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

Not a fan at all! Some GH fragments are formed even by the E. coli process to manufacture rhGH and have to be purified out of the solution. These can somewhat speculatively be linked to an antigenic/immunogenic response that's seen, as in the formation of GH antibodies.

rhGH > *
thanks for your opinion :)
 
There's some reeeeeeally weak data that shows that the dopaminergic and serotonergic systems (rats) are affected by AAS, and slightly better evidence of the influence on the GABA system. AAS deleteriously alter the visuo-spatial centers (this data is decent, and surprising). I'd like @Jin23 to post good data to show a decrease in serotonin from androgens. And when you think about it, you certainly don't want high serotonin with hard training (fatigue). I present data in the book about how rhGH improves a lot of the cognitive harms from AAS.
+1 for another guy who'd pay $20 or so for a book. No need to edit it much, just throw all the shit you know about drugs into a compilation and that's good enough for me.
 
Just wanted to pop this in here. I translated the regimen to about as plain and simple too understand as you possibly can for another thread.

This is the "explain like I'm 5" (ELI5) version:

1. Eat your meal 1-2 hours before, or within 1 hour after pinning your full HGH dose for the day.

2. Workout 2-3 hours after the HGH pin.

3. Eat post workout meal within an hour, maybe 90 mins after you finish your workout. Together this should cause your post workout meal to be approximately 4 hours after your HGH pin.

Facts:
HGH causes insulin to not work so well. This causes your blood sugar to go up. This happens about an hour or two after taking HGH and lasts 5-8 hours depending on your dosage (possibly longer?).

HGH also causes your body to take fat from your fat reserves and free it up, letting it float around in your blood. This means if you exercise at that time, your body can use that fat, burn it, and thus you are preferentially burning MORE FAT than normal because of the HGH.

Lastly, exercise significantly increases insulin sensitivity and allows the nutrients you eat to be transported directly into your MUSCLES rather than floating around your blood to layer be stored as fat!

So, timing your HGH dose around your meal schedule as outlined above helps in many ways:
1. It minimizes/eliminates food intake when your body is insulin insensitive.
2. This prevents you from having such high blood sugar spikes.
3. You exercise when your body has peak HGH levels. This prevents muscle breakdown and burns the most fat.
4. Then you eat after exercising, which mitigates the insulin insensitivity, again preventing high blood sugar spikes and enabling those yummy nutrients to go into your muscles so you can keep the fat that you just burned OFF!

Hopefully this helps some of the folks who aren't as good at translating science-speak to layperson speak :)

@Type-IIx feel free to copy and use this if you ever want and edit or make changes if desired.
Thanks for the ELI5. I have a question about the 4th point if you don't mind. What do you mean by eating migitates insulin insensitivity?
Also, I keep the fat I just burned off?
 
Thanks for the ELI5. I have a question about the 4th point if you don't mind. What do you mean by eating migitates insulin insensitivity?
Also, I keep the fat I just burned off?
Not the eating is mitigating the insulin insensitivity caused by GH, the exercising is doing this
 
Thanks for the ELI5. I have a question about the 4th point if you don't mind. What do you mean by eating migitates insulin insensitivity?
Also, I keep the fat I just burned off?
I wasn't saying eating mitigates insulin insensitivity. It doesn't do that at all. I was saying EXERCISE mitigates insulin insenstivity--acutally it does the opposite lol. As I said, exercise causes GLUT4 to migrated to surface of the cell. This acts as a transporter so that nutrients including sugar and proteins and vitamins, etc., directly into the cell. THIS is what impvoes insulin sensitivity and lowers/prevents a rise in blood sugar drastically.
Not the eating is mitigating the insulin insensitivity caused by GH, the exercising is doing this
Exactly
 
I wasn't saying eating mitigates insulin insensitivity. It doesn't do that at all. I was saying EXERCISE mitigates insulin insenstivity--acutally it does the opposite lol. As I said, exercise causes GLUT4 to migrated to surface of the cell. This acts as a transporter so that nutrients including sugar and proteins and vitamins, etc., directly into the cell. THIS is what impvoes insulin sensitivity and lowers/prevents a rise in blood sugar drastically.

Exactly
Can you explain like I'm extremely stupid?
I mean what does migitating insulin sensitivity mean, and why do we want low blood sugar?
 
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I wasn't saying eating mitigates insulin insensitivity. It doesn't do that at all. I was saying EXERCISE mitigates insulin insenstivity--acutally it does the opposite lol. As I said, exercise causes GLUT4 to migrated to surface of the cell. This acts as a transporter so that nutrients including sugar and proteins and vitamins, etc., directly into the cell. THIS is what impvoes insulin sensitivity and lowers/prevents a rise in blood sugar drastically.

Exactly
Hey @MFAAS ,

What if there is an intra workout with carbs and eaas? Do.you think that the fat loss potential of HGH is still the greatest during the workout period?
 
Hey @MFAAS ,

What if there is an intra workout with carbs and eaas? Do.you think that the fat loss potential of HGH is still the greatest during the workout period?
I mean if you are using a lot of carbs then it will for sure be reduced, possibly nullified entirely. If your goal is fat loss I would avoid that.

However, there still seems to be a special synergy between AAS and HGH that people claim to recomp fat to muscle when dosages are high enough, despite eating not good foods, people consistently report that they don't gain fat, they just gain muscle and seem to get leaner even in a surplus. I am actually experiencing this myself on my current bulk cycle.

Personally, I would avoid too much intra-workout carbs if your goal is fat loss. What you could do is split up your workout so you do some cardio at the time when you'll lose the most fat and then you lift separately? Idk, it's whatever works best for your schedule. I am a big fan of just a banana and some whey isolate like 45 mins before lifting. It just seems to work well for me. Otherwise I just don't eat pre-workout because I probably ate a good meal like 2 hours beforehand anyway. Then I eat a big meal afterwards and feel great.
 
@Type-IIx how much insulin resistance would you develop if you took 4 iu of growth hormone a day, ate 2800 calories and walked 2 hours a day.
This is going to vary wildly depending on individual, what those 2800 calories consist of and how you are eating them (IE, if someone is doing OMAD vs a normal diet of 3-5 meals a day), whether there is snacking occurring or not, etc. I think that Type-IIx will agree that it's really not possible to provide much insight on this question--sorry.

Basically you wouldn't know until you tried it and taken blood marker measurements to determine the deltas before, during, and after.
 
This is my take on it and the first GH available to be was extracted from the pituitary gland of cadavers...I'm old...no I did not try it lol....in simplified terms I have found lower dose GH 5X a week....especially when fasted..takes my bodyfat down to where I have veins in my abs and no noticeable fat. For growth..and this is just MY empirical evidence...3X a week at 10 IU or more helps blow me up. I don't know about studies but it works this way for me time and time again.
 
However, there still seems to be a special synergy between AAS and HGH that people claim to recomp fat to muscle when dosages are high enough, despite eating not good foods, people consistently report that they don't gain fat, they just gain muscle and seem to get leaner even in a surplus. I am actually experiencing this myself on my current bulk cycle.
actually AAS is not even a necessary part of this. From research ive read and personal anecdotal experience HGH is MOST effective not at burning fat (albeit it does aid in that) but rather inhibiting lipogenesis even in the presence of a substantial surplus.

Basically, GH stops your fat cells from storing excess calories as fat. I forget off the top of my head the name of the enzyme mechanism that it accomplishes this by modulating, but i did see research that identified it. So what happens to those excess calories? Not sure BUT my personal experience when eating a large surplus and using HGH is that i get extremely warm. It seems to me the body burns thise excess calories for heat rather than storing them in fat cells. I mean its a night and day difference when im using HGH and bulking i feel very warm all day long compared to not using HGH.

When i lived in a colder climate i was prone to having cold feet in the winter. I noticed the first winter i ever used HGH that my feet never got cold, infact they felt pretty warm as did the rest of my body.

Despite eating ANY size of surplus, i never gain any fat on GH. However i am also an ectomorph so i never rrally gain fat anyways. This may be far more apparent in an endomorph who gain fat really easy and have to run a very conservative caloric surplus. But even on my most aggressive surplus i only seemed to get leaner.
 
This is my take on it and the first GH available to be was extracted from the pituitary gland of cadavers...I'm old...no I did not try it lol....in simplified terms I have found lower dose GH 5X a week....especially when fasted..takes my bodyfat down to where I have veins in my abs and no noticeable fat. For growth..and this is just MY empirical evidence...3X a week at 10 IU or more helps blow me up. I don't know about studies but it works this way for me time and time again.
What dosage are using @5 on 2 off? Fasted in am? When you do 10 IU do you notice in your hands and hold water? I tried 5 IU(split am and pm) and was swollen. What brand have you tried?
 
Some elaboration on why I don't like Ibutamoren (MK-0677; MK-677, informally) much:

Generally, Ibutamoren seems to be characterized by many of the negative effects of GH (e.g. insulin resistance/increased blood glucose, arthralgia/bone pain, edema/fluid retention, etc.) without a substantial (enough, in my view) increase in serum IGF-I (GH response; reflective of its cellular activity).


Informally, I'll highlight the following impressions from the literature:

Ibutamoren did not yield increased functional improvements/QoL (in elderly, rehabilitation). Side effects include increased cortisol, prolactin; musculoskeletal pain and edema (fluid retention); increased insulin resistance; increased appetite [1]. Its results in a double-blind, placebo-controlled study of "healthy obese" subjects were unimpressive: 3kg increase in fat-free mass, no change in visceral nor abdominal fat mass [2]. There is a known partial interference ("blunting") effect of obesity on secretagogue efficacy. In another trial of the same quality on healthy elderly subjects, Ibutamoren yielded a mere 1.1kg increase in fat-free mass (vs -0.5kg control)... no increase in strength, abdominal nor visceral fat mass [3]. This is, to put it mildly, a completely different animal from rhGH (recombinant human growth hormone; Somatropin).


Ibutamoren does have a significant benefit for sleep quality: 25mg daily yielded a 50% increase in stage 4 sleep duration and increased REM duration [1].


Noteworthy, an Ibutamoren trial was halted due to increased congestive heart failure diagnoses (n = 123 total elderly patients undergoing recovery from hip fracture, 4/123 [6.5%] in treatment group suffered congestive heart failure vs 1/123 [1.7%] in the placebo group) [4].

______________________
References:
[1] Sigalos JT, Pastuszak AW. The Safety and Efficacy of Growth Hormone Secretagogues. Sex Med Rev. 2018 Jan;6(1):45-53. doi: 10.1016/j.sxmr.2017.02.004.
[2] Sode-Carlsen R, Farholt S, Rabben KF, Bollerslev J, Schreiner T, Jurik AG, Christiansen JS, Höybye C. Growth hormone treatment in adults with Prader-Willi syndrome: the Scandinavian study. Endocrine. 2012 Apr;41(2):191-9. doi: 10.1007/s12020-011-9560-4.
[3] Nass R, Pezzoli SS, Oliveri MC, Patrie JT, Harrell FE Jr, Clasey JL, Heymsfield SB, Bach MA, Vance ML, Thorner MO. Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults: a randomized trial. Ann Intern Med. 2008 Nov 4;149(9):601-11. doi: 10.7326/0003-4819-149-9-200811040-00003.
[4] Adunsky A, Chandler J, Heyden N, Lutkiewicz J, Scott BB, Berd Y, Liu N, Papanicolaou DA. MK-0677 (ibutamoren mesylate) for the treatment of patients recovering from hip fracture: a multicenter, randomized, placebo-controlled phase IIb study. Arch Gerontol Geriatr. 2011 Sep-Oct;53(2):183-9. doi: 10.1016/j.archger.2010.10.004.
 
This study was on elderly patients with underlining health conditions
Absolutely true that there frequency at which CHF occurred is not directly extrapolable to our population (healthy resistance trained adults, androgen and rhGH users), though we do not want to eviscerate trial data simply because it is not directly in our population as that would leave us with literally nothing to learn from the data and that is dangerous itself, to exclude logical inferences, particularly when there is a plausible physiological mechanism that does apply to our population.

With GH, we know that it causes cardiomyopathy (this is seen with acromegalics for example). We know that Ibutamoren is a potent, orally active Ghrelin mimetic with a considerable half-life that causes GH-like effects, and indeed seems to be fairly characterized as having more potent deleterious side effects than rhGH (i.e., arthralgia/myalgia [musculoskeletal pain], edema [fluid retention], etc.) It's certainly worth a serious consideration whether to use Ibutamoren for those that use androgens that directly cause left ventricular hypertrophy and cardiac dysfunction, as the two (Ibutamoren+AAS) may very well be synergistic in these harmful effects.

We also have the HAARLEM trial data which showed an effect of rhGH+AAS on cardiac morphological changes, i.e., GH use (rhGH+AAS) was associated with a higher left ventricular end-diastolic volume 3D & left ventricular end-systolic volume 3D (mL) post-cycle (T₁), whereas the number (quantity) of AAS used was negatively associated with both.
 
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