Vherny123
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physiology growth IGF1 GH mTOR fructose nutrition looksmax
TL;DR
Thoughts / Suggestions?
This is my theory on optimizing insulin, IGF-1, and mTOR for growth & looks, not medical advice. I’m sharing it for discussion. If you spot gaps, contradictions, or ways to make it more practical, drop your feedback. Always open to refining the approach based on evidence or personal experience.
physiology growth IGF1 GH mTOR fructose nutrition looksmax
TL;DR
- Insulin → follows glucose
- Insulin acutely suppresses GH
- GH → IGF-1
- Insulin is required for liver to respond to GH and produce IGF-1
- Dopamine is a modulator; not a clean “turn on GH” switch
- Leucine + insulin (energy) activate mTOR best; leucine alone in low-energy states is weaker
- Fructose ≠ glucose for anabolic signaling; excess fructose worsens liver fat & insulin resistance
1) Short-term vs long-term GH picture
Post-meal (hours)- Glucose ↑ → Insulin ↑ → GH ↓ (suppression). OGTT is a clinical test that proves this. GH pulses drop after carbs.
Nijenhuis-Noort 2024, Bugalho 2023
- Glucose ↓ → Insulin ↓ → GH ↑. Fasting and sleep give the biggest GH pulses.
- GH alone doesn’t guarantee IGF-1 if the liver lacks insulin signaling → high GH, low IGF-1 happens in type 1 diabetes.
Hollstein 2022
- Adequate calories + portal insulin (fed state over days/weeks) keep liver GH-sensitive → GH → IGF-1 works.
- Acute suppression vs chronic necessity is the nuance most people miss.
2) IGF-1 bioavailability
- Most IGF-1 is bound to IGFBP-3 & ALS → extends half-life & regulates tissue access
- Insulin & nutrition influence IGFBPs/ALS → bioavailable IGF-1 can vary even if total IGF-1 stays similar
Kim 2022
3) Leucine, carbs & mTOR
- Leucine triggers mTORC1 (muscle protein synthesis), but energy & glucose matter
- Leucine + carbs/insulin → bigger mTOR response than leucine alone in low-energy states
- Translation: protein works best with carbs in most contexts
Yoon 2020, Kim 2022
4) Fructose vs glucose
- Fructose → liver → de novo lipogenesis & insulin resistance
- Glucose → systemic insulin spike, anabolic + reward pathways
- For clean GH/IGF signaling: prioritize glucose/complex carbs, avoid excess fructose (sugary drinks, HFCS)
Softic 2017, Geidl-Flueck 2023
5) Dopamine; Modulator, Not GH Switch
- Dopamine drugs can affect GH clinically
- In normal physiology: timing & receptor subtype matter → not reliable to “raise GH → IGF-1”
- Treat dopamine as modulator of appetite, reward, endocrine loops, not a master switch
Jogie-Brahim 2009, PMC9832860
6) Major reviews / key studies
- Insulin suppresses GH acutely / enables hepatic GH action: Nijenhuis-Noort 2024, Bugalho 2023
- Leucine + glucose gate mTOR via LARS1: Yoon 2020, Kim 2022
- Fructose → hepatic fat / insulin resistance: Softic 2017, Geidl-Flueck 2023
- IGF binding proteins & ALS → ternary complex matters: Kim 2022
7) Practical playbook
Height / puberty- Calories drive growth → avoid extreme low-carb or starvation
- Balanced meals with protein + carbs → portal insulin keeps liver GH-sensitive → IGF-1
- Sleep 8 to 9h for GH pulses
- Growth failure suspected → see pediatric endocrinology
- Progressive resistance training priority
- Protein 20 to 40g per meal (whey = leucine-rich), spread across day
- Carbs around workouts → post-workout protein + carb boosts amino-acid uptake
- Cycle AMPK: conditioning / active recovery
- Avoid chronic overfeeding & excess fructose
- Maintain body fat, sleep, stress management
- Cycle mTOR / AMPK: anabolic windows (meals + training) + fasting/cardio for autophagy
8) Practical sample protocol
- Daily: protein 1.6 to 2.0 g/kg, whole-food carbs, avoid sugary drinks
- Training: 3× full-body resistance (progressive), 2× low-intensity cardio
- Per lift day: 25 to 40g whey + 30 to 60g carbs within 1h post workout (performance/growth focus)
- Sleep: consistent 7 to 9h
- 1×/week: longer AMPK session or 16:8 fasting window
9) Safety & limits
- Don’t chase GH pharmacologically unless deficient
- Risks: metabolic, edema, acromegaly-like, cancer risk if predisposed
- Avoid chronic high insulin (sugar grazing); short anabolic spikes ≠ chronic hyperinsulinemia
- Diabetes, liver disease, or endocrine issues → consult endocrinologist
10) Primary sources & reviews
- Nijenhuis-Noort EC et al., GH, Insulin & IGF-1 interplay (2024)
- Bugalho MJ et al., Hyperglycemic Threshold to Suppress GH (2023)
- Yoon I. et al., Glucose + Leucine via LARS1 — Science (2020)
- Kim K. et al., O-GlcNAc LARS1 → mTORC1 (2022)
- Softic S. et al., Glucose vs Fructose hepatic metabolism — JCI (2017)
- Geidl-Flueck B. et al., Fructose → de novo lipogenesis review (2023)
- Kim H. et al., CryoEM IGF-1/IGFBP-3/ALS (2022)
- Jogie-Brahim S., IGFBP-3 biology, Endocrine Rev (2009)
- Hollstein T., Fasting / GH / IGF-1 (2022)
- Softic S., Fructose & hepatic insulin resistance (2020)
Thoughts / Suggestions?
This is my theory on optimizing insulin, IGF-1, and mTOR for growth & looks, not medical advice. I’m sharing it for discussion. If you spot gaps, contradictions, or ways to make it more practical, drop your feedback. Always open to refining the approach based on evidence or personal experience.
