Cycle Design to optimize IGF-1

[Thick500]

running all 6-8iu at night? why not spread throughout the day to get more IGF1 spikes?

I have always been coached when doing anything more the 3 iu split the dose up.....

I used to dose daytime for a year + and as soon as I switched to night time I started to fill out alot better. The insulin resistance in the daytime was no joke and all the GDAs in the world didn't compare to only running at night. I don't have to use insulin in daytime now, pumps in the gym are way better, and food seems to be going where I want it to better than before just based on appearance. I do actually spread it out to 1 pin right before bed and another 3-4 hours later when I wake up to pee.

 

[Thick500]

The problem with guys like Steve (and the reason I don’t follow them) is that they’re making videos for clicks and likes.

He does a good job with his verbiage in the video, but he’s pretty much pitching a risky hypothesis and asking others to try it and see if it works. The drug metabolism conflicts alone make this very risky. But there’s so many other things at play with this medication and using it in bodybuilding for fat loss that we simply don’t know. It’s also hundreds of $300-$500 per bottle.

I am going to bow out here and let you guys keep geeking out in this thread. But remember we have decades of experience and knowledge with clen. There is also no top coach or top bodybuilders out here doing this stuff. Just because we can use science to pitch a hypothesis doesn’t mean it’s the best thing to do- especially in bodybuilding. That is risky.

You have some valid points but I will always feel safer incorporating an FDA approved drug with a known risk profile and substantial peer reviewed literature on humans. Compare this to some bodybuilding staples for many of us that don't meet this criteria, were never FDA approved or still in clinical trials etc.

I'm only n=1 but I've seen nothing but good things and my BPH that had me peeing 6x a night on training days (I train in the evening and fluids galore go down the hatch) which is now no longer a factor. Improved sleep is another thing I can cross off my list.

I agree that the average gym bro shouldn't seek it out and throw it in without a 2nd thought and I appreciate you protecting the community in this way, it really is admirable and honestly not something I have often seen.

 

[Gaintrain]

I used to dose daytime for a year + and as soon as I switched to night time I started to fill out alot better. The insulin resistance in the daytime was no joke and all the GDAs in the world didn't compare to only running at night. I don't have to use insulin in daytime now, pumps in the gym are way better, and food seems to be going where I want it to better than before just based on appearance. I do actually spread it out to 1 pin right before bed and another 3-4 hours later when I wake up to pee.

Got it, personal performance reasons! when I ran 6 iu of GH during the day it was amazing no issues with BG until I reached 10iu per day then insulin was required daily, quickly changed it back to 6iu as I didn't need insulin with that dose, looked and felt great....

We all respond different!

 

[Thick500]

Got it, personal performance reasons! when I ran 6 iu of GH during the day it was amazing no issues with BG until I reached 10iu per day then insulin was required daily, quickly changed it back to 6iu as I didn't need insulin with that dose, looked and felt great....

We all respond different!

Hmmm... I honestly was not great about checking my BG at different dosages when dosing daytime. I just know the dose got high and i was definitely becoming resistant so I switched. There probably is a safe dose where its not impacted significantly. Lowering the dosage is typically not one of the 1st options I entertain

I may start out tomorrow with 3 or 4iu and see how it compares actually

 

[3BILLS]

I’ve kind of been reading into myostatin today, and methods to reduce it and optimize it. I know it’s been discussed some on here, with regards to some of the more experimental types of myostatin inhibitors (which I’m looking to avoid because there’s a lot of unknown health factors and variables), but I did find some interesting safe and natural ways to reduce it

I’ll post it up.

Here’s a safe and effective supplement stack designed to help reduce myostatin and support muscle growth, using widely available and well-tolerated ingredients:

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Safe Myostatin-Reducing Supplement Stack​

Creatine Monohydrate​

• Dosage: 3–5g/day
• Timing: Anytime, preferably post-workout or with a meal
• Benefits: Increases strength and muscle mass, reduces myostatin with training

​

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Whey Protein Isolate​

• Benefits: High in leucine; supports muscle protein synthesis and recovery
• Notes: Opt for a brand with minimal additives and high leucine content.

---

4. Omega-3 Fish Oil (EPA/DHA)​

• Dosage: 1–3g combined EPA/DHA per day
• Timing: With meals (fat helps absorption)
• Benefits: Anti-inflammatory, may indirectly reduce myostatin

---

5. Vitamin D3​

• Dosage: 2,000–5,000 IU/day (based on blood test)
• Timing: With a fat-containing meal
• Benefits: Low vitamin D levels are linked to poor muscle function and possibly higher myostatin
• Notes: Get levels tested to tailor the dose.

^^ now most of these are well known. But I did come across another safe supplement that I’ve never heard of called HMB that seems to be a derivative of leucine. Leucine was a reoccurring mention in some of the reading I did for not only decreasing myostatin but also enhancing muscle protein synthesis (mps) Here’s the information on HMB. I just ordered some today off Amazon and am going to give it a try

HMB and Myostatin: What the Science Says​

• Animal and cell studies have shown HMB can suppress myostatin expression and enhance muscle protein synthesis.
• In human studies, the effect is less direct but promising — HMB helps reduce muscle breakdown, especially in untrained individuals or during caloric deficits.
• HMB also increases IGF-1, which is linked to muscle growth and may indirectly lower myostatin.

---

HMB Summary​

• Dosage: 3 grams per day (split into 2–3 doses)
• Forms: HMB Free Acid (absorbs faster) or HMB Calcium (most common)
• Timing: Around workouts or with meals

---

Stacking HMB with Other Myostatin Inhibitors​

HMB can be part of a synergistic stack:

• Creatine + HMB – enhances strength and muscle protection
• HMB + Epicatechin – potential dual myostatin suppression
• HMB + Protein – amplifies muscle preservation in a deficit

---

Bottom Line:​

HMB is a safe and well-researched supplement that may reduce myostatin and help preserve muscle, especially during stress, aging, or inactivity. Its effects are modest but enhanced when combined with training and other supplements.

Your boy @bbxtreme takes hmb.

After he gets that morning cardio in first though.

#riseandgrind

 

[Gaintrain]

Hmmm... I honestly was not great about checking my BG at different dosages when dosing daytime. I just know the dose got high and i was definitely becoming resistant so I switched. There probably is a safe dose where its not impacted significantly. Lowering the dosage is typically not one of the 1st options I entertain

I may start out tomorrow with 3 or 4iu and see how it compares actually

Yea man I used to have that mind set that more is better! lol not so much anymore....more gear equals more sides.....

 

[Stewie]

@Thick500 what are some other considerations you're looking to optimize?

You kind of having me going down the rabbit hole of the different types of IGF binding proteins and their interactions, and im learning a ton

Have some free time today so I plan to do a much deeper dive on IGF proteins as well as the components of the below chart and how it relates to skeletal muscle

It might be splitting hairs, or irrelevant, but I find this kind of research fun and enjoyable. Just looking for some other topics you've considered

View attachment 226328

Be mindful that there's the possibilities of disruption(s)- insert said reaction pathway[sake of conversation- transcription factor]. You may, or may not have seen I've mentioned this - if a biochemical pathway (charted) directively creates a reaction. This doesn't necessarily mean it will happen. Nor does it tell us how quantitatively un/important it is. Be cognizant we're not living in a vacuum.

I'll pitch one particular transcription factor that's upregulated by uncontrolled OSA- sleep apnea. This isn't taking into account the probability of a laundry list of polypharmacy including nutraceuticals.

If curiosity piques your interest. Take a gander at how HIF1-a (hypoxia-inducible factor-1 alpha), could, theoretically bastardize mTORC1signalling. HIF-1a could very well put the brakes on mTORC1 activity under hypoxia-inducible factors by upregulating REDD1 (regulated in development and DNA damage responses 1). This by itself, could limit anabolic signalling. Under these same hypoxia-inducible factors, through a different pathway that intertwines with metabolism and anabolic pathways that very well could be disrupted; deiodinase activity (thyroid catalyzation) that facilities either activation and deactivation of thyroid hormones- T4, T3, rT3 and both isoforms of T2.

Then we have to account for inflammatory cytokines that theoretically could bastardize a-many more things. All relative to HIF1-a mucking up different hepatic and peripheral IGF-1 transcriptions.

Nevertheless it's good you’re engaging and digesting autodidactic learning

 

[Thick500]

Be mindful that there's the possibilities of disruption(s)- insert said reaction pathway[sake of conversation- transcription factor]. You may, or may not have seen I've mentioned this - if a biochemical pathway (charted) directively creates a reaction. This doesn't necessarily mean it will happen. Nor does it tell us how quantitatively un/important it is. Be cognizant we're not living in a vacuum.

I'll pitch one particular transcription factor that's upregulated by uncontrolled OSA- sleep apnea. This isn't taking into account the probability of a laundry list of polypharmacy including nutraceuticals.

If curiosity piques your interest. Take a gander at how HIF1-a (hypoxia-inducible factor-1 alpha), could, theoretically bastardize mTORC1signalling. HIF-1a could very well put the brakes on mTORC1 activity under hypoxia-inducible factors by upregulating REDD1 (regulated in development and DNA damage responses 1). This by itself, could limit anabolic signalling. Under these same hypoxia-inducible factors, through a different pathway that intertwines with metabolism and anabolic pathways that very well could be disrupted; deiodinase activity (thyroid catalyzation) that facilities either activation and deactivation of thyroid hormones- T4, T3, rT3 and both isoforms of T2.

Then we have to account for inflammatory cytokines that theoretically could bastardize a-many more things. All relative to HIF1-a mucking up different hepatic and peripheral IGF-1 transcriptions.

Nevertheless it's good you’re engaging and digesting autodidactic learning

Well I don't have OSA but I guess this means I need to cancel my Mt. Everest trip and stop choking myself out with a noose when I beat off??

Dammit!! All this time trying to figure out where my gainz have gone, I could've been Mr. O by now

 

[Sectør]

Be mindful that there's the possibilities of disruption(s)- insert said reaction pathway[sake of conversation- transcription factor]. You may, or may not have seen I've mentioned this - if a biochemical pathway (charted) directively creates a reaction. This doesn't necessarily mean it will happen. Nor does it tell us how quantitatively un/important it is. Be cognizant we're not living in a vacuum.

I'll pitch one particular transcription factor that's upregulated by uncontrolled OSA- sleep apnea. This isn't taking into account the probability of a laundry list of polypharmacy including nutraceuticals.

If curiosity piques your interest. Take a gander at how HIF1-a (hypoxia-inducible factor-1 alpha), could, theoretically bastardize mTORC1signalling. HIF-1a could very well put the brakes on mTORC1 activity under hypoxia-inducible factors by upregulating REDD1 (regulated in development and DNA damage responses 1). This by itself, could limit anabolic signalling. Under these same hypoxia-inducible factors, through a different pathway that intertwines with metabolism and anabolic pathways that very well could be disrupted; deiodinase activity (thyroid catalyzation) that facilities either activation and deactivation of thyroid hormones- T4, T3, rT3 and both isoforms of T2.

Then we have to account for inflammatory cytokines that theoretically could bastardize a-many more things. All relative to HIF1-a mucking up different hepatic and peripheral IGF-1 transcriptions.

Nevertheless it's good you’re engaging and digesting autodidactic learning

I definitely appreciate the post and the insight man!

I’ll admit that’s quite a lot for my brain to digest at this time of night as some of that was over my head, but you definitely gave me a few good avenues of reading for tommorow with regards to HIF-1a, mTORC1, and REDD1

 

[Stewie]

I definitely appreciate the post and the insight man!

I’ll admit that’s quite a lot for my brain to digest at this time of night as some of that was over my head, but you definitely gave me a few good avenues of reading for tommorow with regards to HIF-1a, mTORC1, and REDD1

You're welcome. You have a lifetime ahead of you to ease into autodidactic physiology and biochem.

 

[monstaa]

just take gh and stop thinking

 

[KingOfSushi]

Kurt, Dean, and Steve

Which of the three of these guys keeps protocols the most simple and basic, and which one of these three actually has some good results with clients to show?

Something to consider

 

[Thick500]

Which of the three of these guys keeps protocols the most simple and basic, and which one of these three actually has some good results with clients to show?

Something to consider

I don't follow the sport well enough to be able to answer this but I'm sure you are making a valid point. These are not top level coaches.

If Hany was spilling the beans on protocols in his yt channel I would be all on it but training is about all he gets into. My guess is all the top guys are not going to openly discuss the detailed science they are considering. I like John Jewett's stuff but he still holds back quite a bit.

Kurt, Dean, and Steve seem to be covering topics nobody else is and if I hear something that catches my attention I dig deeper. The binding protein topic is something they didn't even have an answer for but more so just discussing their existence and role. Just looking to understand my body better and how it works against my efforts and the $ I dump into it

Are there any podcasts or youtube channels you recommend?

 

[hawkmoon]

Be mindful that there's the possibilities of disruption(s)- insert said reaction pathway[sake of conversation- transcription factor]. You may, or may not have seen I've mentioned this - if a biochemical pathway (charted) directively creates a reaction. This doesn't necessarily mean it will happen. Nor does it tell us how quantitatively un/important it is. Be cognizant we're not living in a vacuum.

I'll pitch one particular transcription factor that's upregulated by uncontrolled OSA- sleep apnea. This isn't taking into account the probability of a laundry list of polypharmacy including nutraceuticals.

If curiosity piques your interest. Take a gander at how HIF1-a (hypoxia-inducible factor-1 alpha), could, theoretically bastardize mTORC1signalling. HIF-1a could very well put the brakes on mTORC1 activity under hypoxia-inducible factors by upregulating REDD1 (regulated in development and DNA damage responses 1). This by itself, could limit anabolic signalling. Under these same hypoxia-inducible factors, through a different pathway that intertwines with metabolism and anabolic pathways that very well could be disrupted; deiodinase activity (thyroid catalyzation) that facilities either activation and deactivation of thyroid hormones- T4, T3, rT3 and both isoforms of T2.

Then we have to account for inflammatory cytokines that theoretically could bastardize a-many more things. All relative to HIF1-a mucking up different hepatic and peripheral IGF-1 transcriptions.

Nevertheless it's good you’re engaging and digesting autodidactic learning

Ah, so now I know why I am so small!
Hopefully my recently acquired CPAP will remedy that.

Seriously that's great information and while I always knew there was some negative impact from OSA it's nice to see how.

 

[Stewie]

Ah, so now I know why I am so small!
Hopefully my recently acquired CPAP will remedy that.

Seriously that's great information and while I always knew there was some negative impact from OSA it's nice to see how.

I'd say you're physique is quite impressively astonishing! Not so much on the small side, admirable to say the least!

The pernicious fallout from uncontrolled sleep apnea can be counterproductive, no doubt.

Opposing as it may be. Model representation, and some seemingly robust literatures in us homo sapiens-sapiens. Chronic activation of hypoxia-inducible factors can run-amok bastardizing several systems. Contrastingly, in acute settings, these same hypoxia-inducible transcription factors can favorably play an important role in regulating skeletal muscle progenitor cells (satellite cells) and skeletal muscle hypertrophy.

Resistance Training Using Different Hypoxic Training Strategies: a Basis for Hypertrophy and Muscle Power Development - Sports Medicine - Open

The possible muscular strength, hypertrophy, and muscle power benefits of resistance training under environmental conditions of hypoxia are currently being investigated.Nowadays, resistance training in hypoxia constitutes a promising new training strategy for strength and muscle gains. The main...

sportsmedicine-open.springeropen.com

 

[SSFITNESS]

Hey all. Long time lurker, rare poster/commenter here looking for some experienced advice.

I've been dieting semi-hard for roughly 8 weeks. 5'10" 220lbs and 8-9%. Going to diet down for another 6-8 weeks to maybe 6% and then rebound blast for 12-16weeks maybe longer. Unless I'm not patient enough and I start this up in 2 weeks who knows.

I've been running generic gh for 2-3 years and currently at 6-8iu per day at night.

I want to optimize my cycle, diet, training etc for the best response to IGF during my growth phase. I've got 2 x 10vial kits of LR3 0.1mg per vial from pharmaqo and 3 kits of Serostim. My concern is IGF binding proteins being high from chronically elevated IGF for the past few years. So... was planning to give the GH a break at some point before I rebound blast to let those protein levels drop considerably but not sure how long that will take (2 weeks, 4 weeks, longer?). I assume there is no other way to achieve this.

Also, would I be shooting myself in the foot running the LR3 with the Serostim? I want to get the most out of both of these products obviously so considering 40 days of LR3 followed (50mcg per day) by 63 days of 6iu Serostim instead of together?

Low dose tren will be present throughout to sensitize IGF-1 receptors. Also Test, Primo, and anadrol for 4 weeks at some point maybe when initial rebound gains slow. I may use EQ if I can get estrogen where I want it (I usually use either primo or eq).

Something around 1g test, 600 primo, 75mg Tren E, and 50mg anadrol.

I also have humalog and Lantus to throw i there, Lantus being known to elevate IGF-1 by binding to the receptors and potentially upregulating IGF receptors. So Lantus everyday?? I have retatrutide to throw in low dose to keep insulin resistance at bay.

Anything else to unregulate IGF-1 receptors and lower the binding proteins?

Should I drop gear to cruise levels before I blast? Had planned to cruise after the rebound. Paul of Anabolic Bodybuilding had great success post show going straight into rebound blast with Lantus, gh, test, primo, and NPP. Thought I would do something similar.

Please offer thoughts, suggestions, any misconceptions or mistakes I have in planning this. I'm 41 with limited growth years ahead of me so have to get a bit nerdy with my setups to see gains, my days of just pin, eat, lift and forget about it to see progress are over for sure.

The best way to get maximum igf1 conversion from your gh is by splitting your dose am pm and only take 2 to 3 days per week. So what's worked well for me and the people I've worked with is 4 iu am upon waking 4iu pm around 2 hours after last meal. This gives the liver a break and simulates it's natural rhythm. The trick is then to put at least 1 day if not 2 in between this keeps you developing insulin insensitivity from the daily gh. Why is that so important, insulin in the master hormone you want all the body's receptors to be working properly otherwise you need to keep taking more and more of everything to get the same result. Tren ace at 75mgs every other day will also help the igf1 take immature satellite cells and develop them into full grown cells