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Dealing with Growth Hormone Insulin Resistance (ameliorating rhGH-induced IR) [Type-IIx]

Naw I'm good. I've done plenty of research, used plenty on different protocols, and have also worked with quite a few well known coaches over the years.

I don't think posting some protocols that have been successful is a big deal. As I stated, most knowledgeable members on the board are already familiar with these interventions.

Not to mention there’s plenty of guys on here who also have clients who still give plenty of free information and/or pros/competitors who also paid for information and they share it on the board…

I totally get TypeII point of view if someone randomly asked him details in a thread or something…

But you’re going to post a new thread/topic and only offer surface information and refuse to go into detail because of clients??

Then why the hell make the thread in the first place??

That’s the part that gets me..
 
Then why the hell make the thread in the first place??
I get the point but the thread is still useful. He listed all kind of different meds one can use to combat insulin resistance, he's just not giving doses which is understandable. Doses can be very individual, so it's not wise to say take x gram of that and you are good.

Some didnt even know all these different kind of medication that can be used and at best only knew metformin.
 
I thought the OP''s post was informative. I can see I'm on the right track in my protocol from a biochemical perspective. I don't need the "paint by numbers" version. I'm not a fan of throwing out numbers either. I can say what has worked for me but I often am concerned that someone else may try my approach with bad results.
 
Some didnt even know all these different kind of medication that can be used and at best only knew metformin.
This would be me. Long history in peds/aas but only last 12 months have I used hgh (as I'm late 40s). Started metaforin at 500mg and had been using 3.5 to 4ius of hgh ED but was eating low carb already, running low-mid tren, and going hypo more than I liked (fasting glucose low to mid 70s) so dropped it. I'll consider it again in the future with some bloods before/after and likely not run with tren.
 
Maybe reductionist and oversimplifying, but what about just relatively large amounts of cardio during offseason? Can that offset some of the gh induced insulin resistance.
Not really, honestly. Bodybuilding-style resistance training is really the ideal means to stress the glycolytic system, and use glucose as an energy substrate to perform work (characterized by short rest intervals between repetitions [with load] that last 30 sec - 1 min); you might characterize that as something approaching glycogen depletion training or anaerobic capacity work. This directly lowers blood glucose, but is not insulin sensitizing.

While zone 2 cardio in particular improves mitochondrial function, which in turn enhances insulin sensitivity, it primarily increases CPT1/carnitine system transporter function (a fatty acid transporter), this is primarily a local adaptation (albeit in skeletal muscle, which constitutes a majority of our tissue) as opposed to the GLP-1 & GIP agonists acting centrally to enhance insulin sensitivity.

We really need centrally-acting insulin sensitizing agents (e.g., GLP-1 & GIP agonists) to counteract more potent drug effects, that are not attached to cardiovascular fitness.

That is to say, the effect of cardio will be modest at best.

I generally see a lot of the chatter promoting cardio to enhance longevity in enhanced bodybuilders as wishful thinking, it could even be construed as magical thinking.

Given that GH induces insulin resistance by increasing circulating FFAs, by acting to enhance HSL activity, increased CPT1 & mitochondrial function really won't serve the task of ameliorating this action of GH (moreover, cardio stimulates HSL).

Slin is like throwing fuel on the fire of rhGH's insulin resistance, in progression to T2DM, given that it induces:
1. central obesity
2. elevated triglycerides; ↓HDL, ↑Apo B, ↓Apo A1 (dyslipidemia)
3. endothelial dysfunction (altered arterial tone ⇒ atherosclerosis)
4. atherosclerosis (factors: platelet adhesion, aggregation, thrombogenecity ⇒ inflammation)
5. hypertension
6. prothrombotic activity

Slin further stimulates VLDL secretion in the liver and directly worsens insulin resistance (as HOMA-IR is a function of blood glucose and blood insulin levels).

AAS induce left ventricular hypertrophy and diastolic function derangement directly. Combined rhGH+AAS quite dramatically increases cardiomyopathy. RhGH directly alters cardiovascular function, induces LVH, etc.

No volume of cardio does anything to ameliorate these direct drug effects.

The sole benefit, as I see it, of cardio for enhanced bodybuilders per se, is by reducing the resistance training-induced increase in arterial stiffness.
 
Not really, honestly. Bodybuilding-style resistance training is really the ideal means to stress the glycolytic system, and use glucose as an energy substrate to perform work (characterized by short rest intervals between repetitions [with load] that last 30 sec - 1 min); you might characterize that as something approaching glycogen depletion training or anaerobic capacity work. This directly lowers blood glucose, but is not insulin sensitizing.

While zone 2 cardio in particular improves mitochondrial function, which in turn enhances insulin sensitivity, it primarily increases CPT1/carnitine system transporter function (a fatty acid transporter), this is primarily a local adaptation (albeit in skeletal muscle, which constitutes a majority of our tissue) as opposed to the GLP-1 & GIP agonists acting centrally to enhance insulin sensitivity.

We really need centrally-acting insulin sensitizing agents (e.g., GLP-1 & GIP agonists) to counteract more potent drug effects, that are not attached to cardiovascular fitness.

That is to say, the effect of cardio will be modest at best.

I generally see a lot of the chatter promoting cardio to enhance longevity in enhanced bodybuilders as wishful thinking, it could even be construed as magical thinking.

Given that GH induces insulin resistance by increasing circulating FFAs, by acting to enhance HSL activity, increased CPT1 & mitochondrial function really won't serve the task of ameliorating this action of GH (moreover, cardio stimulates HSL).

Slin is like throwing fuel on the fire of rhGH's insulin resistance, in progression to T2DM, given that it induces:
1. central obesity
2. elevated triglycerides; ↓HDL, ↑Apo B, ↓Apo A1 (dyslipidemia)
3. endothelial dysfunction (altered arterial tone ⇒ atherosclerosis)
4. atherosclerosis (factors: platelet adhesion, aggregation, thrombogenecity ⇒ inflammation)
5. hypertension
6. prothrombotic activity

Slin further stimulates VLDL secretion in the liver and directly worsens insulin resistance (as HOMA-IR is a function of blood glucose and blood insulin levels).

AAS induce left ventricular hypertrophy and diastolic function derangement directly. Combined rhGH+AAS quite dramatically increases cardiomyopathy. RhGH directly alters cardiovascular function, induces LVH, etc.

No volume of cardio does anything to ameliorate these direct drug effects.

The sole benefit, as I see it, of cardio for enhanced bodybuilders per se, is by reducing the resistance training-induced increase in arterial stiffness.

Does dNPs sensitizing effect full come from the massive glycogen depletion? Or are there other metabolic cascades?

I’m not sure if dnp promotes or diminishes mitochondrial biogenesis…..I just know in rats when they gave them that liver-targeted dnp their metabolic markers improved
 
I get the point but the thread is still useful. He listed all kind of different meds one can use to combat insulin resistance, he's just not giving doses which is understandable. Doses can be very individual, so it's not wise to say take x gram of that and you are good.

Some didnt even know all these different kind of medication that can be used and at best only knew metformin.

No 100%, I really enjoy his posts and his knowledge but in this particular situation it just kind of came off like “I know something you don’t know and I’m not gona tell you” lol 😂

You want to know what’s hilarious about all this though??

Apparently people have a problem with sharing doses/protocols on things that can contribute to being healthier while being enhanced and getting better effects etc…

But people have no problem spouting extremely high and dangerous doses of AAS and other drugs on this board and downplaying constantly how over rated the danger is and that it’s not that big of a deal… lol Whaaaaaaat?? Kinda funny to me..
 
Not really, honestly. Bodybuilding-style resistance training is really the ideal means to stress the glycolytic system, and use glucose as an energy substrate to perform work (characterized by short rest intervals between repetitions [with load] that last 30 sec - 1 min); you might characterize that as something approaching glycogen depletion training or anaerobic capacity work. This directly lowers blood glucose, but is not insulin sensitizing.

While zone 2 cardio in particular improves mitochondrial function, which in turn enhances insulin sensitivity, it primarily increases CPT1/carnitine system transporter function (a fatty acid transporter), this is primarily a local adaptation (albeit in skeletal muscle, which constitutes a majority of our tissue) as opposed to the GLP-1 & GIP agonists acting centrally to enhance insulin sensitivity.

We really need centrally-acting insulin sensitizing agents (e.g., GLP-1 & GIP agonists) to counteract more potent drug effects, that are not attached to cardiovascular fitness.

That is to say, the effect of cardio will be modest at best.

I generally see a lot of the chatter promoting cardio to enhance longevity in enhanced bodybuilders as wishful thinking, it could even be construed as magical thinking.

Given that GH induces insulin resistance by increasing circulating FFAs, by acting to enhance HSL activity, increased CPT1 & mitochondrial function really won't serve the task of ameliorating this action of GH (moreover, cardio stimulates HSL).

Slin is like throwing fuel on the fire of rhGH's insulin resistance, in progression to T2DM, given that it induces:
1. central obesity
2. elevated triglycerides; ↓HDL, ↑Apo B, ↓Apo A1 (dyslipidemia)
3. endothelial dysfunction (altered arterial tone ⇒ atherosclerosis)
4. atherosclerosis (factors: platelet adhesion, aggregation, thrombogenecity ⇒ inflammation)
5. hypertension
6. prothrombotic activity

Slin further stimulates VLDL secretion in the liver and directly worsens insulin resistance (as HOMA-IR is a function of blood glucose and blood insulin levels).

AAS induce left ventricular hypertrophy and diastolic function derangement directly. Combined rhGH+AAS quite dramatically increases cardiomyopathy. RhGH directly alters cardiovascular function, induces LVH, etc.

No volume of cardio does anything to ameliorate these direct drug effects.

The sole benefit, as I see it, of cardio for enhanced bodybuilders per se, is by reducing the resistance training-induced increase in arterial stiffness.

Maybe you can answer this question;

And let me reiterate that I don’t have a problem with you at all and actually really enjoy your posts, especially when I don’t have to read them 23x to understand them (that’s my fault not yours lol).. It’s just how your posts in this thread can be interpreted is all..

So basically you’re saying above that Insulin combined with GH/AAS is significantly more dangerous to health overall than just GH/AAS alone, right??

You also state that AAS contributes to certain cardiovascular changes and HGH on its own contributes to cardiovascular changes and together even worse cardiovascular changes…

May I ask, in your experience; at what dosages and duration have you seen these changes take place??

I ask because I’ve seen you post in the past that 2-4iu is basically a replacement dosage for most people…. And HIV patients have been known to be prescribed 18iu per day..

There’s also plenty of guys on here who use AAS/GH on the responsible side for decades and don’t seem to have these negative changes from the few we’ve seen actually get tested..

Thanks in advance…
 
Buy a banner if you want clients. Or better yet get some of your clients to post on here about you. There are dosages, protocols, recommendations all over this board.
 
Not really, honestly. Bodybuilding-style resistance training is really the ideal means to stress the glycolytic system, and use glucose as an energy substrate to perform work (characterized by short rest intervals between repetitions [with load] that last 30 sec - 1 min); you might characterize that as something approaching glycogen depletion training or anaerobic capacity work. This directly lowers blood glucose, but is not insulin sensitizing.

While zone 2 cardio in particular improves mitochondrial function, which in turn enhances insulin sensitivity, it primarily increases CPT1/carnitine system transporter function (a fatty acid transporter), this is primarily a local adaptation (albeit in skeletal muscle, which constitutes a majority of our tissue) as opposed to the GLP-1 & GIP agonists acting centrally to enhance insulin sensitivity.

We really need centrally-acting insulin sensitizing agents (e.g., GLP-1 & GIP agonists) to counteract more potent drug effects, that are not attached to cardiovascular fitness.

That is to say, the effect of cardio will be modest at best.

I generally see a lot of the chatter promoting cardio to enhance longevity in enhanced bodybuilders as wishful thinking, it could even be construed as magical thinking.

Given that GH induces insulin resistance by increasing circulating FFAs, by acting to enhance HSL activity, increased CPT1 & mitochondrial function really won't serve the task of ameliorating this action of GH (moreover, cardio stimulates HSL).

Slin is like throwing fuel on the fire of rhGH's insulin resistance, in progression to T2DM, given that it induces:
1. central obesity
2. elevated triglycerides; ↓HDL, ↑Apo B, ↓Apo A1 (dyslipidemia)
3. endothelial dysfunction (altered arterial tone ⇒ atherosclerosis)
4. atherosclerosis (factors: platelet adhesion, aggregation, thrombogenecity ⇒ inflammation)
5. hypertension
6. prothrombotic activity

Slin further stimulates VLDL secretion in the liver and directly worsens insulin resistance (as HOMA-IR is a function of blood glucose and blood insulin levels).

AAS induce left ventricular hypertrophy and diastolic function derangement directly. Combined rhGH+AAS quite dramatically increases cardiomyopathy. RhGH directly alters cardiovascular function, induces LVH, etc.

No volume of cardio does anything to ameliorate these direct drug effects.

The sole benefit, as I see it, of cardio for enhanced bodybuilders per se, is by reducing the resistance training-induced increase in arterial stiffness.
Bro, thank you. I'm gonna repay your generosity by asking some more really stupid questions that are probably beneath your paygrade.

What about just not using growth hormone? If you had intermittent cessation and essentially cycled growth hormone the same way you cycled AAS, could you alleviate some insulin resistance?

Keto diets or low/zero carb days/diets... will these do anything to combat insulin insensitivity?

Can insulin sensitivity still get really destroyed just from offseason massing phases with AAS only and/or low dose gh?

Lastly, I have never actually neve run GH full on for a long time, but I've been using mk677 for around 5 months straight. Am I fucking myself up worse than if I'd just been using growth hormone? Is blood glucose elevation a good indicator of how much you're damaging insulin sensitivity?
 
Bro, thank you. I'm gonna repay your generosity by asking some more really stupid questions that are probably beneath your paygrade.

What about just not using growth hormone? If you had intermittent cessation and essentially cycled growth hormone the same way you cycled AAS, could you alleviate some insulin resistance?

Keto diets or low/zero carb days/diets... will these do anything to combat insulin insensitivity?

Can insulin sensitivity still get really destroyed just from offseason massing phases with AAS only and/or low dose gh?

Lastly, I have never actually neve run GH full on for a long time, but I've been using mk677 for around 5 months straight. Am I fucking myself up worse than if I'd just been using growth hormone? Is blood glucose elevation a good indicator of how much you're damaging insulin sensitivity?
I personally had success reducing my am glucose readings by decreasing carb intake and adding more healthy fat . Then got a1c tested and it came back great.
 
Bro, thank you. I'm gonna repay your generosity by asking some more really stupid questions that are probably beneath your paygrade.

What about just not using growth hormone? If you had intermittent cessation and essentially cycled growth hormone the same way you cycled AAS, could you alleviate some insulin resistance?
Absolutely. This is a primary rationale for cyclical use of rhGH, as well as the decrement to GH response (the increase to IGF-I) that diminishes after several months.
Keto diets or low/zero carb days/diets... will these do anything to combat insulin insensitivity?
Well, keto & low carbohydrate (except for the Carnivore-style diets, I suppose) are characterized by high fat/lipid intakes. Recall that GH induces insulin resistance by increasing circulating free fatty acids (by increasing HSL activity).

Keto (with rhGH) accelerates fat loss in energy deficit (due to increased insulin resistance in adipocytes). In fact, GH increases hormone-sensitive lipase (HSL) activity; direct oxidation of FFAs; and suppresses the lipoprotein lipase (LPL) in adipose tissue. But, the increase in blood levels of FFAs (attendant to increased dietary fat intakes) decreases adipose tissue HSL activity, thus reducing hydrolysis of "trapped" triglyceride, despite the insulin resistant effects on the adipocyte (preventing storage of new triglyceride therein)... expect circulating FFAs to be very high. Now, GH likely prevents muscle catabolism by its anticatabolic effects (i.e., net retention of LBM and protein stores during fasting; N, Ca, K retention, though largely in the extracellular matrix).
- But increases to muscular size and strength in an energy surplus (keto) will be relatively slowed relative to an isocaloric balanced or high carbohydrate diet due mostly to lack of glycolytic substrates (again, necessary to support intense resistance training). RhGH use will promote some muscle anabolism by IGF-I-mediated Akt/mTOR activity (again sort of "clawing back" some anabolic potency despite somewhat reduced insulin levels vs. higher carbohydrate intakes).

You could certainly make the argument without looking foolish whatsoever that keto is rational with rhGH for fat loss and even recomp (energy deficit, or at maintenance).

I do, however, believe many of the rationales underpinning keto are eviscerated, at least partly, by rhGH use: i.e., maintaining low insulin levels (increased by rhGH) to promote FA liberation by the utilization of MCTs and ketone bodies to support such; protein sparing by ketone bodies (considering the far more profound effects of rhGH/AAS to effect anticatabolism); and the very fact that rhGH serves lipolytic, recomp, and growth functions better than keto does on an isocaloric moderate-high carbohydrate diet (with improved muscular strength and size increases) renders keto+rhGH suboptimal.
Can insulin sensitivity still get really destroyed just from offseason massing phases with AAS only and/or low dose gh?
AAS are insulin sensitizing (Tren potently so; I suspect Superdrol also). With sane nutrient intakes and voluminous bodybuilding-style resistance training (tension & volume methods), I generally see the off-season as potentially excellent for insulin sensitivity. Perhaps counterintuitively, you might expect the drugs used by most (not saying this is the most rational use), e.g., clen, stimulants (by increasing catecholamine secretion), and high intensity aerobic endurance activity (i.e., cardio) which stimulates catecholamines, and of course rhGH which stimulates HSL, to actually worsen insulin sensitivity during the contest prep.
Lastly, I have never actually neve run GH full on for a long time, but I've been using mk677 for around 5 months straight. Am I fucking myself up worse than if I'd just been using growth hormone? Is blood glucose elevation a good indicator of how much you're damaging insulin sensitivity?
Absolutely, MK0677 (Ibutamoren mesylate) is worse for insulin resistance than rhGH. Relative to rhGH, Ibutamoren's side effect profile is unfavorable: ↑cortisol & prolactin; musculoskeletal pain (myalgia, arthralgia) & edema (fluid retention); ↑insulin resistance (increased blood glucose); ↑appetite. By selectively activating the GHS-R (growth hormone secretatogue receptor), Ibutamoren does confer some cardiovascular and β-cell protective effects (via PI3K/PKB, JNK inhibition) & may be pancreatic regenerative, but it's not great for insulin sensitivity nor improving muscle function (size, strength).
 
@ripriot
I thought banners were for AAS sales and the like, not coaching services. Did you get your mod badge and I missed it? Can you point to where in this thread I solicited clients? I merely addressed a notorious cunt that stated that my thread is useless, and demanded free shit, when I individually tailor doses to clients that I would actually accept to work for. You a freeloader as well?

If someone takes a pros self-reported doses and compounds as a "protocol" (it's not) and straightforwardly uses the same doses and compounds without regard to training status, body mass, etc., well, they are fucking retarded.
 
Maybe you can answer this question;

And let me reiterate that I don’t have a problem with you at all and actually really enjoy your posts, especially when I don’t have to read them 23x to understand them (that’s my fault not yours lol).. It’s just how your posts in this thread can be interpreted is all..

So basically you’re saying above that Insulin combined with GH/AAS is significantly more dangerous to health overall than just GH/AAS alone, right??

You also state that AAS contributes to certain cardiovascular changes and HGH on its own contributes to cardiovascular changes and together even worse cardiovascular changes…

May I ask, in your experience; at what dosages and duration have you seen these changes take place??

I ask because I’ve seen you post in the past that 2-4iu is basically a replacement dosage for most people…. And HIV patients have been known to be prescribed 18iu per day..

There’s also plenty of guys on here who use AAS/GH on the responsible side for decades and don’t seem to have these negative changes from the few we’ve seen actually get tested..

Thanks in advance…
We also have guys that have been diagnosed with congestive heart failure from 20 IU rhGH daily @Biggerp73 . So somewhere in between. Obviously, if you're looking for some clear dose/response for yourself, nobody knows. If I could predict the future, I'd be a trillionaire from the stock market; not posting about drugs on bodybuilding boards.

Cardiomyopathy secondary to chronic GH excess (concentric hypertrophy, increased LV mass [weight of the heart may increase up to 1300 g where < 250 g is normal]) correlates with duration more than dose, though structural changes can occur with short-term GH exposure. It is rare. GH/IGF-I exerts beneficial effects on cardiac growth and function within normal ranges (i.e., a Goldilocks problem: concentrations should be "just right.")

The natural history of cardiomyopathy secondary to chronic GH excess progresses through 3 stages:

1. The early stage is characterized by increased contractility, decreased vascular resistance, and a high cardiac output (not to be confused with systolic or diastolic BP; though systolic BP is a proxy for cardiac output interacting with pressure exerted against the arterial walls)... This stage has no demonstrable morphological abnormalities, although LVH has been observed without any evidence of diastolic dysfunction
2. The intermediate stage is characterized by biventricular hypertrophy, impaired diastolic filling, preserved systolic function at rest, and impaired exercise tolerance
3. In the late stage... cardiac chamber dilation, systolic dysfunction at rest, and congestive heart failure if left untreated

The effects of GH on cardiomyocyte growth and myocardial hypertrophy in GH excess differ from LVH caused by pressure overload. That is to say, controlling BP will not help you here.
 
We also have guys that have been diagnosed with congestive heart failure from 20 IU rhGH daily @Biggerp73 . So somewhere in between. Obviously, if you're looking for some clear dose/response for yourself, nobody knows. If I could predict the future, I'd be a trillionaire from the stock market; not posting about drugs on bodybuilding boards.

Cardiomyopathy secondary to chronic GH excess (concentric hypertrophy, increased LV mass [weight of the heart may increase up to 1300 g where < 250 g is normal]) correlates with duration more than dose, though structural changes can occur with short-term GH exposure. It is rare. GH/IGF-I exerts beneficial effects on cardiac growth and function within normal ranges (i.e., a Goldilocks problem: concentrations should be "just right.")

The natural history of cardiomyopathy secondary to chronic GH excess progresses through 3 stages:

1. The early stage is characterized by increased contractility, decreased vascular resistance, and a high cardiac output (not to be confused with systolic or diastolic BP; though systolic BP is a proxy for cardiac output interacting with pressure exerted against the arterial walls)... This stage has no demonstrable morphological abnormalities, although LVH has been observed without any evidence of diastolic dysfunction
2. The intermediate stage is characterized by biventricular hypertrophy, impaired diastolic filling, preserved systolic function at rest, and impaired exercise tolerance
3. In the late stage... cardiac chamber dilation, systolic dysfunction at rest, and congestive heart failure if left untreated

The effects of GH on cardiomyocyte growth and myocardial hypertrophy in GH excess differ from LVH caused by pressure overload. That is to say, controlling BP will not help you here.

Thanks for the reply;

And yes I remember @Biggerp73 situation, but he was taking closer to 30iu-45iu per day (I recall him saying he was taking 2-3 bottles per day of Meditrope Black Tops which are 15iu each, sometimes higher)… But he was also admittedly taking grams of gear for months and months on end.. I want to say he was also taking around 1g of Trenbolone among other things for like 9 months or something..

I know responses are individual but I’d imagine that taking 2-3g+ of gear and 30-45iu of GH for months and months on end will do something if you’re not genetically gifted like some pros are to be able to handle the drugs..

I know you can’t tell me exactly my individual response but you seem to have a lot of knowledge on these subjects so kinda just looking for a ballpark guideline from your experience..

Like where is it that you start to see these problems??

Sure there are guys who run TRT Test and that’s it but they have dog shit genetics and they’ll get a thrombosis of some kind on that alone and you have guys who can run 5g of gear and 30iu GH for decades and are fairly ok.

But what’s the average of what you’ve seen personally??


Would you say a person with no underlying health issues or genetic issues can reasonably run 500mg-1g of the “safer” AAS with GH between 6-10iu so long as all health parameters are being met with reasonable time off as well down to true TRT doses (say 150mg Test and 2iu GH)??

Have you seen significant health changes in people like that who run gear like that for 3-6 months out of the year but take the other 6-9 months on true TRT doses??

Would you say that the envelope can in fact be pushed a little further and still be relatively safe/healthy without experiencing these negative consequences??

Just curious to get your perspective on where you think, if you were to give a general guideline, that the line should be drawn if health is a concern but still want to make enhanced type of progress… Surely there’s ways to do that and avoid the consequences you speak of as best as possible..

It’s kind of scary to think that you can have perfect blood pressure, health markers and take all kinds of precautions but that these drugs to the damage regardless..
 
@ripriot
a notorious cunt

Can you elaborate on this a little bit further? At least the "notorious" part. I feel that I've made some decent contributions to the board over the years. Not sure why you need to be so hostile towards a long standing contributing member just because I've questioned you on a few of your threads/posts.
 
Can you elaborate on this a little bit further? At least the "notorious" part. I feel that I've made some decent contributions to the board over the years. Not sure why you need to be so hostile towards a long standing contributing member just because I've questioned you on a few of your threads/posts.
Sure, I can elaborate: you are The N-O-T-O-R-I-O-U-S, notorious, C-U-N-T, cunt, mate.
Thanks for the reply;

And yes I remember @Biggerp73 situation, but he was taking closer to 30iu-45iu per day (I recall him saying he was taking 2-3 bottles per day of Meditrope Black Tops which are 15iu each, sometimes higher)… But he was also admittedly taking grams of gear for months and months on end.. I want to say he was also taking around 1g of Trenbolone among other things for like 9 months or something..

I know responses are individual but I’d imagine that taking 2-3g+ of gear and 30-45iu of GH for months and months on end will do something if you’re not genetically gifted like some pros are to be able to handle the drugs..

I know you can’t tell me exactly my individual response but you seem to have a lot of knowledge on these subjects so kinda just looking for a ballpark guideline from your experience..

Like where is it that you start to see these problems??

Sure there are guys who run TRT Test and that’s it but they have dog shit genetics and they’ll get a thrombosis of some kind on that alone and you have guys who can run 5g of gear and 30iu GH for decades and are fairly ok.

But what’s the average of what you’ve seen personally??


Would you say a person with no underlying health issues or genetic issues can reasonably run 500mg-1g of the “safer” AAS with GH between 6-10iu so long as all health parameters are being met with reasonable time off as well down to true TRT doses (say 150mg Test and 2iu GH)??

Have you seen significant health changes in people like that who run gear like that for 3-6 months out of the year but take the other 6-9 months on true TRT doses??

Would you say that the envelope can in fact be pushed a little further and still be relatively safe/healthy without experiencing these negative consequences??

Just curious to get your perspective on where you think, if you were to give a general guideline, that the line should be drawn if health is a concern but still want to make enhanced type of progress… Surely there’s ways to do that and avoid the consequences you speak of as best as possible..

It’s kind of scary to think that you can have perfect blood pressure, health markers and take all kinds of precautions but that these drugs to the damage regardless..
I don't know because I don't have that data, to get that sort of data in a reliable form and in bulk to be able to quantify with statistical methods and determine anything meaningful (significant) with respect to morbidity in enhanced bodybuilding is just not practically feasible, and I cannot answer any of your hypotheticals or questions. Certainly there are modulating factors like genetics and age. You're correct that I was mistaken in the dosage that Biggerp was using, it was 30 IU & 1.5 g Deca. Anyhow, I'm not sure that we should disentangle AAS from rhGH use since the two are almost exclusively used in combination in enhanced bodybuilding.

My own hypothesis is that a lot of guys are probably presently in that first (undetectable) stage of progression to cardiomyopathy from GH excess that are using supraphysiological rhGH; some will progress through to 3 and others will not.

I know it's scary.
 
Absolutely. This is a primary rationale for cyclical use of rhGH, as well as the decrement to GH response (the increase to IGF-I) that diminishes after several months.
Are there any contraindications for using GHRH analogues and/or Ghrelin agonists for this purpose? e.g. replacing GH with secretagogues for a few months out of the year (no idea what reasonable time on/time off would be here), or would this negatively affect resensitization in some way?
 
Absolutely. This is a primary rationale for cyclical use of rhGH, as well as the decrement to GH response (the increase to IGF-I) that diminishes after several months.

Well, keto & low carbohydrate (except for the Carnivore-style diets, I suppose) are characterized by high fat/lipid intakes. Recall that GH induces insulin resistance by increasing circulating free fatty acids (by increasing HSL activity).

Keto (with rhGH) accelerates fat loss in energy deficit (due to increased insulin resistance in adipocytes). In fact, GH increases hormone-sensitive lipase (HSL) activity; direct oxidation of FFAs; and suppresses the lipoprotein lipase (LPL) in adipose tissue. But, the increase in blood levels of FFAs (attendant to increased dietary fat intakes) decreases adipose tissue HSL activity, thus reducing hydrolysis of "trapped" triglyceride, despite the insulin resistant effects on the adipocyte (preventing storage of new triglyceride therein)... expect circulating FFAs to be very high. Now, GH likely prevents muscle catabolism by its anticatabolic effects (i.e., net retention of LBM and protein stores during fasting; N, Ca, K retention, though largely in the extracellular matrix).
- But increases to muscular size and strength in an energy surplus (keto) will be relatively slowed relative to an isocaloric balanced or high carbohydrate diet due mostly to lack of glycolytic substrates (again, necessary to support intense resistance training). RhGH use will promote some muscle anabolism by IGF-I-mediated Akt/mTOR activity (again sort of "clawing back" some anabolic potency despite somewhat reduced insulin levels vs. higher carbohydrate intakes).

You could certainly make the argument without looking foolish whatsoever that keto is rational with rhGH for fat loss and even recomp (energy deficit, or at maintenance).

I do, however, believe many of the rationales underpinning keto are eviscerated, at least partly, by rhGH use: i.e., maintaining low insulin levels (increased by rhGH) to promote FA liberation by the utilization of MCTs and ketone bodies to support such; protein sparing by ketone bodies (considering the far more profound effects of rhGH/AAS to effect anticatabolism); and the very fact that rhGH serves lipolytic, recomp, and growth functions better than keto does on an isocaloric moderate-high carbohydrate diet (with improved muscular strength and size increases) renders keto+rhGH suboptimal.

AAS are insulin sensitizing (Tren potently so; I suspect Superdrol also). With sane nutrient intakes and voluminous bodybuilding-style resistance training (tension & volume methods), I generally see the off-season as potentially excellent for insulin sensitivity. Perhaps counterintuitively, you might expect the drugs used by most (not saying this is the most rational use), e.g., clen, stimulants (by increasing catecholamine secretion), and high intensity aerobic endurance activity (i.e., cardio) which stimulates catecholamines, and of course rhGH which stimulates HSL, to actually worsen insulin sensitivity during the contest prep.

Absolutely, MK0677 (Ibutamoren mesylate) is worse for insulin resistance than rhGH. Relative to rhGH, Ibutamoren's side effect profile is unfavorable: ↑cortisol & prolactin; musculoskeletal pain (myalgia, arthralgia) & edema (fluid retention); ↑insulin resistance (increased blood glucose); ↑appetite. By selectively activating the GHS-R (growth hormone secretatogue receptor), Ibutamoren does confer some cardiovascular and β-cell protective effects (via PI3K/PKB, JNK inhibition) & may be pancreatic regenerative, but it's not great for insulin sensitivity nor improving muscle function (size, strength).


Thank you so much. That is VERY surprising about clenbuterol, stimulants, and high intensity cardio potentially being insulin resistance inducing.

I guess my plan going forward is to drop mk677, use 5ius of generics instead, and use insulin on high days only going into my next offseason phase.


Thanks a lot, Type-IIx!
 

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