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

 

[Type-IIx]

Don't you find the statement that glp-1 agonist are "true insulin sensitizing agents" or that they "improve insulin sensitivity" too misleading?

A true insulin sensitizing agent (like cinnamon for example) would either increase the number of insulin receptors or improve the signaling pathway downstream of the insulin receptor, thus enhancing the cell's response to insulin. Per my knowledge, GLP-1's don't increase GLUT-4 translocation, phosphorylation and they don't enhance PI3K, AKT, etc. nor do they really inhibit the activity of enzymes or processes that work against insulin signaling. The only MOA of indirectly improving insulin sensitivity seems to be a reduction in inflammation, due to a decrease in proinflammatory cytokines (and possibly some microbiome alterations).

An increase in insulin sensitivity implies that per the same unit of insulin, we would see improvements in BG control, so either insulin sensitivity is a more encompassing term than I'm imagining or the term is being used too liberal. Wouldn't you agree that a term like "increasing insulin signaling" is more appropriate or just "improving glucose control"?

Putting it simply, is this just a case of perspective, ie. if one is only monitoring BG levels, a reduction of BG would imply increased insulin sensitivity, but if one was to monitor BG and fasting insulin levels (or perform OGTT with insulin monitoring), "increased insulin sensitivity" would not be the conclusion one would derive at ...

Interested in your thoughts.

No, because these agents tightly couple insulin secretion to glucose, as in per unit of elevated glucose, insulin is secreted; and at euglycemia/normoglycemia, insulin is maintained. As such, they modulate HOMA-IR in a coordinated lockstep. The particularities of mechanisms of action don't matter.

 

[MindlessWork]

How long can these -glutides be safely run from the perspective of people who train? Don't see too much data about the safety of long term use by bodybuilders/gym rats.

 

[Type-IIx]

How long can these -glutides be safely run from the perspective of people who train? Don't see too much data about the safety of long term use by bodybuilders/gym rats.

Mostly, these drugs pose challenges to prone individuals for nausea, diarrhea, decreased appetite, vomiting, constipation, dyspepsia, or abdominal pain, otherwise known, medically, as an upset tummy-wummy.

They are remarkably safe, they practically possess virtually no serious negative side effect for those not among an infinitesimally small group of patients for whom medullary thyroid carcinoma is in their familial or personal history. Even then; thyroid cancer is, if you will permit me some breadth to opine about relative hazards of carcinomas, objectively, not among the worst. Men are already particularly prone to prostate cancer, which AAS & rhGH increase risk for in a compounding fashion. Prostate cancer is one of the very worst carcinomas; similarly bladder cancer, brain cancer especially glioblastomas, etc.

Other hazards:

Pancreatitis risk is small but significant.

Hypoglycemia when combined with insulin and its secretagogues (e.g., sulfonylureas).

Acute kidney injury secondary to severe GI distress.

Severe GI disease in prone individuals.

Worsening of diabetic retinopathy in those patients.

Acute gallbladder disease. Has occurred in clinical trials.

Basically, besides those for whom acute side effects prevent continuing on these drugs (i.e., GI distress, gallbladder/cholelilithiasis infection) & for those in a small sliver of the population who might, maybe face some increased risk for a not terrible carcinoma (the proposed link between these drugs being based on rodent data only but included in hazards due to abundant caution), there really are not any safety concerns for the GLP-1 & GIP agonist incretins, including tirzepatide, which would be excluded by the suffix, -glutides.

Contrast this versus non-testosterone (i.e., synthetic) androgens (anabolic-androgenic steroids; AAS), the risks and side effects of which are so remarkably prevalent and serious, that they are virtually unused by any medical practitioner except in extreme edge cases (e.g., severe burn injury where nothing better is available; hereditary angioedema where nothing better is available; no longer erythropoiesis stimulation because there's something better, no longer anemia because there's something better)... like, maybe in Palestine where more acceptable therapies have been cut off... and, it becomes strikingly apparent that these drugs are exponentially safer than AAS.

 

[MindlessWork]

Thanks for the detailed response @Type-IIx and will keep those factors in mind and very good info for anyone considering running these glp-1's. I am sure more data will come over time as to how truly safe they are for bb'ers and gym rats.

 

[clearheaded]

ya mostly we find out about cancers at the 10-15 year mark which happens RIGHT when patent runs out lol... then as if by magic a new one comes out with what they learned that is safe.... that being said plenty of drugs are never found to have serious sides where is taken from market, but still when we become aware of them even if small seems to be a year or 2 after patent.. perhaps because harder to do research on patented chemicals without companies being involved or less hands in the post marketing data.

 

[Type-IIx]

ya mostly we find out about cancers at the 10-15 year mark which happens RIGHT when patent runs out lol...

Capitalism makes the world go 'round.

FYI: in a slightly above average misanthropic mood at the moment.

I do note, the fact that capitalism vs. philanthropy are so oppositely related is interesting.

then as if by magic a new one comes out with what they learned that is safe.... that being said plenty of drugs are never found to have serious sides where is taken from market, but still when we become aware of them even if small seems to be a year or 2 after patent.. perhaps because harder to do research on patented chemicals without companies being involved or less hands in the post marketing data.

What's your impression of the safety data for this class of drugs versus average? Below average safety? Average safety? Above?

What's you impression of the safety data for synthetic AAS versus average? Below average safety? Average safety? Above?

 

[Type-IIx]

Thanks for the detailed response @Type-IIx and will keep those factors in mind and very good info for anyone considering running these glp-1's. I am sure more data will come over time as to how truly safe they are for bb'ers and gym rats.

TBF, I don't agree that data will come over time as to how truly safe they are for bbers and gym rats, because, the torrent of news media from which people happen upon their "data" reads, presently, like "COUNTERFEIT OZEMPIC KILLED A GUY," etc.

If you think there is any authoritative source of such "data," you're just plain fucked, bro.

Even forum anecdotes are a product of self-selection bias: only those who feel compelled to report something bother posting.

What about the people you never hear from? Ever notice how much traffic vendor pages get versus the rest of the forum? Think about it.

 

[MindlessWork]

TBF, I don't agree that data will come over time as to how truly safe they are for bbers and gym rats, because, the torrent of news media from which people happen upon their "data" reads, presently, like "COUNTERFEIT OZEMPIC KILLED A GUY," etc.

If you think there is any authoritative source of such "data," you're just plain fucked, bro.

Even forum anecdotes are a product of self-selection bias: only those who feel compelled to report something bother posting.

What about the people you never hear from? Ever notice how much traffic vendor pages get versus the rest of the forum? Think about it.

Lol maybe I am just an old worrywart. I have read many of your posts and good stuff. You are up there with @biggerben69 in how detailed and long your posts are. Happy turkey day man!

 

[Type-IIx]

Lol maybe I am just an old worrywart. I have read many of your posts and good stuff. You are up there with @biggerben69 in how detailed and long your posts are. Happy turkey day man!

He seems like a good shit reading through his posts; we've never really crossed paths cause it seems he's more oriented towards the sources.

 

[MindlessWork]

He seems like a good shit reading through his posts; we've never really crossed paths cause it seems he's more oriented towards the sources.

Yep you both are good about your respective subjects...respect.

 

[Jin23]

No, because these agents tightly couple insulin secretion to glucose, as in per unit of elevated glucose, insulin is secreted; and at euglycemia/normoglycemia, insulin is maintained. As such, they modulate HOMA-IR in a coordinated lockstep. The particularities of mechanisms of action don't matter.

I understand the first part, ie. glp's moa, but don't understand the conclusion in the last part, honestly.

1. If post prandial insulin secretion is increased, does this result in lowered fasting glucose down the line and most importantly, fasting insulin will not be elevated (and let's exclude a scenario where the individual undergoes body composition changes)? Seeing how HOMA-IR is calculated via fasting bg and fasting insulin values, the only way for it to improve is obviously via a reduced bg:insulin ratio (not explaining this for you, but for other readers).

2. I speculate most studies on glp's showing improved homa-ir have been done on patients undergoing a fat loss diet? And thus the most important but obvious question: does a glp agonist improve homa-ir, in a lean individual, 10% bf, 22% ffmi, who maintains an eucaloric diet and doesn't basically change anything, no lifestyle changes and thus no body composition changes? So basically; do glp's improve homa-ir irrespective of body composition and lifestyle changes ...

 

[Jin23]

I understand the first part, ie. glp's moa, but don't understand the conclusion in the last part, honestly.

1. If post prandial insulin secretion is increased, does this result in lowered fasting glucose down the line and most importantly, fasting insulin will not be elevated (and let's exclude a scenario where the individual undergoes body composition changes)? Seeing how HOMA-IR is calculated via fasting bg and fasting insulin values, the only way for it to improve is obviously via a reduced bg:insulin ratio (not explaining this for you, but for other readers).

2. I speculate most studies on glp's showing improved homa-ir have been done on patients undergoing a fat loss diet? And thus the most important but obvious question: does a glp agonist improve homa-ir, in a lean individual, 10% bf, 22% ffmi, who maintains an eucaloric diet and doesn't basically change anything, no lifestyle changes and thus no body composition changes? So basically; do glp's improve homa-ir irrespective of body composition and lifestyle changes ...

Forgot to mention suppression of glucagon secretion by glp's. I imagine it would be very hard to exclude this factor ...

 

[Type-IIx]

I understand the first part, ie. glp's moa, but don't understand the conclusion in the last part, honestly.

1. If post prandial insulin secretion is increased, does this result in lowered fasting glucose down the line and most importantly, fasting insulin will not be elevated (and let's exclude a scenario where the individual undergoes body composition changes)? Seeing how HOMA-IR is calculated via fasting bg and fasting insulin values, the only way for it to improve is obviously via a reduced bg:insulin ratio (not explaining this for you, but for other readers).

2. I speculate most studies on glp's showing improved homa-ir have been done on patients undergoing a fat loss diet? And thus the most important but obvious question: does a glp agonist improve homa-ir, in a lean individual, 10% bf, 22% ffmi, who maintains an eucaloric diet and doesn't basically change anything, no lifestyle changes and thus no body composition changes? So basically; do glp's improve homa-ir irrespective of body composition and lifestyle changes ...

1. Yes, 2. Without dietary intervention, patients reduce energy intake voluntarily, because other GLP-1 agonist efects are altered food preferences, increased satiety, delayed gastric emptying; and yet, it is still the primary effect of GLP-1 agonists to couple glucose elevations to insulin secretion.

 

[clearheaded]

just was pointing out that we won't really know until patent runs out..... I was not trying to suggest glp has some extra danger and likely worse case its pros will outweigh cons... BUT plenty of things we thought was safe and turns out to be nasty with chronic use/exposure. I simply wanted to make a point about moderation and caution. even with current spotlight and millions on sema very few horror stories, and would be worse if gave the same amount people Tylenol antibiotics or peanuts as not many serious issues seem to pop up in the media...caveat being media plays alot of the ooo ooo oozempic adds that may not like non proven negative anecdotes hit the MSM that they fund with nearly 50% add revenue IIRC.--


That being said.... just talked to the old man who has kidney disease diabetes overweight etc.... the dr had been talking about ozempic for him but also wanted him to see a specialist before trying something else that helps with diabetes and kidney... not sure what drug that was or if was another GLP... so looked into it and appears may be a fine line for folks with kidney issues as semaglutide appears to accelerate the disease and is non reversible.... perhaps has to do with other factors but if happen to have more data on that id love to hear about it and if its isolated to sema or tirz aswell? he is 82 and going on holiday so I told him prob hold off at least so he is not in a third world country should things go sideways... the case study said those with gastro side effects appear to be the ones who's kidneys are effected..... unsure the mechanism but sorta makes sense if getting dehydrated vomiting and or constipated holding on to 'toxins' longer with decrease kidney function.

anyone notice any differences in bloods esp for kidney function creatine etc after taking sema or glps?

 

[Type-IIx]

just was pointing out that we won't really know until patent runs out..... I was not trying to suggest glp has some extra danger and likely worse case its pros will outweigh cons... BUT plenty of things we thought was safe and turns out to be nasty with chronic use/exposure. I simply wanted to make a point about moderation and caution. even with current spotlight and millions on sema very few horror stories, and would be worse if gave the same amount people Tylenol antibiotics or peanuts as not many serious issues seem to pop up in the media...caveat being media plays alot of the ooo ooo oozempic adds that may not like non proven negative anecdotes hit the MSM that they fund with nearly 50% add revenue IIRC.--


That being said.... just talked to the old man who has kidney disease diabetes overweight etc.... the dr had been talking about ozempic for him but also wanted him to see a specialist before trying something else that helps with diabetes and kidney... not sure what drug that was or if was another GLP... so looked into it and appears may be a fine line for folks with kidney issues as semaglutide appears to accelerate the disease and is non reversible.... perhaps has to do with other factors but if happen to have more data on that id love to hear about it and if its isolated to sema or tirz aswell? he is 82 and going on holiday so I told him prob hold off at least so he is not in a third world country should things go sideways... the case study said those with gastro side effects appear to be the ones who's kidneys are effected..... unsure the mechanism but sorta makes sense if getting dehydrated vomiting and or constipated holding on to 'toxins' longer with decrease kidney function.

anyone notice any differences in bloods esp for kidney function creatine etc after taking sema or glps?

Mostly, these drugs pose challenges to prone individuals for nausea, diarrhea, decreased appetite, vomiting, constipation, dyspepsia, or abdominal pain, otherwise known, medically, as an upset tummy-wummy.

They are remarkably safe, they practically possess virtually no serious negative side effect for those not among an infinitesimally small group of patients for whom medullary thyroid carcinoma is in their familial or personal history. Even then; thyroid cancer is, if you will permit me some breadth to opine about relative hazards of carcinomas, objectively, not among the worst. Men are already particularly prone to prostate cancer, which AAS & rhGH increase risk for in a compounding fashion. Prostate cancer is one of the very worst carcinomas; similarly bladder cancer, brain cancer especially glioblastomas, etc.

Other hazards:

...
Acute kidney injury secondary to severe GI distress.
...
Contrast this versus non-testosterone (i.e., synthetic) androgens (anabolic-androgenic steroids; AAS), the risks and side effects of which are so remarkably prevalent and serious, that they are virtually unused by any medical practitioner except in extreme edge cases (e.g., severe burn injury where nothing better is available; hereditary angioedema where nothing better is available; no longer erythropoiesis stimulation because there's something better, no longer anemia because there's something better)... like, maybe in Palestine where more acceptable therapies have been cut off... and, it becomes strikingly apparent that these drugs are exponentially safer than AAS.

Indeed, it can increase risk of kidney injury, but seems to only present in those that suffer acutely achy tummies.

 

[AlexDavis43]

Yes.

Btw, if you want to gauge insulin sensitivity, it would be much more prudent to use fasting insulin as a biomarker. BG is much higher in the hierarchy of glucose management cascade and is influenced by to many factors to make it a usable biomarker for insulin sensitivity.

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

 

[AlexDavis43]

No, because these agents tightly couple insulin secretion to glucose, as in per unit of elevated glucose, insulin is secreted; and at euglycemia/normoglycemia, insulin is maintained. As such, they modulate HOMA-IR in a coordinated lockstep. The particularities of mechanisms of action don't matter.

There appears to be a disproportionate improvement in efficacy by selectively affecting first phase insulin response.

GLP1 drugs don't simply elevate insulin secretion, but they do it rapidly. I suspect first phase insulin response is critical.

Besides glucose disposal, may influence other pathways; eg, HGP, cancer signaling, neurological, hunger/appetite, et cetera.

No refs for this, but there are some overlapping actions of GLP1 drugs, intranasal insulin, and rapid-acting insulin compared to long-acting insulin preparations.

You may want postprandial insulin secretion to be fast, big, then gone.

@Jin23

 

[Type-IIx]

There appears to be a disproportionate improvement in efficacy by selectively affecting first phase insulin response.

GLP1 drugs don't simply elevate insulin secretion, but they do it rapidly. I suspect first phase insulin response is critical.

Besides glucose disposal, may influence other pathways; eg, HGP, cancer signaling, neurological, hunger/appetite, et cetera.

No refs for this, but there are some overlapping actions of GLP1 drugs, intranasal insulin, and rapid-acting insulin compared to long-acting insulin preparations.

You may want postprandial insulin secretion to be fast, big, then gone.

@Jin23

True; and good info. Have you read my Insulin & skeletal muscle hypertrophy article? I'd appreciate your feedback on that article.

MESO-Rx Exclusive - Insulin and skeletal muscle hypertrophy by @Type-IIx

I am pleased to announce the publication of member @Type-IIx 's first article on MESO-Rx! Type-IIx has been answering your questions on hgh, insulin, dnp and several bodybuilding compounds in the forum for some time. You will appreciate his MESO article as a more detailed treatise on how insulin...

thinksteroids.com

 

[clearheaded]

sore tummy wummy = kidney damage/failure... tomato tomAAhto lol

very much appreciate both of your guys posts, also important to dispel broscience and the harms of such parroted nonsense, great for us newbs.... so TY.

 

[size28s]

I’m diabetic type 2. I hated ozempic. Makes you sick to your stomach and nauseas. I stopped after 2 months. Went back to triseba and metformin