Keicht drug thread 2

Sachlichkeit

Sachlichkeit

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No gatekeeping

In minecraft

follow up of: https://looksmax.org/threads/esoteric-framecel-heightcel-drug-thread.1502129/

Relevant growth related pathways
GH/IGF1 Axis (growth hormone) Stimulator
TGF Beta. similar to myostatin/follistatin muscle cap but de
als with bones as well. Sclupts & stops growth. Regulator
WNT/B cantenin
. Stimulator
FGFR
. Regulator
ESTROGEN.
Not a growth pathway but probably the most important thing to manage when comes to longitudinal growth as it is the major reason growth plates ossify and longitudinal growth stops

These pathways are dictated by genetic expression

Most important pathway is GH/IGF1.

GH/IGF High dose exogenous HGH (8-10) IU/day combined with high protein diet consisting of full amino acid profile. Whey works. 1-1.5g/lb.

TGFB pirfenidone & losartan. Pirfenidone is an anti fibrotic medication used to treat tissue scarring. Short half life. Needs to be dosed 3x/day 600mg per dose. There isn't really any effective affordable way of downregulating TGFB. Losartan & Pirfenidone are the best bet.

WNTB cantenin. KY19382 either injected subcutaneously at 0.25mg pharmaceutical grade or ~0.80mg raw powder ingested orally. see, Literal heightpills 2. ROMOSOZUMAB, Medically approved WNT/B cantenin pathway modulator. 210MG/ injection every month. Carcinogenic, has a maximum of 2 years lifetime use. Will post about it in thread later. KY19832 has better prospects for height gain because of how it targets WNTB, Romo will just make you wide. Easy to source, doesn't decay while being shipped. Kind of expensive ~$400usd/mo

FGFR. Infigratinib. Universally targets FGFR which targets FGFR 3, A mutation of Fibroblast growth factor 3 is what causes dwarfism so inhibition of it allows for normal growth. See, literal heightpills. Pan FGFR inhibition can cause significant vision issues. low dose, not using it chronically, temporarily inhibiting FGFR during the beginning of cycles to kickstart osteoblast proliferation (growing bones) with less resistance from FGFR.

ESTROGEN. If growth plates are open, estrogen will close them. There are a myriad of signals the body can produce that tell growth plates to close but if there is no estrogen the growth plates will not close. Letrozole is the medical gold standard for keeping growth plates open. I mentioned before in an older thread that estrogen is an anti resorptive. It prevents the breaking down of bone. Its crucial for libido, bone health, joint health, brain health, mood regulation. Insane and retarded. So we can't completely eradicate it, it is simply not worth the height gain if any. Raloxifene is a SERM synthetic estrogen modulator that mimics estrogens effects but seems to have negligible effects on growth plates. If that works, it will be the standard for vertical growth as the primary drawback from the use of aromatase inhibitors is how crucial estrogen is for normal function.

High dose androgens during development for male dimorphism

Testosterone has a 1:1 androgenic to anabolic ratio. Anabolism deals with muscle growth, Androgenics deal with dimorphism. Things like fat redistribution, facial hair, even the hooding of eyebrows(I think), secondary sexual characteristics, masculine growth (skeletal V-taper,) deepening of voice, and so on and so forth.

Androgens work synergistically with HGH for growth. Both stimulate osteoblast proliferation, Gear increases height velocity, increase in bone mineral density.

Growth is, low androgens >>> GH starts increasing, sustained linear growth >>> then puberty, high androgens, high GH, Height velocity increases, grow bigger faster >>> tail end of growth, GH decreases, androgens increase, estrogen feedback closes growth plates

Suppress estrogen to abnormal levels while keeping GH and androgens at supraphysiological levels and you will have supraphysiological growth (assuming you are not too old, 13-24, 13-22 whatever)

Trenbolone enanthate & testosterone enanthate

Tren is a non aromatizing steroid originally intended for cattle with a 5:5 androgenic anabolic ratio.
has a harsh side effect profile making it unfit for medical use.

So why use it? It lowers protein requirement for growth and doesn't aromatize which means you don't need to use as much aromatase inhibitors. If you wanted something like the benefits of a gram of test a week without the gram equivalent of DHT you could cut it with 500 test 100 tren which would produce similar results with less hairloss risk.

Testosterone enanthate is just basic primary male sex hormone complete with downstream hormonal profile. DHT is a downstream of Testosterone at a maybe (20%) conversion rate that drives dimorphism MORE than testosterone dose with a 5:0 Androgenic to anabolic ratio. It is the primary cause of hairloss in men.

Testosterone is the best steroid because of the downstream profile. Your brain will develop differently, you will think differently if you are on man made steroid derivative. Enanthate is the ester that extends the half life of the androgen in your body. Injections should be every 4-5 days.

Rest of steroids have their place but we dont care

Androgen ancillaries

Losartan/Telmisartan (blood pressure v important)
GHK CU (skin)
AI's (estrogen management)
Dutasteride/finasteride Hairloss, + skin protection from supraphysiological DHT levels
Topical RU58841, for hairloss. Anti androgen that will prevent hairloss from any androgen
Blood pressure cuff for blood pressure obv
HCG to maintain testicular function. Infertility from steroids is largely cope. HMG is more effective than HCG if you are worried.

Dimorphism is about bones, not muscle. How do we drive a pro osteogenic environment?

1. Prevent resorption using DHT & Estrogen or a synthetic estrogen like raloxifene, Anti resorption drugs like Alendronate
2. HGH & androgens
3. Mechanical tension, exercise
4. diet > High protein, full amino acid profile to fully utilize HGH dosages, Vitamin K2 MK7, Zinc, Calcium, Vit D, & Magnesium

BONE DRUGS

PTH analogs abaloparatide and teriparatide.


Parathyroid hormone analogs cause bone resorption (the breaking down of bones) but then stimulate osteoblast proliferation that outweighs the resorption resulting in a net gain of bone.

Teriparatide is the worse, more risky of the two and should only be used if you have an adverse reaction to abaloparatide. Like romosozumab, these are carcinogenic and have a maximum lifetime use of 2 years. The body will begin to break down the bone built by PTH analogs after treatment so use an anti resorptive drug like alendronate for a literal year.

ANTI RESORPTION

Is severely underrated in bone growth as androgens don't preserve bone, they build it. Raloxifene, estrogen, (DHT, is unique in that sense because it has been shown to retain bone mineral density in the absence of both estrogen in testosterone,) and the Bisphosphonate Alendronate. Preventing resorption means more of our androgen GH gains will go towards accruing mass rather than fighting against the breakdown.

ROMOSOZUMAB

Is the most effective bone drug for thickening/widening. It should be used (if at all) after you reach your desired height because its much better at making you wider, not so much taller. PTH analogs are better for making you taller. Carcinogenic, 2 year lifetime use, Yes it is more effective than PTH analogs

TETRANALOGS/MMP INHIBITORS

THREAD. MMP'S break down collagen scaffolding, Inflammation via gear upregulates them. Low dose MMP inhibitors Doxycycline and minocycline prevent this resulting in more bone gains

HOLY GRAIL OGRE GENE DRUGS

remember, These pathways are dictated by genetic expression.

So instead of individually trying to downregulate or upregulate them, why not just alter the gene expression? Obv this is riskiest, epigenetic permanent effects. WE BALL

Vorinostat enjoyers

3 relevant gene drugs available on open market

1. HDAC inhibitor Vorinostat
2. EZH2 inhibitor Tazmetostat
3. DNMT inhibitor azacitidine & oral azacitidine Onureg

Vorinostat
enhances gene transcription. Allows for more genetic expression, indiscriminately. People pair it with androgens to enhance their masculinizing effect. Think of vorinostat as a megaphone. Though because it universally allows for more genetic expression its not just used for androgens. Chronic use is bad for bones, bad for growth, not to mention ur genes being "unlocked" for long period of time thats obviously not good. I would recommend you cycle it but its anti osteogenic effects on bones and such I think is just being drastically outperformed by the amount of gear these people are blasting and thats how they get away with it.

"Though because it universally allows for more genetic expression its not just used for androgens"

Cognitive Improvement by Vorinostat through Modulation of Endoplasmic Reticulum Stress in a Corticosterone-Induced Chronic Stress Model in Mice
Upregulation of HDAC9 in hippocampal neurons mediates depression-like behaviours (eg. Anhedonia) by inhibiting ANXA2 degradation

Vorinostat (SAHA) May Exert Its Antidepressant-Like Effects Through the Modulation of Oxidative Stress Pathways
Vorinostat Corrects Cognitive and Non-Cognitive Symptoms in a Mouse Model of Fragile X Syndrome
The histone deacetylase inhibitor Vorinostat (SAHA ) alleviates depression-like behavior and normalizes epigenetic changes in the hippocampus during ethanol withdrawal
Early-life stress-induced visceral hypersensitivity and anxiety behavior is reversed by histone deacetylase inhibition (Vorinostat).
Suberoylanilide hydroxamic acid attenuates cognitive impairment in offspring caused by maternal surgery during mid-pregnancy
(Vorinostat) SAHA Improves Depressive Symptoms, Cognitive Impairment and Oxidative Stress: Rise of a New Antidepressant Class

TAZMETOSTAT
removes the epigenetic brake on growth genes present during puberty. That re-exposes the programs that let GH and androgens drive growth and masculinization. In adulthood, EZH2 shuts these genes down, the body genetically shifts into maintenance mode instead of growth. So basically, we turn the programs on, blast androgens, BOOM, second puberty. Whereas vstat will exaggerate this growth.

Taz is generally well tolerated, easier to source, and less risky and more specific than vorinostat though they serve two different purposes. There are some drugs that are just better made than others and taz is one of them.

DNMTI azacitidine & oral azacitidine Onureg

stronger more broad version of tazmetosat. Activates PRE PUBERTY growth programs (such as IGF2 natal version of IGF1 which shuts down in puberty forever.) Obviously the ramifications of genetically resensitizing your body to growth on a childhood/fetal level isn't as promising as it is daunting and risky.

Tazmetostat, selective re-activation of pubertal genes >>>> gene signaling for second partial puberty
Onureg, broad and indiscriminate re-activation of core developmental genes

Making vorinostat bioavailable (will need to source raw powder)
Tazmetostat bottles are already formulated, expensive but feasible for the employed.
Onureg oral version of DNTMI azacitidine probably mega expensive IDK. Aza can be pinned subcutaneously, its cheap and easy to source.

SO

If in puberty & want to "ogremaxx" HDACI

Re-run pubertal programs, Taz

Retarded? Azacitidine

GENE PCT. Post cycle to close genes and reduce genetic damage

SAMe
Methyl-B12
Methyl-Folate
Choline
Creatine

These are all supplements.

Thats all for now, good luck.

1758423426392
 
Last edited:
  • +1
Reactions: hamiwts and CeoVlad
will running romosozumab before reaching desired height hinder reaching goal height. And can i run my vorinostat and tazemetostat at same time?
 
No gatekeeping

In minecraft

follow up of: https://looksmax.org/threads/esoteric-framecel-heightcel-drug-thread.1502129/

Relevant growth related pathways
GH/IGF1 Axis (growth hormone) Stimulator
TGF Beta. similar to myostatin/follistatin muscle cap but de
als with bones as well. Sclupts & stops growth. Regulator
WNT/B cantenin
. Stimulator
FGFR
. Regulator
ESTROGEN.
Not a growth pathway but probably the most important thing to manage when comes to longitudinal growth as it is the major reason growth plates ossify and longitudinal growth stops

These pathways are dictated by genetic expression

Most important pathway is GH/IGF1.

GH/IGF High dose exogenous HGH (8-10) IU/day combined with high protein diet consisting of full amino acid profile. Whey works. 1-1.5g/lb.

TGFB pirfenidone & losartan. Pirfenidone is an anti fibrotic medication used to treat tissue scarring. Short half life. Needs to be dosed 3x/day 600mg per dose. There isn't really any effective affordable way of downregulating TGFB. Losartan & Pirfenidone are the best bet.

WNTB cantenin. KY19382 either injected subcutaneously at 0.25mg pharmaceutical grade or ~0.80mg raw powder ingested orally. see, Literal heightpills 2. ROMOSOZUMAB, Medically approved WNT/B cantenin pathway modulator. 210MG/ injection every month. Carcinogenic, has a maximum of 2 years lifetime use. Will post about it in thread later. KY19832 has better prospects for height gain because of how it targets WNTB, Romo will just make you wide. Easy to source, doesn't decay while being shipped. Kind of expensive ~$400usd/mo

FGFR. Infigratinib. Universally targets FGFR which targets FGFR 3, A mutation of Fibroblast growth factor 3 is what causes dwarfism so inhibition of it allows for normal growth. See, literal heightpills. Pan FGFR inhibition can cause significant vision issues. low dose, not using it chronically, temporarily inhibiting FGFR during the beginning of cycles to kickstart osteoblast proliferation (growing bones) with less resistance from FGFR.

ESTROGEN. If growth plates are open, estrogen will close them. There are a myriad of signals the body can produce that tell growth plates to close but if there is no estrogen the growth plates will not close. Letrozole is the medical gold standard for keeping growth plates open. I mentioned before in an older thread that estrogen is an anti resorptive. It prevents the breaking down of bone. Its crucial for libido, bone health, joint health, brain health, mood regulation. Insane and retarded. So we can't completely eradicate it, it is simply not worth the height gain if any. Raloxifene is a SERM synthetic estrogen modulator that mimics estrogens effects but seems to have negligible effects on growth plates. If that works, it will be the standard for vertical growth as the primary drawback from the use of aromatase inhibitors is how crucial estrogen is for normal function.

High dose androgens during development for male dimorphism

Testosterone has a 1:1 androgenic to anabolic ratio. Anabolism deals with muscle growth, Androgenics deal with dimorphism. Things like fat redistribution, facial hair, even the hooding of eyebrows(I think), secondary sexual characteristics, masculine growth (skeletal V-taper,) deepening of voice, and so on and so forth.

Androgens work synergistically with HGH for growth. Both stimulate osteoblast proliferation, Gear increases height velocity, increase in bone mineral density.

Growth is, low androgens >>> GH starts increasing, sustained linear growth >>> then puberty, high androgens, high GH, Height velocity increases, grow bigger faster >>> tail end of growth, GH decreases, androgens increase, estrogen feedback closes growth plates

Suppress estrogen to abnormal levels while keeping GH and androgens at supraphysiological levels and you will have supraphysiological growth (assuming you are not too old, 13-24, 13-22 whatever)

Trenbolone enanthate & testosterone enanthate

Tren is a non aromatizing steroid originally intended for cattle with a 5:5 androgenic anabolic ratio.
has a harsh side effect profile making it unfit for medical use.

So why use it? It lowers protein requirement for growth and doesn't aromatize which means you don't need to use as much aromatase inhibitors. If you wanted something like the benefits of a gram of test a week without the gram equivalent of DHT you could cut it with 500 test 100 tren which would produce similar results with less hairloss risk.

Testosterone enanthate is just basic primary male sex hormone complete with downstream hormonal profile. DHT is a downstream of Testosterone at a maybe (20%) conversion rate that drives dimorphism MORE than testosterone dose with a 5:0 Androgenic to anabolic ratio. It is the primary cause of hairloss in men.

Testosterone is the best steroid because of the downstream profile. Your brain will develop differently, you will think differently if you are on man made steroid derivative. Enanthate is the ester that extends the half life of the androgen in your body. Injections should be every 4-5 days.

Rest of steroids have their place but we dont care

Androgen ancillaries

Losartan/Telmisartan (blood pressure v important)
GHK CU (skin)
AI's (estrogen management)
Dutasteride/finasteride Hairloss, + skin protection from supraphysiological DHT levels
Topical RU58841, for hairloss. Anti androgen that will prevent hairloss from any androgen
Blood pressure cuff for blood pressure obv
HCG to maintain testicular function. Infertility from steroids is largely cope. HMG is more effective than HCG if you are worried.

Dimorphism is about bones, not muscle. How do we drive a pro osteogenic environment?

1. Prevent resorption using DHT & Estrogen or a synthetic estrogen like raloxifene, Anti resorption drugs like Alendronate
2. HGH & androgens
3. Mechanical tension, exercise
4. diet > High protein, full amino acid profile to fully utilize HGH dosages, Vitamin K2 MK7, Zinc, Calcium, Vit D, & Magnesium

BONE DRUGS

PTH analogs abaloparatide and teriparatide.


Parathyroid hormone analogs cause bone resorption (the breaking down of bones) but then stimulate osteoblast proliferation that outweighs the resorption resulting in a net gain of bone.

Teriparatide is the worse, more risky of the two and should only be used if you have an adverse reaction to abaloparatide. Like romosozumab, these are carcinogenic and have a maximum lifetime use of 2 years. The body will begin to break down the bone built by PTH analogs after treatment so use an anti resorptive drug like alendronate for a literal year.

ANTI RESORPTION

Is severely underrated in bone growth as androgens don't preserve bone, they build it. Raloxifene, estrogen, (DHT, is unique in that sense because it has been shown to retain bone mineral density in the absence of both estrogen in testosterone,) and the Bisphosphonate Alendronate. Preventing resorption means more of our androgen GH gains will go towards accruing mass rather than fighting against the breakdown.

ROMOSOZUMAB

Is the most effective bone drug for thickening/widening. It should be used (if at all) after you reach your desired height because its much better at making you wider, not so much taller. PTH analogs are better for making you taller. Carcinogenic, 2 year lifetime use, Yes it is more effective than PTH analogs

TETRANALOGS/MMP INHIBITORS

THREAD. MMP'S break down collagen scaffolding, Inflammation via gear upregulates them. Low dose MMP inhibitors Doxycycline and minocycline prevent this resulting in more bone gains

HOLY GRAIL OGRE GENE DRUGS

remember, These pathways are dictated by genetic expression.

So instead of individually trying to downregulate or upregulate them, why not just alter the gene expression? Obv this is riskiest, epigenetic permanent effects. WE BALL

Vorinostat enjoyers

3 relevant gene drugs available on open market

1. HDAC inhibitor Vorinostat
2. EZH2 inhibitor Tazmetostat
3. DNMT inhibitor azacitidine & oral azacitidine Onureg

Vorinostat
enhances gene transcription. Allows for more genetic expression, indiscriminately. People pair it with androgens to enhance their masculinizing effect. Think of vorinostat as a megaphone. Though because it universally allows for more genetic expression its not just used for androgens. Chronic use is bad for bones, bad for growth, not to mention ur genes being "unlocked" for long period of time thats obviously not good. I would recommend you cycle it but its anti osteogenic effects on bones and such I think is just being drastically outperformed by the amount of gear these people are blasting and thats how they get away with it.

"Though because it universally allows for more genetic expression its not just used for androgens"

Cognitive Improvement by Vorinostat through Modulation of Endoplasmic Reticulum Stress in a Corticosterone-Induced Chronic Stress Model in Mice
Upregulation of HDAC9 in hippocampal neurons mediates depression-like behaviours (eg. Anhedonia) by inhibiting ANXA2 degradation

Vorinostat (SAHA) May Exert Its Antidepressant-Like Effects Through the Modulation of Oxidative Stress Pathways
Vorinostat Corrects Cognitive and Non-Cognitive Symptoms in a Mouse Model of Fragile X Syndrome
The histone deacetylase inhibitor Vorinostat (SAHA ) alleviates depression-like behavior and normalizes epigenetic changes in the hippocampus during ethanol withdrawal
Early-life stress-induced visceral hypersensitivity and anxiety behavior is reversed by histone deacetylase inhibition (Vorinostat).
Suberoylanilide hydroxamic acid attenuates cognitive impairment in offspring caused by maternal surgery during mid-pregnancy
(Vorinostat) SAHA Improves Depressive Symptoms, Cognitive Impairment and Oxidative Stress: Rise of a New Antidepressant Class

TAZMETOSTAT
removes the epigenetic brake on growth genes present during puberty. That re-exposes the programs that let GH and androgens drive growth and masculinization. In adulthood, EZH2 shuts these genes down, the body genetically shifts into maintenance mode instead of growth. So basically, we turn the programs on, blast androgens, BOOM, second puberty. Whereas vstat will exaggerate this growth.

Taz is generally well tolerated, easier to source, and less risky and more specific than vorinostat though they serve two different purposes. There are some drugs that are just better made than others and taz is one of them.

DNMTI azacitidine & oral azacitidine Onureg

stronger more broad version of tazmetosat. Activates PRE PUBERTY growth programs (such as IGF2 natal version of IGF1 which shuts down in puberty forever.) Obviously the ramifications of genetically resensitizing your body to growth on a childhood/fetal level isn't as promising as it is daunting and risky.

Tazmetostat, selective re-activation of pubertal genes >>>> gene signaling for second partial puberty
Onureg, broad and indiscriminate re-activation of core developmental genes

Making vorinostat bioavailable (will need to source raw powder)
Tazmetostat bottles are already formulated, expensive but feasible for the employed.
Onureg oral version of DNTMI azacitidine probably mega expensive IDK. Aza can be pinned subcutaneously, its cheap and easy to source.

SO

If in puberty & want to "ogremaxx" HDACI

Re-run pubertal programs, Taz

Retarded? Azacitidine

GENE PCT. Post cycle to close genes and reduce genetic damage

SAMe
Methyl-B12
Methyl-Folate
Choline
Creatine

These are all supplements.

Thats all for now, good luck.

View attachment 4131629
Mirin the thread; the real question here though is how many people are actually gonna hop on even one of these :lul:
 
No gatekeeping

In minecraft

follow up of: https://looksmax.org/threads/esoteric-framecel-heightcel-drug-thread.1502129/

Relevant growth related pathways
GH/IGF1 Axis (growth hormone) Stimulator
TGF Beta. similar to myostatin/follistatin muscle cap but de
als with bones as well. Sclupts & stops growth. Regulator
WNT/B cantenin
. Stimulator
FGFR
. Regulator
ESTROGEN.
Not a growth pathway but probably the most important thing to manage when comes to longitudinal growth as it is the major reason growth plates ossify and longitudinal growth stops

These pathways are dictated by genetic expression

Most important pathway is GH/IGF1.

GH/IGF High dose exogenous HGH (8-10) IU/day combined with high protein diet consisting of full amino acid profile. Whey works. 1-1.5g/lb.

TGFB pirfenidone & losartan. Pirfenidone is an anti fibrotic medication used to treat tissue scarring. Short half life. Needs to be dosed 3x/day 600mg per dose. There isn't really any effective affordable way of downregulating TGFB. Losartan & Pirfenidone are the best bet.

WNTB cantenin. KY19382 either injected subcutaneously at 0.25mg pharmaceutical grade or ~0.80mg raw powder ingested orally. see, Literal heightpills 2. ROMOSOZUMAB, Medically approved WNT/B cantenin pathway modulator. 210MG/ injection every month. Carcinogenic, has a maximum of 2 years lifetime use. Will post about it in thread later. KY19832 has better prospects for height gain because of how it targets WNTB, Romo will just make you wide. Easy to source, doesn't decay while being shipped. Kind of expensive ~$400usd/mo

FGFR. Infigratinib. Universally targets FGFR which targets FGFR 3, A mutation of Fibroblast growth factor 3 is what causes dwarfism so inhibition of it allows for normal growth. See, literal heightpills. Pan FGFR inhibition can cause significant vision issues. low dose, not using it chronically, temporarily inhibiting FGFR during the beginning of cycles to kickstart osteoblast proliferation (growing bones) with less resistance from FGFR.

ESTROGEN. If growth plates are open, estrogen will close them. There are a myriad of signals the body can produce that tell growth plates to close but if there is no estrogen the growth plates will not close. Letrozole is the medical gold standard for keeping growth plates open. I mentioned before in an older thread that estrogen is an anti resorptive. It prevents the breaking down of bone. Its crucial for libido, bone health, joint health, brain health, mood regulation. Insane and retarded. So we can't completely eradicate it, it is simply not worth the height gain if any. Raloxifene is a SERM synthetic estrogen modulator that mimics estrogens effects but seems to have negligible effects on growth plates. If that works, it will be the standard for vertical growth as the primary drawback from the use of aromatase inhibitors is how crucial estrogen is for normal function.

High dose androgens during development for male dimorphism

Testosterone has a 1:1 androgenic to anabolic ratio. Anabolism deals with muscle growth, Androgenics deal with dimorphism. Things like fat redistribution, facial hair, even the hooding of eyebrows(I think), secondary sexual characteristics, masculine growth (skeletal V-taper,) deepening of voice, and so on and so forth.

Androgens work synergistically with HGH for growth. Both stimulate osteoblast proliferation, Gear increases height velocity, increase in bone mineral density.

Growth is, low androgens >>> GH starts increasing, sustained linear growth >>> then puberty, high androgens, high GH, Height velocity increases, grow bigger faster >>> tail end of growth, GH decreases, androgens increase, estrogen feedback closes growth plates

Suppress estrogen to abnormal levels while keeping GH and androgens at supraphysiological levels and you will have supraphysiological growth (assuming you are not too old, 13-24, 13-22 whatever)

Trenbolone enanthate & testosterone enanthate

Tren is a non aromatizing steroid originally intended for cattle with a 5:5 androgenic anabolic ratio.
has a harsh side effect profile making it unfit for medical use.

So why use it? It lowers protein requirement for growth and doesn't aromatize which means you don't need to use as much aromatase inhibitors. If you wanted something like the benefits of a gram of test a week without the gram equivalent of DHT you could cut it with 500 test 100 tren which would produce similar results with less hairloss risk.

Testosterone enanthate is just basic primary male sex hormone complete with downstream hormonal profile. DHT is a downstream of Testosterone at a maybe (20%) conversion rate that drives dimorphism MORE than testosterone dose with a 5:0 Androgenic to anabolic ratio. It is the primary cause of hairloss in men.

Testosterone is the best steroid because of the downstream profile. Your brain will develop differently, you will think differently if you are on man made steroid derivative. Enanthate is the ester that extends the half life of the androgen in your body. Injections should be every 4-5 days.

Rest of steroids have their place but we dont care

Androgen ancillaries

Losartan/Telmisartan (blood pressure v important)
GHK CU (skin)
AI's (estrogen management)
Dutasteride/finasteride Hairloss, + skin protection from supraphysiological DHT levels
Topical RU58841, for hairloss. Anti androgen that will prevent hairloss from any androgen
Blood pressure cuff for blood pressure obv
HCG to maintain testicular function. Infertility from steroids is largely cope. HMG is more effective than HCG if you are worried.

Dimorphism is about bones, not muscle. How do we drive a pro osteogenic environment?

1. Prevent resorption using DHT & Estrogen or a synthetic estrogen like raloxifene, Anti resorption drugs like Alendronate
2. HGH & androgens
3. Mechanical tension, exercise
4. diet > High protein, full amino acid profile to fully utilize HGH dosages, Vitamin K2 MK7, Zinc, Calcium, Vit D, & Magnesium

BONE DRUGS

PTH analogs abaloparatide and teriparatide.


Parathyroid hormone analogs cause bone resorption (the breaking down of bones) but then stimulate osteoblast proliferation that outweighs the resorption resulting in a net gain of bone.

Teriparatide is the worse, more risky of the two and should only be used if you have an adverse reaction to abaloparatide. Like romosozumab, these are carcinogenic and have a maximum lifetime use of 2 years. The body will begin to break down the bone built by PTH analogs after treatment so use an anti resorptive drug like alendronate for a literal year.

ANTI RESORPTION

Is severely underrated in bone growth as androgens don't preserve bone, they build it. Raloxifene, estrogen, (DHT, is unique in that sense because it has been shown to retain bone mineral density in the absence of both estrogen in testosterone,) and the Bisphosphonate Alendronate. Preventing resorption means more of our androgen GH gains will go towards accruing mass rather than fighting against the breakdown.

ROMOSOZUMAB

Is the most effective bone drug for thickening/widening. It should be used (if at all) after you reach your desired height because its much better at making you wider, not so much taller. PTH analogs are better for making you taller. Carcinogenic, 2 year lifetime use, Yes it is more effective than PTH analogs

TETRANALOGS/MMP INHIBITORS

THREAD. MMP'S break down collagen scaffolding, Inflammation via gear upregulates them. Low dose MMP inhibitors Doxycycline and minocycline prevent this resulting in more bone gains

HOLY GRAIL OGRE GENE DRUGS

remember, These pathways are dictated by genetic expression.

So instead of individually trying to downregulate or upregulate them, why not just alter the gene expression? Obv this is riskiest, epigenetic permanent effects. WE BALL

Vorinostat enjoyers

3 relevant gene drugs available on open market

1. HDAC inhibitor Vorinostat
2. EZH2 inhibitor Tazmetostat
3. DNMT inhibitor azacitidine & oral azacitidine Onureg

Vorinostat
enhances gene transcription. Allows for more genetic expression, indiscriminately. People pair it with androgens to enhance their masculinizing effect. Think of vorinostat as a megaphone. Though because it universally allows for more genetic expression its not just used for androgens. Chronic use is bad for bones, bad for growth, not to mention ur genes being "unlocked" for long period of time thats obviously not good. I would recommend you cycle it but its anti osteogenic effects on bones and such I think is just being drastically outperformed by the amount of gear these people are blasting and thats how they get away with it.

"Though because it universally allows for more genetic expression its not just used for androgens"

Cognitive Improvement by Vorinostat through Modulation of Endoplasmic Reticulum Stress in a Corticosterone-Induced Chronic Stress Model in Mice
Upregulation of HDAC9 in hippocampal neurons mediates depression-like behaviours (eg. Anhedonia) by inhibiting ANXA2 degradation

Vorinostat (SAHA) May Exert Its Antidepressant-Like Effects Through the Modulation of Oxidative Stress Pathways
Vorinostat Corrects Cognitive and Non-Cognitive Symptoms in a Mouse Model of Fragile X Syndrome
The histone deacetylase inhibitor Vorinostat (SAHA ) alleviates depression-like behavior and normalizes epigenetic changes in the hippocampus during ethanol withdrawal
Early-life stress-induced visceral hypersensitivity and anxiety behavior is reversed by histone deacetylase inhibition (Vorinostat).
Suberoylanilide hydroxamic acid attenuates cognitive impairment in offspring caused by maternal surgery during mid-pregnancy
(Vorinostat) SAHA Improves Depressive Symptoms, Cognitive Impairment and Oxidative Stress: Rise of a New Antidepressant Class

TAZMETOSTAT
removes the epigenetic brake on growth genes present during puberty. That re-exposes the programs that let GH and androgens drive growth and masculinization. In adulthood, EZH2 shuts these genes down, the body genetically shifts into maintenance mode instead of growth. So basically, we turn the programs on, blast androgens, BOOM, second puberty. Whereas vstat will exaggerate this growth.

Taz is generally well tolerated, easier to source, and less risky and more specific than vorinostat though they serve two different purposes. There are some drugs that are just better made than others and taz is one of them.

DNMTI azacitidine & oral azacitidine Onureg

stronger more broad version of tazmetosat. Activates PRE PUBERTY growth programs (such as IGF2 natal version of IGF1 which shuts down in puberty forever.) Obviously the ramifications of genetically resensitizing your body to growth on a childhood/fetal level isn't as promising as it is daunting and risky.

Tazmetostat, selective re-activation of pubertal genes >>>> gene signaling for second partial puberty
Onureg, broad and indiscriminate re-activation of core developmental genes

Making vorinostat bioavailable (will need to source raw powder)
Tazmetostat bottles are already formulated, expensive but feasible for the employed.
Onureg oral version of DNTMI azacitidine probably mega expensive IDK. Aza can be pinned subcutaneously, its cheap and easy to source.

SO

If in puberty & want to "ogremaxx" HDACI

Re-run pubertal programs, Taz

Retarded? Azacitidine

GENE PCT. Post cycle to close genes and reduce genetic damage

SAMe
Methyl-B12
Methyl-Folate
Choline
Creatine

These are all supplements.

Thats all for now, good luck.

View attachment 4131629
Theoretical effects of re activating natal IGF-2 via azacitidine

GH converts to IGF1 which is primary pathway for pubertal/adult growth in human body

2-3x stronger than GH for craniofacial bone remodeling
2x stronger than GH for periosteal bone thickening
negligible for muscle hypertrophy
IGF2 REGULATES facial bone structure development in children. GH does not.

This could theoretically "re-roll" musculature and skeletal structure physique through re structuring the makeup from a top down perspective. The genetic pathway. Because IGF2 regulates growth in such a significant manner, it can SHIFT skeletal and muscular proportions. obv we are blasting androgens it will bias them towards masculine proportioning.

The most obvious should be facial remodeling.
 
No gatekeeping

In minecraft

follow up of: https://looksmax.org/threads/esoteric-framecel-heightcel-drug-thread.1502129/

Relevant growth related pathways
GH/IGF1 Axis (growth hormone) Stimulator
TGF Beta. similar to myostatin/follistatin muscle cap but de
als with bones as well. Sclupts & stops growth. Regulator
WNT/B cantenin
. Stimulator
FGFR
. Regulator
ESTROGEN.
Not a growth pathway but probably the most important thing to manage when comes to longitudinal growth as it is the major reason growth plates ossify and longitudinal growth stops

These pathways are dictated by genetic expression

Most important pathway is GH/IGF1.

GH/IGF High dose exogenous HGH (8-10) IU/day combined with high protein diet consisting of full amino acid profile. Whey works. 1-1.5g/lb.

TGFB pirfenidone & losartan. Pirfenidone is an anti fibrotic medication used to treat tissue scarring. Short half life. Needs to be dosed 3x/day 600mg per dose. There isn't really any effective affordable way of downregulating TGFB. Losartan & Pirfenidone are the best bet.

WNTB cantenin. KY19382 either injected subcutaneously at 0.25mg pharmaceutical grade or ~0.80mg raw powder ingested orally. see, Literal heightpills 2. ROMOSOZUMAB, Medically approved WNT/B cantenin pathway modulator. 210MG/ injection every month. Carcinogenic, has a maximum of 2 years lifetime use. Will post about it in thread later. KY19832 has better prospects for height gain because of how it targets WNTB, Romo will just make you wide. Easy to source, doesn't decay while being shipped. Kind of expensive ~$400usd/mo

FGFR. Infigratinib. Universally targets FGFR which targets FGFR 3, A mutation of Fibroblast growth factor 3 is what causes dwarfism so inhibition of it allows for normal growth. See, literal heightpills. Pan FGFR inhibition can cause significant vision issues. low dose, not using it chronically, temporarily inhibiting FGFR during the beginning of cycles to kickstart osteoblast proliferation (growing bones) with less resistance from FGFR.

ESTROGEN. If growth plates are open, estrogen will close them. There are a myriad of signals the body can produce that tell growth plates to close but if there is no estrogen the growth plates will not close. Letrozole is the medical gold standard for keeping growth plates open. I mentioned before in an older thread that estrogen is an anti resorptive. It prevents the breaking down of bone. Its crucial for libido, bone health, joint health, brain health, mood regulation. Insane and retarded. So we can't completely eradicate it, it is simply not worth the height gain if any. Raloxifene is a SERM synthetic estrogen modulator that mimics estrogens effects but seems to have negligible effects on growth plates. If that works, it will be the standard for vertical growth as the primary drawback from the use of aromatase inhibitors is how crucial estrogen is for normal function.

High dose androgens during development for male dimorphism

Testosterone has a 1:1 androgenic to anabolic ratio. Anabolism deals with muscle growth, Androgenics deal with dimorphism. Things like fat redistribution, facial hair, even the hooding of eyebrows(I think), secondary sexual characteristics, masculine growth (skeletal V-taper,) deepening of voice, and so on and so forth.

Androgens work synergistically with HGH for growth. Both stimulate osteoblast proliferation, Gear increases height velocity, increase in bone mineral density.

Growth is, low androgens >>> GH starts increasing, sustained linear growth >>> then puberty, high androgens, high GH, Height velocity increases, grow bigger faster >>> tail end of growth, GH decreases, androgens increase, estrogen feedback closes growth plates

Suppress estrogen to abnormal levels while keeping GH and androgens at supraphysiological levels and you will have supraphysiological growth (assuming you are not too old, 13-24, 13-22 whatever)

Trenbolone enanthate & testosterone enanthate

Tren is a non aromatizing steroid originally intended for cattle with a 5:5 androgenic anabolic ratio.
has a harsh side effect profile making it unfit for medical use.

So why use it? It lowers protein requirement for growth and doesn't aromatize which means you don't need to use as much aromatase inhibitors. If you wanted something like the benefits of a gram of test a week without the gram equivalent of DHT you could cut it with 500 test 100 tren which would produce similar results with less hairloss risk.

Testosterone enanthate is just basic primary male sex hormone complete with downstream hormonal profile. DHT is a downstream of Testosterone at a maybe (20%) conversion rate that drives dimorphism MORE than testosterone dose with a 5:0 Androgenic to anabolic ratio. It is the primary cause of hairloss in men.

Testosterone is the best steroid because of the downstream profile. Your brain will develop differently, you will think differently if you are on man made steroid derivative. Enanthate is the ester that extends the half life of the androgen in your body. Injections should be every 4-5 days.

Rest of steroids have their place but we dont care

Androgen ancillaries

Losartan/Telmisartan (blood pressure v important)
GHK CU (skin)
AI's (estrogen management)
Dutasteride/finasteride Hairloss, + skin protection from supraphysiological DHT levels
Topical RU58841, for hairloss. Anti androgen that will prevent hairloss from any androgen
Blood pressure cuff for blood pressure obv
HCG to maintain testicular function. Infertility from steroids is largely cope. HMG is more effective than HCG if you are worried.

Dimorphism is about bones, not muscle. How do we drive a pro osteogenic environment?

1. Prevent resorption using DHT & Estrogen or a synthetic estrogen like raloxifene, Anti resorption drugs like Alendronate
2. HGH & androgens
3. Mechanical tension, exercise
4. diet > High protein, full amino acid profile to fully utilize HGH dosages, Vitamin K2 MK7, Zinc, Calcium, Vit D, & Magnesium

BONE DRUGS

PTH analogs abaloparatide and teriparatide.


Parathyroid hormone analogs cause bone resorption (the breaking down of bones) but then stimulate osteoblast proliferation that outweighs the resorption resulting in a net gain of bone.

Teriparatide is the worse, more risky of the two and should only be used if you have an adverse reaction to abaloparatide. Like romosozumab, these are carcinogenic and have a maximum lifetime use of 2 years. The body will begin to break down the bone built by PTH analogs after treatment so use an anti resorptive drug like alendronate for a literal year.

ANTI RESORPTION

Is severely underrated in bone growth as androgens don't preserve bone, they build it. Raloxifene, estrogen, (DHT, is unique in that sense because it has been shown to retain bone mineral density in the absence of both estrogen in testosterone,) and the Bisphosphonate Alendronate. Preventing resorption means more of our androgen GH gains will go towards accruing mass rather than fighting against the breakdown.

ROMOSOZUMAB

Is the most effective bone drug for thickening/widening. It should be used (if at all) after you reach your desired height because its much better at making you wider, not so much taller. PTH analogs are better for making you taller. Carcinogenic, 2 year lifetime use, Yes it is more effective than PTH analogs

TETRANALOGS/MMP INHIBITORS

THREAD. MMP'S break down collagen scaffolding, Inflammation via gear upregulates them. Low dose MMP inhibitors Doxycycline and minocycline prevent this resulting in more bone gains

HOLY GRAIL OGRE GENE DRUGS

remember, These pathways are dictated by genetic expression.

So instead of individually trying to downregulate or upregulate them, why not just alter the gene expression? Obv this is riskiest, epigenetic permanent effects. WE BALL

Vorinostat enjoyers

3 relevant gene drugs available on open market

1. HDAC inhibitor Vorinostat
2. EZH2 inhibitor Tazmetostat
3. DNMT inhibitor azacitidine & oral azacitidine Onureg

Vorinostat
enhances gene transcription. Allows for more genetic expression, indiscriminately. People pair it with androgens to enhance their masculinizing effect. Think of vorinostat as a megaphone. Though because it universally allows for more genetic expression its not just used for androgens. Chronic use is bad for bones, bad for growth, not to mention ur genes being "unlocked" for long period of time thats obviously not good. I would recommend you cycle it but its anti osteogenic effects on bones and such I think is just being drastically outperformed by the amount of gear these people are blasting and thats how they get away with it.

"Though because it universally allows for more genetic expression its not just used for androgens"

Cognitive Improvement by Vorinostat through Modulation of Endoplasmic Reticulum Stress in a Corticosterone-Induced Chronic Stress Model in Mice
Upregulation of HDAC9 in hippocampal neurons mediates depression-like behaviours (eg. Anhedonia) by inhibiting ANXA2 degradation

Vorinostat (SAHA) May Exert Its Antidepressant-Like Effects Through the Modulation of Oxidative Stress Pathways
Vorinostat Corrects Cognitive and Non-Cognitive Symptoms in a Mouse Model of Fragile X Syndrome
The histone deacetylase inhibitor Vorinostat (SAHA ) alleviates depression-like behavior and normalizes epigenetic changes in the hippocampus during ethanol withdrawal
Early-life stress-induced visceral hypersensitivity and anxiety behavior is reversed by histone deacetylase inhibition (Vorinostat).
Suberoylanilide hydroxamic acid attenuates cognitive impairment in offspring caused by maternal surgery during mid-pregnancy
(Vorinostat) SAHA Improves Depressive Symptoms, Cognitive Impairment and Oxidative Stress: Rise of a New Antidepressant Class

TAZMETOSTAT
removes the epigenetic brake on growth genes present during puberty. That re-exposes the programs that let GH and androgens drive growth and masculinization. In adulthood, EZH2 shuts these genes down, the body genetically shifts into maintenance mode instead of growth. So basically, we turn the programs on, blast androgens, BOOM, second puberty. Whereas vstat will exaggerate this growth.

Taz is generally well tolerated, easier to source, and less risky and more specific than vorinostat though they serve two different purposes. There are some drugs that are just better made than others and taz is one of them.

DNMTI azacitidine & oral azacitidine Onureg

stronger more broad version of tazmetosat. Activates PRE PUBERTY growth programs (such as IGF2 natal version of IGF1 which shuts down in puberty forever.) Obviously the ramifications of genetically resensitizing your body to growth on a childhood/fetal level isn't as promising as it is daunting and risky.

Tazmetostat, selective re-activation of pubertal genes >>>> gene signaling for second partial puberty
Onureg, broad and indiscriminate re-activation of core developmental genes

Making vorinostat bioavailable (will need to source raw powder)
Tazmetostat bottles are already formulated, expensive but feasible for the employed.
Onureg oral version of DNTMI azacitidine probably mega expensive IDK. Aza can be pinned subcutaneously, its cheap and easy to source.

SO

If in puberty & want to "ogremaxx" HDACI

Re-run pubertal programs, Taz

Retarded? Azacitidine

GENE PCT. Post cycle to close genes and reduce genetic damage

SAMe
Methyl-B12
Methyl-Folate
Choline
Creatine

These are all supplements.

Thats all for now, good luck.

View attachment 4131629
 

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Theoretical effects of re activating natal IGF-2 via azacitidine

GH converts to IGF1 which is primary pathway for pubertal/adult growth in human body

2-3x stronger than GH for craniofacial bone remodeling
2x stronger than GH for periosteal bone thickening
negligible for muscle hypertrophy
IGF2 REGULATES facial bone structure development in children. GH does not.

This could theoretically "re-roll" musculature and skeletal structure physique through re structuring the makeup from a top down perspective. The genetic pathway. Because IGF2 regulates growth in such a significant manner, it can SHIFT skeletal and muscular proportions. obv we are blasting androgens it will bias them towards masculine proportioning.

The most obvious should be facial remodeling.
Cope
 

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