Ozempic (semaglutide) wtf?

[lukiss96]

So I have finally decided to use it this strange pen, I injected 36 clicks which is 0.5mg (right?) and after couple hours I already feel like I hate eating?

Is it normal? Is it placebo x10 effect? I had this steak on my mind now I don't even want it?

What is food? Do we need to eat? Can I not eat and not die? Am I invincible?

But really though when is it supposed to work and do the effects wear off over time?

Do I need to inject it more frequently
than once a week?

 

[M@NU]

Aww man.. this semaglutide has me bloated to shit. I'm at 1.5mg now. I took 4x bisacodyl and I am gonna take 4x senna/prune. When I get home from work I'm gonna do s colonoscopy protocol with miralax and chug it until I shit my brains out.

start lower or inject a reduced amount more frequently to decrease side effects
i never went above 0,6 in one shot because of the side effects. But i did 0,6mg x 3 a week for some weeks which was good for dropping BW

 

[Rido]

start lower or inject a reduced amount more frequently to decrease side effects
i never went above 0,6 in one shot because of the side effects. But i did 0,6mg x 3 a week for some weeks which was good for dropping BW

Yea. This has happened maybe one other time on semaglutide. It's coming out, just not fast enough. Pretty irritating the miralax will push everything out. I think 10 doses of it should do the trick. I'll do it after I lift and give my previous bisacodyl a chance to work

 

[Pineapples4Puss]

It can be ongoing. I think a break would be good. I stoppes it for 6 weeks but after my hunger was out of control I restarted it.

Original studies were 68 weeks plus


There's nothing that say you can't.

The oral version seems expensive as FUCK. To run for 6+ weeks.

It’s like 60+ bucks a week at 14 mg

 

[Doodle]

The oral version seems expensive as FUCK. To run for 6+ weeks.

It’s like 60+ bucks a week at 14 mg

I know :/ I bought a 30 day supply to try though. Got some unexpected money back so figured I’d give it a shot. Maybe try 7mg for the first week or two and then 14 mg for the remainder?

 

[Pineapples4Puss]

I know :/ I bought a 30 day supply to try though. Got some unexpected money back so figured I’d give it a shot. Maybe try 7mg for the first week or two and then 14 mg for the remainder?

Was considering to try peptide science after some more digging on them.

120 for 3 mg is a little better.

 

[Type-IIx]

@Type-IIx can you explain how it sensitizes you to insulin? I guess it seems paradoxical to me. I would assume, even though it is endogenous, having all that extra insulin would still cause some reduced sensitivity? Maybe not as bad as insulin, but I definitely think it would eventually? Or would this only be true if someone who is stupid and decides to eat a ton of sugar and crap while taking it?

"All that extra insulin?" You seem to equate GLP-1 agonists' mechanism(s) of action to exogenous insulin use (i.e., chronic hyperinsulinemia). In chronic hyperinsulinemia (or "insulin toxicity") a la exogenous slin, the mechanism for decreased insulin sensitivity is diminished autophosphorylation of the IR, and subsequent PI3K-AKT signaling is affected, thereby diminishing GLUT-4 translocation. This is a clear mechanism to induce insulin resistance.

This is wholly inapposite the GLP-1 agonists. The GLP-1 agonists stimulate pancreatic insulin secretion in response to hyperglycemia (and decrease this stimulation as blood glucose levels abate); suppress glucagon secretion (decreasing gluconeogenesis and increasing glycolysis) in a glucose-dependent manner without impairing the normal glucagon response to hypoglycemia; and delay gastric emptying, reducing the rate at which postprandial glucose appears in the circulation. These are factors involved in insulin sensitivity.

 

[Type-IIx]

Can you look over this study glp1 lowers myostatin

Results: Ex-4 suppressed the expression of myostatin (MSTN) and muscle atrophic factors such as F-box only protein 32 (atrogin-1) and muscle RING-finger protein-1 (MuRF-1) in Dex-treated C2C12 myotubes. The suppression effect was via protein kinase A and protein kinase B signalling pathways through GLP-1R. In addition, Ex-4 treatment inhibited glucocorticoid receptor (GR) translocation by up-regulating the proteins of GR inhibitory complexes. In a Dex-induced muscle atrophy model, Ex-4 ameliorated muscle atrophy by suppressing muscle atrophic factors and enhancing myogenic factors (MyoG and MyoD), leading to increased muscle mass and function. In the CKD muscle atrophy model, Ex-4 also increased muscle mass, myofiber size, and muscle function. In addition, treatment with a long-acting GLP-1R agonist, dulaglutide, recovered muscle mass and function in DBA/2J-mdx mice.
Conclusions: GLP-1R agonists ameliorate muscle wasting by suppressing MSTN and muscle atrophic factors and enhancing myogenic factors through GLP-1R-mediated signalling pathways. These novel findings suggest that activating GLP-1R signalling may be useful for the treatment of atrophy-related muscular diseases.
Keywords: Chronic kidney disease; Dexamethasone; Duchenne muscular dystrophy; GLP-1R agonists; Glucocorticoid receptor; Skeletal muscle atrophy.

Amelioration of muscle wasting by glucagon‐like peptide‐1 receptor agonist in muscle atrophy - PMC

Skeletal muscle atrophy is defined as a reduction of muscle mass caused by excessive protein degradation. However, the development of therapeutic interventions is still in an early stage. Although glucagon‐like peptide‐1 receptor (GLP‐1R) agonists, ...

www.ncbi.nlm.nih.gov

That's interesting in that there is yet another novel mechanism of GLP-1 agonists that are beneficial (at least in muscle wasting in a model of glucocorticoid-induced muscle atrophy and Duchenne muscular dystrophy).

MSTN is interesting as it is a pluripotent gene involved in regulation of muscle mass (and instances of total knockout have been shown to induce hyperplasia & hypertrophy in skeletal muscle in mammals) - yet its pluripotent regulation of muscle mass in man has yet to be potently "unlocked" by any of the clinically trialled myostatin inhibitors (Peter Bond wrote an excellent article on the weaknesses of these compounds a couple of years ago that still stands).

As of right now, androgens are the most viable myostatin inhibitors, partly because of MSTN's high sequence homology with, e.g, GDF11, making it difficult to isolate in practice; and partly because AAS function only in part through myostatin as well as by other secondary messenger systems. For example, Testosterone functions via Myostatin, Akt, Notch, etc., in addition to exerting myotrophy via classical AR genomic action and other non-AR mechanisms (e.g., glucocorticoid modulation; aromatization [e.g., promoting growth factor activity]; genomic action including AR tethering by other transcription factors, polyamine biosynthesis & microRNA regulation; nongenomic action including membrane-bound [mARs], AR-SHBG interaction & PKA activity; non-ligand dependent AR action [e.g., IGF-I]).

That was probably excessive to dump on you, but I want to illustrate that as interesting as MSTN is (it truly is), androgens work in part via its inhibition, but are more practically useful than any of the inhibitors (at least those developed thus far) thereof.

 

[Rido]

That's interesting in that there is yet another novel mechanism of GLP-1 agonists that are beneficial (at least in muscle wasting in a model of glucocorticoid-induced muscle atrophy and Duchenne muscular dystrophy).

MSTN is interesting as it is a pluripotent gene involved in regulation of muscle mass (and instances of total knockout have been shown to induce hyperplasia & hypertrophy in skeletal muscle in mammals) - yet its pluripotent regulation of muscle mass in man has yet to be potently "unlocked" by any of the clinically trialled myostatin inhibitors (Peter Bond wrote an excellent article on the weaknesses of these compounds a couple of years ago that still stands).

As of right now, androgens are the most viable myostatin inhibitors, partly because of MSTN's high sequence homology with, e.g, GDF11, making it difficult to isolate in practice; and partly because AAS function only in part through myostatin as well as by other secondary messenger systems. For example, Testosterone functions via Myostatin, Akt, Notch, etc., in addition to exerting myotrophy via classical AR genomic action and other non-AR mechanisms (e.g., glucocorticoid modulation; aromatization [e.g., promoting growth factor activity]; genomic action including AR tethering by other transcription factors, polyamine biosynthesis & microRNA regulation; nongenomic action including membrane-bound [mARs], AR-SHBG interaction & PKA activity; non-ligand dependent AR action [e.g., IGF-I]).

That was probably excessive to dump on you, but I want to illustrate that as interesting as MSTN is (it truly is), androgens work in part via its inhibition, but are more practically useful than any of the inhibitors (at least those developed thus far) thereof.

do you have a gofundme? or patreon? lol

 

[M@NU]

GLP-1 agonists are completely underrated imo.
They still have some effects that couldnt be explained by their known effects until now (e.g. their cardiovascular beneficial effects in non diabetics)
I am sure they will play a major role in disease prevention in future.

 

[Type-IIx]

do you have a gofundme? or patreon? lol

Haha nah, but I'm always happy to work with people on an individual basis for physique enhancement; protocols; etc.

 

[MFAAS]

"All that extra insulin?" You seem to equate GLP-1 agonists' mechanism(s) of action to exogenous insulin use (i.e., chronic hyperinsulinemia). In chronic hyperinsulinemia (or "insulin toxicity") a la exogenous slin, the mechanism for decreased insulin sensitivity is diminished autophosphorylation of the IR, and subsequent PI3K-AKT signaling is affected, thereby diminishing GLUT-4 translocation. This is a clear mechanism to induce insulin resistance.

This is wholly inapposite the GLP-1 agonists. The GLP-1 agonists stimulate pancreatic insulin secretion in response to hyperglycemia (and decrease this stimulation as blood glucose levels abate); suppress glucagon secretion (decreasing gluconeogenesis and increasing glycolysis) in a glucose-dependent manner without impairing the normal glucagon response to hypoglycemia; and delay gastric emptying, reducing the rate at which postprandial glucose appears in the circulation. These are factors involved in insulin sensitivity.

Thank you for clarifying. I wasn't trying to equat orbstate anything. Just understand the mechanisms, which you now xplained well.

So what are the downsides to these substances? Either short term or long term use?

 

[freakyjacked29]

That's interesting in that there is yet another novel mechanism of GLP-1 agonists that are beneficial (at least in muscle wasting in a model of glucocorticoid-induced muscle atrophy and Duchenne muscular dystrophy).

MSTN is interesting as it is a pluripotent gene involved in regulation of muscle mass (and instances of total knockout have been shown to induce hyperplasia & hypertrophy in skeletal muscle in mammals) - yet its pluripotent regulation of muscle mass in man has yet to be potently "unlocked" by any of the clinically trialled myostatin inhibitors (Peter Bond wrote an excellent article on the weaknesses of these compounds a couple of years ago that still stands).

As of right now, androgens are the most viable myostatin inhibitors, partly because of MSTN's high sequence homology with, e.g, GDF11, making it difficult to isolate in practice; and partly because AAS function only in part through myostatin as well as by other secondary messenger systems. For example, Testosterone functions via Myostatin, Akt, Notch, etc., in addition to exerting myotrophy via classical AR genomic action and other non-AR mechanisms (e.g., glucocorticoid modulation; aromatization [e.g., promoting growth factor activity]; genomic action including AR tethering by other transcription factors, polyamine biosynthesis & microRNA regulation; nongenomic action including membrane-bound [mARs], AR-SHBG interaction & PKA activity; non-ligand dependent AR action [e.g., IGF-I]).

That was probably excessive to dump on you, but I want to illustrate that as interesting as MSTN is (it truly is), androgens work in part via its inhibition, but are more practically useful than any of the inhibitors (at least those developed thus far) thereof.

Yeah great reply we see that follistatin is suppressed by androgens specifically testosterone

But glp1 has the actual data at building muscle even in the human trial of dosage of 2.4mg they lost fat and gained muscle no exercise I believe so this must have been suppressed mtsn which is unbelievable so I think 3mg once per week for myostatin lowering benefit is what would be ideal and something to increase gastric emptying to allow one to consume the food like a ghrp which would speed that up

But the hunger loss does ware off over time im currently on semaglutide 1mg per week for type 2.

Another thing myofiber size was increased this is interesting

We need more discussion on this lol

 

[Type-IIx]

Thank you for clarifying. I wasn't trying to equat orbstate anything. Just understand the mechanisms, which you now xplained well.

So what are the downsides to these substances? Either short term or long term use?

None that I am aware of besides financial expense.

 

[Rido]

.

So what are the downsides to these substances? Either short term or long term use?

Short term - Taking a shit

 

[lukiss96]

Only second day on it, but I don't understand why I feel so off.

I feel weaker, kinda light headed, sometimes it's harder to focus vision, feels like my head is under slight pressure, appetite is up and down and I feel like food is taking way longer to be processed, feel like so full like when bulking, also feel heat, food looks bland.

I'm irritable like a bitch on her period, actually not like that, but I'm way more impulsive and more aggressive wtf...

I'm only taking testosterone and equipoise and this nothing else, before adding semaglutide all was good.

Now, I feel like not myself. What is going on? I know you think I'm an idiot, I maybe am, idk.

But everybody reacts so good and gets no sides, so it can't be ozempic can it?

 

[M@NU]

Only second day on it, but I don't understand why I feel so off.

I feel weaker, kinda light headed, sometimes it's harder to focus vision, feels like my head is under slight pressure, appetite is up and down and I feel like food is taking way longer to be processed, feel like so full like when bulking, also feel heat, food looks bland.

I'm irritable like a bitch on her period, actually not like that, but I'm way more impulsive and more aggressive wtf...

I'm only taking testosterone and equipoise and this nothing else, before adding semaglutide all was good.

Now, I feel like not myself. What is going on? I know you think I'm an idiot, I maybe am, idk.

But everybody reacts so good and gets no sides, so it can't be ozempic can it?

whats your blood sugar?

 

[lukiss96]

whats your blood sugar?

Sorry for my ignorance, I don't know and I never bothered to learn about all these things. I just read on meso that ozempic is side effect free and I decided to try it.

I can power through these sides I think, but can I fuck myself up somehow? Should I quit?

 

[Rido]

Sorry for my ignorance, I don't know and I never bothered to learn about all these things. I just read on meso that ozempic is side effect free and I decided to try it.

I can power through these sides I think, but can I fuck myself up somehow? Should I quit?

It's side effect free for the most part but you didn't escalate the dose properly bro...

 

[lukiss96]

It's side effect free for the most part but you didn't escalate the dose properly bro...

I thought 0.25mg was not worth wasting time on...

Just like clen I always start at 60mcg, not 20mcg.

I'm glad that I didn't do worse, I wanted to do 1mg from the start...

I can't believe sides are like this, now my stomach left side slightly hurts.

I feel like moron

 

[Rido]

I thought 0.25mg was not worth wasting time on...

Just like clen I always start at 60mcg, not 20mcg.

I'm glad that I didn't do worse, I wanted to do 1mg from the start...

I can't believe sides are like this, now my stomach left side slightly hurts.

I feel like moron

If you were on the generic I was on. 0.5 would have been fine but one true ozempic I wouldn't have for sure.