Who SHOULDN'T take slin?

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Greatly increases cardiovascular risk and there are extremely strong inverse correlations between basal insulin and lifespan. I recommend everyone read this paper:

Herman, M. E., O’Keefe, J. H., Bell, D. S. H., & Schwartz, S. S. (2017). Insulin Therapy Increases Cardiovascular Risk in Type 2 Diabetes. Progress in Cardiovascular Diseases, 60(3), 422–434. doi:10.1016/j.pcad.2017.09.001

Before the handwaving of "in T2D!" understanding the mechanisms, which I know just bores people, and the constraints on good studies in the bodybuilding population, do believe, there is reason to believe slin has an unfavorable risk-reward for most persons.

When used in combination with AAS and some other stuff, there are additional mechanisms that likely act in concert to increase morbidity risks (elevated triglycerides, endothelial dysfunction, etc.)

Do you have the full paper? Insulin Therapy Increases Cardiovascular Risk in Type 2 Diabetes - PubMed

How dangerous do you think slin is if:
- calories remain the same, at slight surplus for bulking
- user is very lean and insulin sensitive
- used only pre/post workout with rapid acting, like a Milos type protocol?
 
Do you have the full paper? Insulin Therapy Increases Cardiovascular Risk in Type 2 Diabetes - PubMed

How dangerous do you think slin is if:
- calories remain the same, at slight surplus for bulking
- user is very lean and insulin sensitive
- used only pre/post workout with rapid acting, like a Milos type protocol?
Full text, yes. I cannot ascribe a risk/hazard ratio to these hypotheticals (as much as I'd like to be able to). If you want the full text, it is available via SciHub. If you read the paper, you can try to infer the degree or level of cardiovascular risk posed, and whether (I think it does to a significant extent) it applies to healthy, lean bodybuilders.

What I would say is that guys should just be aware of the very real cardiovascular risks of insulin use, so as to be able to consider whether it is worth the tradeoff for them. The risk exogenous insulin poses is compounded (probably synergistically) by AAS use.

This is because elevated triglycerides, endothelial dysfunction, atherosclerosis, hypertension, and prothrombotic activity are all promoted by androgens and contribute to the development of type 2 diabetes. Along with chronic hyperinsulinemia, that contributes to diminished autophosphorylation of the IR, subsequent PI3K-AKT signaling is affected, abating GLUT-4 translocation to the cell surface in muscle and adipose cells. This insulin toxicity (exogenous insulin-induced insulin resistance) is yet another (short-term, apparently reversible) harm to consider as well.
 
I do not have the full paper, but I unfortunately know a lot of Type II diabetics, and they choose insulin rather than a severe calorie restriction.

"But I like carbs," one close friend told me with a laugh.

I am tempted to view the results of that study as having more to do with a whole lifestyle choice rather than the actual use of insulin, and I am not sure it has any application to the use of insulin in bodybuilding if insulin matches the carbs rather than increasing carbs with insulin.

But I don't have the whole study, and I would not understand it as well as you if I did.

Is there nothing to what I wrote above, based on my observations of diabetics? From my own experience it is a self inflicted disease and appears to be the easiest disease in the world to avoid.

There are a number of observations of "cure" by calorie restriction being permanent for those who do not go back to stuffing their face and getting fatter again.

It just seems like the cardiovascular risk would have to be higher for those who continue eating like a Type II diabetic and need insulin. Why is the cardiovascular risk tied to the insulin, as a risk factor all by itself?
 
I do not have the full paper, but I unfortunately know a lot of Type II diabetics, and they choose insulin rather than a severe calorie restriction.

"But I like carbs," one close friend told me with a laugh.

I am tempted to view the results of that study as having more to do with a whole lifestyle choice rather than the actual use of insulin, and I am not sure it has any application to the use of insulin in bodybuilding if insulin matches the carbs rather than increasing carbs with insulin.

But I don't have the whole study, and I would not understand it as well as you if I did.

Is there nothing to what I wrote above, based on my observations of diabetics? From my own experience it is a self inflicted disease and appears to be the easiest disease in the world to avoid.

There are a number of observations of "cure" by calorie restriction being permanent for those who do not go back to stuffing their face and getting fatter again.

It just seems like the cardiovascular risk would have to be higher for those who continue eating like a Type II diabetic and need insulin. Why is the cardiovascular risk tied to the insulin, as a risk factor all by itself?
The study uses statistical and research methods that demonstrate the insulin dose- dependency increasing the cardiovascular risks, as well as highlighting the basic research on insulin showing its direct and pleitropic mechanisms in causing this increased risk (these are physiological mechanisms that apply to humans as a class rather than diabetics as a class). This is aside from the dramatic differences in cardiovascular risk between the same class of type II diabetics on insulin versus other treatments like Metformin or GLP-1 agonists. The dose- dependency of increased CV risk was not small either, it presents a 2- to 3- fold increase in the risk of CV death per 1 unit/kg/day increase, for example.

I think there is absolutely something to what you say above, that lifestyle is a contributor to the early deaths of diabetics in the vast majority of cases. I also think this paper sought to tease out that factor as they understand it as well as we do.

I think that a lot of what bodybuilders do nutritionally and with exercise mitigates some aspect of the risk, but then I think that androgens+insulin probably more than negates that, is my honest view.
 
The study uses statistical and research methods that demonstrate the insulin dose- dependency increasing the cardiovascular risks, as well as highlighting the basic research on insulin showing its direct and pleitropic mechanisms in causing this increased risk (these are physiological mechanisms that apply to humans as a class rather than diabetics as a class). This is aside from the dramatic differences in cardiovascular risk between the same class of type II diabetics on insulin versus other treatments like Metformin or GLP-1 agonists. The dose- dependency of increased CV risk was not small either, it presents a 2- to 3- fold increase in the risk of CV death per 1 unit/kg/day increase, for example.

I think there is absolutely something to what you say above, that lifestyle is a contributor to the early deaths of diabetics in the vast majority of cases. I also think this paper sought to tease out that factor as they understand it as well as we do.

I think that a lot of what bodybuilders do nutritionally and with exercise mitigates some aspect of the risk, but then I think that androgens+insulin probably more than negates that, is my honest view.

I recently got my hands on semaglutide and I can say it does strongly suppress appetite for me. I'm easily at 10% or below and I'd describe my hunger as "extremely strong". 1mg allows me to fast for 12-16 hours with very little hunger.

I'm not sure if it was the drug but I was able to do intense cardio, 16 hours fasted without feeling weak, which normally was impossible at any point in my life. I see no reason to ever stop taking this drug as quality of life for me is based on having very little hunger.

Any idea what the long term consequences might be? I've already read nearly every paper on GLP-1 agonists I could find. It seems to be safe for type-2 diabetes / obese older women, long term, I think.

I hate to sound like an idiot getting excited over the next new thing, but I don't understand why this peptide isn't massively more popular.

The only other drug I'm taking is TRT dose test and dutasteride (for hairloss).
 
I recently got my hands on semaglutide and I can say it does strongly suppress appetite for me. I'm easily at 10% or below and I'd describe my hunger as "extremely strong". 1mg allows me to fast for 12-16 hours with very little hunger.

I'm not sure if it was the drug but I was able to do intense cardio, 16 hours fasted without feeling weak, which normally was impossible at any point in my life. I see no reason to ever stop taking this drug as quality of life for me is based on having very little hunger.

Any idea what the long term consequences might be? I've already read nearly every paper on GLP-1 agonists I could find. It seems to be safe for type-2 diabetes / obese older women, long term, I think.

I hate to sound like an idiot getting excited over the next new thing, but I don't understand why this peptide isn't massively more popular.

The only other drug I'm taking is TRT dose test and dutasteride (for hairloss).
Why do you fast for 16 hours and do cardio when at single digit bodyfat? Just curious.
 
Why do you fast for 16 hours and do cardio when at single digit bodyfat? Just curious.
Oh, I was just testing it out. I read some reports of overweight women claiming to have zero hunger so I wanted to see how far I could push it.

Interesting reading: Semaglutide • r/Semaglutide

Max dose is 2mg, I used 1mg. I thought it wouldn't even have an effect on someone who was lean.

Which begs the question, can an obese person actually have more hunger than someone who is lean?
 
I recently got my hands on semaglutide and I can say it does strongly suppress appetite for me. I'm easily at 10% or below and I'd describe my hunger as "extremely strong". 1mg allows me to fast for 12-16 hours with very little hunger.

I'm not sure if it was the drug but I was able to do intense cardio, 16 hours fasted without feeling weak, which normally was impossible at any point in my life. I see no reason to ever stop taking this drug as quality of life for me is based on having very little hunger.

Any idea what the long term consequences might be? I've already read nearly every paper on GLP-1 agonists I could find. It seems to be safe for type-2 diabetes / obese older women, long term, I think.

I hate to sound like an idiot getting excited over the next new thing, but I don't understand why this peptide isn't massively more popular.

The only other drug I'm taking is TRT dose test and dutasteride (for hairloss).
From what I can tell the GLP-1 agonists are healthy and as of now, they look to be almost devoid of any real long-term health risks. They're probably the future of diabetes treatment.

They're quite popular, and will become more so, but are expensive and are primarily a cutting tool for bodybuilders. Note that agents like clen are anabolic and lipolytic (recomp), so these classic agents are likely to remain popular as they serve different uses. I understand the GLP-1 agonists might serve to raise insulin (I'd say they modulate it) so you could make the argument they promote anabolism, but, not to same degree.
 
From what I can tell the GLP-1 agonists are healthy and as of now, they look to be almost devoid of any real long-term health risks. They're probably the future of diabetes treatment.

They're quite popular, and will become more so, but are expensive and are primarily a cutting tool for bodybuilders. Note that agents like clen are anabolic and lipolytic (recomp), so these classic agents are likely to remain popular as they serve different uses. I understand the GLP-1 agonists might serve to raise insulin (I'd say they modulate it) so you could make the argument they promote anabolism, but, not to same degree.
Have only been using it for about 2 weeks but I no longer see the need to mess with clen/DNP/EC, etc.

Why bother when one can diet on 250-300g of protein a day + fiber and have zero hunger?
 
Have only been using it for about 2 weeks but I no longer see the need to mess with clen/DNP/EC, etc.

Why bother when one can diet on 250-300g of protein a day + fiber and have zero hunger?
I've said it before, I think the GLP-1 agonists are the future (for cutting).
 
I've said it before, I think the GLP-1 agonists are the future (for cutting).

Apparently pfizer, astra, etc. have GLP-1s in the making. Any thoughts on those?

Do you think this will be commonly given out to... everyone in 1st world countries in 10-20 years? It's weird to think you could take any obese person and 1 injection would make it impossible for them to eat more than 2k calories a day without massive effort.

The worst side effect seems to be nausea and that only is reported if people take a huge dose then try to eat a lot of food like normal.
 
Apparently pfizer, astra, etc. have GLP-1s in the making. Any thoughts on those?

Do you think this will be commonly given out to... everyone in 1st world countries in 10-20 years? It's weird to think you could take any obese person and 1 injection would make it impossible for them to eat more than 2k calories a day without massive effort.

The worst side effect seems to be nausea and that only is reported if people take a huge dose then try to eat a lot of food like normal.
Yes, I think these GLP-1 agonists will become part of a standard first-line of treatment for (pre)diabetes/obesity in these countries.
 
Yes, I think these GLP-1 agonists will become part of a standard first-line of treatment for (pre)diabetes/obesity in these countries.
Before I started using semaglutide, I'd go hypo around the 10 hour mark, get intense hunger, feel very weak.

Now it feels like I can't go hypo. I can easily go 16 hours without eating and still lift weights heavy.

Is this in my head, or the GLP-1 doing some weird crap?

tldr; I can't go hypo or feel weak for not eating short term, while before I was an outright slave to eating.
 
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Before I started using semaglutide, I'd go hypo around the 10 hour mark, get intense hunger, feel very weak.

Now it feels like I can't go hypo. I can easily go 16 hours without eating and still lift weights heavy.

Is this in my head, or the GLP-1 doing some weird crap?

tldr; I can't go hypo or feel weak for not eating short term, while before I was an outright slave to eating.
It's very interesting that you can avoid hypoglycaemia with semaglutide, but I absolutely believe it. Perhaps this is chiefly due to delayed gastric emptying as well as its being structurally related to glucagon. While its mechanisms of action involve some suppression of glucagon (which should in theory cause more rapid hypoglycaemia), there is just so much going on with GLP-1 agonists by modulating glucose homeostasis (increased insulin, etc.) that frankly, I don't fully understand how they work, and I don't think anyone understands the full depth and breadth of these compounds yet.
 
It's very interesting that you can avoid hypoglycaemia with semaglutide, but I absolutely believe it. Perhaps this is chiefly due to delayed gastric emptying as well as its being structurally related to glucagon. While its mechanisms of action involve some suppression of glucagon (which should in theory cause more rapid hypoglycaemia), there is just so much going on with GLP-1 agonists by modulating glucose homeostasis (increased insulin, etc.) that frankly, I don't fully understand how they work, and I don't think anyone understands the full depth and breadth of these compounds yet.

I'm losing weight, yes really, on 3600 calories a day. I've been tracking calories almost daily for 10 years and I consider myself extremely accurate. 3400 is more than enough to make me gain, even when I was running 500mg of tren or deca. (Only on TRT now)

I only recently added 4-5 ui a day of generic chinese HGH 7 days ago and the semaglutide was from 14 days ago.

So there is clearly weird shit going on here. Any idea how to figure out what? Maybe run the HGH until the end of the month, then drop it?
 
I'm losing weight, yes really, on 3600 calories a day. I've been tracking calories almost daily for 10 years and I consider myself extremely accurate. 3400 is more than enough to make me gain, even when I was running 500mg of tren or deca. (Only on TRT now)

I only recently added 4-5 ui a day of generic chinese HGH 7 days ago and the semaglutide was from 14 days ago.

So there is clearly weird shit going on here. Any idea how to figure out what? Maybe run the HGH until the end of the month, then drop it?
Are you trying to gain weight? Semaglutide would be incongruent with that goal.
 
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