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

[Type-IIx]

Here is a gift for the Holidays from a likely forthcoming book I am considering releasing, titled Bolus: A Science-Based Guide to recombinant human Growth Hormone (rhGH) for the Athlete, Aesthete, and Aging Gym-goer

This protocol is in direct contravention of the commonly touted 3-5x daily injections of rhGH for lipolysis and the use of GH+fasted cardio for fat loss.

rhGH for lipolysis
Author: Type-IIx

Daily exercise:
Morning or daytime bolus ideally 2-3 hr pre-workout
Single large bolus (≥3IU) for lipolysis: [6] showed lipolysis (blood 3-hydroxy-butyrate) was positively correlated to the peak hGH concentration (r=0.65) for the highest dose (6mcg/kg); [40] showed a significant correlation between the peak GH response to exercise and the post-exercise rise in glycerol measured as area under the curve (r= 0.57,p< 0.04). Also, [69] showed that a single s.c. bolus versus two promotes nighttime FFA liberation.

meal post-workout (4-4.5hr post-bolus), see FFA liberation:


FFA liberation: FFA liberation follows an oscillating, rhythymic pattern for 24 hr post-bolus (palmitate [glycerol] flux)
- Post-5IU rhGH administration subcutaneous vs. jet-injected

The normal 24-hour pattern of FFAs is characterized by high values prior to a meal and low levels post-meal [68]
[5]
________________________
References:
[5] Verhagen, A., Ebels, J. T., Jonkman, J. H. G., & Dogterom, A. A. (1995). Pharmacokinetics and pharmacodynamics of a single dose of recombinant human growth hormone after subcutaneous administration by jet-injection: comparison with conventional needle-injection. European Journal of Clinical Pharmacology, 49(1-2). doi:10.1007/bf00192361
[6] Hansen, T. K., Gravholt, C. H., Ørskov, H., Rasmussen, M. H., Christiansen, J. S., & Jørgensen, J. O. L. (2002). Dose Dependency of the Pharmacokinetics and Acute Lipolytic Actions of Growth Hormone. The Journal of Clinical Endocrinology & Metabolism, 87(10), 4691–4698. doi:10.1210/jc.2002-020563
[40] Wee, J., Charlton, C., Simpson, H., Jackson, N. C., Shojaee-Moradie, F., Stolinski, M., … Umpleby, A. M. (2005). GH secretion in acute exercise may result in post-exercise lipolysis. Growth Hormone & IGF Research, 15(6), 397–404. doi:10.1016/j.ghir.2005.08.003
[68] Laursen, T., Jergensen, J. O. L., & Chrlstiansen, J. S. (1994). Metabolic effects of growth hormone administered subcutaneously once or twice daily to growth hormone deficient adults. Clinical Endocrinology, 41(3), 337–343. doi:10.1111/j.1365-2265.1994.tb02554.x
[69] Jørgensen, J. O. L., Møller, J., Møller, N., Lauritzen, T., & Christiansen, J. S. (1990). Pharmacological Aspects of Growth Hormone Replacement Therapy: Route, Frequency and Timing of Administration. Hormone Research, 33(4), 77–82. doi:10.1159/000181589
_______________________
For those interested in the book, its table of contents (so far) is:
- Objective
- Abbreviations
- Research primer: A 'How To' on interpretation of research
- Contraindications
- Skeletal muscle growth and function
- Skeletal muscle: An endocrine organ
- Hypertrophy
- Mechanisms in hypertrophy
- Conclusions regarding skeletal muscle hypertrophy
- Hyperplasia
- Adult myogenesis
- Satellite cells
- Local mIGF-I and Systemic cIGF-I
- Nitrogen balance and reduced AA proteolysis
- Lipolysis
- Mechanisms in lipolytic activity
- Collagen synthesis
- Collagen Type I & Collagen Type III
- Bone density
- Musculotendinous injury recovery and prevention
- Post-immobilization and post-rehabilitation
- Cognitive function
- Anticatabolism
- Cardiorespiratory endurance
- Anaerobic capacity
- Sprint performance
- Metabolic parameters
- LDL reduction
- Anti-aging and rhGH
- Age-related decline in GH
- Studies
- Lipolysis in elderly
- IGFBPs
- IGFBP-1
- IGFBP-2
- IGFBP-3
- IGFBP-4
- IGFBP-5
- IGFBP-6
- Interindividual variation
- IGF-I/IGFBP-3 ratio
- GHBPs
- Genetic polymorphisms
- d3-GHR
- Women and rhGH
- Plot of IGF-I response to rhGH in adult GHD patients by gender
- Dose-response for women vs men
- Cessation
- Blood pressure
- Pulse pressure
- Intracranial hypertension, i.e., headaches
- Obstructive sleep apnea
- Long-term administration
- Strength
- Withdrawal
- Decrement in serum IGF-I
- Effects on thyroid function
- Anthony Roberts' Article "Thyroid Hormone + Growth Hormone – If You Aren’t Using T4 with Your GH, You’re Not Doing It Right"
- Effects on adrenocortical system
- Organ growth
- Pharmacokinetics & Pharmacodynamics
- SubQ serum GH profile
- IM serum GH profile
- Pulsatile serum GH profile
- GH kinetics
- Effects of estradiol-estrogen, obesity
- Effects of testosterone and aromatizable androgens
- Time-course of changes in response to rhGH administration
- Transient negative feedback inhibition
- cIGF-I changes with administration, withdrawal
- Clinical relevance of cIGF-I
- Practical
- Risk-reward balancing
- Dosages and administration
- Conversion of mcg <=> IU
- General instructions for pharmaceutical rhGH preparations
- Specific products and dosages
- Norditropin
- Genotropin
- Serono Serostim
- Humatrope
- Biodenticals
- Cinnatropin, Jintropin, Kigtropin, Hygetropin
- Generics
- Purity variance within a single batch
- French Testing Group
- Practical protocols
- rhGH for lipolysis
- rhGH for hypertrophy
- Primary RT mode drivers of augmented SC fusion
- combined rhGH and Insulin
- rhGH for musculotendinous healing and post-rehabilitation injury recovery

- combined rhGH and rIGF-I
- rhGH for anti-aging
- Permutations based on limited quantity
- Non-rehabilitative usage
- rhGH for anti-aging
- Testing
- Serum IGF-I
- Analytic laboratory quantitative analysis
- rhGH solutions- What is in the vial or pen?
- Antimicrobial preservative agents
- Considerations
- Theoretical
- Dual Effector Hypothesis supersedes the Somatomedin Hypothesis
- Hyperplasia of skeletal muscle
- Molecular signalling
- AR nongenomic pathway
- Modern theory of 22kDa GH binding at the GHR
- Substrate metabolism
- IGF-I, a myokine promoting a local effort for a global effect
- Pathways and natural pulsatile secretion
- β-adrenergic agonists inhibit GH secretion
- Obesity & rhGH
- Gynecomastia
- Glucose metabolism and insulin resistance
- Hyperglycemia
- Metformin
- Downsides of Metformin
- Insulin
- Rapid-acting, -R type
- Slower-acting, -Log type
- Insulin resistance
- TUDCA
- Calcium levels- hypercalcinemia or hypercalciuria
- Edema and water retention
- Tumor growth and risk of carcinogenesis
- Relevant measures
- Natural baseline measures
- GH
- cIGF-I
- Serum T₄
- Monitoring of rhGH course
- HbA1c and blood glucose monitoring
- Interactions with other drugs or exogenous hormones
- AAS
- AAS Effects on IGFBPs and negative inhibition
- Exogenous Testosterone
- Fluoxymesterone
- Stanozolol
- Oxandrolone
- 5α-DHT
- Metformin
- Estrogen
- Alcohol
- Interactions with endogenous hormones
- Thyroid hormones: TSH, T3, T4
- Testosterone
- Prolactin
- Progesterone
- Health conditions that affect rhGH efficacy
- Related
- Growth hormone secretagogues, i.e. "peptides"
- Secretagogues and obesity

 

[T&H]

I'm not the best with pubmed and interpretation. But I have a few questions if you found studies.

Does hgh provide enhanced additional recovery, whether local muscle or cns, from training and if so at what dose? Tbh, I haven't noticed much or anything personally.

Have you found that hgh can enlarge existing gynecomastia?

What is the true impact of hgh usage to t3/t4 slowdown?

 

[Type-IIx]

I'm not the best with pubmed and interpretation. But I have a few questions if you found studies.

Does hgh provide enhanced additional recovery, whether local muscle or cns, from training and if so at what dose? Tbh, I haven't noticed much or anything personally.

Have you found that hgh can enlarge existing gynecomastia?

What is the true impact of hgh usage to t3/t4 slowdown?

rhGH does promote recovery from exercise including resistance training by procollagenous activity (primarily affecting the extracellular matrix), anticatabolic effects (reduced catabolism of amino acids, improved nitrogen balance), improved sleep (increased slow wave sleep), and improved mitochondrial oxidative capacity.

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.

Yes, GH may enlarge gynecomastia and in some persons cause it outright.

rhGH does reduce extrathyroidal (peripheral) T4 levels by increased peripheral conversion to T3. It thus dysregulates in a sense thyroid function as a rule. It is worth monitoring serum T4 at any dosage increase. There may be a synergistic effect on intramuscular IGF-I (mIGF-I) levels between T4+hGH. This does not mean exogenous T4 is advisable, it means that were it not for the presence of T4 in peripheral tissue, there may not be a mechanism for increased intramuscular IGF-I splice variants to be increased. This is rather theoretical.

 

[GuerillaPete]

Yeah science !

 

[Biggerp73]

Here is a gift for the Holidays from a likely forthcoming book I am considering releasing, titled Bolus: A Science-Based Guide to recombinant human Growth Hormone (rhGH) for the Athlete, Aesthete, and Aging Gym-goer

This protocol is in direct contravention of the commonly touted 3-5x daily injections of rhGH for lipolysis and the use of GH+fasted cardio for fat loss.

rhGH for lipolysis

Morning or daytime bolus ideally 2-3 hr pre-workout

Thanks for this

Single large bolus (≥3IU) for lipolysis:

So here's the evidence...

[6] showed lipolysis (blood 3-hydroxy-butyrate) was positively correlated to the peak hGH concentration (r=0.65) for the highest dose (6mcg/kg);

I'm not sure this is evidence for a single bolus. All it seems to be evidence of is that higher peak concentrations result in more lipolysis.

[40] showed a significant correlation between the peak GH response to exercise and the post-exercise rise in glycerol measured as area under the curve (r= 0.57,p< 0.04).

You'll have to explain why this is evidence for pre-work out being better than any other time (and why it would mean that pre workout alone is better than pre workout plus another dose another time)

Also, [69] showed that a single s.c. bolus versus two promotes nighttime FFA liberation.

This seems like evidence but is nightime FFA liberation alone really enough to conclude the one method is superior to the other? There's a lot more involved in achieving net fat loss over time than just fatty acid liberation

meal post-workout (4-4.5hr post-bolus), see FFA liberation:

View attachment 157904
FFA liberation: FFA liberation follows an oscillating, rhythymic pattern for 24 hr post-bolus (palmitate [glycerol] flux)
- Post-5IU rhGH administration subcutaneous vs. jet-injected

The normal 24-hour pattern of FFAs is characterized by high values prior to a meal and low levels post-meal [68]
[5]

I'm not sure why this is a determining factor or necessarily evidence that dosing a few hours before eating is best

 

[M@NU]

ive heard something like 1,4iu already triggers maximum lipolysis.
Is this true or just some broscience?

 

[Isrrike]

When they say can speed up cancer growth how do you know for sure you don’t have any cancer growing in you? Or is this for people already diagnosed with tumours ?

 

[igfMaster]

Here is a gift for the Holidays from a likely forthcoming book I am considering releasing, titled Bolus: A Science-Based Guide to recombinant human Growth Hormone (rhGH) for the Athlete, Aesthete, and Aging Gym-goer

This protocol is in direct contravention of the commonly touted 3-5x daily injections of rhGH for lipolysis and the use of GH+fasted cardio for fat loss.

rhGH for lipolysis
Author: Type-IIx

Daily exercise:
Morning or daytime bolus ideally 2-3 hr pre-workout
Single large bolus (≥3IU) for lipolysis: [6] showed lipolysis (blood 3-hydroxy-butyrate) was positively correlated to the peak hGH concentration (r=0.65) for the highest dose (6mcg/kg); [40] showed a significant correlation between the peak GH response to exercise and the post-exercise rise in glycerol measured as area under the curve (r= 0.57,p< 0.04). Also, [69] showed that a single s.c. bolus versus two promotes nighttime FFA liberation.

meal post-workout (4-4.5hr post-bolus), see FFA liberation:

View attachment 157904
FFA liberation: FFA liberation follows an oscillating, rhythymic pattern for 24 hr post-bolus (palmitate [glycerol] flux)
- Post-5IU rhGH administration subcutaneous vs. jet-injected

The normal 24-hour pattern of FFAs is characterized by high values prior to a meal and low levels post-meal [68]
[5]
________________________
References:
[5] Verhagen, A., Ebels, J. T., Jonkman, J. H. G., & Dogterom, A. A. (1995). Pharmacokinetics and pharmacodynamics of a single dose of recombinant human growth hormone after subcutaneous administration by jet-injection: comparison with conventional needle-injection. European Journal of Clinical Pharmacology, 49(1-2). doi:10.1007/bf00192361
[6] Hansen, T. K., Gravholt, C. H., Ørskov, H., Rasmussen, M. H., Christiansen, J. S., & Jørgensen, J. O. L. (2002). Dose Dependency of the Pharmacokinetics and Acute Lipolytic Actions of Growth Hormone. The Journal of Clinical Endocrinology & Metabolism, 87(10), 4691–4698. doi:10.1210/jc.2002-020563
[40] Wee, J., Charlton, C., Simpson, H., Jackson, N. C., Shojaee-Moradie, F., Stolinski, M., … Umpleby, A. M. (2005). GH secretion in acute exercise may result in post-exercise lipolysis. Growth Hormone & IGF Research, 15(6), 397–404. doi:10.1016/j.ghir.2005.08.003
[68] Laursen, T., Jergensen, J. O. L., & Chrlstiansen, J. S. (1994). Metabolic effects of growth hormone administered subcutaneously once or twice daily to growth hormone deficient adults. Clinical Endocrinology, 41(3), 337–343. doi:10.1111/j.1365-2265.1994.tb02554.x
[69] Jørgensen, J. O. L., Møller, J., Møller, N., Lauritzen, T., & Christiansen, J. S. (1990). Pharmacological Aspects of Growth Hormone Replacement Therapy: Route, Frequency and Timing of Administration. Hormone Research, 33(4), 77–82. doi:10.1159/000181589
_______________________
For those interested in the book, its table of contents (so far) is:
- Objective
- Abbreviations
- Research primer: A 'How To' on interpretation of research
- Contraindications
- Skeletal muscle growth and function
- Skeletal muscle: An endocrine organ
- Hypertrophy
- Mechanisms in hypertrophy
- Conclusions regarding skeletal muscle hypertrophy
- Hyperplasia
- Adult myogenesis
- Satellite cells
- Local mIGF-I and Systemic cIGF-I
- Nitrogen balance and reduced AA proteolysis
- Lipolysis
- Mechanisms in lipolytic activity
- Collagen synthesis
- Collagen Type I & Collagen Type III
- Bone density
- Musculotendinous injury recovery and prevention
- Post-immobilization and post-rehabilitation
- Cognitive function
- Anticatabolism
- Cardiorespiratory endurance
- Anaerobic capacity
- Sprint performance
- Metabolic parameters
- LDL reduction
- Anti-aging and rhGH
- Age-related decline in GH
- Studies
- Lipolysis in elderly
- IGFBPs
- IGFBP-1
- IGFBP-2
- IGFBP-3
- IGFBP-4
- IGFBP-5
- IGFBP-6
- Interindividual variation
- IGF-I/IGFBP-3 ratio
- GHBPs
- Genetic polymorphisms
- d3-GHR
- Women and rhGH
- Plot of IGF-I response to rhGH in adult GHD patients by gender
- Dose-response for women vs men
- Cessation
- Blood pressure
- Pulse pressure
- Intracranial hypertension, i.e., headaches
- Obstructive sleep apnea
- Long-term administration
- Strength
- Withdrawal
- Decrement in serum IGF-I
- Effects on thyroid function
- Anthony Roberts' Article "Thyroid Hormone + Growth Hormone – If You Aren’t Using T4 with Your GH, You’re Not Doing It Right"
- Effects on adrenocortical system
- Organ growth
- Pharmacokinetics & Pharmacodynamics
- SubQ serum GH profile
- IM serum GH profile
- Pulsatile serum GH profile
- GH kinetics
- Effects of estradiol-estrogen, obesity
- Effects of testosterone and aromatizable androgens
- Time-course of changes in response to rhGH administration
- Transient negative feedback inhibition
- cIGF-I changes with administration, withdrawal
- Clinical relevance of cIGF-I
- Practical
- Risk-reward balancing
- Dosages and administration
- Conversion of mcg <=> IU
- General instructions for pharmaceutical rhGH preparations
- Specific products and dosages
- Norditropin
- Genotropin
- Serono Serostim
- Humatrope
- Biodenticals
- Cinnatropin, Jintropin, Kigtropin, Hygetropin
- Generics
- Purity variance within a single batch
- French Testing Group
- Practical protocols
- rhGH for lipolysis
- rhGH for hypertrophy
- Primary RT mode drivers of augmented SC fusion
- combined rhGH and Insulin
- rhGH for musculotendinous healing and post-rehabilitation injury recovery

- combined rhGH and rIGF-I
- rhGH for anti-aging
- Permutations based on limited quantity
- Non-rehabilitative usage
- rhGH for anti-aging
- Testing
- Serum IGF-I
- Analytic laboratory quantitative analysis
- rhGH solutions- What is in the vial or pen?
- Antimicrobial preservative agents
- Considerations
- Theoretical
- Dual Effector Hypothesis supersedes the Somatomedin Hypothesis
- Hyperplasia of skeletal muscle
- Molecular signalling
- AR nongenomic pathway
- Modern theory of 22kDa GH binding at the GHR
- Substrate metabolism
- IGF-I, a myokine promoting a local effort for a global effect
- Pathways and natural pulsatile secretion
- β-adrenergic agonists inhibit GH secretion
- Obesity & rhGH
- Gynecomastia
- Glucose metabolism and insulin resistance
- Hyperglycemia
- Metformin
- Downsides of Metformin
- Insulin
- Rapid-acting, -R type
- Slower-acting, -Log type
- Insulin resistance
- TUDCA
- Calcium levels- hypercalcinemia or hypercalciuria
- Edema and water retention
- Tumor growth and risk of carcinogenesis
- Relevant measures
- Natural baseline measures
- GH
- cIGF-I
- Serum T₄
- Monitoring of rhGH course
- HbA1c and blood glucose monitoring
- Interactions with other drugs or exogenous hormones
- AAS
- AAS Effects on IGFBPs and negative inhibition
- Exogenous Testosterone
- Fluoxymesterone
- Stanozolol
- Oxandrolone
- 5α-DHT
- Metformin
- Estrogen
- Alcohol
- Interactions with endogenous hormones
- Thyroid hormones: TSH, T3, T4
- Testosterone
- Prolactin
- Progesterone
- Health conditions that affect rhGH efficacy
- Related
- Growth hormone secretagogues, i.e. "peptides"
- Secretagogues and obesity

Will your book be free?

 

[GuerillaPete]

If everyone would wright books who would make bread?

 

[Type-IIx]

Thanks for this

So here's the evidence...


I'm not sure this is evidence for a single bolus. All it seems to be evidence of is that higher peak concentrations result in more lipolysis.


You'll have to explain why this is evidence for pre-work out being better than any other time (and why it would mean that pre workout alone is better than pre workout plus another dose another time)


This seems like evidence but is nightime FFA liberation alone really enough to conclude the one method is superior to the other? There's a lot more involved in achieving net fat loss over time than just fatty acid liberation





I'm not sure why this is a determining factor or necessarily evidence that dosing a few hours before eating is best

So, the primary effect of GH (in the basal state) is to promote lipid mobilization and oxidation as a means of switching substrate utilization from glucose and protein to lipid oxidation. This, then, argues for the primacy of FFA mobilization in its lipolytic effects. Granted, GH promotes lipolytic activity via other minor(!) mechanisms, increased REE, peripheral T4 to T3 conversion, increased sensitivity of adipocytes to catecholamines, etc. Given that a single bolus of rhGH acutely causes insulin resistance within 1-2 h, and these effects disappear after approximately 8 h, this is a strong consideration in favor of a single bolus versus 3 - 5 daily.

So, higher peak concentrations being a correlate to lipolysis clearly argues for a single large bolus, no? Preworkout is best given the benefits for anticatabolism, mitochondrial capacity, etc. from GH and fatty acid oxidation being promoted by exercise may be achieved by the workout. Then, 4 hr post-bolus, the post-workout meal is timed for the natural post-meal reduction in FFA levels.

This protocol is the consequence of logic versus an abundance of cited literature to support each individual "claim." Rather, I felt a single representative cite was sufficient. But I'll be happy to explain the considerations that lead me to each conclusion always.

 

[eery]

ive heard something like 1,4iu already triggers maximum lipolysis.
Is this true or just some broscience?

ive heard that from Joe Jeffery as well.

 

[Type-IIx]

ive heard something like 1,4iu already triggers maximum lipolysis.
Is this true or just some broscience?

It's broscience. There's no theoretical upper limit for the lipolytic effects of exogenous rhGH by dose. 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 (I believe this is the study these guys are referring to). In Hansen they reported glycerol rates of appearance in fat depots (i.e., µM/min).

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).

 

[may2021]

Here is a gift for the Holidays from a likely forthcoming book I am considering releasing, titled Bolus: A Science-Based Guide to recombinant human Growth Hormone (rhGH) for the Athlete, Aesthete, and Aging Gym-goer

This protocol is in direct contravention of the commonly touted 3-5x daily injections of rhGH for lipolysis and the use of GH+fasted cardio for fat loss.

rhGH for lipolysis
Author: Type-IIx

Daily exercise:
Morning or daytime bolus ideally 2-3 hr pre-workout
Single large bolus (≥3IU) for lipolysis: [6] showed lipolysis (blood 3-hydroxy-butyrate) was positively correlated to the peak hGH concentration (r=0.65) for the highest dose (6mcg/kg); [40] showed a significant correlation between the peak GH response to exercise and the post-exercise rise in glycerol measured as area under the curve (r= 0.57,p< 0.04). Also, [69] showed that a single s.c. bolus versus two promotes nighttime FFA liberation.

meal post-workout (4-4.5hr post-bolus), see FFA liberation:

View attachment 157904
FFA liberation: FFA liberation follows an oscillating, rhythymic pattern for 24 hr post-bolus (palmitate [glycerol] flux)
- Post-5IU rhGH administration subcutaneous vs. jet-injected

The normal 24-hour pattern of FFAs is characterized by high values prior to a meal and low levels post-meal [68]
[5]
________________________
References:
[5] Verhagen, A., Ebels, J. T., Jonkman, J. H. G., & Dogterom, A. A. (1995). Pharmacokinetics and pharmacodynamics of a single dose of recombinant human growth hormone after subcutaneous administration by jet-injection: comparison with conventional needle-injection. European Journal of Clinical Pharmacology, 49(1-2). doi:10.1007/bf00192361
[6] Hansen, T. K., Gravholt, C. H., Ørskov, H., Rasmussen, M. H., Christiansen, J. S., & Jørgensen, J. O. L. (2002). Dose Dependency of the Pharmacokinetics and Acute Lipolytic Actions of Growth Hormone. The Journal of Clinical Endocrinology & Metabolism, 87(10), 4691–4698. doi:10.1210/jc.2002-020563
[40] Wee, J., Charlton, C., Simpson, H., Jackson, N. C., Shojaee-Moradie, F., Stolinski, M., … Umpleby, A. M. (2005). GH secretion in acute exercise may result in post-exercise lipolysis. Growth Hormone & IGF Research, 15(6), 397–404. doi:10.1016/j.ghir.2005.08.003
[68] Laursen, T., Jergensen, J. O. L., & Chrlstiansen, J. S. (1994). Metabolic effects of growth hormone administered subcutaneously once or twice daily to growth hormone deficient adults. Clinical Endocrinology, 41(3), 337–343. doi:10.1111/j.1365-2265.1994.tb02554.x
[69] Jørgensen, J. O. L., Møller, J., Møller, N., Lauritzen, T., & Christiansen, J. S. (1990). Pharmacological Aspects of Growth Hormone Replacement Therapy: Route, Frequency and Timing of Administration. Hormone Research, 33(4), 77–82. doi:10.1159/000181589
_______________________
For those interested in the book, its table of contents (so far) is:
- Objective
- Abbreviations
- Research primer: A 'How To' on interpretation of research
- Contraindications
- Skeletal muscle growth and function
- Skeletal muscle: An endocrine organ
- Hypertrophy
- Mechanisms in hypertrophy
- Conclusions regarding skeletal muscle hypertrophy
- Hyperplasia
- Adult myogenesis
- Satellite cells
- Local mIGF-I and Systemic cIGF-I
- Nitrogen balance and reduced AA proteolysis
- Lipolysis
- Mechanisms in lipolytic activity
- Collagen synthesis
- Collagen Type I & Collagen Type III
- Bone density
- Musculotendinous injury recovery and prevention
- Post-immobilization and post-rehabilitation
- Cognitive function
- Anticatabolism
- Cardiorespiratory endurance
- Anaerobic capacity
- Sprint performance
- Metabolic parameters
- LDL reduction
- Anti-aging and rhGH
- Age-related decline in GH
- Studies
- Lipolysis in elderly
- IGFBPs
- IGFBP-1
- IGFBP-2
- IGFBP-3
- IGFBP-4
- IGFBP-5
- IGFBP-6
- Interindividual variation
- IGF-I/IGFBP-3 ratio
- GHBPs
- Genetic polymorphisms
- d3-GHR
- Women and rhGH
- Plot of IGF-I response to rhGH in adult GHD patients by gender
- Dose-response for women vs men
- Cessation
- Blood pressure
- Pulse pressure
- Intracranial hypertension, i.e., headaches
- Obstructive sleep apnea
- Long-term administration
- Strength
- Withdrawal
- Decrement in serum IGF-I
- Effects on thyroid function
- Anthony Roberts' Article "Thyroid Hormone + Growth Hormone – If You Aren’t Using T4 with Your GH, You’re Not Doing It Right"
- Effects on adrenocortical system
- Organ growth
- Pharmacokinetics & Pharmacodynamics
- SubQ serum GH profile
- IM serum GH profile
- Pulsatile serum GH profile
- GH kinetics
- Effects of estradiol-estrogen, obesity
- Effects of testosterone and aromatizable androgens
- Time-course of changes in response to rhGH administration
- Transient negative feedback inhibition
- cIGF-I changes with administration, withdrawal
- Clinical relevance of cIGF-I
- Practical
- Risk-reward balancing
- Dosages and administration
- Conversion of mcg <=> IU
- General instructions for pharmaceutical rhGH preparations
- Specific products and dosages
- Norditropin
- Genotropin
- Serono Serostim
- Humatrope
- Biodenticals
- Cinnatropin, Jintropin, Kigtropin, Hygetropin
- Generics
- Purity variance within a single batch
- French Testing Group
- Practical protocols
- rhGH for lipolysis
- rhGH for hypertrophy
- Primary RT mode drivers of augmented SC fusion
- combined rhGH and Insulin
- rhGH for musculotendinous healing and post-rehabilitation injury recovery

- combined rhGH and rIGF-I
- rhGH for anti-aging
- Permutations based on limited quantity
- Non-rehabilitative usage
- rhGH for anti-aging
- Testing
- Serum IGF-I
- Analytic laboratory quantitative analysis
- rhGH solutions- What is in the vial or pen?
- Antimicrobial preservative agents
- Considerations
- Theoretical
- Dual Effector Hypothesis supersedes the Somatomedin Hypothesis
- Hyperplasia of skeletal muscle
- Molecular signalling
- AR nongenomic pathway
- Modern theory of 22kDa GH binding at the GHR
- Substrate metabolism
- IGF-I, a myokine promoting a local effort for a global effect
- Pathways and natural pulsatile secretion
- β-adrenergic agonists inhibit GH secretion
- Obesity & rhGH
- Gynecomastia
- Glucose metabolism and insulin resistance
- Hyperglycemia
- Metformin
- Downsides of Metformin
- Insulin
- Rapid-acting, -R type
- Slower-acting, -Log type
- Insulin resistance
- TUDCA
- Calcium levels- hypercalcinemia or hypercalciuria
- Edema and water retention
- Tumor growth and risk of carcinogenesis
- Relevant measures
- Natural baseline measures
- GH
- cIGF-I
- Serum T₄
- Monitoring of rhGH course
- HbA1c and blood glucose monitoring
- Interactions with other drugs or exogenous hormones
- AAS
- AAS Effects on IGFBPs and negative inhibition
- Exogenous Testosterone
- Fluoxymesterone
- Stanozolol
- Oxandrolone
- 5α-DHT
- Metformin
- Estrogen
- Alcohol
- Interactions with endogenous hormones
- Thyroid hormones: TSH, T3, T4
- Testosterone
- Prolactin
- Progesterone
- Health conditions that affect rhGH efficacy
- Related
- Growth hormone secretagogues, i.e. "peptides"
- Secretagogues and obesity

How about removing the exogenous gh entirely and running CJC-1295 Ipamorelin?

​

 

[may2021]

When they say can speed up cancer growth how do you know for sure you don’t have any cancer growing in you? Or is this for people already diagnosed with tumours ?

This is the big concern with gh which is why I've been experimenting more with CJC-1295 Ipamorelin

 

[may2021]

And I've read somewhere there's a greater potential for general calcification - including the pineal gland... i.e., leading to dementia/Alzheimer's which, you'll never hear about in body building.

 

[Cherokee]

It's broscience. There's no theoretical upper limit for the lipolytic effects of exogenous rhGH by dose. 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 (I believe this is the study these guys are referring to). In Hansen they reported glycerol rates of appearance in fat depots (i.e., µM/min).

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).

How popular is Growth Hormone in the Weigh lifting, body building, sports community? I never knew it was used this much, till I started dabbling in this community. Has anyone ever did any surveys?

 

[Type-IIx]

@Isrrike @may2021

I won't deny a logical connection between elevated serum IGF-I and the pathogenesis of certain neoplasms. It is a relevant risk-balancing consideration (which I specifically enumerate in the book such that people can appropriately balance risks).

What I can say is that:
A 2019 position paper by anti-aging skeptical European Journal of Endocrinology, after consultation with industry, essentially concluded that there is insufficient evidence to demonstrate a relationship between legitimate rhGH treatment and risk of cancer or mortality. The relationship, however, is confounded by the far greater mortality posed by conditions rhGH is used to treat (e.g., idiopathic/childhood GHD, HIV/AIDS wasting) long-term, and thus follow up measurement is biased by the positive influence of rhGH treatment on mortality and life expectancy.

This is not intended as a directly relevant conclusion for persons undertaking supraphysiological rhGH courses. Rather, it presents a conservative view of the evidence including the most robust data on longitudinal follow-up available.

 

[Isrrike]

@Isrrike @may2021

I won't deny a logical connection between elevated serum IGF-I and the pathogenesis of certain neoplasms. It is a relevant risk-balancing consideration (which I specifically enumerate in the book such that people can appropriately balance risks).

What I can say is that:
A 2019 position paper by anti-aging skeptical European Journal of Endocrinology, after consultation with industry, essentially concluded that there is insufficient evidence to demonstrate a relationship between legitimate rhGH treatment and risk of cancer or mortality. The relationship, however, is confounded by the far greater mortality posed by conditions rhGH is used to treat (e.g., idiopathic/childhood GHD, HIV/AIDS wasting) long-term, and thus follow up measurement is biased by the positive influence of rhGH treatment on mortality and life expectancy.

This is not intended as a directly relevant conclusion for persons undertaking supraphysiological rhGH courses. Rather, it presents a conservative view of the evidence including the most robust data on longitudinal follow-up available.

Ok take my money when’s the book going to be released?

 

[Biggerp73]

So, the primary effect of GH (in the basal state) is to promote lipid mobilization and oxidation as a means of switching substrate utilization from glucose and protein to lipid oxidation. This, then, argues for the primacy of FFA mobilization in its lipolytic effects.

It seems possible that FFA mobilization isn't necessarily a reflection of lipid oxidation, for example, a certain dose may elicit more more mobilization but not necessarily more oxidation.

Granted, GH promotes lipolytic activity via other minor(!) mechanisms, increased REE, peripheral T4 to T3 conversion, increased sensitivity of adipocytes to catecholamines, etc. Given that a single bolus of rhGH acutely causes insulin resistance within 1-2 h, and these effects disappear after approximately 8 h, this is a strong consideration in favor of a single bolus versus 3 - 5 daily.

But some level insulin resistance is probably playing a part of the fat loss mechanics here, isn't it? I could conceive of arguments for saying you want to have the insulin resistance 24/7

So, higher peak concentrations being a correlate to lipolysis clearly argues for a single large bolus, no?

Well it would indicate that one treatment with a higher peak would be better than one treatment with a lower peak, but it doesn't necessarily mean that one high peak is better than two low peaks.

Also, the idea that higher peak = better would seem to argue in favor of IM rather than subq.

Preworkout is best given the benefits for anticatabolism, mitochondrial capacity, etc. from GH and fatty acid oxidation being promoted by exercise may be achieved by the workout. Then, 4 hr post-bolus, the post-workout meal is timed for the natural post-meal reduction in FFA levels.

I don't quite understand the reason for wanting to sync up with the natural post meal reduction in FFA

 

[Type-IIx]

It seems possible that FFA mobilization isn't necessarily a reflection of lipid oxidation, for example, a certain dose may elicit more more mobilization but not necessarily more oxidation.


But some level insulin resistance is probably playing a part of the fat loss mechanics here, isn't it? I could conceive of arguments for saying you want to have the insulin resistance 24/7


Well it would indicate that one treatment with a higher peak would be better than one treatment with a lower peak, but it doesn't necessarily mean that one high peak is better than two low peaks.

Also, the idea that higher peak = better would seem to argue in favor of IM rather than subq.


I don't quite understand the reason for wanting to sync up with the natural post meal reduction in FFA

FFA (serum) is a reflection (a proxy) for lipid mobilization, training may be used to induce beta oxidation, there are benefits from GH in the post-training replenishment of triglyceride stores. What you do with that is dependent on your training.

What's your argument for 24/7 insulin resistance?

This protocol calls for as large a bolus as affordable/tolerable, and a second dose can be administered at nighttime (pre-sleep). I would argue this evidence convincingly demonstrates one high peak is better than two low peaks.

As for IM: I do not disagree, the issue is that we do not have insight into its pharmacokinetics/pharmacodynamics and it's less comfortable for most; given that subq is effective, comfortable, and we do have insight into its PK/PD, I opt for that. This does not foreclose the use of IM, and the book has plenty of protocols that DO call for IM administration over subq in certain use cases.

Timing of the meal 4-4.5 h post-bolus is for appetite and energy homeostasis.

As I've mentioned before, my view is that rhGH practical use falls into the following categories:
I) lipolysis
II) growth/anabolism
III) anti-aging
IV) post-rehabilitation/return from immobilization

with permutations based on limited dosage:
i) non-rehabilitative usage (lipolysis/recomp)
ii) anti-aging