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

Thank you for all the very interesting info. I am happy to purchase your book, once it’s ready.

Question: For max lipolysis and min insulin resistance, how would you structure the post-cardio meal (2iu Pharma GH)?
Practically irrelevant given the more potent drug effects. Strictly to your question (for max lipolysis and min insulin resistance), a whey protein shake or flavorless BCAA solution (mixed in water). But that's not very practical.
 
Good afternoon @Type-IIx

I have some doubts.

I apologize if they have already been answered, but my English is very basic, I rely on Google translate:

1 - I am forced to stop training because I am having surgery for an inguinal hernia. The question is, does it make sense to apply 3 or 4 IU of HGH after the operation? I mean if it can help me in some way in the postoperative period or if it will harm me. Is it wasting money for not training?

2 - Since I won't be able to train, I'm going to follow a ketogenic diet because it works for me personally. Does following a ketogenic diet have any problems with HGH? Is it counterproductive?

Many thanks in advance to anyone who wants to contribute their experience.

Greetings!
 
From my understanding, lipid oxidation is the limiting factor of “burning fat”. GH mobilizes lipids into the blood, where it needs to be used as energy, hence the reason for your pretraining protocol.

My question is, how long do FFA remain in plasma before they are recycled and stored?

Sleeping burns roughly 300-400 calories over 6-8hrs. Similar to a typical cardio session.

So why is GH taken an hr or two before training more lipolytic than taken pre-sleep, a few hours after a low carb dinner. Then fasted cardio is done the following morning. This way you have GH benefits of sleep+ morning cardio and have waited long enough to avoid most of the insulin resistance. About 10+ hrs from injection time to first meal.

What am I missing here.
 
From my understanding, lipid oxidation is the limiting factor of “burning fat”. GH mobilizes lipids into the blood, where it needs to be used as energy, hence the reason for your pretraining protocol.

My question is, how long do FFA remain in plasma before they are recycled and stored?

Sleeping burns roughly 300-400 calories over 6-8hrs. Similar to a typical cardio session.

So why is GH taken an hr or two before training more lipolytic than taken pre-sleep, a few hours after a low carb dinner. Then fasted cardio is done the following morning. This way you have GH benefits of sleep+ morning cardio and have waited long enough to avoid most of the insulin resistance. About 10+ hrs from injection time to first meal.

What am I missing here.
You believe that it is necessary to measure the time-course of re-esterification? I don't see why that's necessary to quantify here. Fast? Who cares.

The reason that this protocol provides for GH in that time span is basically illustrated in the original post.

GH taken pre-training is more lipolytic than taken pre-bed because the energy expenditure of sleep is definitionally just your RMR. The use of liberated FA stores from fat cell preferentially as energy substrates during low intensity aerobic exercise reflects reduction, largely, of fat cell lipid. I don't know who told you that sleep = cardio in terms of energy expenditure, but it's clearly false (since exercise-activity thermogenesis + RMR > RMR).
 
You believe that it is necessary to measure the time-course of re-esterification? I don't see why that's necessary to quantify here. Fast? Who cares.

The reason that this protocol provides for GH in that time span is basically illustrated in the original post.

GH taken pre-training is more lipolytic than taken pre-bed because the energy expenditure of sleep is definitionally just your RMR. The use of liberated FA stores from fat cell preferentially as energy substrates during low intensity aerobic exercise reflects reduction, largely, of fat cell lipid. I don't know who told you that sleep = cardio in terms of energy expenditure, but it's clearly false (since exercise-activity thermogenesis + RMR > RMR).
What i was getting at is that if it’s pre bed, you’re utilizing energy while sleeping AND morning cardio as opposed to just a one or two hour training session. All the while getting the benefit of better sleep (to most people) and avoiding the window of insulin resistance.

I mentioned the re-esterification because i read a study about how caffeine mobilizes lipids but 66% get recycled and stored.

 
What i was getting at is that if it’s pre bed, you’re utilizing energy while sleeping AND morning cardio as opposed to just a one or two hour training session. All the while getting the benefit of better sleep (to most people) and avoiding the window of insulin resistance.

I mentioned the re-esterification because i read a study about how caffeine mobilizes lipids but 66% get recycled and stored.

There are definitely benefits to performance and lipolysis during exercise that persist from nighttime administration. What you absolutely forego, though, are these more acute changes in serum FFAs that can be used as the preferred energy substrate using zone 2/LISS exercise. You read the title post, right? It's self-contained, succinct.

Albeit tangential, if 1/3 of mobilized lipid is then used as energy to perform work (whether that's just an increase to RMR, to maintain homeostasis with elevated core temp, breathing rate, etc., or applied to formal exercise) after caffeine ingestion... isn't that a fucking fantastic result?

GH even more potently than caffeine mobilizes stored lipid into the circulation, we know its pharmacodynamics, and we can use that to our advantage by depleting the free fatty acids with a particular exercise modality & intensity.
 
There are definitely benefits to performance and lipolysis during exercise that persist from nighttime administration. What you absolutely forego, though, are these more acute changes in serum FFAs that can be used as the preferred energy substrate using zone 2/LISS exercise. You read the title post, right? It's self-contained, succinct.

Albeit tangential, if 1/3 of mobilized lipid is then used as energy to perform work (whether that's just an increase to RMR, to maintain homeostasis with elevated core temp, breathing rate, etc., or applied to formal exercise) after caffeine ingestion... isn't that a fucking fantastic result?

GH even more potently than caffeine mobilizes stored lipid into the circulation, we know its pharmacodynamics, and we can use that to our advantage by depleting the free fatty acids with a particular exercise modality & intensity.
On that point, how beneficial would HIIT type conditioning still be for oxidizing the liberated FFA from HGH administration? 15s sprint-60s rest for 15-20-ish minutes for example.

And you probably covered it but is there an upper limit to HGH dose for this purpose? Maybe realistic upper limit if not theoretical? And in case it doesn't get said enough, we always appreciate your contributions.
 
There are definitely benefits to performance and lipolysis during exercise that persist from nighttime administration. What you absolutely forego, though, are these more acute changes in serum FFAs that can be used as the preferred energy substrate using zone 2/LISS exercise. You read the title post, right? It's self-contained, succinct.

Albeit tangential, if 1/3 of mobilized lipid is then used as energy to perform work (whether that's just an increase to RMR, to maintain homeostasis with elevated core temp, breathing rate, etc., or applied to formal exercise) after caffeine ingestion... isn't that a fucking fantastic result?

GH even more potently than caffeine mobilizes stored lipid into the circulation, we know its pharmacodynamics, and we can use that to our advantage by depleting the free fatty acids with a particular exercise modality & intensity.
That’s all great but there are downsides I find hard to manage.
When fatty acids are released from adipose tissue as a result of lipolysis stimulated by exogenous HGH injection, they can be taken up by cells throughout the body and used as a source of energy. So far so good but if they are not immediately used for energy, several things can happen:

  1. They may be re-esterified: If there is an excess of energy in the body, the free fatty acids released from lipolysis may be taken up by adipose tissue again and re-esterified into triglycerides for storage.
  2. They may be metabolized by other tissues: Fatty acids released from lipolysis can also be taken up by other tissues, such as the liver, and used to synthesize glucose or ketone bodies for energy.
  3. They may contribute to insulin resistance: In cases where there is already an excess of free fatty acids in the blood, the accumulation of fatty acids released from lipolysis can contribute to insulin resistance.
  4. They may contribute to oxidative stress: Fatty acids released from lipolysis can also be subject to oxidation, which can produce reactive oxygen species (ROS) that can damage cells and contribute to oxidative stress.
From a practical perspective, how do I know that I’ve used up all or most of the fatty acids released by GH?
Secondly, lipolysis is very individual as far as I understand and can range from several hours up to 24-48h which makes the management of using up all available fatty acids in the bloodstream even more complicated?
 
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
Great, thanks!!
 
IV) post-rehabilitation/return from immobilization


I was in bed for almost 4 months.. Haven't been the same ever since. Will hgh help me recover?
 
That’s all great but there are downsides I find hard to manage.
When fatty acids are released from adipose tissue as a result of lipolysis stimulated by exogenous HGH injection, they can be taken up by cells throughout the body and used as a source of energy. So far so good but if they are not immediately used for energy, several things can happen:

  1. They may be re-esterified: If there is an excess of energy in the body, the free fatty acids released from lipolysis may be taken up by adipose tissue again and re-esterified into triglycerides for storage.
  2. They may be metabolized by other tissues: Fatty acids released from lipolysis can also be taken up by other tissues, such as the liver, and used to synthesize glucose or ketone bodies for energy.
  3. They may contribute to insulin resistance: In cases where there is already an excess of free fatty acids in the blood, the accumulation of fatty acids released from lipolysis can contribute to insulin resistance.
  4. They may contribute to oxidative stress: Fatty acids released from lipolysis can also be subject to oxidation, which can produce reactive oxygen species (ROS) that can damage cells and contribute to oxidative stress.
From a practical perspective, how do I know that I’ve used up all or most of the fatty acids released by GH?
Secondly, lipolysis is very individual as far as I understand and can range from several hours up to 24-48h which makes the management of using up all available fatty acids in the bloodstream even more complicated?
These are all risks of GH per se. Practically, you cannot quantify how much of these FFAs you've used nor determine precisely your individual rate nor sum total of lipolysis.

I fail to see these arguments that you have made as anything other than a very well thought out Perfect Solution Fallacy, given the fact that the protocol as described does what is intended; it preferentially reduces body fat.
 
On that point, how beneficial would HIIT type conditioning still be for oxidizing the liberated FFA from HGH administration? 15s sprint-60s rest for 15-20-ish minutes for example.

And you probably covered it but is there an upper limit to HGH dose for this purpose? Maybe realistic upper limit if not theoretical? And in case it doesn't get said enough, we always appreciate your contributions.
The point of diminishing returns with respect to rhGH dose & lipolysis has not been established, using doses up to 16 IU. See A GH and fat loss protocol (rhGH lipolysis) that is science-based

HIIT would be less effective than LISS/zone 2.
 
IV) post-rehabilitation/return from immobilization


I was in bed for almost 4 months.. Haven't been the same ever since. Will hgh help me recover?
I'm going to have to remove that chapter from the book, this goes to other posters as well, it's medical advice that I cannot give. There's no practical use, anyway, of rhGH for these applications, you're not missing out on anything. Put another way, if rhGH was actually effective at this, it'd be a part of rehab and such - well, it's not.
 
I'm going to have to remove that chapter from the book, this goes to other posters as well, it's medical advice that I cannot give. There's no practical use, anyway, of rhGH for these applications, you're not missing out on anything. Put another way, if rhGH was actually effective at this, it'd be a part of rehab and such - well, it's not.
So the miraculous healing of some athletes that would take normally 6 months and they do it in 3 is not due to growth hormone ?
That was the speculation for ligament tears and such .
 
So the miraculous healing of some athletes that would take normally 6 months and they do it in 3 is not due to growth hormone ?
That was the speculation for ligament tears and such .
Any nonamateur athlete's recovery practices, that would be managed by a team of professionals like a sports medicine doctor, physiotherapist, team doctor, and coaching staff at least, would not be something you'd be privy to. These are confidental and subject to legal protections under trade secrecy laws. RhGH is prohibited by WADA and virtually every single domestic testing agency. You haven't the slightest notion about what athletes do or do not do that involve rhGH.
 
Any nonamateur athlete's recovery practices, that would be managed by a team of professionals like a sports medicine doctor, physiotherapist, team doctor, and coaching staff at least, would not be something you'd be privy to. These are confidental and subject to legal protections under trade secrecy laws. RhGH is prohibited by WADA and virtually every single domestic testing agency. You haven't the slightest notion about what athletes do or do not do that involve rhGH.
They can exit the testing pool to my knowledge as they don't compete (think Conor McGregor) and once healed they re enter the testing pool .
Also hgh is hard to detect many athletes have admired using it while tested and not failed tests(Mirko Crocop)
Edit: does wada or usada really want to catch them?
I don't think so….

View: https://youtu.be/p6H7aRlosmE
 
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