A GH and fat loss protocol (rhGH lipolysis) that is science-based

[JG1234]

And I no longer care to buy your "book" that I can only assume is filled with baseless conclusions such as "There's no theoretical upper limit for the lipolytic effects of exogenous rhGH by dose" while citing a paper whose authors themselves make no such claim.

Yep that makes two of us. IIx, sorry if I hurt your book sales. But to quote the author….”Don’t Care”.

It is a book that doesn’t exist anyways.

 

[AlexDavis43]

Read what you quoted fully. 0.2 IU/kg = 20 IU for a 100 kg bodybuilder. Math, bro. What if? It doesn't, read the paper.

Paging @ChaseIrons: 18 IU/d and >100 kg?

 

[AlexDavis43]

Are you drawing this conclusion by comparing the lipolytic effects of GH dosages from multiple studies? Because that seems tenuous at best.

Tenuous but definitely not worthless. This is part of how we start to figure shit out.

 

[Oakley6575]

Re: normal FFA liberation in the basal/fasted/fed states

Is this a study you linked or what? If so, I don't see it in the OP. Can you elaborate?

 

[AlexDavis43]

Is this a study you linked or what? If so, I don't see it in the OP. Can you elaborate?

This isn't controversial. FFA/lipolysis is suppressed by mixed meal consumption. That's basal/fasted vs fed right there.

 

[Oakley6575]

This isn't controversial. FFA/lipolysis is suppressed by mixed meal consumption. That's basal/fasted vs fed right there.

I don't see anyone saying otherwise. Not sure if you read my post wrong or what you are responding to..? I don't understand his response of "Re: normal FFA liberation in the basal/fasted/fed states" when asking him to respond to my post below:

Since the chart was posted showing FFA dropped after eating a meal at the 4 hour mark, I'm assuming his protocol is based on that. But what would happen if the meal wasn't eaten? I'm assuming FFA would continue to rise.

If that would be the case, why not take the bolus prebed so the FFA's are high all night, and wake up and do fasted cardio?

 

[Oakley6575]

Also, you asked @ChaseIrons to chime in here and I think he might have the same thought as me. He has run his 18iu prebed, and has tested splitting the dose up in different variations and in his own thread he has stated he didn't see any better fat loss splitting the dose.

I think he said when be blasts again, he is going back to a bolus prebed.

 

[AlexDavis43]

But what would happen if the meal wasn't eaten? I'm assuming FFA would continue to rise.

No. It levels off. Does not continue to rise indefinitely.

 

[AlexDavis43]

Also, you asked @ChaseIrons to chime in here and I think he might have the same thought as me. He has run his 18iu prebed, and has tested splitting the dose up in different variations and in his own thread he has stated he didn't see any better fat loss splitting the dose.

I think he said when be blasts again, he is going back to a bolus prebed.

There is a reply button. I just used it, so people know what I'm replying to.

 

[Oakley6575]

No. It levels off. Does not continue to rise indefinitely.

At what hour does it stop rising after a meal? Do you have a chart?

The charts I’m seeing show FFA’s to continue to rise in a fasted state for over 24 hours. And that is without GH.

 

[readalot]

Whereas a frequently cited paper by Hansen, et al. (2002) using a microdialysis technique to measure IV-administered doses up to 6µg/kg corresponding to endogenously (pulsatilely) secreted concentrations (the IV bolus at these concentrations is used to mimic pulsatile release) or just above endogenous levels and lipolysis. This would be congruent with replacement rhGH dosages, or 1.458IU for an 81kg male

https://academic.oup.com/view-large/figure/53399448/eg1028901003.jpeg

Time serum concentration curves of the lipid intermediates FFAs, BOH, and glycerol following GH administration are depicted in Fig. 3. Regarding FFAs and BOH there were significant dose-response effects when comparing the iAUCs following 0, 1, and 3 μg/kg−1 GH, whereas there were no differences between the responses following 3 and 6 μg/kg−1 GH. With glycerol the iAUCs following 1, 3, and 6 μg/kg−1 GH were comparable, but all were significantly larger than following 0 μg/kg−1 GH. Irrespective of GH dose, there were no correlations between the observed changes in the lipid intermediates and age or any of the measures of body composition. The resulting increase in BOH following the highest GH dose was positively correlated to the peak GH concentration (r = 0.65, P < 0.005) and negatively correlated to MCR (r = −0.50, P < 0.05), but otherwise there were no significant correlations between the changes in serum lipid intermediates and GH pharmacokinetics.

Although alterations in GH levels undoubtedly induce significant within-subject differences in lipolysis, as indicated by the clear dose-response relationship, the major determinant of subject-to-subject variations in the overall lipolytic response may therefore be differences in the catecholaminergic tone.

 

[readalot]

In a more relevant study, Healy ML, Gibney J, Pentecost C, Croos P, Russell-Jones DL, Sönksen PH, Umpleby AM. Effects of high-dose growth hormone on glucose and glycerol metabolism at rest and during exercise in endurance-trained athletes. J Clin Endocrinol Metab. 2006 Jan;91(1):320-7. doi: 10.1210/jc.2005-0916. Epub 2005 Nov 1. PMID: 16263834., that looked at high dose subq-administered rhGH, demonstrating substantial differences in glycerol concentrations (µM/L in serum) between the up to 16IU daily group and placebo post-exercise. Here, glycerol concentrations differ markedly (<100 µM/L in placebo vs. ~300µM/L at 60-min post-exercise 0.2IU/kg rhGH dose).

Healy 2006

Effects of High-Dose Growth Hormone on Glucose and Glycerol Metabolism at Rest and during Exercise in Endurance-Trained Athletes

Abstract. Context: Recombinant human-GH (r-hGH), in supraphysiological doses, is self-administered by athletes in the belief that it is performance enhanci

academic.oup.com

This study did not address the question of whether supraphysiological GH enhances exercise performance in GH-replete subjects. Exercise capacity is reduced in GHD subjects and improved after GH replacement (12, 13, 52). Fat is an important fuel during mild to moderate exercise, and increased fatty acid availability could theoretically prolong exercise by sparing limited carbohydrate stores (53, 54). However, despite an increase in lipolysis and fatty acid availability, there was no effect of GH on fat oxidation during exercise in either the current study or that reported by Lange et al. (19). These observations can be explained by studies that have reported that increased availability of FFA during low to moderate intensity does not lead to a further increase in fat oxidation (55, 56). Additional evidence that the observed metabolic effects of supraphysiological GH are not reflected in improved athletic performance comes from three recent studies. Berggren et al. (57) administered supraphysiological GH for 28 d to healthy active normal subjects and found no change in VO2max or maximal power output during cycling. In the study reported by Lange et al. (19), GH administration led to a significant increase in plasma lactate during 90 min of cycling at 65 and 75% of VO2max during GH administration that was associated with reduced exercise performance in some subjects. Hansen et al. (58) observed no effect of GH administration on fat oxidation in well-trained subjects during 120 min of cycling at 55% of VO2max, despite a marked increase in lipolysis. Although these observations argue against a beneficial effect of supraphysiological GH during exercise, we cannot rule out a potentially advantageous effect of GH administration in the posttraining setting. For example, increased fatty acid concentrations postexercise could be advantageous in replenishing muscle triglyceride stores.

Hansen 2005

No effect of growth hormone administration on substrate oxidation during exercise in young, lean men

The purpose of this study was to examine the effects of increased fat availability induced by growth hormone (GH) administration on the oxidative metabolism during exercise. Seven well-trained males (age 25 ± 2 years (mean ±); peak oxygen ...

www.ncbi.nlm.nih.gov

The main purpose of the present study was to examine if an increased availability of fatty acids induced by GH administration prior to exercise would change the substrate oxidation pattern during subsequent moderate intensity exercise in trained individuals. We expected that increased accessibility of fatty acids would increase the fat oxidation rate during exercise, as it has been observed at rest in earlier human studies after acute GH administration (Møller et al. 1990a, 1992a, b, 1993; Bak et al. 1991; Jørgensen et al. 1994; Lange et al. 2000), or when the availability of fatty acids has been enhanced by intravenous infusion of lipids (Intralipid) with heparin (Romijn et al. 1995; Odland et al. 1998). However, this hypothetical relationship could not be confirmed by the present results. Although GH administration increased plasma NEFA substantially during exercise, it had no effect on fat oxidation during exercise. This is in contrary to the Randle Cycle (Randle et al. (1994), but perfectly in line with the crossover concept of Brooks & Mercier (1994), which describes that during exercise glycolysis in human skeletal muscles dominates and down-regulates fatty acid entry into the TCA cycle, probably by acting on CPT1 via malonyal-CoA or by other means (Brooks & Mercier 1994).

The increased availability of NEFA in the present study after GH administration did not increase the use of fat as a fuel in energy metabolism, even though the dose of GH (29–39 µg kg−1 or 173–380 µg (kg fat mass)−1) was in the same range as in the studies at rest in the literature, where increases in fat oxidation have been observed (Møller et al. 1990a, 1992a, b, 1993; Bak et al. 1991; Jørgensen et al. 1994; Lange et al. 2000). Three explanations seem reasonable: (1) the method used to detect changes in fat oxidation was not sensitive enough, (2) the elevated metabolic rate during exercise limited the use of fat as a fuel, and/or (3) the increased availability of glucose after the meal in the present study overrode the effect of the increased availability of fatty acids.

In conclusion, no additional increase in relative fat oxidation during exercise at a moderate intensity was observed after acute GH administration to young trained subjects. Unchanged fat oxidation was observed, despite an increase in availability of NEFA for the active skeletal muscles. Thus, under circumstances where a carbohydrate-rich meal is ingested in the hours before exercise, fat oxidation is not limited by the availability of fatty acids induced by acute growth hormone administration. The present findings are in accordance with the view that CHO oxidation has a dominating regulatory role during exercise, even with a substantially enhanced level of fatty acids in the blood.

 

[readalot]

Related: lipolysis vs fatty acid oxidation

Possible Mechanisms to Explain Abdominal Fat Loss Effect of Exercise Training Other Than Fatty Acid Oxidation

The abdominal fat-reducing effect of exercise training is well-supported by scientific studies according to a current meta-analysis of data collected from image-based tools (DEXA or MRI). The underlying mechanism explaining this favorable outcome remains controversial. Increased fatty acid...

www.frontiersin.org

12 articles.

https://www.frontiersin.org/articles/10.3389/fphys.2020.575363
https://www.frontiersin.org/articles/10.3389/fphys.2021.685166

 

[Oakley6575]

@readalot, thanks for posting all this info. It's definitely contradictory to any GH fat loss protocol.

 

[readalot]

@readalot, thanks for posting all this info. It's definitely contradictory to any GH fat loss protocol.

Sure. However, my intention was not to contradict the idea of a GH fat loss protocol.

For example, from the 3rd link in post 693 above (see bold):

Lipolysis appears to be more relevant with fat loss than fatty acid oxidation. Exercise increases plasma epinephrine levels at high intensities (Mora-Rodriguez and Coyle, 2000). Epinephrine stimulates lipolysis and inhibits the esterification of triglycerides via adrenergic receptors of adipocytes (Reilly et al., 2020), leading to release of free fatty acid from adipose tissue into circulation (Urhausen et al., 1994). Long-term adrenergic stimulation (i.e., clenbuterol and ractopamine) has been shown to decrease fat mass and increase muscle mass without changes in food intake and body temperature (Page et al., 2004). Abdominal adipocytes show much higher lipolytic response to epinephrine than gluteal adipocytes, which may partly explain the commonly observed abdominal fat loss response to high-intensity exercise training (Wahrenberg et al., 1989; Thompson et al., 2012).

The physiological significance of the enhanced release of fatty acids from lipolysis without the corresponding increase in fatty acid oxidation during and after exercise remains unclear. However, a proposed role of adipocyte-derived fatty acids in tissue repair has been recently described elsewhere (Shook et al., 2020). Fatty acids (e.g., eicosapentaenoate, linoleate, α-linolenate, γ-linolenate, and arachidonate) have been found to accelerate wound healing (Ruthig and Meckling-Gill, 1999). In addition, vascular structure formation can be enhanced by fatty acids, which is mediated by increasing reactive oxygen species and activating endothelial NOS synthase (Taha et al., 2020). Both findings implicate a possible role of elevated fatty acid concentrations in the repairing mechanism of exercise-induced tissue damage.

My intended point is this is complex material and the idea of no upper limit on GH dose response for fat loss does not seem congruent with the data we have available. For harm reduction the above has significant implications.

 

[readalot]

Dose-response is individualized, but do consider that 2IU 5 days weekly is less than the average (mean) weekly production of a healthy 22 - 28 year old male. So a lot of the dosages I see are very low and often are mere replacement

There's no theoretical upper limit for the lipolytic effects of exogenous rhGH by dose.

Continuing from post 695. As shown, the OP mentions this. Your dose response will come down to your genes so the tradeoff between potential fat loss vs. harm must be weighed as you escalate your GH dose.

Repeating from post 691:

Although alterations in GH levels undoubtedly induce significant within-subject differences in lipolysis, as indicated by the clear dose-response relationship, the major determinant of subject-to-subject variations in the overall lipolytic response may therefore be differences in the catecholaminergic tone.

Minimum effective dose. Probably doesn't hurt to be sub 10% BF before you try to use GH for fat loss anyway. Seems like a great tool for fat loss for people who are already ripped.

Frontiers | Growth Hormone as a Potential Mediator of Aerobic Exercise-Induced Reductions in Visceral Adipose Tissue

www.frontiersin.org

This finding may help further explain why individuals with obesity and reduced CRF, who on average have elevated levels of FFAs (König et al., 2003; Boden, 2008), exhibit impaired GH secretion and action, as their ability to uptake and oxidize FFAs is reduced (Kim et al., 2000).

Lipid oxidation is reduced in obese human skeletal muscle - PubMed

The purpose of this study was to discern cellular mechanisms that contribute to the suppression of lipid oxidation in the skeletal muscle of obese individuals. Muscle was obtained from obese [body mass index (BMI), 38.3 +/- 3.1 kg/m(2)] and lean (BMI, 23.8 +/- 0.9 kg/m(2)) women, and fatty acid...

pubmed.ncbi.nlm.nih.gov

https://journals.physiology.org/na101/home/literatum/publisher/physio/journals/content/ajpendo/2000/ajpendo.2000.279.issue-5/ajpendo.2000.279.5.e1039/production/images/large/h11100162001.jpeg

https://journals.physiology.org/action/downloadFigures?id=F1&doi=10.1152/ajpendo.2000.279.5.E1039

The main finding of the present study was that both long- and medium-chain fatty acid oxidation was depressed at the level of the mitochondria in the skeletal muscle of obese individuals. The rate of long-chain (palmitate) fatty acid oxidation is at least partially dependent on transport across the mitochondrial membranes via CPT-1 (16-18, 24, 25, 30).

In conclusion, the oxidation of both long- (palmitate and palmitoyl carnitine) and medium- (octanoate) chain fatty acids were reduced in skeletal muscle homogenates from obese subjects. Muscle CPT-1 activity was reduced with obesity, which may at least partially explain the decrement in palmitate oxidation. The decrease in palmitoyl carnitine, however, implies a post-CPT-1 defect such as a reduction in oxidative capacity via reduced mitochondrial content. In support of a reduction in mitochondrial content, muscle citrate synthase and β-HAD activities were lower, while PFK activity was elevated in the skeletal muscle of obese individuals. These data suggest that there are defects at several levels in the catabolic process for lipids in obese skeletal muscle mitochondria. These findings also provide a possible explanation for the reduced reliance on lipid oxidation seen in obese individuals.

First things first. Don't throw everything at the issue from the get go. Use diet and exercise. If you are good, then great. Add in the TRT/"TRT" to hit next plateau. Good? OK. Not Good and want to be a mutant? Then move on to bust the next plateau. What I don't understand is throwing everything all at once at an issue that should be solved in sequential steps with escalating levels of potential harm.


Also throwing this graph up again cause I think it is so darn cool:

Now Obese Getting back into the gym and moving again?

Did you start losing weight yet? I think this thread can go dormant until the day (if it ever happens) that you start actually doing something.

thinksteroids.com

Fundamental different operating points when it comes to fat loss for obese/diabetic vs "normal" person. Getting your waist circumference to height ratio down before using drugs will greatly increase the probability of good results from the drugs.

 

[Ex0shear]

 

[Amgiji]

Continuing from post 695. As shown, the OP mentions this. Your dose response will come down to your genes so the tradeoff between potential fat loss vs. harm must be weighed as you escalate your GH dose.

Repeating from post 691:


Minimum effective dose. Probably doesn't hurt to be sub 10% BF before you try to use GH for fat loss anyway. Seems like a great tool for fat loss for people who are already ripped.

Frontiers | Growth Hormone as a Potential Mediator of Aerobic Exercise-Induced Reductions in Visceral Adipose Tissue

www.frontiersin.org

Lipid oxidation is reduced in obese human skeletal muscle - PubMed

The purpose of this study was to discern cellular mechanisms that contribute to the suppression of lipid oxidation in the skeletal muscle of obese individuals. Muscle was obtained from obese [body mass index (BMI), 38.3 +/- 3.1 kg/m(2)] and lean (BMI, 23.8 +/- 0.9 kg/m(2)) women, and fatty acid...

pubmed.ncbi.nlm.nih.gov

https://journals.physiology.org/na101/home/literatum/publisher/physio/journals/content/ajpendo/2000/ajpendo.2000.279.issue-5/ajpendo.2000.279.5.e1039/production/images/large/h11100162001.jpeg

https://journals.physiology.org/action/downloadFigures?id=F1&doi=10.1152/ajpendo.2000.279.5.E1039

First things first. Don't throw everything at the issue from the get go. Use diet and exercise. If you are good, then great. Add in the TRT/"TRT" to hit next plateau. Good? OK. Not Good and want to be a mutant? Then move on to bust the next plateau. What I don't understand is throwing everything all at once at an issue that should be solved in sequential steps with escalating levels of potential harm.


Also throwing this graph up again cause I think it is so darn cool:

Now Obese Getting back into the gym and moving again?

Did you start losing weight yet? I think this thread can go dormant until the day (if it ever happens) that you start actually doing something.

thinksteroids.com

Fundamental different operating points when it comes to fat loss for obese/diabetic vs "normal" person. Getting your waist circumference to height ratio down before using drugs will greatly increase the probability of good results from the drugs.

"What I don't understand is throwing everything all at once at an issue that should be solved in sequential steps with escalating levels of potential harm."

I assume that is a rhetorical question meant to disparage people who act in a way you find needlessly reckless but in case it's a legitimate question.

two reasons

1 efficacy.

body fat is a self-sustaining problem the most extreme option can be the only thing that works at all,
after all the defects at several levels in the catabolic process for lipids in obese skeletal muscle mitochondria also decrease the effectiveness of doing it the "old fashioned way".
if the sledgehammer barely makes a dent telling people to punch it with their bare hands won't work any better.

reason 2 time


the effectiveness of most drugs and people's tolerance to them goes down with age.
something that if you took it at 25 could be paradigm changing could do next to nothing at 35,

doing it in steps takes years, potentially too many years if you could be 25 years old for 10 years that would be fine but as that's not the case,
any action now is better than the "right" action later, after it's too late to be of much use anymore.

 

[AlexDavis43]

I don't see anyone saying otherwise. Not sure if you read my post wrong or what you are responding to..? I don't understand his response of "Re: normal FFA liberation in the basal/fasted/fed states" when asking him to respond to my post below:

At what hour does it stop rising after a meal? Do you have a chart?

The charts I’m seeing show FFA’s to continue to rise in a fasted state for over 24 hours. And that is without GH.

Gotcha. Not sure the hourly, but FFAs level off. Looks like a few days. See study by Cahill:

 

[readalot]

disparage people

not my intent as I have been in their shoes wrt obesity. Clearly if they have tried the other steps and it is not working then the MED hasn't been identified yet. I was thinking of convenience or perhaps good but uniformed intentions instead of desperation. Anyway to be clear...more power to anyone who is trying to address obesity.

Thanks for your thoughts. I appreciate your perspective.

A potential concern with gh use in obese folks is the water weight. Would be a bummer to have someone get discouraged and commit type II error thinking they aren't losing fat when instead they are holding extra water. Seeing that scale not budge can mess with your head.

Some of the logs on here have been instructive; fortunately there has been some good advice given.