their doping substance, that's how they're going to take it. They're going to take it IV. They're not going to go to Starbucks and get a dentate before they enter the Olympic Marathon, right? They're going to take it that way, just like, you know, the blood doping with the blood cells, right? So that would be my guess, that would be absolutely banned.
Speaker 2 18:38
My question is, like, I remember I asked Dr white this too. But why would blood doping even be like? Because it's technically your own blood Well, it could
Speaker 1 18:47
be either you can either harvest your own cells, or you could have a match donor, which is dangerous, even more dangerous, I mean, blood doping, is it's so dangerous to begin with because you're increasing cells, right? So it increases your risk of clots, even if you're using your own cells, right? But that's very common. Well, what they do now is they use Erythropoietin, right? Which is a, which is a med that they inject intravenously, rather than like doping with cells, they take a rethrow point.
Unknown 19:21
Can't they just train a higher elevation also?
Speaker 1 19:24
Well, they could, if they were able to, like, if they geographically, could do that. But your
Speaker 3 19:32
opinion, right? Compared to like, other drugs, like,
Unknown 19:36
how, how good
Speaker 1 19:39
is, when you say good, you mean like for performance, for like doesn't come close, you'd have to take a lot. You have to take a lot. That's why I don't think it would ever be banned, right?
Unknown 19:55
It's silicon, like a dentist.
Unknown 20:01
Cyclic AMP, what did you say there was
Speaker 2 20:02
a slide. It was talking about like cyclic adenosine and increase
Unknown 20:09
year, what we were doing, glycogenolysis,
Speaker 2 20:14
year, things like two slides.
Speaker 1 20:19
Yeah, so that's cyclic AMP, right? Cyclic adenosine monoplastic. That's cyclic AMP, two
Unknown 20:28
different things, though.
Speaker 2 20:30
Question on the last test, I know there was something about like so it only does it directly affect both directly affect a dental lean cyclase and cyclic AMP or cyclic AMP, just the result. Because I know it's like a no
Speaker 1 20:44
directly up regulate both. Okay, right? It's upregulate both of these. There's a, I made a new study guide, and it's on bright space for the exam, exam five. I think this is right, so you can pull it off. Bright space. No, it's fine. Somebody backed me out the window. I backed you already,
Unknown 21:13
yeah, because I do you enough.
Unknown 21:18
You're like the secretary of the class.
Speaker 1 21:21
Anything else? Okay, the research symposium is going on. Students are going to be by their posters, downstairs, posters, and ask them really hard questions
Unknown 21:36
about their Research yesterday.
Unknown 21:53
Guy, Nick ain't getting no punches. How many of you are involved in that?
Speaker 1 22:12
Okay, let's think about this. Let me just give me, give me 30 seconds to look in the head so we didn't have class on the 20th got a wire. That would mean that I would have Wednesday and Friday and then the following Monday, which is the 27th right.
Speaker 1 0:00
Fever, headaches, right? I had a splitting headache yesterday, and I took two NSAIDs because I thought cerebral spinal fluid was going to drip out of my ears. It was hurting so bad, right? This is a big one that we're going to talk about arthritis. This is the big one with athletes, sports injuries, right? And then some women, when it's their time of the month, they take them for menstrual cramps. So I mentioned aspirin is in this class, and it is right. But what? What makes aspirin a little bit different? What do we know about aspirin? You're telling me that's right, it's a waste Blood Center, and what he means by that is it's used to inhibit the clotting of blood. So if someone's at risk for blood clots, they may be told to take an aspirin today, right? Because that will decrease their risk of having a stroke or a heart attack. But there's a correlation with using aspirin, because it does decrease the placement now with sports anemia, which is gi beauty, and that could exclude an athlete from being able to compete if this happens to them. So you have to be cautious. And it's all about the dosage, which we're going to talk about. Anybody ever know anybody that had any issues with aspirin? So here are a list of commonly used NSAIDs, white people, and you again, jump off the page to you? Ibuprofen, yeah, is that your instead of choice? Okay? Anybody else have an n set of choice? Neroxin prescription or over the counter, like a leave, right? So I like to leave non prescription. So this is interesting. See my little note here. Some have been known could cause water retention. This is a fact. So when I was competing, you know, I had injuries from my earlobe to my big toe.
Unknown 2:17
I got prescription naproxen.
Speaker 1 2:22
I got on the scale the next day, I was four pounds heavier, right? I held significant water from the prescription naproxen. Now the over the counter, naproxen is a leaf. I can take a lead. No water retention at all, right? I am very, very sensitive. I'm very my friend this morning. I'm very water sensitive, right? So I just couldn't take that, even though the prescription nephropathy was probably stronger, probably would have helped me with my injuries a little bit more. Being in the sport that I was in, having four pounds of water on you was not going to be beneficial, right? So I had to get off that, get on the over the counter, right? Anybody else have one on here that you prefer over another? Let me see this show of hands. How many of you take NSAIDs on a regular basis? Of course, how many of you take it? Like, episodically, like, if you have a headache, kept here, okay, how about in the training room? Do they monitor the NSAIDs? Like, you only allowed a certain amount. You can take as much as you want. Like, what happens over there? Wild West. I mean, nah, they don't lock up. Okay? So Courtney, give me before we can talk anymore about understand what prostaglandins are. So prostaglandins are made in our body by this enzyme called cyclooxygenase, or the Cox enzyme. And there are two of them. There are the Cox one and the Cox two, right? So these enzymes make prostaglandins, and then the prostaglandins are what promote the pain, the fever, the inflammation. Okay. Now, the Cox one enzyme produces prostaglandins that support platelet function and protect the lining of the stomach. There's a good thing. So prostaglandins are just it's not all bad stuff, right? They do good stuff too. So only the prostaglandins that come from the Cox one enzyme control your support your platelet count, make sure it doesn't drop too low, right? And protect the lining of your stomach, but not the prostaglandins from the cups too. So these are functions of prostaglandin So, like I said, not all bad, right? Prostaglandins, they they do contraction and relaxation of smooth muscle. So smooth muscle is in our blood vessels, right in our GI tract, prostaglandins do vasodilation and vasoconscious blood vessels, so that helps us to control our blood pressure. Right? When arteries dilate, blood pressure goes down. When arteries are strict, blood pressure goes up, and sometimes we need it to go up if you're bleeding, right? You need constriction to keep your blood pressure from bottoming out. But we're going to focus mostly on what's in the red box here when we talk about insects today. So we're going to talk about how the prostaglandins promote the inflammation and the pain and the fever, how they support the function of the platelets with the blood clotted, right? How they protect the lining of the stomach from acid, right? So remember, those are only from the prostate gland. Is from the toxin. Any questions so far? Yeah. Is that why they tell you that? Yeah. So now let's talk about prostaglandins versus NSAIDs. So when you take an NSAID, you block the Cox enzyme. That's what the drug does. So if the Cox enzyme is blocked, the prostaglandins cannot be formed. So therefore it reduces the inflammation and the pain in the fever, and those are primarily the reasons why you all take them, right? You've got pain, you've got an injury, and there's inflammation, right? So soon as you swallow that pill, it's going to block the Cox enzyme, and that's what's going to reduce all those symptoms for you. Now here's the thing. You take that NSAID, that ibuprofen, that, naproxen, whatever is your NSA of choice, you're going to block that Cox one enzyme too. You block both. You block the Cox one, you block the Cox two, and when you block the Cox one, you're no longer making the prostaglandins that support the platelet function and protect the lining of the stomach from acid. So now you're at risk. Now let me say this. Devon, you had your hand up. You take in cells, right? How many milligrams do you take at one shot, 500 500 Okay, anybody else? How many
Speaker 1 7:23
take 1000 at a shot? Okay, those are, this is getting a little high, but that's a therapeutic dose, right? 200 to 400 like a pill is usually, in general, one pill is usually around 200 milligrams, okay, you can get them higher. You can get them higher, but in a therapeutic dose, a lot of the things I'm going to tell you, you're not at risk, okay. But here's the thing, if you take them daily, if you take them a couple of times a day, now you're starting to be at a little bit higher risk. So when you take that n set of choice, when you take that n set of choice, you block both of those COX enzymes, so you've reduced your pain, your fever, your inflammation, whatever you're taking it for, but you're also blocking the protection of the stomach and the platelet function. So NSAIDs can cause ulcers in your stomach. Those are called gastric ulcers, and they can promote bleeding. So here we go. That is a gastric ulcer, okay, that is the stomach, and that is an ulcer on the stomach. It is like a festering boil. Anybody have an ulcer? Okay, here we go. That is my stomach. That is the ulcer that lives in my stomach. Now I took a lot of insects. I took a lot of insects. I had seven herniated discs. I had a Tor meniscus in my knee. I had a lot going on leading into that last Olympia that I did a um, I took a lot of pain. I took a lot 1000 milligram pills, and I took it several times a day to get Friday I was training four hours a day. Okay, now, the second I stepped off stage at the day, I stopped taking so good thing for me is I don't have an addictive
Unknown 9:45
nature to me, right? So I could just stop.
Speaker 1 9:50
But I had to go in for I had to go in for a colonoscopy. And they decided, since they were taking me in there for that that they were going to do an endoscope. So they were just shoving tubes everywhere they could, right? So I come out of, I'm like, coming out of the anesthesia. And the doctor is like, over top of me with this picture, and she's like, What do you take for your ulcer? And I was like, like, trying to wake up. I push her. I go, What are you saying? Right? She goes, this is one of the worst guests or holsters I've ever seen. What do you take for this? And I go, that's, that's not me. You have the wrong picture, right? I didn't even know I had this answer because, because my diet is so clean, right? So normally, if you have an ulcer and you eat like spicy food, or you drink a lot alcohol, those are things that are going to let you know you have an ulcer and you're going to have burning from here all the way up, right? I didn't have any of that, so I was like, wow, I have an ulcer. So they had to test it for eight pyroid bacteria. I didn't have that. I had to go on Prilosec for a little bit. But I still have it. And here's how I know I have it.
Unknown 11:15
Every once in a while,
Speaker 1 11:18
I like to have a Diet Coke, okay? And when I get that Diet Coke, I like chugging, and it's like, all right, there's an ulcer, right? Like, it's like instant fire in my chest, right? So that's the only, that's the only time I remember I have an ulcer. Well, it's the only time, once in a while, very infrequently, I will wake up in the middle of the night and I and I mean so much pain. I mean, like I can't breathe, pain. So I go to the refrigerator and I keep a bottle of that liquid shock my lanta, right Bay locks that you ever drink that stuff. I just take it and I chug it, right? It's disgusting, but it instantly suits it instantly, like coats your and it just soothes your esophagus and your stock, and the pain goes away immediately. So this happens, Mr. Bateman, be careful with the 1000 milligrams, right? Because that that's what mine were, 1000 milligrams. One shot, 1000 milligrams. I took it like four times a day, right? Which is the other reason why I had to have the colonoscopy, because you take too much of that stuff and you're not going to shit anymore. So now, how do we get around this from happening? So these drugs are really, really, really, really popular with people with arthritis, because when you have arthritis, that's 24/7, that's chronic, constant pain. So they have prescription meds that fall under the category of selective Cox two inhibitors. So a selective Cox two inhibitor is an NSAID that only blocks the Cox two enzyme. So the prostaglandins made by the Cox one enzyme, they're the ones that protect the platelets and the lining of the stomach, they will still get produced, right? So the ones that fall under these selective Cox twos are Celebrex, right? Mobix or Meloxicam, same thing, and Vioxx. Ever heard of these?
Unknown 13:33
That's because you don't have arthritis yet you will,
Speaker 1 13:40
ironically, is there any wood? It's not what this wood? I don't have any arthritis. I cannot believe I arthritis is genetic. I'm absolutely convinced of it. I don't have any arthritis. I don't know how. I don't know how, but praise the Lord. All right, so
Unknown 14:02
these are by prescription only.
Unknown 14:06
But here's the controversy around that
Speaker 1 14:11
they are well known to inhibit endothelial function. So what do we know? Well, maybe we don't know. I probably had mentioned it, but you're really going to know it next semester when we do cardiovascular the endothelial lining of an artery is where nitric oxide gets released, and nitric oxide is very potent vasodilator, right? So when you have an impaired endothelial function, it means nitric oxide is not going to get released, so you're not going to have dilation, and you're going to have more constriction. And when you have more constriction, you are at much higher risk of having a heart attack, right?
Unknown 14:57
So Vioxx,
Speaker 1 15:01
Vioxx was the drug of choice in the 90s. Right? The drug of choice in the 90s, early 2000s it was the most popular prescribed NSAID, selective Cox, two inhibitor for people with arthritis. And it worked and it worked, but there were almost 150,000 people that died from a cardiac related event because of the endothelial function being impaired.
Speaker 1 15:41
They they died of heart attacks. They died of strokes, right? Because it was all about constriction was happening. Blood clots were being formed. So Vioxx was recalled on September 30, 2004 I remember when this was happening, because they would have the FDA is the one that pulled it. They had news conferences on TV, and I remember it as clean as day. They had, like a panel of FDA people and a big room, oh, I swear to God, all senior citizens and like a microphone set up in the center, and just people in line to get up to the microphone to plead for them not to take Vioxx off the market, and how it was helping them so much with their arthritis, right? So they let people speak. But the end of the day, Vioxx got pulled so now you still have movix Meloxicam and Celebrex on the market. There's a warning on the bottles that this can happen, but the incident of it happening is very, very much less than it was with Vioxx. All right, so let's talk about NSAIDs and platelet aggregation. So we know that platelets are blood cells that help our blood to clot. That is a good thing, because when you're bleeding, you need to be able to form a clot to be able to stop bleeding, right? But some of these NSAIDs can affect the way the platelets work, and innate not able us to form clots. How many of you have ever had surgery of any kind? I don't care what the surgery is. So you were told, whether you remember it or not, to stop any and all supplements or medications about a week before, seven to 10 days before the surgery, right? Remember this? This is why I'm going to tell you why. Because if you were taking anything, and it's not just n sets, like there's some vitamins minerals that inhibit platelet, right, they won't be able to stop bleeding during the surgery, right? So they need you to have that all out of your system before you go in. So remember when we talked about, this is a great story, guys. So remember when we talked about analog steroids, and I told you that guys that take synthetic testosterone, it starts to mess with their natural production of testosterone, right? And what did I tell you? Happens to them? Gynecomastia, right? They start getting breast tissue. Okay? So do uh,
Unknown 18:47
my husband, that is not him.
Speaker 1 18:51
I just needed to find a picture of the driven inch too. I don't know who this is. Had to have. He went on. He did diner surgery with your
Unknown 19:04
early 2000s really early 2000s
Speaker 1 19:07
we pretty much just got married. Talk about in sickness and in health taking that valve. Good God. So he goes in for the surgery. He comes out with the drainage tubes, except his tubes. Inserted his tubes so he was cut like here. So his tubes actually inserted here, one on each side, the tube with the bowl at the end. Okay, so, and people get these drainage tubes for many, many different types of sort of like liposuction, you're going to come out with drainage tubes. If you have, like, a lumpectomy from breast cancer, you're going to come out with drainage tubes. Right? The drainage tubes, you want to make sure that they're draining right? So each day, these should fill up with fluid. So we had to check his tubes, like the next morning make sure they're filled up. So my
Unknown 20:06
husband's a big dude. He's a tough dude.
Speaker 1 20:15
Like he's useless when the dog shits on the carpet, like all the things, right?
Unknown 20:22
So the next morning,
Speaker 1 20:25
I knew he wasn't going to be able to do it, so we go in the bathroom, and I he's standing there, and I look down at the tubes, and they're empty.
Unknown 20:36
So I say to myself,
Speaker 1 20:39
so he's standing right, so the tub, the shower behind, and he's standing here, and I'm thinking to myself, Okay, I get him sit down, because when I tell him this, if he falls, so I go sit down
Unknown 20:53
on the edge of the tub for a second,
Speaker 1 20:56
because I immediately looked at the bulb, saw the Randy, and just kind of looked up a little bit, and I saw his chest,
Unknown 21:04
and his chest was gigantic,
Speaker 1 21:07
red, filled with blood. So I said, sit down. You have two giant hematomas that have formed, and they have to call they're probably gonna have to take you back into surgery. So I call. They go get them up to this hospital immediately. I'll meet you there. So we dig up. He goes, I'll call tell them you're coming in. We go to the hospital. They're waiting for us. They take them right back into surgery. The surgeon says to me, I need a surgeon. And he goes, we'll be in an hour.
Unknown 21:45
Three and a half hours later,
Unknown 21:48
he comes out. Surgeon just looks at me, I'm like,
Speaker 1 21:56
and this is because he never stops taking his NSAIDs prior to any surgery. He goes, I couldn't get the bleeding stopped. He goes, I would get it stopped on one side. I'd go to the other and start bleeding again. He goes, midway through, I had the lab come in to run in blood. I want to see a platelet count. He goes, he goes, finally, I used the free spray. He goes, I finally got it to stop bleed, right? You want to talk about a wimp. He's like, in a fetal position, like, right? But so my story here is, this is real, right? This really happens. So if you have to have surgery, listen to them. Stop taking any of your supplements, stop taking your NSAIDs. It does greatly decrease your platelet count, and you will not stop bleeding in the middle of surgery, but that was a nice thing to show you what life would look like if you came out of gyne. All right. So if you are taking NSAIDs, even if you're kind of like taking therapeutic dosages, because, you know, everybody's different, and some people are more sensitive if you start to see that, oh, you just ran into the desk. Oh, my God, now you have a giant bruise on your leg. That's not normal, right? So you might be experiencing this platelet aggregation from even a therapeutic dose of NSAIDs, right? So if you start to see bruising more readily, you should lower the dose, right or discontinuing for a little bit of time. But we don't see this on these Cox two inhibitors, rights and movinx. We don't really see any of that platelet aggregation happening, and they are known for less bleeding and fewer ulcers than any of the other NSAIDs. Okay, questions on anything so far. So how do you Well, you won't know. I'm going to tell you. How do these NSAIDs affect metabolism? So here we go. Nudge Sam. Sam, yes, yes. Hi. All right, so again, with therapeutic dosages, none of this should happen. I'm not going to say that it won't ever happen, but it should happen, right? But if you are taking toxic dosages, what are toxic dosages? Here you go. That that's not hard to do. Guys, I just told you I was taking 4000 milligrams a day, maybe more. So this is not hard to do, right, especially if you've got Jason, you say you take 1000 is that in one pill? You just two? Okay? So they come in, 400 500 800,000 milligrams have tablets, right? So this could be really easy to do, so with toxic dosages. Here's a bunch of stuff that could happen. There could be uncoupling of oxidative phosphorylation. What does that mean? It means that complex four and five of the electron transport chain are not really talking anymore, right? They become uncoupled, which means what happens in complex four. Anybody remember complex four is where two electrons get dropped off, they combine with oxygen, and they make two water molecules that sit there and wait because the eight complex five is that ATP synthase, where the protons enter, three protons enter, they combine with the water, right? We make ATP. Well, that's not happening anymore, right? That's not happening happening at these toxic dosages when the oxidative phosphorylation becomes uncoupled.
Unknown 25:45
Okay? So
Unknown 25:48
if that happens, you're not
Speaker 1 25:52
using electron transport, things are going to get backed up, right? Things are going to get backed up. You're going to have lower endurance performance, lower vo two. And then this starts to happen. So now remember, if we move backwards, you've got electron transport chain, you've got citric acid cycle. So the two key rate limiting enzymes of the citric acid cycle get inhibited, isocitrate dehydrogenase and alpha ketoglutarate dehydrogenase, so now they're inhibited, which means the citric acid cycle is slowed down and the electron transport chain is slowed down, right? So now we're going to see interference with all areas of metabolism. So let's see. Let's tell the story together. So oxidative phosphorylation is citric acid cycle and electron transport chain, and that is now not really working for us. So what's your body going to switch to to try and make ATP from? Where do we make the lactic acid? What pathway anaerobic glycolysis, your body is immediately going to switch to anaerobic glycolysis, right? But you're going to start making a bunch of lactate, right? Because the pyruvate, it can get converted to acetyl CoA. But can the acetyl CoA get into the central gap? No, no. So it's gonna be lactate. It's gonna be lactate. So now we're becoming more acidic, right? Your body's gonna start trying to make more glucose. You're gonna have glycogenolysis increasing. You're gonna try to break down all your storage glycogen, but it's all gonna go to lactate, and eventually that's gonna be depleted. So now we can't even use glycolysis. So now what's going to happen? Your body's going to switch to fats. It's going to start trying to make ATP from fats. So what's going to increase? Well, okay, yeah, but lipolysis is going to increase, right? Lipogenesis is going to go down. Lipolysis is going to increase. We're going to start breaking down all these stored triglycerides. We've got all these pre fatty acids. They're getting into the mitochondria. They're going through beta oxidation. They're becoming acetyl CoA. And the acetyl CoA gets this exact and what can't do it. So then what happens? They go to become ketones, right? So now we're making more ketones, so now we've got even more acid, right? So this is you guys told me in the next two slides, that's exactly what happens. The first thing that happens is your body's going to switch to anaerobic glycolysis, right? It's going to start breaking down stored glycogen using free glucose, but it's all going to turn to lactic acid. Okay, because the pyruvate can become Acetyl Co acetyl CoA can get so then the body tries to switch to fats. So you're going to have decreased lipogenesis. We're not going to form triglycerides, because we're going to just be breaking them down like crazy. Lipolysis is going to increase. We're going to make acetyl CoA through beta oxidation, but that acetyl CoA can't get into the citric acid cycle, so we're going to start having more ketones made, and that's going to lead to ketoacidosis, until you come off the NSAIDs right. Come off the NSA, then your body will go back, right? But there's a big metabolic crisis happening. If you, if you take these therapies, toxic dosages at me, look, you take toxic doses for a day, a couple days, you're probably good, but if you take it all the time, there's a good chance that this is going to start happening. And how do you know this is happening? Well, if your performance starts to go down, if you're winding, if you start, if you get here, you're going to start becoming a little bit symptomatic. Remember, keto, ketoacidosis symptoms. You kind of feel like you have the flu. You might smell a little fruity, right? All those things. How about protein metabolism? So you're going to probably have.
Regards, Devon Johnson