Dr. Dean: Best Steroid Doses & Compounds, GH, & Living Long

Speaker 1 Dr. Dean St.
Martin, renowned for his knowledge of bodybuilding pharmacology, PhD in synthetic chemistry, and product formulator for supplement needs.

Speaker 1 He is a renowned pharmacologist for his no-nonsense approach and open-ended transparency in bodybuilding and the dangers associated.

Speaker 2 Every step you take is either going to lead you towards ease or towards dis-ease. You could make it where an ante fits better over cipinate.

Speaker 2 Those genetic changes could dictate whether you're a good responder to a certain ester drug, regardless. The fast or slow metabolizer recovered comes from liver genetics, the CYPs.

Speaker 2 Guys in the 90s were basically, well, if he's taking four vials of parabolin, I'm going to do five.

Speaker 1 What's the craziest thing you've heard in terms of abuse?

Speaker 2 10 plus grams of testosterone. For one thing, you sort of applaud, well, where did you find space to eject that volume? But on the other side, you have a spillover.

Speaker 2 Like when you're trying to carve up or a show, you've got a sweet spot where you're going to have glycogen build within your muscle tissue without the excess water retention.

Speaker 2 Where the spillover then is interacting with aromatase, interacting with 5-alphreductase, oxidative stress.

Speaker 2 I hate using the phrase cosmetic compound, but it almost changes how fluid is distributed into your skin cells.

Speaker 2 When you're very low body fat, when you add it in, how your skin changes a rougher texture to your skin, but it's the fact that the skin is actually not as hydrated as it normally would be.

Speaker 2 And you sort of then see very dry striations, especially around the chest, the shoulders.

Speaker 2 What happens with orals is they could potentially interfere with how bile is made within the liver and then obviously bile is stored in the gallbladder and a lot of the digestive upsets with orals how we sort of try and offset that then is by improving bile viscosity so totke or udke and then maybe using if you're on a certain dose for a longer period of time and now it's not yielding a benefit sometimes it can be lifestyle that's impacting how you gain muscle mass where you're not sleeping properly bile flow acid health digestion slows down indirectly it can come from the drugs themselves Where taking a break naturally resolves some of that roadlock now, all of a sudden,

Speaker 1 how you doing, brother? You look fucking badass with that on you.

Speaker 2 Well, I'd say nine days ago, I wasn't in the same condition as I am now. And then a week before that, I guess

Speaker 2 we're lucky with what we have with medicine to be able to get something fixed so quickly.

Speaker 1 Yeah.

Speaker 2 But I knew

Speaker 2 as soon as I got punched in the face, I knew my nose was broke. It was like, it wasn't even one of those ones where you ask someone, oh, is my nose broke?

Speaker 2 You just felt my nose was over here.

Speaker 2 Fuck.

Speaker 1 Yeah, that's rough.

Speaker 2 And I mean,

Speaker 2 I was lucky in that whatever way it broke, all the blood started going down the back of my throat rather than all over the mats. And so that was a lot easier to manage trying to get the hospital over.

Speaker 2 Not trying to stop blood pissing out of my face.

Speaker 2 Oh, God.

Speaker 2 That's fucking hardcore.

Speaker 2 There was a doctor at the event. So yeah, for people who didn't know, I decided to return to martial arts after 11 years with my brother.

Speaker 1 And we win a fucking championship.

Speaker 2 I went to the WKA World Championship. So my brother's a very successful kickboxer.

Speaker 2 We introduced him at a very early age. Like my growing up, I done karate, and then I sort of left martial arts.

Speaker 2 And then my brother convinced me when we put him into kickboxing at 10 to go back to kickboxing as a martial art.

Speaker 2 I'd done it on and off, and then sort of left in,

Speaker 2 I can't even remember now the year. I think it must have been

Speaker 2 2012, 2011 to do bodybuilding. I had smashed my ankle training prior to that.
That was the whole thing that got me into bodybuilding was kickboxing.

Speaker 2 And so

Speaker 2 with no sort of plans now, finishing competing, you know, still training. My brother was sort of at me of, you should come back to kickboxing.

Speaker 2 And like in your head, you're thinking, well, I've got no goal. When you've got no physique goal to speak, you're like, well, what challenge can I put on myself to train for? So

Speaker 2 why not go back to martial arts where it all began?

Speaker 1 So, right, that's badass, dude.

Speaker 2 Yeah, I mean, it was fun up until like there's 20 minutes left in the 20 seconds left in the final, I should say.

Speaker 3 And

Speaker 2 I dodged the kick, went into counter with a punch to the guy's stomach.

Speaker 2 And I just felt this fist come across my face and counter from my punch to his stomach. And

Speaker 2 yeah, we knew straight away. Like, I just looked at the ref.
The ref ended up calling the match and disqualifying the other guy because it wasn't full contact.

Speaker 2 Like, had I have gone into full contact and got my nose broke, I could have said, oh, well, it's on me for that happening. But

Speaker 2 it was just annoying because that just then put me into A and E and the hospital, and then having to figure out DNT.

Speaker 2 One of the biggest risks when you break your nose is if your septum in the middle gets a hematoma, you're at big risk of like your septum dying basically. So,

Speaker 2 your septum is made of cartilage, and there's not very good blood flow to it. So, if it fills with if it fills with a hematoma, it can starve itself of nutrient delivery.

Speaker 2 so

Speaker 2 i i sort of knew this from years ago but when you're in the sort of moment of it you're not really thinking about it and the event doctor said to my brother when we were getting ready to leave the event to go to a and e

Speaker 2 um he was like to my brother don't tell him but there's a risk here that he needs to be seeing asap through a ct scan to make sure he doesn't have a septum hematoma or how badly it was sort of broken across

Speaker 2 And afterwards, when the CT scan came back clear, my brother said to me, you know, all afternoon after the doctor said it to me, that was like the biggest risk in my head.

Speaker 2 That I'm thinking, God, if he only knows what he's potentially at risk of without even realising.

Speaker 2 But it's like, it's one of those things that I've gotten injured in the past, I've gotten hurt.

Speaker 2 You just have to accept the situation for where it is and just pray that you're going to get seen to quite quickly an accident, an emergency.

Speaker 3 And,

Speaker 2 you know, hats off in Sheffield, where we're in the UK.

Speaker 2 What was funny was we turned up to the doctor at the event said to us, there's a local hospital that has

Speaker 2 a minor injuries unit. If there's any hospital you want to get injured, it's to go to that one, Hallamshire Royal Hospital.

Speaker 2 We turned up, it was like it took a 15-minute Uber to get to this hospital. We walk in at 6 p.m.

Speaker 2 And the receptionist says, oh, this minor injuries clinic closes at 8 p.m. And we were like, so what happens if it gets to 8 p.m.? Oh, we just closed and you're sent home.

Speaker 2 I'm like, looking at him, going, what? And she's like, yeah, x-ray everywhere here closes 8 p.m.

Speaker 2 We won't be able to do anything until tomorrow. I said, well, is there another accident and emergency? And she said, oh, yeah, Sheffield, like Northern General Hospital is another 15-minute Uber.

Speaker 2 That has an A and E that's open 24 hours. So hopped in another Uber.
So like, we're wasting time here trying to get to

Speaker 2 get to hospital. So yeah, thankfully when we got to the hospital within two hours they had the CT scan done.

Speaker 2 They were fairly confident that the CT was clear.

Speaker 2 But they, because we flew over, I didn't even know if I could fly back in a plane that maybe I'd have to stay in the UK to have the sort of surgery with the NHS.

Speaker 2 NHS consultant came after staying in hospital overnight on the Friday and he he basically came to me Saturday morning and he said,

Speaker 2 you know, normally if that had occurred and I was present as a consultant and I had a good confidence level that was just like a break, a community break across,

Speaker 2 you could quickly push it back in place. But he said, if it's not done immediately, then you have to wait four or five days for the inflammation to settle to go in and break it back into place.

Speaker 2 So,

Speaker 2 yeah, I mean, I had on my social media, like I said, some of these injuries are going to happen to us in life.

Speaker 2 I ended up in an ENT ward that evening after I was waiting to see that consultant to be allowed to fly home. And

Speaker 2 I was in a ward with three other guys. And obviously, by the time they admitted me into the hospital, it was like half 12 at night after midnight.
The three guys in the room are asleep.

Speaker 2 And so the next morning, I got talking to one of the gentlemen. He was in his 80s.
And like, he then turns around to me and says, We're all in here waiting on cancer treatment.

Speaker 2 And that, you know,

Speaker 2 puts things into perspective that your nose break isn't the biggest problem in the room. That there's three guys there who are receiving, you know, quite serious treatment and care.

Speaker 2 That it really then makes you,

Speaker 2 you know, it was very somber. I got talking to this guy.
He was telling me I traveled to Northern Ireland. He knew, you know, where we live and everything.

Speaker 2 And then at

Speaker 2 3 p.m. on saturday afternoon by the time they ran blood to check that i'd lost a lot of blood so they wanted to make sure that i was okay to be discharged

Speaker 2 by the time the blood results came back and i was allowed to leave the hospital it you know reflecting on saying goodbye to these guys miss ward who are you know undergoing like

Speaker 2 throat cancer you know therapies that you really then put things into perspective how grateful you are that although you've had like a

Speaker 2 you know shit accident you know know in the in the in the bigger universe and the scheme of things that your your problem is probably relatively small to someone else's so that you know that's been that's been a good lesson to to help reframe and remind you that whilst things happen to you a lot of worse things happen to other people

Speaker 1 yeah

Speaker 1 yeah the reframing is extremely important something that i appreciate whenever i um my family and i travel to the philippines about every other year when i was a child because that's not really a perspective that most kids get to get, I guess.

Speaker 2 So

Speaker 2 I'm sure that's it's always nice to like travel back home.

Speaker 2 Like obviously my father's from Mauritius, so we've traveled to Mauritius a couple of times and you know that again reframes how different sort of the Western world is versus what happens in other other cultures and countries that

Speaker 2 we we traveled there two years ago in 2023, and the last time I was there prior to that was like 2005.

Speaker 2 And so, the difference in those 18 years of what sort of happened culturally

Speaker 2 shows that obviously that sort of developing side of the world is catching up very quickly. But it again, it reframes everything, the comforts that we have at home versus what

Speaker 2 other countries may not have as quickly developed as us.

Speaker 1 Yeah, right.

Speaker 2 Combat sports have some level of need to satisfy aggression.

Speaker 2 I guess that's sort of where when I moved from kickboxing into bodybuilding, the aggression was against a piece of equipment in the gym rather than

Speaker 2 someone on the mats with you. And, you know, that's,

Speaker 2 you know,

Speaker 2 but there has to be like with weightlifting and bodybuilding, there's a place for controlled aggression and then there's a place for where you where you leave it behind.

Speaker 2 And that's what I loved with the beauty of bodybuilding was was you could go in the gym and you could effectively

Speaker 2 take out frustrations on a piece of equipment based on what your logbook is saying. You have to beat.

Speaker 2 But it's important that what's said and done in the gym is left behind, that you don't carry that aggressive behavior out of the gym environment.

Speaker 1 Right. Yeah.
I bet it's super interesting now, too, though,

Speaker 1 that

Speaker 1 you've been delving into this space for, what is it called, the enhanced games. Yeah.
Has there been any like evolution in that since the last time we spoke?

Speaker 2 Not really. I've stepped away a little bit from it

Speaker 2 in terms of like my advisory position. I've had too much going on.

Speaker 2 Dr. Imran Khan and Dr.
Gehramer Escalante are still involved.

Speaker 2 To my knowledge,

Speaker 2 from the inside out, there is still a lot of discussion going on surrounding,

Speaker 2 I guess, what is a fair protocol to use.

Speaker 2 And, like we highlighted in the last conversation, I find it just very difficult to frame

Speaker 2 the word safety because, to be honest, if you're putting like safe protocols in place, we know bodybuilding, none of this is safe. And it'd be silly to try and portray it as safe.

Speaker 2 Like, we're looking at it at a responsible level. We're competing in a responsible fashion.

Speaker 2 With that in mind, you know,

Speaker 2 would someone's risk threshold be lower than another's? Yeah, of course. But, you know, I think one of the main arguments I brought up last year in Oxford was

Speaker 2 how do you define

Speaker 2 one man's success? It could be poisonous, but are they going to care?

Speaker 2 You know, if we're setting world records that have never been achieved by athletes, like the whole, you know, if you won a gold medal at the Olympics and you died in five years, would you take the medal?

Speaker 2 You know, a lot of this is setting history whilst it's tainted a little bit. And I don't really agree with it.

Speaker 2 When you look at when they done the public event or like the launch of the games in Las Vegas back in the summer, and they done the, you know, the sprint record for swimming,

Speaker 2 even trying to like

Speaker 2 sift through what a lot of mainstream media were doing. Even in Ireland, it was under radio where it was sort of being tainted.
That, oh, yeah, but that was with drug use.

Speaker 2 It's you know, it's like that stigma of how we approach like hormone optimization and discussions like that. That

Speaker 2 I'm not sure why the angle is there. Maybe it's from a level of people going out and doing silly things based on what they see.
And again,

Speaker 2 that was another fair criticism I brought up of

Speaker 2 one of the ethics of the enhanced games is whatever they

Speaker 2 whatever they do with the athletes will be publicly made available so in terms of the protocols they run one of the things that was hinged on was transparency of of information so if whatever swimmer takes whatever protocol and achieves a world record this is what they've done there's transparency rather than trying to mask it behind coaching practices and training which which isn't to take away from that being a a positive driver of someone's success.

Speaker 1 Still an important facet, but

Speaker 1 like I mean,

Speaker 1 people would just avoid talking about it altogether.

Speaker 2 Yeah. And so one of the things with the enhanced games was to be like critically transparent in, I guess, one of their end goals is like human evolution.

Speaker 2 I don't think we sort of touched on that in the last conversation, but it's like transhumanism of how we, how we evolve. the species really is you know one of their overarching goals

Speaker 3 um

Speaker 2 and even when you look at at enhanced games, I was part of a discussion panel in Oxford when we were having this sort of conference with all the experts. And

Speaker 2 enhancement can mean external enhancements versus like internal what you put in your body, like drugs or peptides or whatever. Like external enhancements can be like bionics.

Speaker 2 So,

Speaker 2 you know, and we're heading into a slippery slope here of like one of the things that was in their charter was you couldn't, like,

Speaker 2 you, you couldn't create any form of,

Speaker 2 I guess you could say, like, humiliation of your body, where you could not go in and, like, chop your leg off to get a robotic leg for the aspect of performance enhancements.

Speaker 2 That's like viewed morally and ethically wrong.

Speaker 2 But, you know, if we're releasing data where someone has an exoskeleton or whatever, you know, slowly over time, people are crazy. They'll do crazy things.

Speaker 2 You have to be very careful on what you're promoting with

Speaker 2 that transparency of information. So

Speaker 2 I've sort of stepped away. Dr.
Dan Turner is obviously the lead when it comes to

Speaker 2 the Athlete Safety Committee. He might be someone very interesting to get on the podcast.

Speaker 1 Okay.

Speaker 1 What did you say his name was again?

Speaker 2 Dan Turner. Dr.
Dan Turner.

Speaker 1 Dr. Dan Turner.
Okay. Gotcha.

Speaker 2 He'd be obviously the lead on

Speaker 2 strategy for athlete safety. So

Speaker 2 he'd be someone very interesting. I've had good conversations with him prior to Oxford and in Oxford

Speaker 2 on where they're sort of standing now. Because obviously we're heading into now nearly the start of 2026.

Speaker 2 Like before we know it, I think May or June is when you have the first set of games planned for in Las Vegas. It's not going to be long coming around.

Speaker 2 Wow.

Speaker 1 Wild. That's going to be insane.

Speaker 2 Hmm.

Speaker 1 The bionics thing is extremely interesting because that's something that I've always.

Speaker 1 I remember when I was watching Teen Titans as a teenager, and I'm like, honestly, I want to get in bionics.

Speaker 1 And literally, the reason I'm in California is because I was going to do my master's in biomechanical engineering at UCSD.

Speaker 1 Instead, I just decided to put the substances in myself, try to make myself a taste.

Speaker 1 I mean, that would be insane. Just

Speaker 1 to,

Speaker 1 I don't know, I can't even facet the thought of like, how would you,

Speaker 1 how would you standardize that, you know?

Speaker 2 Yeah, I mean, how, how I brought it up, like, well, it wasn't actually me that brought up the discussion. It was, I forget his name now.

Speaker 2 I'm very bad with remembering names, but he was, he was one of the heads of WALA for doping control, for blood doping,

Speaker 2 an Australian guy. Apologies, I can't remember your name, but we had a we were on this expert panel together.

Speaker 2 And he brought up the aspects of, you know, breaking world records, wearing external enhancements. And I never even thought about it, but like running shoes is an external enhancement.

Speaker 2 Like when you look at runners and the science that goes into runners, it's incredible. You know, naively, I wasn't even thinking of this.

Speaker 2 He was on about, you know, like running suits, runners, goggles, et cetera.

Speaker 2 And then it sort of slowly led into, you know, transhumanism of like I brought up the aspect of like archery with we already have you know neuralink and and other technologies coming out that eventually have like an artificial AI retina where like your eye is replaced where like you know if you're doing archery or shooting it's telling you you know move your hand two degrees left and now fire.

Speaker 2 Does that, you know, take away the element of like marksmanship then, where you have to actually train, a hand-eye coordination to shoot a gun, and you've got a piece of tech sitting inside your eyeball that's telling you how to shoot perfectly?

Speaker 2 You know, that

Speaker 2 we're sort of laughing. I think this is all science fiction.
And probably, you know, back in like the 70s and 80s, it would have been

Speaker 2 that sort of very Terminator-esque.

Speaker 1 It's totally possible.

Speaker 2 The way things are progressing with AI in terms of how AI is thinking and returning information.

Speaker 2 You know, that's something that I've watched closely in terms of like what is AI capable of doing when you try and set the limits? If you sort of, if you let it run unhinged, even medically,

Speaker 2 what will it,

Speaker 2 I guess, return back as a source of information? I guess it's when you use like some of the thinking models within OpenAI and ChatGPT,

Speaker 2 it's very

Speaker 2 responsible in how it returns information.

Speaker 2 And I think that might have been a new update, to be honest, in terms of how it thinks now that prior with ChatGPT,

Speaker 2 you could coax some things out of it

Speaker 2 hypothetically. And now it will only hinge off strict guidelines and will cite the strict guideline references,

Speaker 2 which is a good thing, because then it means that there's some level of accountability to the information it's gathering.

Speaker 2 But then it sort of questions you, well,

Speaker 2 something like that in terms of gatekeeping and an honest discussion, it's being biased a little bit.

Speaker 2 But on the other side, having clear established rules, you know, overcomes hopefully some of the safety concerns.

Speaker 2 Because obviously, when you look at some of the inventors of the technology speaking on podcasts,

Speaker 2 security and how this is capable of evolving is quite scary when you think about it.

Speaker 1 Yeah, scary and freaking epic.

Speaker 2 Yeah, yeah.

Speaker 2 On two sides, 100%.

Speaker 2 It's just, it's almost like that Terminator-esque sight of you don't want to get to the point where the machines think they can take over. Yeah.

Speaker 1 Speaking of standardizing, though, all of this, including the enhanced games, I love that last time, especially in the first podcast, we discussed slow versus fast metabolizers and respective steroid doses,

Speaker 1 which was widely loved by the audience and myself too, because I think it's something that hasn't been stated very often or at least

Speaker 1 expounded on in the past, because there's just this like very easy,

Speaker 1 this common perception that if you take more doses or if you take higher doses, then you're going to have a one-up on your competition.

Speaker 1 But we each have our own, I'd say, potential sweet spot, depending on what the drawbacks are. And obviously these drawbacks are in variance depending on what our genetics are as well.

Speaker 1 So it's, it's, it's definitely like a game of like shooting a dart in the dark, unless maybe you get your genetics tested or whatever.

Speaker 1 But I mean, getting the data, I think getting the data that we've been doing personally, which all of us have been doing as bodybuilders or even coaches, you could say, have been doing with their clients is probably the most important part.

Speaker 1 But I also appreciate that we talked about oxidative stress being a primary driver of a lot of these diseases.

Speaker 1 And that's why real bodybuilding, like eating healthy, sleep, rest, cardio, et cetera, is a whole lifestyle that includes healthy habits done consistently that most people don't do consistently.

Speaker 1 And now finally, the industry is openly talking and discussing supplementation, longevity interventions, and blood work and a bunch of scans and everything that's important.

Speaker 1 So, I think we're definitely evolving,

Speaker 1 especially with bodybuilding, which I think is a beautiful thing because, you know, back then in the 90s, you'll hear stories of the guys just taking all the stacks that they got from their coaches, never getting their blood work done ever, ever, bro.

Speaker 1 And it's just, it blows my mind that, like, even some of these guys are still alive today, but obviously not in the greatest condition.

Speaker 1 So, imagine that we're doing all of these inventions, all of these oxidative stress interventions.

Speaker 1 I just feel like, I don't know, man, I feel like unless we're really, unless we're,

Speaker 1 unless we're dealt with some pretty shitty genetics, we should be okay.

Speaker 2 Yeah, I mean,

Speaker 2 it's definitely turning into a more

Speaker 2 open discussion of risk tolerance. But now, that risk tolerance isn't like any, mini, miny, mo of let's just keep opening the dose until side effects, whether they're physical, mental,

Speaker 2 I guess, biological towards digestion, etc.

Speaker 2 We're now at a place where we can probably use genetics, so we can use some level of pharmacogenetic genomics, which is basically using your genetics to understand how pharmacology interacts in your body.

Speaker 2 And like we then have to view pharmacology as two branches. We've got pharmacokinetics of how the drug basically moves through the body between administration all the way to elimination.
right

Speaker 2 but on the other side you've got pharmacodynamics which is basically how does the drug interact in your body you know at a receptor level how does it how does it bind how how does it create changes in your your genome or cellularly and so the first one's like how your body interacts with how your body changes or interacts with the drug and then the second one's like how the drug interacts and changes with your body right correct so like when you sort of look at let's take injectable testosterone, because an injectable testosterone versus an oral steroid will have two different pharmacokinetics.

Speaker 2 So, when you inject something, you are bypassing the sort of gut-first pass of having to absorb something, you know, from the stomach into the intestine and from the intestine to the liver, and then from the liver out into systemic circulation.

Speaker 2 With an injectable, you're you're sort of

Speaker 2 you've got

Speaker 2 ADMAI, which is like the

Speaker 2 acronym for pharmacokinetics, and that's administration, distribution, metabolism, and excretion.

Speaker 2 And what some people actually then say between, you know, administration, you've got absorption occurring afterwards.

Speaker 2 So really, it's like administration, liberation, distribution, metabolism, excretion.

Speaker 2 You administer the drug, it's liberated, it's distributed through your tissues, you know, throughout all your body.

Speaker 2 It's then metabolized by the liver for either secondary metabolic effects or for excretion, making it more easier for your body to get rid of in your uri in your feces.

Speaker 2 Genetically, for something like an injectable testosterone, you've got the ester attached. So now you've got maybe genetics in terms of how do you cleave that ester away.

Speaker 2 So, one of the main esters or esterases, the enzymes that take the ester away, is PDE7B, phosphodesterase 7B.

Speaker 2 Dr. Scott Stevenson has done some lovely podcasts on this if people sort of search for it with TinkBig.
But with PD7B,

Speaker 2 we have to view enzymes have a 3D shape in terms of how our body makes them. We have the genetics, which is the recipe, and we have the translation of the recipe into the protein.

Speaker 2 With PD7B, this is sort of what my contextualization of of it is: why some people respond better to enantate versus cipionate.

Speaker 2 This whole age-old argument of, you know, what testosterone ester is better between cipionate and enantate.

Speaker 2 Cipionate has a five-membered ring, it's big and bulky. Enantate has a long carbon chain and it can rotate in space and it's very flexible.

Speaker 2 If you've got an enzyme, PD7B, which is going to cleave that ester away to leave you with the parent testosterone, so when you inject testosterone and enantate, you're taking it for the parent testosterone and then the ester is just cleaved off and metabolized.

Speaker 2 PD7B, because it's got that 3D confirmation, you could make it in a certain shape where enantate fits better over cipinate.

Speaker 2 And now you've got either faster ester clearance, so the ester is being cleaved off quicker.

Speaker 2 and you're sending the drug into circulation, the testosterone from the depot into circulation, or it's slower and it's causing post-injection pain, where the ester is sitting in that depot of the skin.

Speaker 2 With that in mind, those genetic changes could dictate whether you're a good responder to a certain ester, you know, drug regardless.

Speaker 2 So then you've got, obviously, the parent compound is cleaved after the ester. So the ester is one element of pharmacokinetics.

Speaker 2 The injection depot has some level of pharmacokinetics as well, of where you inject the ester.

Speaker 1 So, whether it's the delt, the glute, delta, the glute, right?

Speaker 2 You know, we're going to have different distribution speeds, and that's based on like the fat content and how to

Speaker 2 basically when you inject an oily depot, it spreads out along the fibers, or in theory, that's what should happen. It should spread out along the fibers.

Speaker 2 If it's sort of localized and just sits as a big bolus, then the drug delivery might actually be a little bit slower than spreading out over a larger surface area when you create that injection depot.

Speaker 1 I thought I saw some graphs stating that

Speaker 1 doing injections in the glute seem to be more optimal in terms of like absorption, like overall absorption. And

Speaker 2 there is a good study that looked at, I believe it was with Nandrolone, I think. Now you're putting me on the spot.

Speaker 2 And it looked at the absorption, well, the serum plasma level that was achieved or the area under the curve

Speaker 2 with different injection sites.

Speaker 2 It was either an angelone or testosterone.

Speaker 2 I'll look up the study. I can send a link to you afterwards.
But yeah, there was clear, distinct changes in how the drug was distributed into the body based on where it was injected.

Speaker 2 Now, bear in mind, I think,

Speaker 2 again, from

Speaker 2 off the top of my head, knowledge-wise, whilst there was differences between, say, the delt and the glute,

Speaker 2 statistically, it was quite small in terms of the change. That,

Speaker 2 yeah, one is more optimal than the other. But in the bigger scheme of things, compliance is the bigger thing that drives how a drug is administered to someone.

Speaker 2 Whether it's easier for it to put a needle in the glutes or to put a needle in the delt, whenever there's sort of

Speaker 2 flexibility allows, some people might prefer to do a delt IM shot over a glute shot, but then we have to bear in mind that there's probably a lot more fat tissue within the glute than the delts.

Speaker 2 So, again, the absorption speed from the delt

Speaker 2 is normally viewed faster than the glute because of the depot that's formed in the glute.

Speaker 2 Again, I'll send a paper on this. It's been a while since I read that paper.

Speaker 2 But, you know, that of itself adds a layer of adding on to your genetics and of how quickly the drug is released for it to interact with esterases as well.

Speaker 2 So,

Speaker 2 you know, as soon as that parent drug is released into the bloodstream, you're now looking at it's being distributed through the body.

Speaker 2 So, you've got like your volume of distribution, how the drug is being put out into circulation, whether that's on carrier proteins like albumin or sex hormone, binoglobulin, or as free testosterone.

Speaker 2 We have to view, obviously, SHBG is linked to genetics to an extent, and your liver health.

Speaker 2 Albumin is linked to your liver and kidney health. They're going to interfere with your free testosterone depending on how much is being made.
So, again, that's a layer of genetics.

Speaker 2 And then you've got, obviously, the free

Speaker 2 hormone testosterone either permeating into cells to interact with an androgen receptor, interact with aromatase, interact with 5-alpha reductase, or interact with a CYP metabolic enzyme that breaks it down, or a hydroxylase, or whatever sort of

Speaker 2 sulfation or glucronidation, or whatever

Speaker 2 enzyme it interferes with, or interacts with, I should say,

Speaker 2 you're going to see a change that drug distribution as well in terms of what you expect to get from X amount of dose of testosterone to what's actually yielded in serum.

Speaker 2 So,

Speaker 2 I guess if you know your genetics and you've delved into your CYP enzymes,

Speaker 2 how well or how heavy do you express CYP19A, which is aromatase?

Speaker 2 How much CYP3A4 you make, which is one of the main oxidation enzymes that breaks down testosterone,

Speaker 2 your distribution of 5-alpha-reductase versus

Speaker 2 5-beta-reductase, the other converting enzyme,

Speaker 2 you could probably, you know, assess based on like your natural blood work, how well you're going to respond with a standard dose, like let's say 250 milligrams that's been studied in the literature or 600 or whatever.

Speaker 2 You then have a bigger base to play off where it's not like, let's just put X dose in and see what happens with estrogen. What side effects happen? Does blood pressure go up?

Speaker 2 Having your genetics to begin with, you know, you'll know instantly, do I have ACE2

Speaker 2 overexpression? Am I going to have to use an A or B prophylactically before I even have to measure my blood pressure? You know, do I have that risk to consider?

Speaker 2 Do you have to look at overexpression of aromatase? So, you're planning strategies to mitigate estrogen going up.

Speaker 2 5-alphreductase, androgenic alopecia,

Speaker 2 you know, before you even decide to go down this path,

Speaker 2 genetics, I believe, or pharmacogenetics or genomics

Speaker 2 gives you almost like you know the cheat codes of how well is this going to go for you based on how your body's responded naturally.

Speaker 1 And that's why people should get their data and put it into Prometheus and genetic genie like us.

Speaker 2 You know, put it put into that. And then you've got like, you've got

Speaker 2 AI-driven softwares, you know, Joe Cohen. I've spoken to him a couple of times at like BioHacking Events.
He owns Self-Decodes.

Speaker 2 They have an in-depth platform where their

Speaker 2 algorithm does a lot of in-depth analysis of SNPs that are constantly being published. So it's like a subscription service.
That

Speaker 2 instantly, you know, gives you, like you said,

Speaker 2 on one side, how well is this going to go from a physique enhancement perspective? What can I sort of expect to happen in my body with this drug interacting?

Speaker 2 But on the other side, it lets you sort of see, well, let's say you have genetics towards higher Apo B

Speaker 2 or you have

Speaker 2 genetic underexpression of GST or GGT or SOD. These are all enzymes that make, you know, glutathione, superoxide dismutase, you know, your main antioxidant generating enzymes in your body.

Speaker 2 That if you have an underexpression or these things don't operate as well as they should in your body, that instantly tells you again that your whole strategy of bodybuilding has to be anchored on like reducing oxidative stress or strategies that are going to support your body first and foremost, but then offset the oxidative stress that maybe lifestyle is going to induce, let alone the drugs.

Speaker 2 It's, you know, it's, it's, I think,

Speaker 2 versus when I first started bodybuilding back in like 2007, 2008 in college, I'm, I'm reading, you know, I've made jokes on a post before of like reading men's health magazines and you know, you're sort of naive to what goes on with some of the things.

Speaker 2 We're now in

Speaker 2 an era, I guess, of like there is this open transparency of what people are doing. There's accessibility to the information, there's accessibility to private testing.

Speaker 2 You know,

Speaker 2 it's hard to say that

Speaker 2 it shouldn't be difficult to do performance enhancement like in a relatively risk reduction fashion, given everything that's available to someone.

Speaker 2 You know, you're not trying to have to learn from experience, like you said, where guys in the 90s were basically,

Speaker 2 well, if he's taking, you know, four vials of parabola and I'm going to do five. You know, there's,

Speaker 2 and I guess what we're lucky is a lot of these guys who competed back then are slowly opening a little bit towards what practices were done back in the 90s versus what's going on today.

Speaker 2 And, you know, I've spoken to a good few, and, you know, in terms of like what people perceive or dosages back then versus what I've seen done in the last 10 years,

Speaker 2 you know,

Speaker 2 it's black and white that their level of abuse is quite different to what abuse has evolved in the last 12, 15 years beyond the 90s.

Speaker 1 What's the craziest thing you've heard

Speaker 1 in terms of abuse?

Speaker 2 Like

Speaker 2 10 plus grams of testosterone.

Speaker 1 So that's where I came from.

Speaker 2 Which I feel like we knew that. You know, I

Speaker 2 for one thing,

Speaker 2 you sort of applaud, well, where did you find space to inject that volume? But on the other side,

Speaker 2 like you said, there's a sweet spot. In my view,

Speaker 2 you have like a spillover.

Speaker 2 Like when you're trying, like when you're trying to carb up for a show, you've got a sweet spot where you're going to have glycogen filled within your muscle tissue without the excess water retention or the spillover.

Speaker 2 And you're trying to, like, there is no perfect calculation. Anyone asks you, well, what should I eat to carb up for a show?

Speaker 2 Over time, you'll get to know roughly based on your body weight, well, how much glycogen can I hold, you know, from being flat to full, or based on visual look, X amount of carbohydrates gives me this body weight and this visual look with fluid and electrolytes.

Speaker 2 You're sort of trying to take that science and then apply it to, you know, a certain way of

Speaker 2 how am I going to create the most optimal set point without causing a spillover?

Speaker 2 Where the spillover then is interactomate aromatase, interactomate 5-alphreductase, oxidative stress, or, you know, quite frankly,

Speaker 2 just metabolizing the drug and excreting it unused, where like your body then just has no use for it and it'll just excrete it out.

Speaker 1 When you're saying glycogen from increasing,

Speaker 1 have you seen where guys are taking too much gear and then they just look like they're like water bags on stage? But not like water bags because like the estrogen's high or anything like that.

Speaker 1 It's because they're just so saturated. The muscles are so full.
There's so much pressure, but it's like it's like a balloon, right?

Speaker 1 Like any wrinkles, any details that are within the muscle have just kind of like shallowed out because the muscles just being so fucking,

Speaker 2 I don't know, full, full, full iced.

Speaker 2 I guess we have to, you have to view what impacts that. And that it's fluid movement based on electrolyte distribution.
And,

Speaker 2 you know, this spillover that I'm talking about,

Speaker 2 aromatase, 5-alpha ductase, these are all

Speaker 2 the common or known things that we'd expect drugs to interact with, androgens to interact with.

Speaker 2 But

Speaker 2 all steroid molecules can interact or cross-interact with other steroid nuclear receptors.

Speaker 2 So now you've got androgens being able to cross-talk with mineral corticoid receptors or glucocorticoid where we see this reduction in cortisol expression or or cortisol impact.

Speaker 2 The mineral corticoid interaction is basically going to affect your aldosterone and your sodium retention.

Speaker 2 More so that, like, sodium increases,

Speaker 2 fluid increases within your blood volume. So, you have extracellular increase in fluids.

Speaker 2 Potassium, estradiol change how fluid move into tissue. So, normally it's potassium that creates a full muscle in terms of the fluid being held inside the tissue, and then estrogen

Speaker 2 estrogen-one of estrogen's impacts is a change is interfacial fluid distribution of

Speaker 2 you know the space between your skin cells where that fluid gets distributed between the sketch the skin cells themselves.

Speaker 2 There,

Speaker 2 you know, in terms of like dosages, I won't have a dose to say, but this is obviously what you're on about: an interaction of an unwanted interaction that then ruins the look.

Speaker 3 Um, That

Speaker 2 quite often with bodybuilding, yes, we want to be full and sort of pumped on stage, but that's also one of the aspects of when you are pumping up prior to getting on stage, you don't

Speaker 2 to

Speaker 2 not like dumb it down, but you don't want to over pump yourself to the point where you lose that detail where you've just basically expanded the muscle and you've lost.

Speaker 2 you know, detail can matter in some shots that can make you look look more impressive. You might look full as anything and you hit a crab most muscular or

Speaker 2 hands in front most muscular and you look crazy full. But in other shots, you're losing bits of detail between like your tricep separation or your tricep striations.

Speaker 1 And you have to adjust this based off the division too, right? Like you look at,

Speaker 1 and I think the most obvious one is just comparing men versus women, for example.

Speaker 1 Men in classic, men in open bodybuilding, you don't want to like, most of them don't want to hit their legs, you know, within a week out of show.

Speaker 1 show you also want to pump out your legs but you look at wellness you look at bikini and they're pumping up their glutes and they're pumping up their quads and whatever because they want it full like with less detail right

Speaker 1 um and then i think same can be said but you kind of have to analyze what your physique looks like and where maybe your physique accentuates special genetics like oh man like i have like very diced

Speaker 1 I don't know, I have very diced arm separation or something. And the judges like this when they hit a side chest.

Speaker 1 I think that's not something you want to lose if you want to take like you want to take advantage of that.

Speaker 2 Yep. Really depends.
Yeah, it does. And I mean, I, you know, over time with competing myself, you, you learn what's sort of like the sweet spot.

Speaker 2 And I always laugh for guys like pumping up for like 30, 40 minutes prior to get on stage.

Speaker 2 You know, when I, when I first started competing in my first sort of two years, you thought, okay, yeah, I need to make sure I'm properly pumped.

Speaker 2 You know, you'd spend about 30 minutes getting pumped before you got on stage.

Speaker 2 The harder you pose and the longer you're out on stage, the quicker you start to, you know, if you're if you know how to pose properly and correctly with you know proper isometric posing, you quickly start pumping up on stage where you've got you know, even coming off stage, if you've been posing your leg so hard,

Speaker 2 the next day it's not, you know, it hasn't been uncommon for me to feel like I've gone through a leg workout

Speaker 2 out.

Speaker 1 I mean, my left calf is always shot afterwards. Always.

Speaker 2 Back in 2022, the second last competitive season,

Speaker 2 Aaron Casey was overseeing my training. Aaron's like an osteopath rehab specialist.

Speaker 2 About three weeks before the Irish Nationals, I like strained my adductor doing like a backdouble bicep the way you like twist your hamstring into your adductor.

Speaker 2 And that for like two weeks prior to that show my leg train was like goblet squats with like dumbbells and doing ordls with a kettlebell he was like you're gonna have to protect that because it was just obviously being low body fat hard isometric contractions you know you're gonna you can end up with injuries doing hard posing that people you know like you said they're their calf it's not uncommon when you're on stage you get a whopper cramp in your calf where you almost don't want to flex your calf when you're doing like back double biceps or rare lat spreads because you you know, if I'm going to do it, I'm how dehydrated potentially can be, that is this going to lock and you're sort of limping then for the rest of the day.

Speaker 1 Yeah,

Speaker 1 yeah,

Speaker 1 the dehydration part scares me every time I go on stage.

Speaker 1 Real quick, guys. So, while I was looking at the YouTube analytics, I actually saw that 85% of you guys that watch this channel are not subscribed.

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Speaker 1 And if you decide to purchase anything from any of these companies, it will help immensely for me by using my code and this way i can travel to other guests and also upgrade an equipment to make this podcast bigger and better for you guys uh going off of that actually um and i'm glad we discussed the glycogen thing because it's something that's always been fun for me to discuss with like top coaches like stefan gienzel and patrick toor because uh

Speaker 1 You know, you'll get those comments and like a like a reel or something saying like, oh man, more gear is better.

Speaker 1 And these are normally the guys that like on stage with like veins are covering their quad striations, and then you can't see the separation.

Speaker 1 There's like there's a level of too much, you know, because

Speaker 1 the prettiest physique is the physique that wins, not just the most fucking geared-out physique. And I think that's the wrong conception.

Speaker 2 Yeah, I mean, like, again, coming back to my own personal experience, um, Colin Raisedrich was, you know, like my prep coach, one of my good friends, and we sort of bounced ideas.

Speaker 2 You know, I tell him what I thought in terms of like stack setup and whatever.

Speaker 2 If we knew, you know, in terms of visual,

Speaker 2 I know from experience how my body responds to something like growth hormone, you know, in terms of that, that fullness.

Speaker 2 That

Speaker 2 if I want to be as dry and separated as possible on stage, I have to play everything in advantage of keeping that glucocorticoid activation under control or aldosterone effects.

Speaker 2 Growth hormone for me, if I wanted to be crazy full,

Speaker 2 how I sort of look in some of the reels of when I hit most musculars training back then, that's the effect, that sort of bubbly look with growth hormone.

Speaker 2 Is that going to be the most pleasing thing to have when you're doing something like classic bodybuilding or classic physique?

Speaker 2 Not really. You know, like you said,

Speaker 2 it looks visually impressive. You hit it in the gym, you look bursting forward, there's all veins coming out of your shoulders and biceps.

Speaker 2 But if that detail on your back or your hamstring glue tie-in disappears from from that small little film of fluids,

Speaker 2 you could lose based on condition, no matter how pretty your physique was. And I always knew my, you know, my asset was condition and anything that would impair that.

Speaker 2 But in saying that, there were times where I've done, you know, open bodybuilding in terms of like a weight division, and you wouldn't be sort of hinged off having to take that out.

Speaker 2 I think 2022, I done the under 90 class of the IFBB nationals rather than doing classic bodybuilding. And that was one of the shows where, you know, I said to Carl, let's just keep it in.

Speaker 2 I'd already won Mr. Ireland with PCA in classic bodybuilding.
This was just the show I'd sort of committed to and the run afterwards.

Speaker 2 So let's just keep it in and bring a much fuller looking physique for, you know, stage photos to keep.

Speaker 2 But like you said, it's like if you put in these drugs genetically, you know, touching back on it, how the drug distributes from the body or how it's absorbed.

Speaker 2 How it's metabolized and excreted will then put impacts on

Speaker 2 your,

Speaker 2 I guess, the substrates of your body. So, in terms of like sulfates, glutathione,

Speaker 2 how well your filtration of those metabolites is, outputting them from your urine.

Speaker 2 What's the likelihood of some of these metabolites getting stuck in the body in terms of like in your fat tissue? And this is where historically some guys failed drug tests because

Speaker 2 metabolites of drugs stay around in the body, and that's because they distribute back into tissues. And so the detection time of those tissues is, you know, 40 to 60 days for some compounds.

Speaker 2 But it's not uncommon that you could have a failed drug test, you know, a year and a half, two years later.

Speaker 2 If some of that drug has been distributed into tissue,

Speaker 2 that you lose body fat in terms of the fat cell shrinks, releases its content, and what was stuck inside that fat cell were fat-soluble hormones or hormone metabolites that now you fail a drug test because you've done drugs two years ago or whatever.

Speaker 2 You have to bear that in mind, you know, when you're looking at how drugs are metabolized from your body, that there's always potentially a small amount to get stuck, which is,

Speaker 2 you know, not to put strategies out there, but you know, maintaining low body fat levels in theory saves away some of that potential risk risk of failing a test in years' time.

Speaker 2 You know, on top, on top of that, I guess, just to really briefly touch on it, then is your receptor interactions,

Speaker 2 the genetics that drive that of like

Speaker 2 the faster, slow metabolizer recovered comes from liver genetics, the CYPs. So, that's genetic genie.

Speaker 2 The other ones,

Speaker 2 you know, in terms of like genetics, it's very hard to get an accurate picture on your genetics genetics of,

Speaker 2 I guess, your

Speaker 2 androgen receptor deficiency. And what we're talking about here are the fingers within the receptor that allow to take the drugs, which are like the zinc binding claw.

Speaker 2 So when people talk about this CAG repeats,

Speaker 2 CAG repeats are what dictate

Speaker 2 how well you create this binding claw in the androgen receptor.

Speaker 2 That of itself,

Speaker 2 you could have an amazing

Speaker 2 genetic response to drugs in terms of like,

Speaker 2 let's just say, for example, a slow metabolizer. So you need to take less drugs.
They stay in your body longer. In theory, then that achieves a higher therapeutic level when you take an average dose.

Speaker 2 So let's say. 250 milligrams is creating double the expected serum level.

Speaker 2 But now you've been dealt shorthanded to genetics and your CAG repeats, where now your angium receptor's efficiency is quite poor.

Speaker 2 The only way you might overcome that then, if you think about it, is by putting more drugs in to try and create successful interactions with the receptor.

Speaker 2 So you almost bully the probability of an interaction, whereas a normal person doesn't probably have to think about that in terms of the interaction of the molecule to the receptor.

Speaker 2 So that's where then someone on terriers great drug metabolism genetics, but dynamically, they have really poor response where their cells are.

Speaker 2 If you want to put it in a simple term, androgen resistant, where the receptor is not functioning as well as it could.

Speaker 1 Would you have any recommendations as how someone can determine this for themselves?

Speaker 2 I think

Speaker 2 there's a couple of places in

Speaker 2 Europe that do it. I think there's a lab in Norway.
And I think,

Speaker 2 to my knowledge, there's a few in the US that do it.

Speaker 2 There's one guy who's wrote a great book

Speaker 2 and a close friend of mine,

Speaker 2 Thomas Anderson. He has a great post for all of the links of where you can get the CAG repeat testing done.
And

Speaker 2 again, I'll send you his profile. You're going to put in the links below.
I'm sure he'll be happy. He has a really good anabolic encyclopedia book that he wrote that goes into all the drug profiles.

Speaker 2 I think Merrick might offer it. I think Steve was saying before when we discussed on a podcast that they offer a CJG genetic test.

Speaker 2 And then it's interpreting whether you have shorter or longer repeats.

Speaker 2 How efficient the finger is at docking the hormone into it.

Speaker 3 Okay.

Speaker 2 With that, you know, again,

Speaker 2 if you do your pharmacogenomics and you do your CAG repeats and you have all this information,

Speaker 2 you sort of reduce the risk of then having to think of, oh, well, I'm just going to take five grams of gear and see what happens.

Speaker 2 Yeah.

Speaker 2 Yeah.

Speaker 1 Going off of you discussing your prep and also discussing abuse in the 90s versus now, I think a lot of people can take a lot of value from your own prep and compound uses, even though obviously,

Speaker 1 as we discussed before, muscularity is a big variable when it comes to like what you're going to dose for yourself.

Speaker 1 So, you know, it's, I'm sure, like, what you take and what I take is still a completely different league than the typical top pros.

Speaker 1 But would you mind sharing your own personal compound choices and uses for your last prep? Because I think out of anyone that I would ask, you'd probably be the most health conscious, I would assume.

Speaker 2 Yeah, well, I mean, that last prep and

Speaker 2 last time I competed,

Speaker 2 you were just looking at a physiological base of testosterone. So it was one, two, five test D.

Speaker 2 And then we

Speaker 2 prior to sort of committing in my mind to competing,

Speaker 2 I had 300 milligrams of primo enantate in sort of for six weeks as like a muscle building phase. Bear in mind, I had

Speaker 2 my estrogen sitting around at 90 picomole within

Speaker 2 UK measurements, which is,

Speaker 2 I'd say,

Speaker 2 2020 in US terms. I'm really bad at doing conversion, but we're sort of looking at mid-range, basically.

Speaker 1 So, you're someone that like you can titrate up your DHC like primo to about twice your testosterone base.

Speaker 2 Well,

Speaker 2 for me, genetically, I have high CYP19A expression.

Speaker 2 When I was in puberty, I had gyno, like puberty gyno, that was taken care of in my early 20s. And that was, again, when I delved into my genetics, there was the CYP19A expression.

Speaker 2 And my mother had a history of benign tumors in her breasts that had to be surgically removed. So I knew that genetically, aromatase for me is going to be an enemy to have to consider.

Speaker 2 An enemy in terms of like keeping it strictly controlled because it's going to impact my physique, it's going to impact my neurochemistry, you know, all these things that estrogen plays into, positive and negative.

Speaker 1 Okay.

Speaker 2 That 125

Speaker 2 sort of served as an anchor that I knew was predictable.

Speaker 2 And then any change that came from blood work that was predictable based on that was coming from the other things that were going in on top, which was obviously Primo E at 300.

Speaker 2 To be honest, we ran that for

Speaker 2 started prep the middle of May. I think it was the 14th of May, it was a Monday.
I'd just gotten back from vacation.

Speaker 2 And then the Northern Irish show that I won the overall at, that I think was like the 7th of July. So it was maybe eight weeks later.

Speaker 2 When I made the decision to compete in that show,

Speaker 2 I think

Speaker 2 we were seven weeks into prep. And I said it to Cal, and we sort of then thought, okay, well, let's add in a very low dose.

Speaker 2 of trend that we've covered before and that was quite literally 40 milligrams 10 milligrams prior to training. And I was only training four days per week.

Speaker 2 And then we put in 20 milligrams of Winstrawl on those training days as well. So I think total androgen dose for that overall was 600 milligrams, I think.

Speaker 2 It was very low.

Speaker 1 And how much did you weigh at what height?

Speaker 2 I was, I'm 176 centimeters, so I'm class B for classic physique. And I weighed in for that BPA show, I was

Speaker 2 just under 90 kilos. I was 89.5 kilos, which I think is like just under 200 pounds.

Speaker 2 So, and then you can see in the shots, like I'm pretty much down to where I was before, straight glutes, deep condition.

Speaker 2 After that, the sort of goal, that was just like, let's just enter for the crack. You know, it's, it's an hour and a half drive.

Speaker 2 I'm, I'm pretty much where I want to be for the, the aim was to do the Two Bros Emerald Cup, which was like two days before our family vacation.

Speaker 2 And how I, you know, approached the prep to my wife was: well, you can't stop me getting in shape for our holidays, but if I decide to compete and keep things, you know, family, work, everything balanced, it's just a holiday diet.

Speaker 2 That show, after the BPA,

Speaker 2 I think there was another, so that was July, you had all of July into the start of August. I think about five weeks between that show and the actual target show.

Speaker 2 From that point, after that show, I think we added in 20 milligrams of Anavar on top of the windstrowl. More so from an ergogenic perspective to maintain train intensity, maintain lift intensity.

Speaker 2 And bear in mind, my training style since 2022, Aaron, was reps and reserve. So the whole thing about volume, volume was as low as you could imagine.

Speaker 2 Train intensity, stopping two reps in reserve, but like true, two reps and reserve, where you know, I'm getting into these dodgy reps.

Speaker 2 That, you know, like by the end of it, I think again, I was like, sub 700 total, taking into account like the Winstrawl Trend,

Speaker 2 the Anover,

Speaker 2 the base of testosterone 125 stayed steady all the way through, and then the 300 Primo stayed the same all the way through.

Speaker 2 We discussed, me and Steve, 2022's prep. 2022's prep was 300 tests, 600 Primo, and 300 mast dron, and then sort of the similar dosages of TREN and

Speaker 2 anovir and winterl. So, you know, taking that into perspective, that was, you know, nearly, I think, 1,400 milligram total with everything layered in on top of the 300, 600, 300.

Speaker 2 This time round, there was no mast drawn.

Speaker 2 The testosterone was half.

Speaker 2 The, you know, the oral setup and the trend was pretty similar to 2022, which improved to me in terms of like cosmetic benefit.

Speaker 2 The estrogen-lowering ability of Primabolin in terms of what it does to dearomatase enzyme expression in theory was enough to keep me looking dry.

Speaker 2 I didn't need to add in, you know, what you'd classically run with, you know, your test trend masks for a contest prep.

Speaker 2 But also showed me, you know, relative to

Speaker 2 stage weight, 2022, I competed roughly around 88 kilos,

Speaker 2 and last year I competed roughly at the same weight. You know, my lowest weigh-in was 87 when we really pushed drying us for the final like BPA championships, the like British championships.

Speaker 2 It just showed me that, you know,

Speaker 2 I could probably have lowered that Prima Bowl into around 150 in theory and probably not seen any real change

Speaker 2 performance-wise or cosmetically.

Speaker 2 300 was sort of like I was at 125.

Speaker 2 I was running 300 for six weeks, like an off-season prior to starting prep.

Speaker 2 That

Speaker 2 what that sort of was yielding was, okay, well, this was a nice dosage. But again, it shows you that even with all the data that we have,

Speaker 2 it's still an arbitrary number based on what you're perceiving.

Speaker 2 You know, like I said, in hindsight, even looking at the data, 2022 is 600, 2024 2024 is 300, and in theory, could I've gone a bit lower? And we're sort of starting to then see

Speaker 2 maybe when we're looking at drug use and PrEP,

Speaker 2 people lose sight of the fact that you're using the drugs to maintain muscle mass, not build muscle mass.

Speaker 2 So the dosages of PrEP in theory should be way, way lower than where they were in your off season when you're actually trying to enhance muscle protein synthesis.

Speaker 2 And so that was like an last year, that was this sort of aha moment of when I decide I'm going to prep. I thought,

Speaker 2 you know,

Speaker 2 if I'm going to do this, do I need to go exponentially high with dosages versus where I am heading into the prep, you know, one, two, five tests, 300 mass, 300 primo? Do I need Mastron?

Speaker 2 Do I need Trend?

Speaker 2 You then realize, well, when you're making these decisions of, oh, it's prep time, now it means more drugs.

Speaker 2 You know, that's classic old school thinking of renowned prep. Here's our like RIP blend.

Speaker 2 You know, in the UK, you've got like RIP blend, where in the vial, you've got, you know, testoprope, mastoprope, and tranesety,

Speaker 2 which is the classic, like, old-school way of, you know, just take one meal of rip blend every other day, heading into a show, and you'll be fine.

Speaker 2 It

Speaker 2 showed me that when we're looking at prep, we have to be very, you know, objective of

Speaker 2 do we need half of the dosages that we've done in the offseason heading into prep.

Speaker 2 Some might argue yes, because obviously you've got a predictable response, you've held a certain body weight, and the goal is to hold as high a body weight as possible whilst reducing the body fat.

Speaker 2 But on the other side of it, that dosage again could have been just something that you escalated to based on numbers on a piece of paper, like body weight and and how you felt in the gym and your progress, that you might be able to take a step back and go, well, maybe we could half that compound and see what happens.

Speaker 2 Interesting.

Speaker 2 You know,

Speaker 2 it's one of those ones where when you

Speaker 2 suggest the lowering of dose, it's almost like blasphemy. No, we should be going the other way.

Speaker 2 And

Speaker 1 I feel like that's very counter to what maybe 90% of the industry believes at the moment, or at least enforces.

Speaker 1 So I guess what I'd have to ask, just

Speaker 1 as a devil's advocate is

Speaker 1 i guess what other data do you feel like you have other than uh your personal anecdote that

Speaker 1 it may be potentially true that your prep doses should be lower than your off-season because i find that most bodybuilders pro bodybuilders these days will run a lower off-season dose

Speaker 1 because of just how low how prolonged that off-season is and to maintain relatively okay markers, I guess.

Speaker 1 And then as prep rolls around, you know, you're like, okay, I understand that some of these things are not going to be good for, say, my liver or blood markers, other relative blood markers.

Speaker 1 But, you know, hopefully the cardio and everything else that we're doing is going to help manage that.

Speaker 2 So I

Speaker 2 view it like this, because once you start framing it this way, it sort of makes sense, the viewpoint of less grogs.

Speaker 2 In a prep setting, you've got a classic stressful scenario. You're eating less food, you're hyper-fixated on your performance towards an end goal of getting on stage.

Speaker 2 And if it's to get a pro card and everything that sort of comes from that

Speaker 2 personal expectation of achieving that goal, that guys then tend to do excessive cardio, do more than they should, do more working sets or work within the gym, thinking that more work will equal a better outcome.

Speaker 2 And

Speaker 2 that's not to say that it's not true, but there comes a point where you have to be very careful of the fine line between driving

Speaker 2 the accelerator too hard on the expected outcome versus being a little bit more intelligent with how you're approaching fatigue management overall.

Speaker 2 I hate this bloody word, you know, where guys like, oh, we should manage fatigue, but

Speaker 2 if

Speaker 2 you are doing, you know, drop sets and intensifiers and this, that, and the other training, beyond like your standard,

Speaker 2 I don't know, meat and potatoes of maintaining strengths within a reputable rep range. Again, I'm not coming in being an exercise expert.

Speaker 2 I can only speak for what I've done personally, and when I helped other guys with some level of coaching,

Speaker 2 you want to do, you know,

Speaker 2 as lazy as it is, the most

Speaker 2 effective volume or the least effective volume that's going to hold that muscle mass in your body. And that's it.

Speaker 2 And be very strategic in your analysis of: have I done enough in the gym today to maintain chest volume, arm density, blah, blah, whatever, you know, leg, leg.

Speaker 2 And this was all, this all came from Aaron, to be honest, because I was the typical like me head of, you know, I told on the anabolic round table the time I nearly cleaved myself in a leg press trying to beat the logbook, but two weeks out to a show that

Speaker 2 you know, when

Speaker 2 Aaron told me about like reps and reserve and you know, intelligent tempo training and everything, like like being

Speaker 2 still lifting heavy, but lifting smartly, I guess

Speaker 2 the first when we approached that in an off-season perspective, I grew just as well as like going in and doing like top set, back off set.

Speaker 2 So, he'd set like two, two or three sets in terms of volume for an exercise,

Speaker 2 two

Speaker 2 to one rep in reserve. So, never going to that failure rep.

Speaker 2 And I know you know, Paul Carter puts out a lot of good content on this.

Speaker 2 That sort of stopping at one rep in reserve, as mentally frustrating in the beginning as it was, where you're like, I should be really getting to the point where I'm grinding out that last rep.

Speaker 2 2022's prep, I told him, this is cheating. We were two weeks out from the first show.
I said, this is cheating. I don't even feel tired.
My sleep is amazing. You know, my mood.

Speaker 2 That year I had a lot of expectation on myself that mentally, yes, I was a bit distressed.

Speaker 2 Taking that same approach into last year,

Speaker 2 I realized, you know, that fatigue management where you're still lifting heavy, still lifting heavy and strong, but you're not going to those reps that are going to cause unnecessary fatigue.

Speaker 2 When you get to that point of unnecessary fatigue, appetite and recovery demands increase. So naturally, you're going to feel more hungry.
Your sleep is affected because you're hungry.

Speaker 2 and there's a recovery aspect in your body where your body's telling you to feed it to recover more yep

Speaker 2 That then enters the scenario where you then bully that recovery by adding in more drugs.

Speaker 2 I'm going to mask this fatigue and under recovery with more drugs, which is going to let me train better and stronger, but in the long haul is creating more systemic stress, to speak, in that your appetite is still going to be very high.

Speaker 2 Your body's screaming at you to feed it, to recover adequately. But now the drugs are making you do more volume with the added mental expectation on top of yourself to do more and be better.

Speaker 2 That you then start start to realize perhaps the increase in dosages during a prep is to mask the mismanagement of fatigue or being smart in your approach of how you're going to approach training and your fat loss.

Speaker 2 And that was like the light bulb moment last year where I was like, okay, mitochondrial efficiency, you're able to create more energy density so that there's less oxidative stress.

Speaker 2 You've higher numbers of mitochondria, feed that adequate glucose to maintain training efficiency.

Speaker 2 And now you're into a position where actually I probably need less drugs because the system is less stressed. I'm still hitting,

Speaker 2 you know, this is where I argued in the beginning about like milligram per kilogram dosing, where people are saying, oh, you should take three milligrams per kilogram testosterone, and that's sports TRT.

Speaker 2 And you sort of look at it and you go, well, we don't have a measure of how much density of androgen receptors you have per kilogram body weight. So, that argument eventually fizzles.

Speaker 2 That you're

Speaker 2 like that, you're trying to anticipate where's the sweet spot

Speaker 2 for recovery in a prep setting.

Speaker 2 And

Speaker 2 you'd be surprised, you know, this is you know, anyone out there that is falling into that trap of more drugs. How about potentially less drugs and understanding fatigue management, looking at

Speaker 2 how you're training.

Speaker 2 Is your training truly effective?

Speaker 2 Or is there a biased attachment that you feel under pressure that you have to do more in the gym?

Speaker 2 I used to get anxiety, I remember when I was younger about leg days because I'd be like

Speaker 2 looking at the logbook and thinking, how am I getting, you know, I don't know, eight reps with seven plates aside in this hack squat, and you're like four weeks out from a show and you're looking and you're going, this, you know, and to be brutally honest, if I didn't hit it, you know, you'd throw a strap.

Speaker 2 You know, I competed back then in my late 20s with my wife. You'd be just in such a bad mood that you feel like a failure.

Speaker 2 You feel like you didn't achieve what you were supposed to based on the logbook.

Speaker 1 Or like you're losing muscle or something.

Speaker 2 Yeah. And then you're like, well, it's the whole session thrown out.
But like you realize it's just one small little thing.

Speaker 2 And perhaps it's actually telling you, well, actually, Dean, you're quite effed here. You know, in terms of fatigue, sleep,

Speaker 2 under nutrition or malnutrition, you know, in terms of glycogen and everything else.

Speaker 2 Perhaps that's a sign to really pay attention to your training. And but the reverse with Dennis,

Speaker 2 don't train like a pussy.

Speaker 2 Like, not not to be like too harsh, but

Speaker 2 reps and reserve, you still have to understand where your limits are and how you train effectively, but you're not going into those depths of despair where you're realizing I've created enough mechanical tension within this muscle to maintain this volume and structure.

Speaker 2 Move on.

Speaker 1 That's why I really appreciate what Chris Tuttle discussed with me regarding training in

Speaker 1 your prep phase. Because, you know, a lot of us believe, oh shit, like we need to maintain a level of a volume and stimulus to maintain our muscle mass.

Speaker 1 But I mean, the fact is that you're, as you're, as you're lowering your energy intake,

Speaker 1 your recovery is going to be hindered too. But the recovery is the most important part.
So it's okay to reduce the volume. It's okay to have a lower level of overall volume and stimulus.

Speaker 1 And that's kind of what you have to do to do it correctly.

Speaker 1 So he said, like, I think for Jordan Hutchinson, maybe it was like, I don't remember the exact percentage, but maybe it was around like 75 to 80% of Jordan's like off-season volume.

Speaker 1 He was hitting during prep. And he was recovering fine.
He was recovering great. And then you look at him on stage and he looks absolutely phenomenal, which is great because

Speaker 1 that's proper management when it comes to bodybuilding. But the one thing I'd have to say is

Speaker 2 I think

Speaker 1 my argument against your point is that I feel like

Speaker 1 I don't feel like when it comes to the drug intake that we can, even though

Speaker 1 I do want to press nowadays that lower doses can be used than the past, I think it's still so variable that it'll depend on the person and when they're at, whether or not the prep cycles is going to be lower than the off-season cycles.

Speaker 1 Like, I'll see some guys who are like, who've built a ton of muscle mass in their off-season already, and now they're still building muscle mass at a lower rate, but they don't need to titrate up those doses.

Speaker 1 And one of those examples, I think, for example, is Martin Fitzwater, who's been running 750 tests base. consistently throughout all his offseasons.

Speaker 1 Obviously, he has another secondary compound on top of that, which is EQ. But

Speaker 1 then when it comes to actual prep,

Speaker 1 it's like, all right, well,

Speaker 1 now we got to adjust the doses based off of your recovery and how much you're losing.

Speaker 1 And if you are losing more than we expect, then maybe it is important for us to titrate up this oral a little bit or something like that.

Speaker 2 Yeah, I mean,

Speaker 2 the way you have to view it like you're,

Speaker 2 you know, really beautifully explained, there's

Speaker 2 you need,

Speaker 2 if you don't satisfy the androgen receptors that are being occupied by drugs in terms of like within muscle tissue.

Speaker 2 So you've got android receptors inside your muscle tissue that are being occupied by androgens, which are given the cellular signal for either muscle protein synthesis, nitrogen retention,

Speaker 2 reducing glucocorticoid expression, etc.

Speaker 2 I'm not saying that you go in and you slash dosages in terms of like, oh yeah, well, run half-term prep, because even when you look at my prep, it started at 125 and 300, and then there was another edition with Trent and Winshall, and there's another edition with Anivar.

Speaker 2 So I'm actually going up in dose

Speaker 2 relative to where my physique is, where I'm finding, you know, recovery. I'm still performing really well, but I know now I'm at a place where,

Speaker 2 again,

Speaker 2 if I was to be truly objective,

Speaker 2 when Anivar went in with five,

Speaker 2 six weeks ago, prior to the Emerald Cup. Did I have to go in based on where my training performance was? Probably not.
I probably could have been, you know,

Speaker 2 let's back off here. But knowing that you're in that fine balance of where the physique was, body fat-wise, how training numbers were maintaining, it was just another sort of

Speaker 2 card to play

Speaker 2 at that time. But again, patience could have paid off and we could have went, actually,

Speaker 2 let's just wait another couple of weeks.

Speaker 2 And that's that's sort of you know, the approach here is: I'm not going to argue that you don't need a lot of drugs for a prep because that would be silly to say.

Speaker 2 And I've seen it with pro-bodybuilders, but for the average amateur, just have a real

Speaker 2 base your drug usage off objective data rather than subjective and emotional.

Speaker 2 I'm 10 weeks out from the show, so now I have to add in this compound and I have to increase the dose.

Speaker 2 You sort of have to look at your physique, look at the numbers, look at your body fat level, look at your output.

Speaker 2 You know, look at a bigger picture of does it make sense that that compound has to go in? You know, where's recovery if you add in more,

Speaker 2 I guess, androgens, COMT expression, slow down of COMT, we now have impacts on sleep, we have impacts on mood.

Speaker 2 There's a fine balance, and this is why I love that

Speaker 2 it's so inter-individual in the responses. That my setup and your setup are going to be completely different.

Speaker 2 You could run what I used last year, and it might actually end up where your physique looks way, way worse.

Speaker 2 And

Speaker 2 that's where you can never cookie colour, give a blanket cycle to someone, and go, This is what you do.

Speaker 2 All I will say is just don't be afraid to give yourself time for prep, prep, obviously, but play on the side of less, maybe more to begin with, and have that option of escalating up if needs be.

Speaker 1 I'm totally with that too.

Speaker 1 Going off of that, actually, I have an experiment to share with you that for this,

Speaker 1 I did three shows for this season. Third show is in like

Speaker 1 it's like tomorrow.

Speaker 1 And basically,

Speaker 1 so Patrick Tor,

Speaker 1 I'm open about just releasing my cycle. Basically, it was a 600 test prop, 600 mast,

Speaker 1 mass P,

Speaker 1 Trend, 100 milligrams of Trend Ace. He wanted 150, but I hackled him down to 100 just because I do get my night sweats and a little bit of insomnia from it.

Speaker 1 So I'd prefer just not to have to deal with that. So what's 50 milligrams less of Trend, really, you know? And then 50 mills of Provirin

Speaker 1 two times a day.

Speaker 1 And then that was basically the cycle. And for me, I was like, holy shit, no orals except for the the provider, like no actual hard orals.

Speaker 1 That's kind of surprising because I've always ran orals for all my preps.

Speaker 1 Even my very first prep that I won my pro card was actually no injectables, just windstroll and halo testing, which is a long story. But

Speaker 1 I've never not ran Windstroll before.

Speaker 1 And obviously, we implemented a little Halo in the last couple of weeks, but I just never implement, never didn't implement Windstroll. And so I had this discussion with him.

Speaker 1 He's like, we're going to keep it off. So the first show, we kept it off.
And I looked very defined. I was very dry.
And my lowest weight was about 179.

Speaker 1 And then afterwards, from the feedback from the audience, as well as some of the judges, basically I was like the smallest one on stage. I'm 18 pounds below the weight cap.

Speaker 1 I also looked the least, maybe like full with the least pop compared to the people.

Speaker 1 And, you know, the judges aren't going to say, oh, you look like you took the last, the least gear, but my friends and other people in the audience that I knew are open to telling me that.

Speaker 1 So they're like, yeah, bro, especially out of the top five, you definitely look like you were taking probably the least amount of gear out of all these guys.

Speaker 1 So I asked Patrick and I confronted him about it. And he's like, yes, that's a fact.

Speaker 1 You're probably running about half of a normal Olympian stack right now.

Speaker 1 But slow and steady wins the race. And that's how Patrick likes to roll: you know, he starts slow with all his clients.
And then obviously builds up as a relationship builds up as well.

Speaker 1 I convinced him to let me experiment with adding Winchstroll. And so luckily, Winstroll is the only variable.
so I can see how it changes.

Speaker 1 And so we added windstrol for three weeks at the last show at 37.5 megs a day, which would be 25,

Speaker 1 1.5 times with 25 megs, which means I actually literally like opened up a cap of 25 megs and split it in half and took that as a second dose each day.

Speaker 1 And I think that was probably the best look.

Speaker 1 And that's the interesting thing. It's like, did it affect

Speaker 1 my training and my recovery. I really didn't notice hardly a difference, to be honest.
But when it came to the actual aesthetics and the actual look, I looked fuller and a little tighter.

Speaker 1 There were certain parts of, like, for example, glute striations that maybe didn't look quite as deep, but they also didn't look as loose, if that makes sense. Like, there was a tighter look to it.

Speaker 1 And then now, for this last show, I up it to 50 milligrams a day. And now, this is going to be six weeks on Winstrel.
The first three weeks was 37.5, the last three weeks is 50 milligrams. And

Speaker 1 my weight at its lowest is probably around 184. when we drop all the compound when we drop all the um injectables and the gh i would say it's probably closer to about 182.

Speaker 1 so maybe so i've gained probably about like two pounds of just water weight in general from being on windstrol regardless of how dry and how lean i'm pushing it um and that definitely shows in the pop But uh, whenever I did up the 50 milligrams, and now that it's been six weeks on Winstroll, I'm noticing certain things about my look and my digestion.

Speaker 1 And my digestion has taken a hit. The GI tract doesn't feel as healthy.
I'm having more

Speaker 1 gas and it's slower. And then also,

Speaker 1 before I took the windstrol, people were telling me that I looked very healthy. People were telling me my skin looks great.

Speaker 1 And I was getting that from multiple different people that didn't know each other at different times.

Speaker 1 And now it's not that no one has, it's not that people are saying that I don't look good, but I have acne on my chest now and I have acne on my back now.

Speaker 1 And the water retention in my cheeks is a lot higher than it was before, because before I had just sunken cheeks the entire time. So it's like

Speaker 1 I've noticed, I don't know if that's oxidative stress or increasing liver damage or if that's just introst like glycogen from the intake of Winstrel, all of these variables.

Speaker 1 But to me, I would say, man, I think I found like a perfect balance. Like next time, I'm probably just going to run 37.5

Speaker 1 for six weeks. And

Speaker 1 if I have to do multiple shows, I'm not going to start six weeks before my first show.

Speaker 1 I'm going to make it so that my last show has six weeks of Winstrall in it because at a certain point, it starts hurting me.

Speaker 2 Yeah, yeah. I mean, that's, I discussed this before.
Someone asked me about Winstrawl. Winstrawl, from my perspective,

Speaker 2 I hate using the phrase cosmetic compound, but like you sort of said, Winstrahl, we don't have any data to really say

Speaker 2 how it works, but we can, you know, from your experience, how I viewed it on my physique,

Speaker 2 it almost

Speaker 2 changes how

Speaker 2 fluid is distributed into your skin cells.

Speaker 2 It's one of those ones, like you said, when you're very low body fat, when you add it in,

Speaker 2 there's just this how your skin changes in terms of like a

Speaker 2 rougher texture to your skin, but it's the fact that the skin is actually not as hydrated as it normally would be, and you sort of then see

Speaker 2 very

Speaker 2 dry striations, especially like around the chest, around your shoulders.

Speaker 2 What's happening in your case, potentially, if we look at what happens with orals, is they can potentially interfere with how bile is made within the liver, and then obviously bile is stored in the gallbladder and released from the gallbladder.

Speaker 2 That

Speaker 2 a lot of the digestive upsets with orals, when you look at mechanisms, when you postulate mechanisms of what ties in, they affect bile, which then is secondary messaging signals towards

Speaker 2 ghrelin regulation and obviously leptin.

Speaker 2 That

Speaker 2 when we have impaired bile flow,

Speaker 2 it upsets our gut microbiome because bile is basically what's a lubricant for the digestive tract moving everything along.

Speaker 2 Obviously, if we have

Speaker 2 slow intestinal motility where food isn't moving as quickly, you will have

Speaker 2 digestive distress to speak, where food is being fermented more easily than if it's passing through quicker,

Speaker 2 which will cause bloating and distension, to speak.

Speaker 2 That

Speaker 2 potentially, how we sort of try and offset that then is by improving bile viscosity, which is sort of your bile acids, so totke or odke, where we need a relatively high concentration of totke and odke to support that bile viscosity.

Speaker 2 And then maybe using synthetic bile like ox bile, which is very identical to a human's own bile.

Speaker 2 And now what you're doing doing is you're providing a level of lubricant and emultification of dietary fats in your digestive tract, whilst also offsetting if your digestion has become more poor, where there's reflux or there's a lack of appetite where you just don't feel like eating because your stomach just feels off.

Speaker 2 Those mechanisms of running a relatively clinical dose of todka, you know, 1200 to 1600 milligrams of todka, I don't know if that's in your health setup currently, and ox bile might overcome some of those issues with the bile flow.

Speaker 1 Um, I do have totka in the in the program. Uh,

Speaker 1 what about Bt and HCl?

Speaker 1 How do you feel about that? So, I know that's more for protein, but

Speaker 2 with the stomach acidity, again, it's really important for your overall digestive health because I guess

Speaker 2 a really nice way of putting gut health is your stomach is a sterilization tank of acid. Your gut is filled with alkaline like bicarbonate.
So it's still quite low in pH.

Speaker 2 We're talking like pH five, pH six, still below water at seven.

Speaker 2 But your stomach is designed to kill and sterilize bacteria that could even come from your oral microbiome from your mouth. Again, your mouth is a pH of 6.5 to 7, so it's neutral in theory.

Speaker 2 Depending on obviously what you eat, that acidity can change. But you're constantly swallowing saliva that has oral bacteria within it, into your stomach.

Speaker 2 Stomach should have high enough acidity to sterilize and kill that bacteria. If your stomach's acidity in terms of the hydrogen content of your stomach, which is where the HCl comes from, changes,

Speaker 2 you're going to see changes potentially in how you digest protein. You need a low enough pH of your stomach to activate pepsin and trypsin to chemically break down proteins.

Speaker 2 Effectively, if you don't chemically break down proteins properly, you're expecting your gut to pick up the slack, but your gut bacteria may then start

Speaker 2 putrefying, if you want to put it that way, that back that

Speaker 2 bad bacteria, I hate that word,

Speaker 2 but you end up with then, obviously, with the creation of sulfur gas, depending on the bacteria, it tends to be the metanogens or proteobacteria that produce hydrogen sulfide and methane gas.

Speaker 2 If your stomach acidity isn't low enough, you're going to see issues with protein digestion.

Speaker 2 And that could be effectively as well slow gut motility, where food doesn't leave your stomach quick enough.

Speaker 2 Common things that you might experience with low stomach acidity can be reflux.

Speaker 2 The way I try and explain it is your stomach has a set volume of like two and a half liters to three liters.

Speaker 2 With gastric juices. When you put food into your stomach, like throwing a load of rocks into a bucket of water, the volume rises of the fluids.

Speaker 2 Obviously, to accommodate the volume of the food you've eaten in with the fluids.

Speaker 2 If you've got poor stomach acidity, where the the acid level isn't low enough

Speaker 2 what potentially you're going to see then is that stomach volume increases and takes a longer time for chime, for whatever's being chemically mixed around the stomach to pass into the small intestine.

Speaker 2 And if that volume increases, now it's touching off the sphincter at your esophagus, giving you the sensation of heartburn because your gastric juice is still acidic.

Speaker 2 It's just that the volume has increased.

Speaker 2 That when you have low stomach acidity, it can give you the signs or symptoms of high stomach acidity, too much acid being made.

Speaker 2 And so you'd have to look at things that are potential signs of low stomach acidity or poor digestion. That's like poor protein digestion or malnutrition, brittle nails, burping,

Speaker 2 what are other things?

Speaker 2 I guess excessive gas production.

Speaker 2 affects where the food goes into the small intestine where it hasn't been digested chemically properly in the stomach.

Speaker 2 But also the fact fact that you could have bacteria from the oral microbiome arriving in the stomach and getting the chance to pass into the small intestine, which is now a more basic pH in line with your mouth,

Speaker 2 which then can contribute to these bacteria contributing to dysbiosis. The bacteria is in an overgrown state versus where it should be naturally.

Speaker 2 And so,

Speaker 2 with gut health, people often view, you know, and you've probably had Austin's thout on before, Austin Staut was very clear with gut and that, that dysbiosis doesn't necessarily mean that there's pathogenesis, which is disease.

Speaker 2 Dysbiosis can create a level of discomfort.

Speaker 2 If that discomfort is linked to pathogenesis, where you have like leaky gut and endotoxin or lipopolysaccharide coming from your normal bacteria into your your body because of the like tribal war that's going on with this biosis

Speaker 2 then you have to go back to like this sequential link of well

Speaker 2 how did how did this imbalance happen in the first place and in theory the stomach is the first sterilization tank the liver health or gallbladder and bile is like your second sterilization

Speaker 2 that the two of them are so so critical you know when you're looking at digestive discomfort with most bodybuilders,

Speaker 2 most of it's driven by having low stomach acidity, in my view, that

Speaker 2 you're then bullying more food in on top of a chemical digestion problem, where the reverse is probably back off on foods,

Speaker 2 correct the chemical digestion problem, correct if there is dysbiosis. It can be difficult to address naturally.

Speaker 2 You might need some level of targeted therapy to work with, you know, a functional practitioner or a medical doctor or whatever

Speaker 2 that can target based on stool testing, okay, yes, there's a pathogenic bacteria present that is correlating the symptoms.

Speaker 2 Most people that go through like gut healing protocols that are based on supplements rather than data and you know, an outcome that's driven by data end up with gut problems where they, you know, they take supplements like olive leaf extract or oregano oil or whatever,

Speaker 2 which do have some spectrum of activity to killing bad bacteria. Again, I don't like that word, but bacteria that's causing you discomfort.

Speaker 2 As soon as you stop using these things, and even antibiotics, if you use antibiotics for SIBO or small intestinal bacteria overgrowth, unless you correct the patterns that led to that bacteria getting into your body, which is your sterilization tanks, your bile health, and ultimately your stomach acidity, you're just inviting more of it to be swallowed back in and start growing again.

Speaker 2 So, you know, every sort of gut strategy has to fix digestive problems and improve the

Speaker 2 strategy of respecting that acidity in the stomach before you even then think of using whatever herb or antibiotic to address the gut bacteria if needed.

Speaker 2 So, yeah, I think betaine ATL,

Speaker 2 what you've got is trimethylglycine or betane, which is a recycler of homocysteine in the body. So it helps your body convert it back to methionine for methylation.

Speaker 2 It's useful as well. It's an osmolite, so it helps with improving electrolyte distribution in your body.

Speaker 2 What you're doing there is you're taking a four-dohydrochloride salt aspect of the betaine.

Speaker 2 So you're putting HCl directly into the stomach as a salt form to improve the hydrogen content of the stomach.

Speaker 2 When you look at

Speaker 2 the output of stomach acids that you create per day,

Speaker 2 off the top of my head, it's about

Speaker 2 0.15 molar in concentration,

Speaker 2 which is a relatively,

Speaker 2 I guess.

Speaker 2 Looking at the acidity of HCl, it's a relatively strong acid molarity. That's sort of the amount of molecules in a liter of fluid molarity.

Speaker 2 Or moles per liter, I should say, without getting into chemistry.

Speaker 2 With the stomach, from that aspect, when you take betaine HCl,

Speaker 2 in order to achieve about 5%

Speaker 2 of the acidity of your stomach with betaine HCl.

Speaker 2 And I'm a bit nerdy, so I do calculations like this.

Speaker 2 You're looking at between five to ten capsules of betaine HCl to achieve around 0.02 to 0.04 molar of hydrogen, which contributes to acidity. So to contribute to about 5%,

Speaker 2 5 to 10% of your stomach's acidity.

Speaker 2 You're looking at between 5 and 10 capsules of betaine HCl. If you've got an issue with stomach acidity, and that's lowballing in at the very bottom end of like a 5%

Speaker 2 adjustment on top of what you should be making daily. The problem with pataine HCL, you know, when you look at it, what you're doing there is you're increasing stomach acidity.

Speaker 2 That you have to be very careful. If you have

Speaker 2 undiagnosed peptic ulcers or bleeding, you're creating a bigger acid pool, which is going to eat quicker into that that ulceration. Or if you've got H.

Speaker 2 pylori, which is a bacteria that does live in a lot of people's guts, if that is the thing that is contributing to the ulceration and more stomach acid being pumped out to allow it to proliferate, you're making that problem much worse.

Speaker 2 So

Speaker 2 it's a useful thing if someone does have potential low stomach acid. It could be a strategy they might

Speaker 2 consider, but being mindful that you know there is pros and cons that

Speaker 2 you don't want to just start taking a load of betaine H cell because on the other side,

Speaker 2 betaine, which is the other side of the hydrochloride salt, plays into methylation.

Speaker 2 So now you can be speeding up methylation or the conversion of methionine to Sami by putting a big chunk of betaine into your body. So it's

Speaker 2 you can get hydrochloride in liquid formats. There are

Speaker 2 you know, certain supplements where you dilute that into water, you know, five or 10 drops or whatever, based on the concentration of the product to try and get some level of acidity into your stomach.

Speaker 2 The same way people view apple cider vinegar as something that helps with stomach acidity.

Speaker 2 Useful, but like anything, and supplements, there's just it's a double-edged sword. There's pros and cons to it.

Speaker 1 You often hear coaches say during prep, for example,

Speaker 1 or at least you often see them implementing something to keep androgenicity high. So I was wondering if you can explain the benefits to higher

Speaker 1 androgenicity or an androgen ratio. Like, what is the reasoning behind this?

Speaker 2 That is a very good question. I guess

Speaker 2 when we look at

Speaker 2 studies that investigate serum balance between testosterone and estrogen,

Speaker 2 in theory, the ratio that's maintained optimally or should be maintained optimally within the serum is approximately one estradiol for every 200 testosterone.

Speaker 2 That's sort of the estrogen to androgen ratio.

Speaker 2 I guess

Speaker 2 when you do that calculation based on serum, testosterone, and serum estradiol,

Speaker 2 one flaw of that in an anabolic steroid setting is

Speaker 2 most of these compounds aren't detectable in bloods. So you're never going to get a serum level of what's Tren or what's primobol or mastron doing to your serum androgen level.

Speaker 2 The best assumption, in my view, that you can make is

Speaker 2 let's say, for example,

Speaker 2 you're taking

Speaker 2 150 milligrams of testosterone,

Speaker 2 and that is creating an androgen to estrogen ratio in your bloodstream of 200 to 1. Let's just call these arbitrary numbers.

Speaker 2 My

Speaker 2 reductionists, so we're going to make assumptions here, is that for every other 150 milligrams of another androgen, you're adding an extra 200 to that ratio.

Speaker 2 So if you've got 150 primobolin, based on that reductionist calculation, and this isn't strictly correct because you have to view what happens to primabolin when it gets metabolized and interacts in the body, et cetera.

Speaker 2 But trying to understand how that weighted strategy is happening,

Speaker 2 you then have to then realise, well, if you've got this balanced ratio of in the bloodstream, because again, inside your cells is a completely different picture,

Speaker 2 of 200s to one,

Speaker 2 adding in another 150 now takes you to 400s to one, which

Speaker 2 then as you add more androgens in this sort of androgen balance,

Speaker 2 you can be heading towards more androgenic side effects. So like this sort of spillover that we talked about, where now the molecule,

Speaker 2 you know, this is the whole thing around selective androgen receptor modulators.

Speaker 2 We just want to interact with the androgen receptor inside muscle tissue and disregard every other tissue of the body, whether it's hair, skin, immune cells, whatever.

Speaker 2 If you now improve that ratio

Speaker 2 and androgenic side effects start to become apparent, where you're now interacting with skin, hair, etc.

Speaker 2 That

Speaker 2 in theory,

Speaker 2 you've made again, it's an extrapolated calculation because you can't measure what's in the bloodstream. You're then making the assumption that by doubling that balanced 200 to 1 to 400 to 1,

Speaker 2 whilst you now are in a more androgen-dominant environment, which in theory lowers estrogenic side effects or counteracts some of the effects of estrogen, you're now heading towards more androgenic side effects.

Speaker 2 Most bodybuilders

Speaker 2 probably do care about the hair and don't really take care of it until it's too late.

Speaker 2 And then the other side, they sort of just accept some level of acne as being a consequence of what happens with androgens.

Speaker 2 Maybe the other strategy there is once the androgen side effects start to manifest, that

Speaker 2 it's sort of a subtle way of telling you that that balance is out of control.

Speaker 2 And by calculating, like I said, your testosterone to estrogen ratio in your serum, you can try and make extrapolations off where your testosterone level is for an X dose and try and

Speaker 2 mirror or manipulate that value based on your androgens.

Speaker 2 It's quite often, you know, someone could be taking

Speaker 2 TRT, 125 tests, testosterone and estrogen on bloods looks good. So that ratio is 200 to 1.

Speaker 2 But they're not thinking about the extra 300 or 400 milligrams of primo that's stacked in on top of that serum testosterone, that that ratio is moving more towards androgenicity than a balanced, favorable point.

Speaker 2 Because again, if we're below 200 to 1,

Speaker 2 in tier, you're making more estrogen. relative to your serum testosterone, which can bring estrogen side effects.
So

Speaker 2 there's a sweet spot, but when you start adding in androgens on top, that androgenic ratio gets very skewed because it's an assumption calculation.

Speaker 2 And you're trying to use that assumption to correlate to something that is potentially happening physically, hair loss or side effects or whatever.

Speaker 1 Okay, gotcha.

Speaker 2 Yeah.

Speaker 2 What way would you view it or what's sort of been the classic way of viewing it? Because I might have a completely different way of viewing it.

Speaker 1 No, no,

Speaker 1 I think

Speaker 1 we're pretty on point, but

Speaker 1 I just always found it interesting that

Speaker 1 I made the argument that I wanted to keep the trend low, for example.

Speaker 1 And he made an argument of adding in another compound or increasing it to a certain dose just to keep the androgen level where he wanted it.

Speaker 1 And I think that's always interesting to me because when I think about a high androgen level, I'm thinking about a lot of the side effects that are associated.

Speaker 2 Yeah, you're thinking of the bigger picture, like it's

Speaker 1 really

Speaker 1 the benefits, I guess.

Speaker 2 Yeah, you're thinking cautiously of when I put this extra, you know, when we're talking 50 milligrams,

Speaker 2 when you work out the number of molecules in a certain dosage of a drug based on like molecular weight and the the weight of the substance you're ingesting,

Speaker 2 you know,

Speaker 2 to put it in perspective,

Speaker 2 10 milligrams of anovar is like quintillion, trillion, billion in terms of like molecular number. But like, we'd look at 10 milligrams of anovar and think, God, it's a very small dose.
But it's

Speaker 2 like it's

Speaker 2 like 10 to the power of 18. You're like, you've got 18 zeros after your number.

Speaker 2 It's huge. And we tend to dissociate where, like, you're seeing there, but sure, it's only 50 milligrams of TREN.

Speaker 2 That 50 milligram is, like I said, quintillion, billion, trillion added interactions in your body, whether that's androgen receptor, liver, skin, hair, whatever, brain.

Speaker 2 You're thinking of it logically:

Speaker 2 is that extra 50 milligrams all going to go to my muscle? And that's the strategic way of thinking about it: of

Speaker 2 what's my benefit-to-risk ratio of these added interactions from this drug dose.

Speaker 2 And you don't have a predictability. You might have some level of gut instinct that, you know,

Speaker 2 I'm pretty sweet with where I am now.

Speaker 2 If we had another 50 milligrams, like you said, now I'm going to have unwanted brain interactions, which are driving catecholamines up, which are going to cause insomnia. It's going to slow down COMT.

Speaker 2 It's going to affect your estrogen metabolism and affect your methylation and your magnesium stores. And there's a big knock-on there that you're thinking of it logically logically.
Of well,

Speaker 2 50 milligrams on paper sounds like a small number in the grand scheme of when we're talking like grams of gear.

Speaker 2 But truly, what does that 50 milligrams bring me positive over the other negatives that you're thinking about?

Speaker 2 Yeah.

Speaker 1 If you haven't gotten your test, if you haven't gotten yourself tested for methylation problems, when would you recommend someone take methylfolate?

Speaker 1 If any, I'm assuming you would be like, oh, just get tested first.

Speaker 2 I mean, this is where genetic testing,

Speaker 2 some people,

Speaker 2 I wouldn't say prey on it, but if you end up with having, let's say, MTHF4 genetics, so metal tetrahydrofolate reductase, where

Speaker 2 you

Speaker 2 aren't as efficient at creating the required metal

Speaker 2 aspect to generating methionine.

Speaker 2 So folate and B12, metal folate, metal B12 play off homocysteine to recycle it back to methionine. So,

Speaker 2 they do a chemical conversion process to recycle homocysteine back to methionine, which then creates SAM-E-S-Adenosyl methionine, which is your metal donor.

Speaker 2 If you get your genetics tested and you find that you have MTHF4 in terms of a poorly functioning MTHF4, so that recycling of homocysteine back to methionine is poor,

Speaker 2 I don't think you need genetics to tell you that problem. You just check your blood work.
Your serum, homocysteine, will tell you how well are you pushing homocysteine back to methionine.

Speaker 2 And functionally, the levels of homocysteine that are often recommended for optimal methylation is between eight and nine. That's sort of the sweet spot.

Speaker 2 With that, you know, you're then seeing optimal conversion where you have balanced folate in B12 from your nutrition or from supplementation, pushing homocysteine back to methionine if it's in that sort of optimal range of eight to nine.

Speaker 2 If you have MTHF4 and you don't check homocysteine and you take a load of folate in B12, you could then feed into over-methylation, which has its own problems versus under-methylation.

Speaker 2 You know, over-metallation can play into insomnia,

Speaker 2 mood disturbance in terms of like volatile moods.

Speaker 2 It's

Speaker 2 like any supplements, I wouldn't just chuck in

Speaker 2 a high dose of metal folate, metal B12, just on the off chance that you could be metal donor,

Speaker 2 like deficient, or to improve the efficiency of methylation.

Speaker 2 A crude way of testing this,

Speaker 2 and this was something I learned from a seminar from Dr. Ben Lynch, who's a great expert on methylation.
Again, people for following.

Speaker 3 He

Speaker 2 has basically said that you can sort of test how well your methylation is operating, and that

Speaker 2 if you take Sam E prior to bed and it doesn't cause insomnia, so you take Sam E, like 200, 400 milligrams of Sam E before bed, so let's say 7 p.m., 8 p.m.,

Speaker 2 and you fall asleep, no problem, you're probably metal donor deficient.

Speaker 2 If it goes the other way and causes insomnia, you now have an excess of metal donors, or you're over-methylating.

Speaker 2 That

Speaker 2 some of the things that deplete metal donors in the body, vitamin B3 or niacin, can help to sort of quench over-methylation.

Speaker 2 That is crude tests: you take your SAME, and then if you have insomnia, you take a dose of niacin to try and clear out the excess metal donors.

Speaker 2 But

Speaker 2 I've never suggested someone just do crude tests. Yeah, it's useful

Speaker 2 if you don't want to fork out money on a blood test. Fair enough.
But

Speaker 2 just check homocysteine and that way it'll give you an accurate idea. You know, you're going to get your serum folate and

Speaker 2 B12 on your general blood panel normally.

Speaker 2 But what's in your blood doesn't necessarily mean what's being used by your tissue. So you have to view the blood as what is in your bloodstream, not as what's inside your cells.

Speaker 2 If we have high amounts of homocysteine in your blood, it's come from your cells and that recycling capacity. So, you now know, okay, well, I need folate and B12 to improve that recycling.

Speaker 2 That, you know, that stands your folate and B12 and serum could look good, but your homocysteine could be above eight or nine, meaning that you probably could benefit from an increase from your nutrition, whether that's green leafy vegetables thereof, or using a supplement.

Speaker 2 Just like I said, with methylation and menthol donors,

Speaker 2 you can't hit a point where it causes worse problems than under methylation. Like you go from low mood to actual like mania or aggressiveness or insomnia, that there's a fine balance there.
But

Speaker 2 genetics, it's probably one of the ones, like this is a great point you brought up.

Speaker 2 Your genetics don't necessarily mean that you've got a problem that you need to fix with MTH or 4 if your nutrition is satisfying your genetics.

Speaker 1 Okay, got it. The motherfucker gene.

Speaker 2 Yeah.

Speaker 1 All right. Before we go to the QA, I just want to ask because I totally forgot earlier, but you said you were mentioning abuse now versus the 90s.
What do you see

Speaker 1 regarding abuse now?

Speaker 2 Abuse.

Speaker 1 Just regarding, or even just regarding use in general?

Speaker 2 I guess

Speaker 2 maybe it's things are underdosed,

Speaker 2 but you know, there are

Speaker 2 I've seen in terms of like

Speaker 2 what

Speaker 2 other coaches have with like clients coming to them using personally before they coach this person

Speaker 2 where the person's on like three to four thousand milligrams of total androgens and their physique doesn't reflect what that dose

Speaker 2 should create.

Speaker 2 What they're taking is completely bunk, which can often sometimes be the case,

Speaker 2 or there's just this delusion. You know, yes, we know from Bazin's study that you take testosterone and you're going to see an increase in

Speaker 2 fat-free mass. I'm not going to say laying tissue because fat-free mass is how it's accurately calculated.

Speaker 2 Increase in people who took testosterone and didn't necessarily resistance train.

Speaker 2 That there's almost this assumption that, like that, you take more gear, you're going to get bigger, but not have to do the work.

Speaker 2 And to be honest, with

Speaker 2 how accessible information is now and it becoming, you know, openly talked about, like we began the conversation, seeing someone take 2,000 milligrams of testosterone and think, oh, if I take that dose, I'm going to be their size based on what they observe in a social capacity.

Speaker 2 Not realizing that, you know, there's been years of muscular development to get to that person's physique, the routines and habits that play into it and everything else.

Speaker 2 It's, I guess, years ago, it was the reverse.

Speaker 2 It was like, I'm going to take this really high dose because in theory it makes sense the more i take the better i get whereas the other side of it is they're seeing guys use high dosages publicly or discuss publicly and think that that's the acceptable dose that has to be taken to start with

Speaker 1 until until a coach tells them okay well perhaps what you're doing here is quite excessive and let's go back to basics yeah i like uh i like chris and jordan hutchinson's example of how they titrated it up after a long period of time off and those low dosages were extremely effective for him um do you feel like there is a

Speaker 1 what was i going to ask um

Speaker 1 like what what is the term that you would can what what is the term that you would use for

Speaker 1 i guess

Speaker 1 uh tolerance buildup or like resistance to um

Speaker 1 resistance to

Speaker 1 reaction or benefit of a certain dose

Speaker 1 like i think kurt uses the word homeostasis

Speaker 1 but I don't know.

Speaker 1 Interesting to use.

Speaker 2 I guess homeostasis would infer like your body's own natural balance. And I'm not going to argue, you know, what someone perhaps uses as a definition.

Speaker 2 I guess

Speaker 2 when you reach a point

Speaker 2 of

Speaker 2 no further return from a drug dosage,

Speaker 2 in my view, from a pharmacology perspective, you've reached drug dosing saturation.

Speaker 2 So

Speaker 2 when drugs are being designed and developed, and we're looking at how X drug causes Y effect,

Speaker 2 you do have empirical dosing, which is basing on body weight. So you dose it in animals, and then you go, okay, well, the human equivalent dose from the animal is this.

Speaker 2 And so you start your clinical trial roughly around your human equivalent dose.

Speaker 2 If it passes safety clearance for a small

Speaker 2 random control trial,

Speaker 2 what you'll often see is

Speaker 2 they'll kick that human equivalent dose and then observe the effects. It's not like, oh, this dose is this many molecules, which will fit this many receptors.

Speaker 2 It's still sort of scaled from the assumption of what we've observed effect-wise cellularly from cells to animals and then to humans you end up with a dose response curve so you you know you start off low you see no effect and you start to see some effect some effect and that that saturation curve see it keeps going up at some point your your drug response curve hits a point where you see

Speaker 2 i guess optimal outcome in terms of like balanced interactions where we're we're interacting with the receptor efficiently to create whatever effect. Let's just say, let's just say a pain medication.

Speaker 2 You're seeing a reduction in pain symptoms from X dose.

Speaker 2 You keep increasing the dose.

Speaker 2 You're not necessarily increasing the outcome of the symptom. You're now increasing the drug's concentration where it's spilling over into other aspects of the body.

Speaker 2 So now you're into saturation basically. And at that point,

Speaker 2 saturation, your curve can fall basically into low therapeutic level. So you've got your therapeutic index, which is like a window where you have effects.

Speaker 1 Do you mind if I interject real quick?

Speaker 2 Yeah.

Speaker 1 Do you feel like that's like, is that associated though, with just if you're on the same dose over a long period of time and then you start reaping less and less benefits?

Speaker 2 So if you're doing that, I guess if you're on the same dose for a longer period of time and you're seeing no further benefit

Speaker 2 in terms of

Speaker 2 homeostasis,

Speaker 2 that would infer that your body's metabolism, to speak, has balanced itself to the drug exposure.

Speaker 2 So you're now seeing no further rate of gain of muscular tissue, if that's the outcome of anabolic steroids,

Speaker 2 because of a balance in potentially energy in, energy out, which

Speaker 2 I'm not an expert here, and I'm not going to know I know the data inside out, but you know, there's a lot of people arguing that you need very little in terms of energy surplus to gain muscle tissue.

Speaker 2 Is that going to be the optimal rate of gain in terms of like time it takes to gain? Um, I can't, I've got nothing to argue there, so I just listen to what people are more experts than me on.

Speaker 2 But

Speaker 2 if you're on a certain dose for a longer period of time and now it's not yielding a benefit, you then have to realize: then, are you at that

Speaker 2 drug saturation level where the androgen receptors are being occupied maximally?

Speaker 2 And in order to elicit a change, you need either more androgen receptors, so you increase the dose, which up-regulates the androgen receptor,

Speaker 2 or you take a break where you reduce the drug exposure. Androgen receptor levels have

Speaker 2 it's not like

Speaker 2 insulin where the receptor internalizes off the surface of the cell. But by reducing the dose and the exposure to the compound,

Speaker 2 further downstream some of the genetic road stops that could be interfering with gene transcription to cause more muscle mass to be developed, folestatinum and whatever else,

Speaker 2 taking that break might allow that drug to become therapeutic again, if you want to use that word. You know, you've got that therapeutic window where the drug is creating the effect you want.

Speaker 2 Beneath that therapeutic window, there's no effect, or you just, you're not no optimal effect. And above that window, you're into toxicity or unwanted interactions.

Speaker 2 I'd probably prefer, like,

Speaker 2 from a drug perspective, that you're at saturation, that you're, you're now, you're now at a point where

Speaker 2 if you put more drugs in, more androgen molecules, you're going to elicit more androgen receptors being made.

Speaker 2 Does that increase in androgen receptors mean you're going to gain more muscle mass or muscle tissue in theory

Speaker 2 from anecdotal reports and history? In theory, it does go up. But then there's all the other things that put

Speaker 2 a stop on the rate of muscle gain as well.

Speaker 1 I thought the rise in androgen receptors was from the increase in muscle mass over time. So

Speaker 2 as you increase,

Speaker 2 to my knowledge, I've never seen that, but I could be wrong. And

Speaker 2 I'd be openly happy to read on that. To my view,

Speaker 2 the increase in androgen receptors that comes from the increase in the drug concentration, which increases the androgen receptor, response or the regulation of the protein to create more receptors.

Speaker 2 The more receptor you create, the more genetic signals you send to the nucleus to increase muscle density.

Speaker 2 But, like you said, the more muscle you gain, and the more androgen receptors interior you have in your body, which then comes back to what we talked about:

Speaker 2 whilst I said you might need lower drug concentrations, you still need to be hitting how many androgen receptors inside that muscle to maintain its genetic response.

Speaker 2 So, I think

Speaker 2 where you hit this balance of diminishing returns, where you're left with a choice of either up the drugs

Speaker 2 or you

Speaker 2 take a step back and lower the exposure,

Speaker 2 it's not that

Speaker 2 the receptor down-regulates.

Speaker 2 We've enough papers and evidence to suggest this doesn't happen, that the androgen receptor down-regulates like an insulin receptor, where an insulin receptor becomes desensitized. It's just that

Speaker 2 everything on top of it i guess you know heavy training high food volumes everything else sometimes it can be a lifestyle that's impacting how you gain muscle mass where you're not sleeping properly bile flow acid health digestion slows down that

Speaker 2 indirectly can come from the drugs themselves where taking a break naturally resolves some of that road block and now all of a sudden you can eat again you can sleep you can recover from training.

Speaker 2 You might deload where you're pushing your body hard, and that deload from training results in a rebound in PRs or an increase in training

Speaker 2 intensity because of your rest of the body.

Speaker 2 I think when you hit that point of diminishing returns, either something is affecting rate of muscle gain genetically, that I don't know the

Speaker 2 ins and outs from a muscle protein synthesis perspective of what everything that feeds into halting muscle protein synthesis.

Speaker 2 That it's either something like that or it's environmental that's halting you.

Speaker 2 Like you've hit drug saturation, is basically what I'd be hinging on, rather than the body has gained some level of like balance or

Speaker 2 symbiotic relationship of balance where the androgens are balancing out metabolism that the body's just happy to stay where it is.

Speaker 2 If that was the case,

Speaker 2 further increasing the dose wouldn't overcome that homeostatic curve, to speak, because

Speaker 2 balance has been achieved. So your body sort of then sat in a place where it's able to keep things steady.

Speaker 2 You know, when we're looking at homeostatic levers,

Speaker 2 you get a temporary shift in one direction, but quite quickly it's brought the body brings it back into balance really quickly.

Speaker 2 Like the kidneys, you can, with fluid manipulation and electrolyte manipulation, you can artificially suppress anti-diuretic hormone before a show.

Speaker 2 But as soon as you sort of reduce those strategies, the body's homeostatic set point is like 12, 20 hours.

Speaker 2 that all of a sudden now you're retaining fluid for a while while the body balances out from that, you know that that balance.

Speaker 2 So, homeostasis tends to mean that the body comes back to balance very quickly.

Speaker 2 That doesn't necessarily happen with a high drug concentration if you want to speak in it strictly that way, but it could be a nice way of explaining something in a more simple fashion and you know, drug receptor saturation, or you know, you've hit the limit on that therapeutic window, if you want to even call it a therapeutic window.

Speaker 1 Gotcha.

Speaker 1 I truly believe that

Speaker 1 after talking to all the figures that I've discussed these topics with the coaches and the athletes, I truly believe that coming off is the right answer.

Speaker 1 I think in terms of at least being optimal for not just like long-term health, but also long-term overall gains, it just seems to be a better marker.

Speaker 1 Plus, I've experimented myself with the rebound phase last year. Honestly, I don't think it was as

Speaker 1 I don't think the reward was as good as I thought it was going to be.

Speaker 1 To be honest, I feel like I actually had a greater reward when I took a long health phase and just off of everything for a good long period of time and then jumped back on.

Speaker 1 And I just felt like it was a lot more optimal then. So

Speaker 2 that's going to be the new.

Speaker 2 You have to view what's happening in the health phase. You're reducing drug exposure.

Speaker 2 So on one side, you are taking some level of molecular stress away from your body, but moving into a health phase to speak, in terms terms of how they're normally set up from a coaching perspective,

Speaker 2 it's normally like lower training intensity. Not that we're fluffing training, but there's lower training intensity.
Food tends to fall into either a maintenance or just above maintenance level where

Speaker 2 you're eating to appetite, where you're not starving hungry.

Speaker 2 You're happy with a level of body fat gain, which brings you back to your genetic, you know, there's an example of homeostasis. You have a genetic set point of body fat that

Speaker 2 your body will naturally try and gravitate back to, where that's you know, through increased appetite to get you to eat.

Speaker 2 Which, over time, the more disciplined you are and the more metabolically flexible you are, you can change that set point.

Speaker 2 But you're always going to try and gravitate back to that natural where you're like, whatever, eight to ten percent body fat without throwing numbers out there, but you're eating three, three and a half thousand calories.

Speaker 2 You're in a much more optimal environment from a lifestyle perspective that everything else just follows beyond there then. So you're not,

Speaker 2 the reduction in drug dose plays into your lifestyle as well as into your biology as well.

Speaker 1 Yeah.

Speaker 1 I've been training for over 15 years now, and I was too lazy to track anything training-wise for about the first 10 years Cause science-based training is for pussies.

Speaker 1 But I kept hitting plateaus from burnout, fatigue, joint issues, and injuries, and other factors that at the time I didn't really fully understand.

Speaker 1 Realizing not everyone is built to handle the intense, insane workload and injury resilience as Tom Platts and Ronnie Coleman, sadface.

Speaker 1 I wanted to speedrun that shit, but the reality is, dudes that have always known their body best are the ones that have been lifting for at least a decade. Shit takes a long ass time to figure out.

Speaker 1 I started tracking all my training on the notes app on iPhone because I don't know what paper is. Until recently, I started using the RP Hypertrophy app.

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Speaker 1 Well-educated coaches have always cost $250 to $500 or more a month. I'm paying $500.

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Speaker 1 It'll base this on your pump, how fatigued you feel, how your joints feel, and more. It takes in everything to account.

Speaker 1 None of which I took into account in college because the only accounting I did was counting how many dumpies were in my class.

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Speaker 1 Yeah, I think it was really cool to see Terrence, Terrence, and both Jordan gain so much after they took so much time off of training stimulus and obviously PED stimulus, too.

Speaker 1 So, I mean, it sounds very promising.

Speaker 1 Plus, just having like,

Speaker 2 I don't know,

Speaker 1 world seems to run best when it's running cycles.

Speaker 2 That is true. I mean,

Speaker 2 going back to the 90s,

Speaker 2 watching, you know,

Speaker 2 I grew up in the era where we watched bodybuilding DVDs

Speaker 2 that, you know, people shared around and watching, you know, Kevin Lavron's Maryland muscle mayhem, muscle machine, whatever it was called.

Speaker 2 And, you know, Kevin was the classic example of like

Speaker 2 would compete, do Mr. Olympia,

Speaker 2 do a little bit of tour, and then take six, six months off, five, six months off, and then just rebound back into the next Mr. Olympia.

Speaker 1 And it's hard to believe like some of these numbers that they give, like five, six months off. It's super hard to believe, but

Speaker 1 it's, it does seem consistent over all the people that do take long breaks that they gain the most mass. It's, it, it feels so contradictory because, like, you want to just fucking run year-round.

Speaker 1 But I mean, same thing with caffeine and all the other substances we use, right? Like, I will cycle anything that, anything that helps

Speaker 1 my

Speaker 1 well, I guess I'm not cycling enough because it's not working really well enough for peak week, but I will cycle on things that'll uh help my like brain, my um brain quality and my thought process well.

Speaker 1 And if I run it every day, it doesn't work. It doesn't like alpha brain, um, caffeine, any of these things, they just over time it's like it just starts hitting this,

Speaker 2 yeah, you know what I mean? Uh, yeah, you you don't see that the

Speaker 2 like the stimulus uh response being as as high as it should. I think, you know, the other side of the view,

Speaker 2 I've done this personally

Speaker 2 back in 2005. I'm trying to remember now, years.
2015, I took like four months off bodybuilding. I sort of,

Speaker 2 I don't know, just

Speaker 2 the monotony of being a bodybuilder for day in, day out for three years.

Speaker 2 I just, I don't know, I couldn't, mentally, I couldn't bring myself to go train in the gym, you know, as

Speaker 2 blasphemous as it is, I, I maybe trained maybe once a week, if I felt like doing it, between like January and April. And then

Speaker 2 eventually, you know, the love, you know, you're doing like one session every few weeks, you sort of then start to appreciate training in the gym and appreciate training for what it does for you mentally and physically.

Speaker 2 That

Speaker 2 like anything, if you're,

Speaker 2 you know, if you're a rock star and you're touring every

Speaker 2 like week of the year and you're playing multiple shows per week, I'm sure eventually the buzz of playing to the solo stadium wears off where

Speaker 2 the tour fatigue, you know, your performance on stage as a musician.

Speaker 2 wanes off where they take breaks because they don't want to look at their instruments and that's why sometimes you know, I guess looking at very popular bands, it can be years between albums because of the touring demands and then trying to fit writing and recording in a studio when you're already fatigued from such a high performance output.

Speaker 2 It could be the same, you know, bodybuilding, you're doing this, you're thinking about it all the time. If your goal is to become professional,

Speaker 2 your daily habits and routines revolve around it, that eventually, you know,

Speaker 2 your mind could be one of the limiting factors where

Speaker 2 taking a break away from it gives you that sort of stimulus. That when you go back to it, it's more beneficial for you, as you know, paradoxical as

Speaker 2 you're saying.

Speaker 1 Yeah.

Speaker 1 How do you feel about GH timing? Where do you stand on that?

Speaker 2 I've always said a growth hormone should ideally be timed before bed, in line with how it's prescribed.

Speaker 2 I guess

Speaker 2 my viewpoint

Speaker 2 was: if you're doing it fasted in the morning time before cardio,

Speaker 2 knowing about the distribution of how growth hormone is absorbed, you know,

Speaker 2 pharmacokinetic-wise, it takes about one and a half to two hours for growth hormone to peak in your body exogenously when you injected sub-Q.

Speaker 2 It's much, much quicker with IM, Although, in theory, the argument between IM and sub-Q

Speaker 2 area under the curve of the actual serum level over time is roughly similar between sub-Q and IM.

Speaker 2 With

Speaker 2 doing it in the morning time, my

Speaker 2 caveat to that proposition is

Speaker 2 people are going to wake up, go to the fridge, take

Speaker 2 one unit of growth hormone, let's say, as a very low lipolytic dose, if you want to put it that way,

Speaker 2 and then go do their cardio fasted within like 20-30 minutes, drive to their gym or go out to their garage, wherever, and do their cardio.

Speaker 2 But that lipolytic window from the increase in growth hormone from the injection they've given themselves before the cardio is really only starting to peak in their body about an hour and a half, two hours after they've injected it.

Speaker 2 So, unless you're strategically getting up two two hours earlier to inject your growth hormone, go back to bed, to then get up for your cardio when it's peaking in terms of lipolysis

Speaker 2 or serum level, because obviously lipolysis doesn't switch on with growth hormone.

Speaker 2 I just always viewed growth hormone as being this

Speaker 2 physiological aid towards recovery.

Speaker 2 There's no doubt from what we've observed, you know, anecdotally that

Speaker 2 changes happen in terms of hyperplasia with satellite cells, the higher your IGF-1 exposure is, not necessarily growth hormone.

Speaker 2 But

Speaker 2 if you're taking it all throughout the day in terms of split dosage,

Speaker 2 then

Speaker 2 you're,

Speaker 2 I guess, coaxing

Speaker 2 somatostatin to increase in tandem. So you're always going to blunt how your body's releasing its own natural growth hormone.

Speaker 2 That's fine if you want to commit to a strategy where every few hours you're going to pulse in two or three units of growth hormone.

Speaker 2 That's fine. But then you have to view that

Speaker 2 before you go to bed and you take your dose, your timed dose, you're taking two or three IUs of growth hormone every three or four hours, let's say, as one peak is rolling off after about six or seven hours.

Speaker 2 You're putting in another dose a half the time, basically.

Speaker 2 When you go to sleep that night, you're relying on what you've injected over what you could capably produce naturally based on your circadian rhythm and your somatotrophs in your body.

Speaker 2 That

Speaker 2 there's nothing wrong with that, but you have to commit to that strategy all the time of continuously pulsing rotom and otherwise somatostatin is going to be blocked in your natural output.

Speaker 2 Viewing it that way, that

Speaker 2 increase in lipolysis with that continuous exposure to growth hormone at

Speaker 2 let's say optimal levels. Let's say we're doing two or three I use of growth hormone every few hours, which was done in the past as a strategy with insulin.

Speaker 2 Lipolysis,

Speaker 2 I think lipolysis is something that

Speaker 2 is obviously our end goal as bodybuilders getting on stage of releasing fatty acids to fuel our body.

Speaker 2 The reverse with those

Speaker 2 chronic fatty acids oxidation can have metabolic effects that impacts our insulin sensitivity due to the increase in fatty acids in our bloodstream, but also affects our mitochondrial work and how we utilize glucose in the mitochondria as well.

Speaker 2 So you're downstream creating some level of glucose resistance or a preference to burn fatty acids,

Speaker 2 which then can starve cells with glucose utilization, which can cause health problems or can create metabolic problems.

Speaker 2 My view on it is to use growth hormone prior to bed

Speaker 2 as a replacement strategy, in that on average, you're going to make

Speaker 2 depending again genetics,

Speaker 2 some research suggests on body weight, but again, I don't really believe body weight, but this is how it's scaled and dosing with growth hormone and dose response curves.

Speaker 2 That on average, you're making anywhere from like 1.5 I use

Speaker 2 up to maybe four IUs of growth hormone at night, four I use being like the very top,

Speaker 2 but also that's then further underlined by your IUGF-1 score and your Z score of where you fall in the populations level.

Speaker 2 So, obviously, IGF-1, we can measure IGF-1, we can get a relative understanding of what conversion process is happening from the GH you've taken exogenously.

Speaker 2 But it's more important to sort of see, well,

Speaker 2 where was my initial baseline IGF?

Speaker 2 And where has it moved to with whatever dose in terms of therapy? And what you're looking for is your Z score to go up anything above two

Speaker 2 in terms of like standard deviation of where you are versus the population is considered supraphysiological igf

Speaker 2 if if you're doing it before bed you're understanding that it takes three to four hours to peak in your system and this is where where it's prescribed for people have kick axe or muscle ways to do it eight

Speaker 2 you're understanding that you dose before bed knowing that three to four hours into sleep you're getting this big maximal peak of growth hormone.

Speaker 2 With that, you have the opportunity, based on circadian rhythm, as the drug level is peaking from the injection, to still produce some growth hormone from your circadian output.

Speaker 2 Because there shouldn't be anything limiting somatostatin, maybe

Speaker 2 grelin impacts from the food you've eaten and your nutrition.

Speaker 2 But you have this window of maybe the first hour and a half of your deep sleep, which is obviously your most physically respirative part of sleep, which we think

Speaker 2 before we move into the later stages of REM and light sleep,

Speaker 2 that you're getting your body's own natural production of growth hormone and then adding the injected growth hormone on top. So you're getting like a one plus one effect.

Speaker 2 You've got your own body's natural production and then you're getting a peak from whatever dose you choose to use with growth hormone.

Speaker 2 And then as you wake up the next morning, because of the clearance profile based on circadian rhythm, what you've injected starts to clear as you wake up.

Speaker 2 So, the lipolysis that's happened in your sleep from the increase in growth hormone is now starting to roll off into daytime when you're more active.

Speaker 2 You've got muscular contractions influencing insulin sensitivity and glucose transport, that you're not creating this sort of

Speaker 2 blurred signal, I guess, of excessive lipolysis because of the increased growth hormone level in your body.

Speaker 2 It doesn't mean that dosing it multiple times throughout the day or doing IM injections, which some people, you know, argue and theory against. When you look at the research,

Speaker 2 the whole point of a sub-Q versus IM injection was compliance. You know,

Speaker 2 growth hormone deficiency is in pediatric populations, in children.

Speaker 2 It's a little bit easier to, compliance-wise, administer a sub-Q injection to either Thai muscle with a very short needle gauge or to the abdomen than it is getting a deeper needle and injecting it into the muscle.

Speaker 2 There's a lot more trauma. And to be honest, if you want this child to take this medication to proliferate bone tissue and whatever to grow to proper stature, they have to take this

Speaker 2 medication for a long period of time.

Speaker 2 Any sort of deviation to compliance becomes a negative. So, whilst I am, when you look at the data, results in a higher peak but a shorter window,

Speaker 2 when you view it versus

Speaker 2 sub-Q,

Speaker 2 you get a slower peak,

Speaker 2 well, a lower peak, I should say, but a slower distribution. That the area under the curve, when you draw a dose response curve, you do IM, you get a big peak and then you come down.

Speaker 2 So you have this shaded area where the peak goes up really high, but drops down really quick.

Speaker 2 If you do sub Q, you get this smaller peak, but it's over hours upon hours. So when we shade in the area underneath the curve, it's relatively similar between IM and sub-Q.
So

Speaker 2 IM generates a big, massive peak, a higher serum level,

Speaker 2 but rolls off quicker. Yeah.

Speaker 2 Sub-Q creates a lower serum level, but it's over a longer period of time. So some of the arguments are basically that you get a higher serum level with IM with whatever dose you choose.
Let's put

Speaker 2 four IUs versus four IUs sub Q.

Speaker 2 Yes, you're getting a higher serum level of growth hormone from the IM injection.

Speaker 2 Does that serum level mean more growth hormone receptor interactions versus the lower serum level over a longer period of time?

Speaker 2 You then have to then classically look at, well, what's the IGF that's being yielded directly from that area under the curve?

Speaker 2 And when we look at the area under the curve towards drug response, they're relatively the same.

Speaker 2 So it then comes back to, like I said, you get a big peak for IM, which is one of the arguments, which is valid.

Speaker 2 You get a big serum level, but that doesn't necessarily mean you're going to get a higher IOGF-1 serum level,

Speaker 2 and that that's more appropriate than a lower serum IogF1 level over a longer period of time.

Speaker 2 I'm not an expert in terms of the kinetics when it comes to IOGF-1, but having a higher level of IOGF-1 can invite then more binding proteins to be made, which then reduces the bioavailability of the IGF-1.

Speaker 2 Having a

Speaker 2 lower peak level, but a longer exposure could increase binding protein levels as well, reducing the bioavailability.

Speaker 2 I think

Speaker 2 there's just two camps. I don't sit in either one of them of, you know, you have to IM or you have to sub-Q.

Speaker 2 have to do it before bed you have to do it you know before fast at cardio i think looking at logically what happens when you take the drug, you have to then think, well, what am I gaining?

Speaker 2 Like what we talked about with the 50 milligrams of extra trend.

Speaker 2 If I do that GH I am in the morning before my fasted cardio, but I specifically on purpose do it about an hour and a half before that fasted cardio.

Speaker 2 So I'm going to fast for an hour and a half, let that big peak level happen.

Speaker 2 Is that peak and GH and the lip polysis that's

Speaker 2 induced from that high growth hormone level going to directly mean that over that 24-hour period, you're oxidizing more fatty acids

Speaker 2 versus not doing it until you go to bed that night?

Speaker 2 I don't think there's arguments for and against either. But in my view, based on how it's been administered to

Speaker 2 patients who need it as a therapy, it's always been before bed based on IM, it creates a higher peak level with too quick acting.

Speaker 2 When it's done sub-Q, it mirrors the circadian output of growth hormone of how it's produced, you know, peak nighttime, you know, 1 a.m. to 2 a.m., whatever, and then rolls off before you wake up.

Speaker 2 That sub-Q is designed to mirror how you make it naturally.

Speaker 2 And it just made sense that then, if you're going to utilize it, do it as a replacement whereby if your deep sleep is affected for whatever reason where you're a very light sleeper you've got kids you've got a stressful job that you don't get proper deep sleep or your sleep is very fragmented you have undiagnosed apnias

Speaker 2 you're you're using that as like

Speaker 2 a strategy to ensure that you have an optimal growth hormone level during your sleep for cellular repair and everything that growth hormone hormone plays into.

Speaker 2 So I don't think either argues

Speaker 2 argument is wrong. It's just thinking logically, well, what happens to the drug when it's done either way?

Speaker 1 Do you believe, Kurt's research, that

Speaker 1 I am

Speaker 1 there's 30% less growth hormone absorbed?

Speaker 2 I have never seen that paper, to be fully honest.

Speaker 2 Again, I'm not going to argue what someone says,

Speaker 2 but in terms of an

Speaker 2 inflammatory response that comes from

Speaker 2 growth hormone injected into the muscle interior,

Speaker 2 I guess

Speaker 2 looking at how growth hormone is constituted, it's an aqueous solution.

Speaker 2 So

Speaker 2 residency time of something that is aqueous, let's say we do inject it into a muscle cell, into muscle tissue, and into the muscle cell. Not even like

Speaker 2 we have to be very careful in how we view what's being spoken at here because

Speaker 2 injecting something into a muscle

Speaker 2 in theory, and this is abstract thinking, even though you've gone into the actual muscle tissue,

Speaker 2 you're going to have spaces between cells. So, in theory, you might not put the needle.
And so, what I'm trying to get people to visualize here is piercing straight into a muscle cell itself,

Speaker 2 rather than the space around muscle cells.

Speaker 2 I have not seen research

Speaker 2 that argues that it doesn't occur, so I can't argue or refute. And, you know,

Speaker 2 having

Speaker 2 absence of evidence doesn't mean that it doesn't occur. We have to, you know, if there is some place where it's come from, just because I can't find evidence of it, doesn't mean it can't occur.

Speaker 2 Similarly, we should have evidence to support if it does occur.

Speaker 2 But if something is injected into a cell specifically, like growth hormone

Speaker 2 and it's inside the cytoplasm of that cell, this is what again I want you to think about,

Speaker 2 I'd just see it potentially just leaving the cell because it has nothing to interact with with inside the cell. The growth hormone receptor is on the surface.

Speaker 2 So

Speaker 2 I'm not going to go against if it does occur, maybe that's why you see

Speaker 2 potential responses.

Speaker 2 But like I said, between IM and sub-Q, when you look at the area under the curve between the two administration methods, the area under the curve is relatively the same, which tells us that

Speaker 2 the availability or

Speaker 2 the release of the drug in both cases, the concentration, the total concentration delivered is the same.

Speaker 2 It's just IM delivers it quicker and higher versus sub-Q.

Speaker 1 Gotcha. Okay.

Speaker 1 What about GH post-workout to increase hypertrophy?

Speaker 2 Again,

Speaker 2 when you inject it, let's say you inject it locally.

Speaker 2 That's not to say there's not growth hormone receptors within like your biceps, but really what's causing the hyperplasia, we know is IgF-1, like local IGF-1 production from mechanical tension and then global IGF-1 conversion from the liver.

Speaker 2 If you do it, you know, post-workout

Speaker 2 and you inject intramuscularly into, say, a body part you want to grow, let's say your biceps, you want bigger biceps.

Speaker 2 Does that increase in growth hormone concentration locally, does that occur?

Speaker 2 Again, we have to view that an intramuscular injection peaks much quicker than a sub-Q,

Speaker 2 which means it peaks in serum,

Speaker 2 not peaks locally. So peaks in serum mean that your whole body has an increase in growth hormone level.

Speaker 2 Which isn't necessarily going going to contribute to an increase in growth from the bicep that you've trained.

Speaker 2 Does that stand for something like recombinant IgF1 or IGF-1 LR3 or IGF1 DES?

Speaker 2 Perhaps there's some strategy there of injecting locally into the site that has been trained that has seen an increase in IGF-1 expression from mechanical tension.

Speaker 2 But

Speaker 2 again,

Speaker 2 it's a water-based compound which will go into serum very quick once injected, which then goes to other parts of the body. So, what you're trying to catch there, it's like anecdotally,

Speaker 2 BPC-157, TB500, were always told to be injected at the site of injury, like injected as close as you can to that torn tendon or ligament.

Speaker 2 Not something you want to be telling someone who's had like a tendinograph operation of like having tendon reattached or whatever to start sticking needles in close to the injury site to get it to repair.

Speaker 2 It's water-based, so it diffuses and then it diffuses into circulation, into systemic circulation. So anything that's water-based injection-wise is going to move through tissues very quickly.

Speaker 2 You know, things that are lipophilic, you know, fat-loving-like

Speaker 2 steroid oils, they're going to pass much slower because they're getting held.

Speaker 2 Their distribution or their affinity to stay in the tissue is much higher. So, when you've got water-based compounds,

Speaker 2 even trying to time it around

Speaker 2 like training to improve a body part, eventually it's going into systemic circulation. Some of it's going to act locally.

Speaker 2 So, yeah, if you inject BPC157 into an injured tendon, you're going to get interactions of that peptide locally as it diffuses from where you've injected it.

Speaker 2 But surely enough, all of those molecules head out into the bloodstream and just get distributed everywhere.

Speaker 1 That

Speaker 2 it's probably easier to put something like that into sub-Q from a compliance perspective. Again, you don't want to be telling someone with surgery, start sticking needles in where you've had surgery.

Speaker 2 Putting it into somewhere that allows them to take it daily

Speaker 2 without objection is a better strategy long term. Again, you're not causing trauma locally.
So, yeah, I think

Speaker 2 any sort of strategy in the past of like

Speaker 2 timed use,

Speaker 2 maybe

Speaker 2 increlex or IGF-1 does

Speaker 2 locally trait after you've trained.

Speaker 2 You can see some logic to it.

Speaker 2 But

Speaker 2 I just don't think, you know,

Speaker 2 how we're viewing it and how the molecule would move into distribution that you're getting any local benefit.

Speaker 2 But that's not to say increasing IGF-1 from an injection of IGF-1 isn't going to yield benefit because it certainly would.

Speaker 1 Right. Okay.
Awesome. Gotcha.
Well, I feel freaking terrible because

Speaker 1 I need to get my meal in because it's big week now. And I'm sure that it's really late for you considering that we started at like 8 p.m.
your time. But

Speaker 1 I don't know. If you're up for it in the future, we got a lot of questions for you.

Speaker 1 As normal, because everyone always wants to know things from Dr. Dean.
But a bunch of stuff about like mitochondrial supports and kidney health and other organ health and management. So I don't know.

Speaker 1 If you're ever up to coming on the podcast again, say in the next couple of months or so, I think that'd be freaking awesome.

Speaker 2 Absolutely. I'm sure that that question list probably just gets longer and longer from podcast to podcast.

Speaker 2 So yeah, maybe next one we just go straight into QA that rather than tangents on digestive health and everything else, I'd be happy to do that.

Speaker 1 Yeah, that'd be awesome, man. Because I'm sure we can expound on it even further and just keep going on on other topics that are very related.
So thanks for coming coming on, brother.

Speaker 1 Thank you so much. That was amazing.
And I think that was so much information and value that it's always new for everyone. So, everyone's always very happy to hear from you.

Speaker 2 Yeah, I'm delighted that there's such a demand. I'm always happy to come and have great conversations with you, Niall.
So, yeah, let's do more in the future.

Speaker 1 Hell yeah. Thank you, brother.
Is there anywhere that you would like to share with the audience? Maybe anywhere they can find you or anything you'd like to promote?

Speaker 2 I guess

Speaker 2 Instagram, DNSTM, is my Instagram that I've heard before. Supplement Needs is our company in the UK.
So supplementneeds.co.uk.

Speaker 2 Unfortunately, I have gotten a lot of flack from US followers. We've had to stop shipping to the US for the time being with customs and everything, which has been something I'm trying to overcome.

Speaker 2 So apologies there. But anyone who's, you know, on the European side, they can check out our website.

Speaker 1 Hell yeah. All right.
Bet.

Speaker 1 And

Speaker 1 I don't know if the answer has changed since the last few podcasts that we had, but if you were to disappear from the world tomorrow and you had one message you could send to the entire world today,

Speaker 2 what would the message be?

Speaker 2 I think it'll stay the same. I think forever, it's always going to be protect your future health.
Always

Speaker 2 like I'm so pleased with today's conversation of when it's all like, oh, well, let's put 15 milligrams of tread in. You're thinking, what negatives are going to happen here, right?

Speaker 2 And more drugs means more success. So

Speaker 2 every

Speaker 2 little,

Speaker 2 I can't remember who said it in terms of like who's originally quoted with saying it.

Speaker 2 So, apologies, but I read before that every step you take is either going to lead you towards ease or towards disease.

Speaker 2 So, that I think is a brilliant quote: of just every little small action you take daily plays into the bigger picture. That sometimes you might not see it.

Speaker 2 And like I said, with the hospital and the guy is there with critical illness, it just anchors you back into the presence of taking care of yourself as a priority from a longevity perspective pays off in the long run.

Speaker 1 Awesome. Well, thank you so much again.

Speaker 2 Thank you. That was awesome, bro.
Speak to you soon.

Speaker 1 Yeah, I hope you get some rest tonight.

Speaker 2 You too.

Speaker 2 Sure, Emil. Bye.