MESO-Rx Exclusive Ozempic and Mounjaro for bodybuilders - more than just weight loss drugs

[MESO-Rx Administrator]

@Type-IIx explains the benefits of GLP-1 and GIP agonists like Semaglutide and Tirzepatide, as true insulin sensitizing agents. how they are different from other weight loss drugs, and the benefits as partitioning agents for bodybuilders.

I'm sure you've read a lot about Ozempic, Wegovy, and Mounjaro for overweight sedentary people in the mainstream media but if you want to read about the use of these drug from a bodybuilding perspective, read on:

Semaglutide and Tirzepatide are More Than Just Weight Loss Drugs

Learn how GLP-1 and GIP agonists like Semaglutide and Tirzepatide enhance insulin sensitivity, preserve muscle mass and reduce fat stores.

thinksteroids.com

 

[Jin23]

Sure but fasting and 2-hour postprandial glucose are decent indicators and a million times more convenient.

Ideally we'd want a two-step hyperinsulinemic euglycemic clamp but there's a balance between convenience, relevance, sensitivity, importance, et cetera.

@29trt

Unfortunately, I'm going to remain a bit autistic on this topic. While I do agree on the practicality aspect, I can't agree on the validity of it's measured outcomes, which then makes it a moot point altogether. It seems like you all are trying to superimpose data taken from huge epidemiological studies on a very specific, mechanistic/pharmacodynamic query. Which honestly doesn't make a lot of sense, as this are two completely different discourses. You can't apply intra-discourse logic from there to here.

Sure, seeing an improvement in homa-ir in a general population cohort study is a huge plus and the nuances of how and why aren't that important as bg management and all it's relevant outcomes have improved. But that can't be your answer to a narrow mechanistic query. Same goes for the fasting bg argument ... Deriving to a conclusion about improved insulin resistance from a lowered fasting bg makes sense only in a very specific controlled environment.

For illustration purposes; if my fasting glucose is 5.6 and I take metformin, which lowers hepatic glucose release, and the next day my fasting bg is 5.2, are you going to surmise improved insulin resistance? Same with glp agonists, they lower glucagon levels which in turn also decreases hepatic glucose release. Is my insulin resistance improved in a 24h timeframe?

An improvement in homa-ir is a broad signifier. Primarily it signifies an improvement in glucose management, period. But the improvement in glucose management can then be a result of a myriad of factors, only one of which can be an improvement of insulin sensitivity. And tissues being insulin sensitive is something very different then just having lowered hepatic glucose release or more insulin.

But why, why care about this if an improvement in homa-ir is really good enough and that's all that matters? Again, since when has this place not cared about exact mechanisms of action? Isn't this basically all that we do here, bicker about the very specific micro nuances of said drugs moa's? We are biohacking and exact mechanisms of action matter to us. Well, at least they do to me ...

 

[Type-IIx]

Unfortunately, I'm going to remain a bit autistic on this topic. While I do agree on the practicality aspect, I can't agree on the validity of it's measured outcomes, which then makes it a moot point altogether. It seems like you all are trying to superimpose data taken from huge epidemiological studies on a very specific, mechanistic/pharmacodynamic query. Which honestly doesn't make a lot of sense, as this are two completely different discourses. You can't apply intra-discourse logic from there to here.

Sure, seeing an improvement in homa-ir in a general population cohort study is a huge plus and the nuances of how and why aren't that important as bg management and all it's relevant outcomes have improved. But that can't be your answer to a narrow mechanistic query. Same goes for the fasting bg argument ... Deriving to a conclusion about improved insulin resistance from a lowered fasting bg makes sense only in a very specific controlled environment.

For illustration purposes; if my fasting glucose is 5.6 and I take metformin, which lowers hepatic glucose release, and the next day my fasting bg is 5.2, are you going to surmise improved insulin resistance? Same with glp agonists, they lower glucagon levels which in turn also decreases hepatic glucose release. Is my insulin resistance improved in a 24h timeframe?

An improvement in homa-ir is a broad signifier. Primarily it signifies an improvement in glucose management, period. But the improvement in glucose management can then be a result of a myriad of factors, only one of which can be an improvement of insulin sensitivity. And tissues being insulin sensitive is something very different then just having lowered hepatic glucose release or more insulin.

But why, why care about this if an improvement in homa-ir is really good enough and that's all that matters? Again, since when has this place not cared about exact mechanisms of action? Isn't this basically all that we do here, bicker about the very specific micro nuances of said drugs moa's? We are biohacking and exact mechanisms of action matter to us. Well, at least they do to me ...

I think that if there's any superimposition going on here, it's that you are superimposing your opinion about superiority of certain mechanisms vs. others onto the discourse, to be fair. I'm not here for biohacking bro; but I respect your right to bicker about MOAs, it brings an interesting element to the conversation and lets us hash through mechanisms, however valuable. Many of us basically enjoy this thought exercise I think.

 

[Jin23]

I think that if there's any superimposition going on here, it's that you are superimposing your opinion about superiority of certain mechanisms vs. others onto the discourse, to be fair. I'm not here for biohacking bro; but I respect your right to bicker about MOAs, it brings an interesting element to the conversation and lets us hash through mechanisms, however valuable. Many of us basically enjoy this thought exercise I think.

Sure, to each their own - and yeah I think so too, we're all here to stretch our PFC synapses.

 

[Spaceman Spiff]

@Type-IIx

I just noticed you referenced Lyle Mcdonald, What is your opinion of him?


I know he types like a dick but I like him lol. Always followed his info since I was a kid

 

[Type-IIx]

@Type-IIx

I just noticed you referenced Lyle Mcdonald, What is your opinion of him?


I know he types like a dick but I like him lol. Always followed his info since I was a kid

Very knowledgeable about nutrition. He basically brought the importance of leptin from the scientific to the fitness/nutrition realm, and this article is sort of a homage to that; giving credit where it is due. Even with regards to training, and certainly nutrition, he was saying things 20 years ago that is only now being hashed out by Western academics and being validated empirically by practitioners.

He is clearly influenced by Duchaine. His Ultimate Diet is basically an improvement of Duchaine's BodyOpus. You might view him fairly as an early protegé of Duchaine that broke out on his own.

There are few individuals smarter than these guys in our field.

He's not a perfect human; he's not always right about topics outside of his wheelhouse, including drugs; but he's probably always right about factual matters within his subject matter expertise.

 

[JG91]

Since clen increases insulin resistance, and GLP1 agonists increase insulin sensitivity, doesn't that mean the two work synergistically?

 

[Type-IIx]

Since clen increases insulin resistance, and GLP1 agonists increase insulin sensitivity, doesn't that mean the two work synergistically?

Since systemic insulin resistance is unfavorable per se, you might say that they work at odds with one another.

For features like (e.g., synovial joint) fluid balance, you might say that stanozolol (Winstrol; Strombaject) & oxymetholone (Anadrol) act complementarily in principle (1 + -1 = 0) because they lead to a "middling out" of behaviour.

Synergistic action (1 + 1 > 2) refers to effects on the same end-point (e.g., muscle size) occurring by different mechanisms (e.g., decreased GR number & increased IGF-IEc expression).

Additive action (1 + 1 = 2) refers to everything else, i.e., effects on the same end-point occurring by the same mechanisms (e.g., 2 AAS that both increase IGF-IEc activity).

 

[AlexDavis43]

Very knowledgeable about nutrition. He basically brought the importance of leptin from the scientific to the fitness/nutrition realm, and this article is sort of a homage to that; giving credit where it is due. Even with regards to training, and certainly nutrition, he was saying things 20 years ago that is only now being hashed out by Western academics and being validated empirically by practitioners.

He is clearly influenced by Duchaine. His Ultimate Diet is basically an improvement of Duchaine's BodyOpus. You might view him fairly as an early protegé of Duchaine that broke out on his own.

There are few individuals smarter than these guys in our field.

He's not a perfect human; he's not always right about topics outside of his wheelhouse, including drugs; but he's probably always right about factual matters within his subject matter expertise.

Tl;dr: Lyle has been consistently more right than wrong for longer than many people in this space.

I haven't been following him for years because I care about his dog videos or mental wellness (not to be a dick, but I have no idea who this person is).
I usually fast forward to exercise science content.

 

[Jin23]

Since clen increases insulin resistance, and GLP1 agonists increase insulin sensitivity, doesn't that mean the two work synergistically?

Not to passive aggressively oppose Type's point of view but ... This isn't maths; it's biology. You have to look at the underlying mechanisms, as one mechanism might override the other one and thus either make it irrelevant or just less effective.

For instance: beta receptor activation increases cAMP which opposes the whole intracellular insulin cascade signaling pathway and glp agonists don't directly oppose this mechanism.

Beta receptor activation increases liver glucose output, where more insulin does lower blood glucose levels, but can you really call this lowering insulin resistance? If you was to use clen and started pinning insulin, would you call this lowering insulin sensitivity?

Beta agonists can also increase lypolisis, obviously, it's why you use them, and this means increased FFA release - which does directly oppose insulin action but again, can you call simply increasing insulin levels decreasing insulin resistance?

Calling glp1 agonists "insulin sensitizing" is imo dubious at best because as discussed previously, glp agonist mostly just upregulate insulin secretion but don't effect the whole insulin signaling cascade directly. Thus calling glp1 agonists insulin sensitizing agents is more a mater of perspective, ie. the discourses point of view from which you're presenting your argument.

But anyway, however simplistic my argument is, it should make the point clear: that this is biology and you have to look at underlying mechanisms.

 

[Type-IIx]

Not to passive aggressively oppose Type's point of view but ... This isn't maths; it's biology. You have to look at the underlying mechanisms, as one mechanism might override the other one and thus either make it irrelevant or just less effective.

For instance: beta receptor activation increases cAMP which opposes the whole intracellular insulin cascade signaling pathway and glp agonists don't directly oppose this mechanism.

Beta receptor activation increases liver glucose output, where more insulin does lower blood glucose levels, but can you really call this lowering insulin resistance? If you was to use clen and started pinning insulin, would you call this lowering insulin sensitivity?

Beta agonists can also increase lypolisis, obviously, it's why you use them, and this means increased FFA release - which does directly oppose insulin action but again, can you call simply increasing insulin levels decreasing insulin resistance?

Calling glp1 agonists "insulin sensitizing" is imo dubious at best because as discussed previously, glp agonist mostly just upregulate insulin secretion but don't effect the whole insulin signaling cascade directly. Thus calling glp1 agonists insulin sensitizing agents is more a mater of perspective, ie. the discourses point of view from which you're presenting your argument.

But anyway, however simplistic my argument is, it should make the point clear: that this is biology and you have to look at underlying mechanisms.

I guess you weren't kidding when you said you would remain autistic on this topic.

 

[clearheaded]

I thought high insulin levels meant insulin resistance though?(or at least highly probable and only way of measure is it not?) ie blood sugar may be fine but ur pancreas is working to hard which than leads to diabetes(the real issue)

anyhoo...

 

[Type-IIx]

I thought high insulin levels meant insulin resistance though?(or at least highly probable and only way of measure is it not?) ie blood sugar may be fine but ur pancreas is working to hard which than leads to diabetes(the real issue)

anyhoo...

High (especially fasting) insulin levels are a signal associated with insulin resistance (by definition IR is when we become resistant to the effects of insulin & this is marked by chronic hyperinsulinaemia), and incretins like semaglutide & tirzepatide don't cause high insulin, unlike what Jin23 seems to think. These are antidiabetes drugs.

 

[Jin23]

High (especially fasting) insulin levels are a signal associated with insulin resistance (by definition IR is when we become resistant to the effects of insulin & this is marked by chronic hyperinsulinaemia), and incretins like semaglutide & tirzepatide don't cause high insulin, unlike what Jin23 seems to think. These are antidiabetes drugs.

Did I say they cause high insulin? I'm not going through the tread ... But if I did, I definitely didn't mean to. We're only talking about increased postprandial insulin secretion, I don't understand how and why this became unclear.

 

[Type-IIx]

Did I say they cause high insulin? I'm not going through the tread ... But if I did, I definitely didn't mean to. We're only talking about increased postprandial insulin secretion, I don't understand how and why this became unclear.

Somewhere between cinnamon and PFC synapses I must have lost the plot. I must be getting dumb. I think I'll sign off for today & perhaps restimulate my neural plasticity and come back to a Meso that isn't gunning for me. Here's to hopin'!

 

[Jin23]

Somewhere between cinnamon and PFC synapses I must have lost the plot. I must be getting dumb. I think I'll sign off for today & perhaps restimulate my neural plasticity and come back to a Meso that isn't gunning for me. Here's to hopin'!

Hey, cinnamon is the real deal! : D Idk if you've ever tried it, but if you do, get a concentrated extract it will drop your BG big time and the good part is it's moa. I can send you some research if you'll be interested ...

 

[29trt]

Hey, cinnamon is the real deal! : D Idk if you've ever tried it, but if you do, get a concentrated extract it will drop your BG big time and the good part is it's moa. I can send you some research if you'll be interested ...

cinnamon really? I thought there were studies were the effect on BG was nonexistant.. and if I remember right there was some toxicity or something related to high dosages
don't get me wrong I'm all for alternatives to metformin and glp1 for BG and I've been using cinnamon for years but small dosages...

 

[AlexDavis43]

High (especially fasting) insulin levels are a signal associated with insulin resistance (by definition IR is when we become resistant to the effects of insulin & this is marked by chronic hyperinsulinaemia), and incretins like semaglutide & tirzepatide don't cause high insulin, unlike what Jin23 seems to think. These are antidiabetes drugs.

[emphasis added by me]

Definitely higher first phase insulin response but 24-h AUC insulin exposure may be reduced.

 

[AlexDavis43]

cinnamon really? I thought there were studies were the effect on BG was nonexistant.. and if I remember right there was some toxicity or something related to high dosages
don't get me wrong I'm all for alternatives to metformin and glp1 for BG and I've been using cinnamon for years but small dosages...

I can't tell if y'all kidding, but there are several positive studies on cinnamon and insulin sensitivity (1, 2, 3).

My only tip is that if any of those studies entice you to try cinnamon, make sure it is the right type of cinnamon and dose.

@29trt is your source for cinnamon toxicity that TikTokker? jk (info on coumarin and cassia here). I'm having trouble making the calculations, but it seems like a shit-ton of cinnamon is necessary to reach those levels.

@Jin23 @Type-IIx

 

[Smashshit]

Hey, cinnamon is the real deal! : D Idk if you've ever tried it, but if you do, get a concentrated extract it will drop your BG big time and the good part is it's moa. I can send you some research if you'll be interested ...

I’d be interested if you don’t mind sending it to me as a t2d I’m always looking to learn more and look for better or healthier alternatives

 

[clearheaded]

lol tik tok... SCARY how they can just slowly make people mindless or perhaps just to make people not trust ANY media, or perhaps more likely divide .. my fav was girls sister said % precipitation means that % of the area gets rain... lol learned on tik tok... IDIOTS, or perhaps just FAR to trusting...

anyhoo, every plant produces toxins, some taste good to us, some give us nice buzz, some of them are anti fungal (we are closely related to fungus so what kills fungus often will harm mammals too) etc, but every taste and smell is basically defence mechanism to keep animals and/or pests away... from oregano to lemon peel and tonic water its all 'toxic', its just about dosage... of course BB world likes to overdo everything, moderation in ALL THINGS will keep u GTG. think turpentine vs dry rosemary or pine needle tea...