SUGAR, IGF-1, MTOR - optimising glucose for max growth? INFO

[gayspringtrap993]

@HEXEDRONE What if you mix, say, raspberries or strawberries with sugar? Glucose is a good conductor of vitamin C.

no need in additional vitamin c and berries outside summertime

 

[gayspringtrap993]

however sugar can blunt human growth hormone, which is of course bad if you prioritize height. What’s your opinion about this

yeah can blunt but only if you get insulin resistance i heard

 

[gayspringtrap993]

Can you give a list of foods for maximum optimality?

u can just use glucose powder its cheaper and its 100% glucose and not white sugar thats everywhere and 50% fructose 50% glucose

 

[theübermenschboy]

SUGAR, IGF-1, MTOR​

sugar diet, pablo diet, etc etc.

HERES THE INFO DUMP

View attachment 3664672

HOW DOES IGF-1 WORK ALONGSIDE INSULIN?​

1. Insulin indirectly increases IGF-1 via GH (Growth Hormone) signalling​

• GH stimulates IGF-1, mostly in the liver
• GH needs insulin to do this
• In low-insulin states (fasting, starvation), GH goes up, but IGF-1 drops

2. Insulin directly supports IGF-1 production (even independent of GH)​

• Even without GH, insulin increases:
  • IGF-1 mRNA expression
  • IGF-binding proteins (like IGFBP-3)
• Most active in high-carb, fed states

3. Insulin modulates IGF-1 activity​

• It raises IGFBP-3 and ALS (acid-labile subunit)
• These stabilise and carry IGF-1 in the blood
• More usable IGF-1 circulating = better growth signalling

MTOR VS AMPK​

*	mTOR (mechanistic Target of Rapamycin)	AMPK (AMP-activated Protein Kinase)
Triggers	Nutrients (protein, leucine), insulin, IGF-1, high energy (ATP)	Low energy (AMP:ATP ↑), fasting, exercise, metformin, berberine
Function	Growth, anabolism, synthesis	Catabolism, cleanup
Brain	Enhances neuroplasticity (but too much is excitotoxicity)	Promotes neuroprotection, autophagy, anti-aging
Muscle	Promotes hypertrophy	Makes more mitochondria, endurance
Fat	Promotes lipogenesis	Promotes lipolysis
Cell Metabolism	↑ protein & lipid synthesis, ↓ autophagy	↓ protein synthesis, ↑ autophagy, ↑ glucose uptake
Link	AMPK inhibits mTOR	mTOR blocks some AMPK-induced autophagy
Skin	oily skin, acne	clearer skin, less inflammation

• Therefore, when optimising growth, you have to consider the tradeoffs
• Activating mTOR (like through sugar) provides growth, but higher risk of cancer, acne, and ageing

View attachment 3664666
Note tall people

mTOR Overactivation Risks:

• ↓ Autophagy, ↑ Cellular junk
• ↑ Cancer risk
• ↑ Acne, sebum production
• ↓ Insulin sensitivity (if chronic)

LEUCINE?​

This study says that leucine activates mTOR better than sugar, but they also mentioned how glucose is almost necessary to maximise leucine intake for activation of mTOR pathways and growth. High protein diet with almost no carbs will NOT give you sufficient growth, therefore.

Spoiler: EXTRACT FROM STUDY

Experiments using somatostatin, which prevents secretion of a number of growth factors, including insulin, suppressed leucine-induced phosphorylation of S6K1 and 4E-BP1, suggesting that the response is partially modulated by growth factors. Furthermore, in diabetic rats, muscle protein synthesis is thought to be reduced by ∼65% compared with starved nondiabetic controls. Leucine supplementation caused partial recovery of this; however, muscle protein synthesis was still abnormally low, supporting the notion that insulin is required for a maximal response to leucine

Glucose helps LARS1 detect leucine and activate mTORC1, but only if there’s enough energy in the cell

CARBS FOR IGF 1 DIET​

In adult female pigs, dextrose and sucrose combined with lactose stimulated higher insulin responses (therefore igf 1 production) compared to control diets


In growing thoroughbreds (horses), a sugar and starch-rich diet gave higher plasma IGF-1 levels during rapid growth phases compared to a fat and fibre-rich diet


Prepubertal female cows fed lots of starch and sugar showed increased serum IGF-1 concentrations to spike growth


Sugar supplementation in growth retarded calves led to elevated blood glucose and IGF-1 levels, and improved overall growth performance


Sugar → Insulin ↑ → IGF-1 ↑ → Growth ↑

• This effect is most prominent during rapid growth phases or growth-delayed states in animal models

DIABETES​

Fructose may induce inflammation and increase cortisol production, leading to insulin resistance


Chronic cortisol overproduction could be a cause of type 2 diabetes, as numerous interventions that decrease cortisol show antidiabetic effects, while factors increasing cortisol are associated with type 2 diabetes development

• Eat glucose for better spikes in insulin to promote dopamine secretion and reducing cortisol (more near bottom of thread)
• Minimise cortisol through phosphatidylserine, GABAergic supplements, and don’t let blood sugar drop too low or too often as it can spike it
• Possibly cycle mTOR with AMPK activation for cell clean up and regeneration

CANCER​

Some possible risks of cancer can occur from mTOR overactivation and excess cell growth, however

GLUCOSE vs FRUCTOSE
​

Prioritise glucose over fructose to maximise spikes

FRUCTOSE

• It doesn’t raise blood glucose much, so no major insulin spike
• Fructose goes straight to your liver and gets turned into fat and other stuff instead of being used for energy like glucose (bypasses glycolysis)
• Raises cortisol in excess, increases AMPK short term due to AMP:ATP ratio going up

GLUCOSE

• Also, glucose can spike dopamine short-term and benefit hormones, and that spike is greater than from fructose​
• Activates D1 receptors (beneficial for mTOR and other hormones, including GH and Test)​
• Can suppress D2 autoreceptors (even more dopamine release)
• Glucose → insulin ↑ → dopamine ↑ → GH ↑ → IGF-1 ↑​
• Check this thread for more info based on dopamine and test/GH:​

Spoiler: DOPAMINE, GABA, TEST & GH

Dopamine, GABA, Test & GH

reupload needed formatting + new info D O P A M I N E Dopamine is an essential neurotransmitter that greatly benefits us in terms of survival through its effect on motivation. However, it also has effects on testosterone and growth hormones. LOCATIONS WHERE DOPAMINE HITS Hypothalamus...

looksmax.org

Spoiler: BASIC GLUCOSE VS FRUCTOSE TABLE

Sugar Type	Glucose	Fructose	Notes
Table sugar (sucrose)	50%	50%	1:1 glucose + fructose
Honey	~35–40%	~35–40%	Also has water + trace stuff
Fruit	Varies	High	Mostly fructose with fibre
Starch (rice, bread, potatoes)	100%	0%	Pure glucose (as long chains = slow digestion)
Dextrose powder	100%	0%	Pure glucose, fast-acting
Maltodextrin	Glucose polymers	0%	High GI, glucose-heavy

FINAL STUFF​

View attachment 3664727

• Maximising insulin, mTOR and IGF-1 for growth can be done by eating meals/high carbs every 2 hours or less to counteract the crashes
• Rice seems to spike blood sugar the lowest and therefore give less of an insulin response

TLDR?

• Frequent glucose-based meals
• High insulin → High IGF-1 → Pulsed mTOR
• Avoid excess fructose
• Glucose boosts dopamine which is beneficial for hormones and growth
• Especially beneficial during rapid growth phases
• Minimise cortisol to reduce chance of diabetes, as even person with good diet but high cortisol can develop it
• Sugar diet etc may be legit, but higher glucose content is more effective compared to fructose
• Leucine needs sugar to be effective
• Cycle between AMPK and mTOR pathways to not wreck body (to minimise side effects from mTOR overactivation and reintroduce sensitivity)

thoughts?

I am impressed a lot. Very good thread .

 

[weepmeep]

sub5 thread

 

[ILikeNihari123]

SUGAR, IGF-1, MTOR​

sugar diet, pablo diet, etc etc.

HERES THE INFO DUMP

View attachment 3664672

HOW DOES IGF-1 WORK ALONGSIDE INSULIN?​

1. Insulin indirectly increases IGF-1 via GH (Growth Hormone) signalling​

• GH stimulates IGF-1, mostly in the liver
• GH needs insulin to do this
• In low-insulin states (fasting, starvation), GH goes up, but IGF-1 drops

2. Insulin directly supports IGF-1 production (even independent of GH)​

• Even without GH, insulin increases:
  • IGF-1 mRNA expression
  • IGF-binding proteins (like IGFBP-3)
• Most active in high-carb, fed states

3. Insulin modulates IGF-1 activity​

• It raises IGFBP-3 and ALS (acid-labile subunit)
• These stabilise and carry IGF-1 in the blood
• More usable IGF-1 circulating = better growth signalling

MTOR VS AMPK​

*	mTOR (mechanistic Target of Rapamycin)	AMPK (AMP-activated Protein Kinase)
Triggers	Nutrients (protein, leucine), insulin, IGF-1, high energy (ATP)	Low energy (AMP:ATP ↑), fasting, exercise, metformin, berberine
Function	Growth, anabolism, synthesis	Catabolism, cleanup
Brain	Enhances neuroplasticity (but too much is excitotoxicity)	Promotes neuroprotection, autophagy, anti-aging
Muscle	Promotes hypertrophy	Makes more mitochondria, endurance
Fat	Promotes lipogenesis	Promotes lipolysis
Cell Metabolism	↑ protein & lipid synthesis, ↓ autophagy	↓ protein synthesis, ↑ autophagy, ↑ glucose uptake
Link	AMPK inhibits mTOR	mTOR blocks some AMPK-induced autophagy
Skin	oily skin, acne	clearer skin, less inflammation

• Therefore, when optimising growth, you have to consider the tradeoffs
• Activating mTOR (like through sugar) provides growth, but higher risk of cancer, acne, and ageing

View attachment 3664666
Note tall people

mTOR Overactivation Risks:

• ↓ Autophagy, ↑ Cellular junk
• ↑ Cancer risk
• ↑ Acne, sebum production
• ↓ Insulin sensitivity (if chronic)

LEUCINE?​

This study says that leucine activates mTOR better than sugar, but they also mentioned how glucose is almost necessary to maximise leucine intake for activation of mTOR pathways and growth. High protein diet with almost no carbs will NOT give you sufficient growth, therefore.

Spoiler: EXTRACT FROM STUDY

Experiments using somatostatin, which prevents secretion of a number of growth factors, including insulin, suppressed leucine-induced phosphorylation of S6K1 and 4E-BP1, suggesting that the response is partially modulated by growth factors. Furthermore, in diabetic rats, muscle protein synthesis is thought to be reduced by ∼65% compared with starved nondiabetic controls. Leucine supplementation caused partial recovery of this; however, muscle protein synthesis was still abnormally low, supporting the notion that insulin is required for a maximal response to leucine

Glucose helps LARS1 detect leucine and activate mTORC1, but only if there’s enough energy in the cell

CARBS FOR IGF 1 DIET​

In adult female pigs, dextrose and sucrose combined with lactose stimulated higher insulin responses (therefore igf 1 production) compared to control diets


In growing thoroughbreds (horses), a sugar and starch-rich diet gave higher plasma IGF-1 levels during rapid growth phases compared to a fat and fibre-rich diet


Prepubertal female cows fed lots of starch and sugar showed increased serum IGF-1 concentrations to spike growth


Sugar supplementation in growth retarded calves led to elevated blood glucose and IGF-1 levels, and improved overall growth performance


Sugar → Insulin ↑ → IGF-1 ↑ → Growth ↑

• This effect is most prominent during rapid growth phases or growth-delayed states in animal models

DIABETES​

Fructose may induce inflammation and increase cortisol production, leading to insulin resistance


Chronic cortisol overproduction could be a cause of type 2 diabetes, as numerous interventions that decrease cortisol show antidiabetic effects, while factors increasing cortisol are associated with type 2 diabetes development

• Eat glucose for better spikes in insulin to promote dopamine secretion and reducing cortisol (more near bottom of thread)
• Minimise cortisol through phosphatidylserine, GABAergic supplements, and don’t let blood sugar drop too low or too often as it can spike it
• Possibly cycle mTOR with AMPK activation for cell clean up and regeneration

CANCER​

Some possible risks of cancer can occur from mTOR overactivation and excess cell growth, however

GLUCOSE vs FRUCTOSE
​

Prioritise glucose over fructose to maximise spikes

FRUCTOSE

• It doesn’t raise blood glucose much, so no major insulin spike
• Fructose goes straight to your liver and gets turned into fat and other stuff instead of being used for energy like glucose (bypasses glycolysis)
• Raises cortisol in excess, increases AMPK short term due to AMP:ATP ratio going up

GLUCOSE

• Also, glucose can spike dopamine short-term and benefit hormones, and that spike is greater than from fructose​
• Activates D1 receptors (beneficial for mTOR and other hormones, including GH and Test)​
• Can suppress D2 autoreceptors (even more dopamine release)
• Glucose → insulin ↑ → dopamine ↑ → GH ↑ → IGF-1 ↑​
• Check this thread for more info based on dopamine and test/GH:​

Spoiler: DOPAMINE, GABA, TEST & GH

Dopamine, GABA, Test & GH

reupload needed formatting + new info D O P A M I N E Dopamine is an essential neurotransmitter that greatly benefits us in terms of survival through its effect on motivation. However, it also has effects on testosterone and growth hormones. LOCATIONS WHERE DOPAMINE HITS Hypothalamus...

looksmax.org

Spoiler: BASIC GLUCOSE VS FRUCTOSE TABLE

Sugar Type	Glucose	Fructose	Notes
Table sugar (sucrose)	50%	50%	1:1 glucose + fructose
Honey	~35–40%	~35–40%	Also has water + trace stuff
Fruit	Varies	High	Mostly fructose with fibre
Starch (rice, bread, potatoes)	100%	0%	Pure glucose (as long chains = slow digestion)
Dextrose powder	100%	0%	Pure glucose, fast-acting
Maltodextrin	Glucose polymers	0%	High GI, glucose-heavy

FINAL STUFF​

View attachment 3664727

• Maximising insulin, mTOR and IGF-1 for growth can be done by eating meals/high carbs every 2 hours or less to counteract the crashes
• Rice seems to spike blood sugar the lowest and therefore give less of an insulin response

TLDR?

• Frequent glucose-based meals
• High insulin → High IGF-1 → Pulsed mTOR
• Avoid excess fructose
• Glucose boosts dopamine which is beneficial for hormones and growth
• Especially beneficial during rapid growth phases
• Minimise cortisol to reduce chance of diabetes, as even person with good diet but high cortisol can develop it
• Sugar diet etc may be legit, but higher glucose content is more effective compared to fructose
• Leucine needs sugar to be effective
• Cycle between AMPK and mTOR pathways to not wreck body (to minimise side effects from mTOR overactivation and reintroduce sensitivity)

thoughts?

Just spam sugar every once in a while and your good