A sober look at HGH

When I take testosterone I'm taking something that directly stimulates muscle protien synthesis.

That doesn't mean if it raises my blood pressure it doesn't work. That would be a side effect. Something to the side of the effect I want.

However raising my blood glucose is HGH working. It's the literal effect of the drug by stimulating FFA release and by increasing gluconeogenesis in the liver (and my reducing GLUT4 sensitivity in the muscle tissue).

Now you're saying because I can't manage this or don't like it somehow I'm not using the drug properly.

What I am saying is:
Given the effect of HGH is to create a diabetogenic state I don't see how the minor gain in anabolism justifies the risk for me.

It will do this to everyone. You can take drugs to offset this (polypharmacy), but in the end unless you have GH deficiency it will harm your health long term.

HGH is very profitable for these companies. If it had any use outside the very narrow scope it's being used for now they WOULD have pushed for it.

I'll drop it after this, because:

1) doesn't look like you're gonna budge on this topic;

2) it might appear like I'm telling people GH is healthy and everyone should take it like a vitamin. I'm absolutely not saying that.

3) I think GH for anti-aging is bullshit -- "game changer!" said by someone who started HRT around the same time they started GH, where TRT is obviously doing all the heavy lifting

First, this.

Yes, GH creates a diabetes-like phenotype. Not to be confused with a step toward actually developing T2D.

In the relevant context, insulin sensitivity is restored when you stop GH; the source you cited of kids being treated with GH, having insulin resistance post treatment was included as a throwaway line in their paper - no acknowledgment of confounding by the kids' underlying pathology; did they have insulin resistance before GH therapy too (untested)? How long after GH d/c was IR measured (not specified)? Besides being in a completely different context (GHD kids vs healthy adults), those questions are critical to support the notion that GH causes T2D.

Further, in comparison with actual type 2 diabetes, one of the better theories (imo) of the cause, which explains T2D in both obese and lean people, is energy toxicity & personal fat threshold

Both skinny people & fat people with T2D have fatty liver; fat people without diabetes don't have fatty liver; there are not many exceptions to the fatty liver → T2D link

GH treatment reduces fatty liver

Yes you get high blood glucose readings but this is different from the underlying pathophysiology of T2D

:::end rant:::
 
I'll drop it after this, because:

1) doesn't look like you're gonna budge on this topic;

2) it might appear like I'm telling people GH is healthy and everyone should take it like a vitamin. I'm absolutely not saying that.

3) I think GH for anti-aging is bullshit -- "game changer!" said by someone who started HRT around the same time they started GH, where TRT is obviously doing all the heavy lifting

First, this.

Yes, GH creates a diabetes-like phenotype. Not to be confused with a step toward actually developing T2D.

In the relevant context, insulin sensitivity is restored when you stop GH; the source you cited of kids being treated with GH, having insulin resistance post treatment was included as a throwaway line in their paper - no acknowledgment of confounding by the kids' underlying pathology; did they have insulin resistance before GH therapy too (untested)? How long after GH d/c was IR measured (not specified)? Besides being in a completely different context (GHD kids vs healthy adults), those questions are critical to support the notion that GH causes T2D.

Further, in comparison with actual type 2 diabetes, one of the better theories (imo) of the cause, which explains T2D in both obese and lean people, is energy toxicity & personal fat threshold

Both skinny people & fat people with T2D have fatty liver; fat people without diabetes don't have fatty liver; there are not many exceptions to the fatty liver → T2D link

GH treatment reduces fatty liver

Yes you get high blood glucose readings but this is different from the underlying pathophysiology of T2D

:::end rant:::

Also came across this, where insulin sensitivity upon discontinuation of GH was assessed directly (albeit at only 1 time point: 6 months later)

3-7 IU/d GH treatment for 6 years, insulin sensitivity returned to normal (link)

It was kids born small for gestation age, treated on average from 6 to 12 years old; so different context / grain of salt etc
 
Thanks for commenting Sampei I always enjoy reading your posts.

Everyone responds differently. My igf1 got that high on 2iu of HGH per day. I guess it's individual sensitivity.

Glad it's working for you.
I would never walk around for long period of time with an igf1 of 500+ so yes in your case I wouldn't use HGH at all.

I use the dosage I do because my igf1, increase is very low and I enjoy the side benefit without having a massive igf1 and the risk associated with is.

As I said, everyone need to tailor their drug usages and dosage around their individual response.
 
Im running it with reta to help rhe insulin issue.

Im testing next week to see where 3iu lands my igf1 and will get fasting insulin and glucose done at the same time.
 
Banana.... thanks for starting this thread. As someone new to using hgh, it's been a good, mostly civil debate on the dangers vs benefits of taking hgh. Learning a lot from this from both sides of the argument, and I appreciate the discussion. I'm nearing a month on 3ius taken mainly for health benefits as I just turned 50, and anxiously awaiting an igf 1 test to see if my ginormous head is at risk of getting even ginormous-r. If so, going to have a whole pile of wasted hgh that I won't be continuing to use. But so far, nothing of note save for a little finger tingling at night, but glucose levels haven't reacted that much thankfully.
 
Banana.... thanks for starting this thread. As someone new to using hgh, it's been a good, mostly civil debate on the dangers vs benefits of taking hgh. Learning a lot from this from both sides of the argument, and I appreciate the discussion. I'm nearing a month on 3ius taken mainly for health benefits as I just turned 50, and anxiously awaiting an igf 1 test to see if my ginormous head is at risk of getting even ginormous-r. If so, going to have a whole pile of wasted hgh that I won't be continuing to use. But so far, nothing of note save for a little finger tingling at night, but glucose levels haven't reacted that much thankfully.
If you want a mostly positive take on HGH search up @Ghoul 's posts.

I'm kinda cynical...
 
Banana.... thanks for starting this thread. As someone new to using hgh, it's been a good, mostly civil debate on the dangers vs benefits of taking hgh. Learning a lot from this from both sides of the argument, and I appreciate the discussion. I'm nearing a month on 3ius taken mainly for health benefits as I just turned 50, and anxiously awaiting an igf 1 test to see if my ginormous head is at risk of getting even ginormous-r. If so, going to have a whole pile of wasted hgh that I won't be continuing to use. But so far, nothing of note save for a little finger tingling at night, but glucose levels haven't reacted that much thankfully.
Im on 3iu as well
43 years old. Im getting igf1 fasting insulin and glucose checked next week.

Pretty sure it takes years of supraphysiologic levels to start growing the head. Organs grow faster from my understanding. And even then it take high igf1 levels as well.

Id love to run it indefinitely but I won't.
 
This abstract is amazing:
In evolutionary terms, GH and intracellular STAT 5 signaling is a very old regulatory system. Whereas insulin dominates periprandially, GH may be viewed as the primary anabolic hormone during stress and fasting. GH exerts anabolic effects directly and through stimulation of IGF-I, insulin, and free fatty acids (FFA). When subjects are well nourished, the GH-induced stimulation of IGF-I and insulin is important for anabolic storage and growth of lean body mass (LBM), adipose tissue, and glycogen reserves. During fasting and other catabolic states, GH predominantly stimulates the release and oxidation of FFA, which leads to decreased glucose and protein oxidation and preservation of LBM and glycogen stores. The most prominent metabolic effect of GH is a marked increase in lipolysis and FFA levels. In the basal state, the effects of GH on protein metabolism are modest and include increased protein synthesis and decreased breakdown at the whole body level and in muscle together with decreased amino acid degradation/oxidation and decreased hepatic urea formation. During fasting and stress, the effects of GH on protein metabolism become more pronounced; lack of GH during fasting increases protein loss and urea production rates by approximately 50%, with a similar increase in muscle protein breakdown. GH is a counterregulatory hormone that antagonizes the hepatic and peripheral effects of insulin on glucose metabolism via mechanisms involving the concomitant increase in FFA flux and uptake. This ability of GH to induce insulin resistance is significant for the defense against hypoglycemia, for the development of “stress” diabetes during fasting and inflammatory illness, and perhaps for the “Dawn” phenomenon (the increase in insulin requirements in the early morning hours). Adult patients with GH deficiency are insulin resistant—probably related to increased adiposity, reduced LBM, and impaired physical performance—which temporarily worsens when GH treatment is initiated. Conversely, despite increased LBM and decreased fat mass, patients with acromegaly are consistently insulin resistant and become more sensitive after appropriate treatment.

Source: attached

Another cool one:
It should be underlined that the proposed potential of insulin resistance and hyperinsulinemia to promote protein conservation merely rests on circumstantial evidence that high levels of insulin restrict protein breakdown and increase protein synthesis. Unlike cardiovascular morbidity, which in general affects people at the grand parental stage, famine poses a greater threat to human survival because all age groups are inflicted andreproductionisjeopardized. Thecyclingbetweenfeastand famine is regulated by insulin building up glycogen and fat, insulin and GH building up protein, and GH with low insulin levels triggering fat mobilization and utilization.

I'm guessing this is how HGH works in bodybuilding. Creating a state of insulinemia that blocks catabolism.

This quote would suggest that the anabolism or nitrogen retention is caused by insulinemia and/or IGF1:
Patients with type 1 diabetes exhibit elevated and fluctuating GH levels, in particular when poorly controlled (176); it has been estimated that poorly controlled patients [glycosylated hemoglobin (HbA1c) 12%] are characterized by 2to 3-fold elevated GH levels with a secretory pattern similar to fasting in normal subjects (177). At the same time, serum IGF-I levels are reduced in poorly controlled patients (178), which may be caused by a combination of a negative nitrogen balance and low portal insulin levels (179, 180). It is, in turn, likely that the low IGF-I levels cause or contribute to the increased GH secretion via classic feedback mechanisms.
So there is no argument that HGH causes insulin resistance. It's mechanistic of how it evolved. The only question is does that mean it increases the risk of T2D.
Despite these effects, GH may further impair insulin sensitivity. This is not surprising when considering that daily sc administration of GH is unable to mimic the endogenous pattern resulting from pituitary GH release, which allows insulin to actin dependently due to postprandial suppression of GH. With more prolonged GH therapy, the favorable effects on body composition may offset the direct insulin antagonistic effects, in particular if attention is paid to avoid overdosing. Insulin resistance as a side effect to GH administration is no less surprising than the risk of hypoglycemia with insulin therapy.

I think I've sufficiently answered the question for myself.
 

Attachments

This abstract is amazing:


Source: attached

Another cool one:


I'm guessing this is how HGH works in bodybuilding. Creating a state of insulinemia that blocks catabolism.

This quote would suggest that the anabolism or nitrogen retention is caused by insulinemia and/or IGF1:

So there is no argument that HGH causes insulin resistance. It's mechanistic of how it evolved. The only question is does that mean it increases the risk of T2D.


I think I've sufficiently answered the question for myself.
if attention is paid to avoid overdosing. Insulin resistance as a side effect to GH administration is no less surprising than the risk of hypoglycemia with insulin therapy.

Yeah you just did ;)
 
I jumped on the HGH hype train back in the day and now my fridge is loaded, both ugl and pharma like Seros and Headon. It’s literally chilling next to the eggs.

So quitting isn’t really on the table. At this point I’m just trying to “use inventory responsibly.” I still remember when GH was being sold as the Holy Grail of everything. Youth, recovery, fat loss, enlightenment… so of course I bought in.

And because I clearly don’t learn, I also jumped on the SS-31 hype. So now my “health phase” looks like this: Test E 250, GH 2iu, SS-31 5mg, Reta 6mg, Epitalon 5mg for 20 days. Basically a longevity starter pack. We’re about to be optimized and feel like a million bucks… or at least convince ourselves we do.

Alright, that was a tangent. Back to it.
SS -31 is great even without test

But better with gh

How does one "feel" epithalon? I gave up after 2 shots.
 
SS -31 is great even without test

But better with gh

How does one "feel" epithalon? I gave up after 2 shots.
Still on the fence about SS-31, but it’s only been 6 days. Staying at 5mg for now, might bump it to 10mg later. As for Epithalon, I had my doubts too, but after just 2 shots, I slept like a rock. Woke up feeling like I actually hit REM sleep for once, and the dreams were vivid as hell. Could be placebo, could be magic, but I’ve got 18 days left so I’m definitely finishing the cycle. Don't give up after 2 shots.
 
Still on the fence about SS-31, but it’s only been 6 days. Staying at 5mg for now, might bump it to 10mg later. As for Epithalon, I had my doubts too, but after just 2 shots, I slept like a rock. Woke up feeling like I actually hit REM sleep for once, and the dreams were vivid as hell. Could be placebo, could be magic, but I’ve got 18 days left so I’m definitely finishing the cycle. Don't give up after 2 shots.
Huh. Your dose is also 10x mine. Gotta try that

Without ss-31: 3 days of running at high zone 2, cannot recover, threw my back out reaching for tp in the toilet.

With ss-31: after the 4 weeks of no training, back halfway better went to run again. Didn't stop for three months. As long as there was 5 mg in the system (bw 77kg) eod, could run everyday.

Switched to 3 times a week running because bodyweight dropped to 70kg.

Prior to this i had no cardio since 2020. Injecting this i didn't need months of training.
 
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