Masteron vs halo for dimo

[burntboats]

looking for some dimo right now and stanolone is virtually impossible to source here in canada, at least as far as my research went, as nobody has it in their catalogue. Would mast or halo provide the same degree of dimo facial bone wise/ shoulder broadness as dht? im also looking to run these compounds without a base to avoid local aromatization at gps

 

[India lover 52]

hmm a compound with an androgenic rating of 25 or one of the most liver toxic compounds you can't run for more than a few weeks

DHT derrivs only provide any androgenic activity by binding to SHBG and freeing up more DHT and free test in your system

if you want andrognecitiy then high test or tren are the only ways to go if your worried about muhhh plates or whatever take letrozole which pretty much turns off your estrogen or use tren + trt

obviously pure dht would work too but you have to run hundreds of mgs to saturate 3α-HSD and allow the dht to bind to androgen receptors in skeletal muscle plus its expensive as fuck

 

[burntboats]

hmm a compound with an androgenic rating of 25 or one of the most liver toxic compounds you can't run for more than a few weeks

DHT derrivs only provide any androgenic activity by binding to SHBG and freeing up more DHT and free test in your system

if you want andrognecitiy then high test or tren are the only ways to go if your worried about muhhh plates or whatever take letrozole which pretty much turns off your estrogen or use tren + trt

obviously pure dht would work too but you have to run hundreds of mgs to saturate 3α-HSD and allow the dht to bind to androgen receptors in skeletal muscle plus its expensive as fuck

im surprised to hear people say that dht is expensive as from what I gathered it should be easy as hell to synthesize in a lab and you get like 80+ yield.
What about dht gel? I heard plenty of people say they got considerable facial bone gains from it.
From what I understand letrzole systemically lowers (or even shuts down as you said) estrogen conversion but doesn't stop local aromatization in growth plates, wouldn't that stunt growth? my only concern is dimo tbh (facial structure/frame/height) that's why im looking to avoid stuff like tren but also I heard a lot of people recommend against it

 

[India lover 52]

im surprised to hear people say that dht is expensive as from what I gathered it should be easy as hell to synthesize in a lab and you get like 80+ yield.
What about dht gel? I heard plenty of people say they got considerable facial bone gains from it.
From what I understand letrzole systemically lowers (or even shuts down as you said) estrogen conversion but doesn't stop local aromatization in growth plates, wouldn't that stunt growth? my only concern is dimo tbh (facial structure/frame/height) that's why im looking to avoid stuff like tren but also I heard a lot of people recommend against it

topical steroids have horrible blood level stability and exert mostly local effects instead of entering circulation

you read a troll post about someone trying to convince you to rub dht gel on your face, which would cause collagen loss and extreme acne


... what do you think local aromatization is? there are not many aromatase enzymes in your growth plates in the first place the majority are in subq fat tissue but using a fully unselective ai which nukes over 99% of aromatase enzymes in your body would nuke the AE's in your growth plates too... which is not really a good thing as you need estrogen for igf conversion and nuking it that hard with letrozole would be a net negative for bone growth/formation unless you were running grams of testosterone with it

tren or high test for dimo, tren upregulates igf 1 through multiple mechanisms so it is more potent for bone growth, it also has extreme nutrient partitioning effects and does not bloat you like testosterone, its a little bit worse for your brain than test what usually do is low tren + high test for some of the tren benefits but having the majority of the androgenic load come from testosterone but its up to you if the tradeoff is worth it

 

[aac21]

topical steroids have horrible blood level stability and exert mostly local effects instead of entering circulation

you read a troll post about someone trying to convince you to rub dht gel on your face, which would cause collagen loss and extreme acne


... what do you think local aromatization is? there are not many aromatase enzymes in your growth plates in the first place the majority are in subq fat tissue but using a fully unselective ai which nukes over 99% of aromatase enzymes in your body would nuke the AE's in your growth plates too... which is not really a good thing as you need estrogen for igf conversion and nuking it that hard with letrozole would be a net negative for bone growth/formation unless you were running grams of testosterone with it

tren or high test for dimo, tren upregulates igf 1 through multiple mechanisms so it is more potent for bone growth, it also has extreme nutrient partitioning effects and does not bloat you like testosterone, its a little bit worse for your brain than test what usually do is low tren + high test for some of the tren benefits but having the majority of the androgenic load come from testosterone but its up to you if the tradeoff is worth it

you have good takes and points but i will correct you on some things.

halo can be taken long term on low doses and with a proper anc protocol. doctors gave it to basically toddlers and overall they were healthy after stopping.

Estrogen is involved in the GH/IGF-1 axis, and estrogen can influence GH secretion and IGF-1 biology.

But “estrogen is required for IGF conversion” isn't a correct description of the physiology.

Under supraphysiological doses of GH, (15iu ed) your IGF-1 will push the upper threshold (750 - 1050) typically. Independent of estrogen.

And no do not take grams of testosterone in the growth phase. This will seal your plates shut before you know it. Extra substrate = quicker fusion regardless of any AI. I dont care if you are taking 100mg of letrozole. (You would just die before growing taller.)

And masteron is not ran solo for dimo, its paired with proviron to lower SHBG.

Tren is obviously on a different league and doesnt pair up with typical dimo cycles unless managed exceptionally, but its obviously at a cost. Neurotoxicity, mental instability, heart problems, and many more to list. Also have to throw the kitchen sink in for the ancs on tren.

 

[burntboats]

topical steroids have horrible blood level stability and exert mostly local effects instead of entering circulation

you read a troll post about someone trying to convince you to rub dht gel on your face, which would cause collagen loss and extreme acne


... what do you think local aromatization is? there are not many aromatase enzymes in your growth plates in the first place the majority are in subq fat tissue but using a fully unselective ai which nukes over 99% of aromatase enzymes in your body would nuke the AE's in your growth plates too... which is not really a good thing as you need estrogen for igf conversion and nuking it that hard with letrozole would be a net negative for bone growth/formation unless you were running grams of testosterone with it

tren or high test for dimo, tren upregulates igf 1 through multiple mechanisms so it is more potent for bone growth, it also has extreme nutrient partitioning effects and does not bloat you like testosterone, its a little bit worse for your brain than test what usually do is low tren + high test for some of the tren benefits but having the majority of the androgenic load come from testosterone but its up to you if the tradeoff is worth it

interesting, first time hearing about estrogen playing a role in the liver igf 1 and gh secretion pathway, could you elaborate on that, and what do you mean conversion?

I have a little order some gh in the mail that's why im planning to buy some androgens along side it

is a tren only cycle a thing or is it completely not worth it? I also just read some dudes post on mtren and how it's hella potent as an androgen. and how would either of them pair up with a pan kinase inhibitor like erda? im assuming it would improve the sides since improved recovery speed and potential

 

[India lover 52]

you have good takes and points but i will correct you on some things.

halo can be taken long term on low doses and with a proper anc protocol. doctors gave it to basically toddlers and overall they were healthy after stopping.

Estrogen is involved in the GH/IGF-1 axis, and estrogen can influence GH secretion and IGF-1 biology.

But “estrogen is required for IGF conversion” isn't a correct description of the physiology.

Under supraphysiological doses of GH, (15iu ed) your IGF-1 will push the upper threshold (750 - 1050) typically. Independent of estrogen.

And no do not take grams of testosterone in the growth phase. This will seal your plates shut before you know it. Extra substrate = quicker fusion regardless of any AI. I dont care if you are taking 100mg of letrozole. (You would just die before growing taller.)

And masteron is not ran solo for dimo, its paired with proviron to lower SHBG.

Tren is obviously on a different league and doesnt pair up with typical dimo cycles unless managed exceptionally, but its obviously at a cost. Neurotoxicity, mental instability, heart problems, and many more to list. Also have to throw the kitchen sink in for the ancs on tren.

you technically CAN take halo long term if you do all of that shit but why would you? even something like winstrol would be pretty much the same as low halo but actually anabolic as well

estrogens bind to ERα in liver hepatocytes which increase SOCS-2 mRNA and protein abundance, which actually inhibit igf conversion at low doses but in superphysological doses the relationship inverts because it displaces SOCS1 and SOCS3 which are stronger JAK2 inhibitors and also binds all availble helper protiens (Elongin B/C and Cullin-5) which all couple together to form a functional E3 ubiquitin ligase ring, which destroys the gh receptor.

and even at non supraphysological doses

15 is FAR above the supraphysiological dose of hgh, yes technically your body will produce up to like 10 ius for a breif period of time between 16-17 however HGH's natural half life is 10-20 minutes while exogenus HGH's is 20-30 minutes IV, however everybody does it subq which extends the absorption half life to 2.3-5 hours because of depot pharmokenetics of subq administration and the clearence time from 1-2 hours to 12-24 hours which obviously your liver will produce more igf with a sustained hgh signal compared to natural short pulses which are rate limited by liver hepatocyte processing speed

fearmongering, letrozole doesn't do anything past its prescribed dose because it already nukes 99 something % of aromatase enzymes any more would just be causing side effects

if you did the math then running 2 grams on letrozole would aromatase less than 200mg of testosterone which is a physiological dose for some people, and if that would close your plates than everybodys plates would close as soon as they entered puberty

dnr sides tren is fun asf honestly a better reason to run it than for muhh dimo, life is about having fun after all

 

[burntboats]

you have good takes and points but i will correct you on some things.

halo can be taken long term on low doses and with a proper anc protocol. doctors gave it to basically toddlers and overall they were healthy after stopping.

Estrogen is involved in the GH/IGF-1 axis, and estrogen can influence GH secretion and IGF-1 biology.

But “estrogen is required for IGF conversion” isn't a correct description of the physiology.

Under supraphysiological doses of GH, (15iu ed) your IGF-1 will push the upper threshold (750 - 1050) typically. Independent of estrogen.

And no do not take grams of testosterone in the growth phase. This will seal your plates shut before you know it. Extra substrate = quicker fusion regardless of any AI. I dont care if you are taking 100mg of letrozole. (You would just die before growing taller.)

And masteron is not ran solo for dimo, its paired with proviron to lower SHBG.

Tren is obviously on a different league and doesnt pair up with typical dimo cycles unless managed exceptionally, but its obviously at a cost. Neurotoxicity, mental instability, heart problems, and many more to list. Also have to throw the kitchen sink in for the ancs on tren.

thanks for your insight too. that's pretty much what I heard about tren.
I'm planning to do about 10 iu's of gh so that's pretty close to the upper threshold like you said, so im assuming I won't have to worry about estrogen being too low?

could a mast and mesterolone (provision) cycle only pass for dimo? im assuming it'll also have an estrogen suppressive effect because it'll lower total and free t right?

that's why I appealed of stanolone(DHT) at first cuz it would help with dimo AND suppress estrogen so I could save on ai's. also it doesn't even have to seem side effects of ed or depression or testosterone production shutdown once the dot clears the system or anything like that usually comes with synthetic aas like tren but since I can't effectively source it I turned to dht derivatives ( aka Masteron/halostatin)

also do you have any knowledge or a hypothesis if it would it be a good idea to run it with a pan fgfr kinase inhibitor like erda or (more selective) infigratinib with mast and prov??? or would It be better to run erda with gh and then stop the erda and keep the gh but add mast and prov to recover from the sides of erda?

im kind of going above and beyond trying to optimize height here considering my advanced bone age

 

[India lover 52]

interesting, first time hearing about estrogen playing a role in the liver igf 1 and gh secretion pathway, could you elaborate on that, and what do you mean conversion?

I have a little order some gh in the mail that's why im planning to buy some androgens along side it

is a tren only cycle a thing or is it completely not worth it? I also just read some dudes post on mtren and how it's hella potent as an androgen. and how would either of them pair up with a pan kinase inhibitor like erda? im assuming it would improve the sides since improved recovery speed and potential

read my post above and in addition to that high doses of testosterone will cause the hypothalamus and pituitary to produce more HGH however this effect does not happen if you are taking a high dose aromatase inhibitor because it is reliant on local aromatisation in the brain

yes tren + trt is a thing its usually used as a bare bones cut stack because you will loose almost 0 muscle at any caloric intake and if your not worried about gaining mass you can starvemaxx without withering away and eat like 500 cals a day

mtren is a meme its just liver toxic tren JFL literally 0 reason to ever run it compared to a equivalent dose of tren, even if your taking it pre wo tren base and tren no ester exist but either way theres better pre wo androgens than any trens

 

[aac21]

you technically CAN take halo long term if you do all of that shit but why would you? even something like winstrol would be pretty much the same as low halo but actually anabolic as well

estrogens bind to ERα in liver hepatocytes which increase SOCS-2 mRNA and protein abundance, which actually inhibit igf conversion at low doses but in superphysological doses the relationship inverts because it displaces SOCS1 and SOCS3 which are stronger JAK2 inhibitors and also binds all availble helper protiens (Elongin B/C and Cullin-5) which all couple together to form a functional E3 ubiquitin ligase ring, which destroys the gh receptor.

and even at non supraphysological doses

15 is FAR above the supraphysiological dose of hgh, yes technically your body will produce up to like 10 ius for a breif period of time between 16-17 however HGH's natural half life is 10-20 minutes while exogenus HGH's is 20-30 minutes IV, however everybody does it subq which extends the absorption half life to 2.3-5 hours because of depot pharmokenetics of subq administration and the clearence time from 1-2 hours to 12-24 hours which obviously your liver will produce more igf with a sustained hgh signal compared to natural short pulses which are rate limited by liver hepatocyte processing speed

fearmongering, letrozole doesn't do anything past its prescribed dose because it already nukes 99 something % of aromatase enzymes any more would just be causing side effects

if you did the math then running 2 grams on letrozole would aromatase less than 200mg of testosterone which is a physiological dose for some people, and if that would close your plates than everybodys plates would close as soon as they entered puberty

dnr sides tren is fun asf honestly a better reason to run it than for muhh dimo, life is about having fun after all

Unfortunately aromatization isnt testosterone amount × percentage of aromatase inhibition its based of various UNACCOUNTABLE factors

You'd need to account for testosterone concentrations, tissue-specific aromatase activity, pharmacokinetics, substrate availability, and estrogen production.

Everyone aromatizes differently
Physiological puberty isn't equivalent to pharmacological testosterone exposure + pharmacological aromatase inhibition.

Your cellular signalling logic is partly correct for GHR, but you forgot that simply IGF-1 is what derives bone growth, not GHR. Countless studies backing increased FAH markers with letrozole + GH, arimidex + GH, Aromasin + GH. Better than GH monotherapy.

Again estrogen does not partake directly into GH > IGF-1 axis. Many studies show blood serum IGF skyrocketing just simply because of GH subq administration.

 

[India lover 52]

thanks for your insight too. that's pretty much what I heard about tren.
I'm planning to do about 10 iu's of gh so that's pretty close to the upper threshold like you said, so im assuming I won't have to worry about estrogen being too low?

could a mast and mesterolone (provision) cycle only pass for dimo? im assuming it'll also have an estrogen suppressive effect because it'll lower total and free t right?

that's why I appealed of stanolone(DHT) at first cuz it would help with dimo AND suppress estrogen so I could save on ai's. also it doesn't even have to seem side effects of ed or depression or testosterone production shutdown once the dot clears the system or anything like that usually comes with synthetic aas like tren but since I can't effectively source it I turned to dht derivatives ( aka Masteron/halostatin)

also do you have any knowledge or a hypothesis if it would it be a good idea to run it with a pan fgfr kinase inhibitor like erda or (more selective) infigratinib with mast and prov??? or would It be better to run erda with gh and then stop the erda and keep the gh but add mast and prov to recover from the sides of erda?

im kind of going above and beyond trying to optimize height here considering my advanced bone age

mast itself is a non selective SERM so it will control estrogen up to a reasoanble test dose

every single androgen will shut down your htpa if you run it long/hard enough to actually cause any changes, hpta shutdown is fearmongered asf tho take hcg if your worried but we don't even know the % of young male who's hpta will be permenantly damaged from steroid use as 100% of study participants have recovered in under a year lol unless your blasting for decades without hcg or your 60 years old with 176ng/dl test don't worry about shutdown its honestly a good thing less risk of a accidental pregnancy and just take hmg if u want kids on cycle

masteron is a really weak androgen and already crashes shbg i would pick one or the other not provirion and mast but either way 2 weak androgens are going to do nothing for dimo besides shut you down while your on them which means you will have low e2 side effects and all the steroid side effects without any of the benefits lol


what do you mean a good idea? yes stacking a fgfr inhib will increase bone growth with any androgen but i would never touch it because of sides and i've ran high tren + adrol for months

either way u need a trt base so u dont have crashed e2 and also some stronger androgens, if u want strong AR affinity without aromatisation your only options are tren or dhb/dhts but the latter 2 act as functional ai's which means u can crash your e2 if your test ratio is too skewed

so you can go the dhb/dht way and test your e2 ultra sens very frequently or trt + tren and let it rip

 

[aac21]

mast itself is a non selective SERM so it will control estrogen up to a reasoanble test dose

every single androgen will shut down your htpa if you run it long/hard enough to actually cause any changes, hpta shutdown is fearmongered asf tho take hcg if your worried but we don't even know the % of young male who's hpta will be permenantly damaged from steroid use as 100% of study participants have recovered in under a year lol unless your blasting for decades without hcg or your 60 years old with 176ng/dl test don't worry about shutdown its honestly a good thing less risk of a accidental pregnancy and just take hmg if u want kids on cycle

masteron is a really weak androgen and already crashes shbg i would pick one or the other not provirion and mast but either way 2 weak androgens are going to do nothing for dimo besides shut you down while your on them which means you will have low e2 side effects and all the steroid side effects without any of the benefits lol


what do you mean a good idea? yes stacking a fgfr inhib will increase bone growth with any androgen but i would never touch it because of sides and i've ran high tren + adrol for months

either way u need a trt base so u dont have crashed e2 and also some stronger androgens, if u want strong AR affinity without aromatisation your only options are tren or dhb/dhts but the latter 2 act as functional ai's which means u can crash your e2 if your test ratio is too skewed

so you can go the dhb/dht way and test your e2 ultra sens very frequently or trt + tren and let it rip

very interesting, fearmongering erda sides but ran high dose tren and adrol.

 

[India lover 52]

Unfortunately aromatization isnt testosterone amount × percentage of aromatase inhibition its based of various UNACCOUNTABLE factors

You'd need to account for testosterone concentrations, tissue-specific aromatase activity, pharmacokinetics, substrate availability, and estrogen production.

Everyone aromatizes differently
Physiological puberty isn't equivalent to pharmacological testosterone exposure + pharmacological aromatase inhibition.

Your cellular signalling logic is partly correct for GHR, but you forgot that simply IGF-1 is what derives bone growth, not GHR. Countless studies backing increased FAH markers with letrozole + GH, arimidex + GH, Aromasin + GH. Better than GH monotherapy.

Again estrogen does not partake directly into GH > IGF-1 axis. Many studies show blood serum IGF skyrocketing just simply because of GH subq administration.

GHR is what stimulates igf production lol


literally nobody said hgh doesn't increase igf??? your just making up shit for the sake of aruging atp


"Physiological puberty isn't equivalent to pharmacological testosterone exposure + pharmacological aromatase inhibition."

explain the mechanism then lol this sounds like chatgpt

"You'd need to account for testosterone concentrations, tissue-specific aromatase activity, pharmacokinetics, substrate availability, and estrogen production."

also sounds like ai, if you actually researched you would realise how little aromatase enzymes are in ur growth plates jfl also you worded this in such a vauge and said a whole lot of words but didn't really say anything way that im convinced you chatgpted this lol you obviously don't understand any of the mechanism you have not listed any specific enzymes or anything ur just making shit up from chatgpt

 

[India lover 52]

very interesting, fearmongering erda sides but ran high dose tren and adrol.

hmm cancer drug that can make you blind vs two drugs that have been approved for human use and are commonly used in bodybuilding with decades of human data

stfu chatgpt warrior

 

[aac21]

GHR is what stimulates igf production lol


literally nobody said hgh doesn't increase igf??? your just making up shit for the sake of aruging atp


"Physiological puberty isn't equivalent to pharmacological testosterone exposure + pharmacological aromatase inhibition."

explain the mechanism then lol this sounds like chatgpt

"You'd need to account for testosterone concentrations, tissue-specific aromatase activity, pharmacokinetics, substrate availability, and estrogen production."

also sounds like ai, if you actually researched you would realise how little aromatase enzymes are in ur growth plates jfl also you worded this in such a vauge and said a whole lot of words but didn't really say anything way that im convinced you chatgpted this lol you obviously don't understand any of the mechanism you have not listed any specific enzymes or anything ur just making shit up from chatgpt

im trying to tell you that letrozole even at its clinical dose wont affect igf-1 levels signifincatly. i am getting a bloodtest in 3 days so just wait gupps. i am on 2.5 letrozole and 14 gh

lets say even if there are low aromatase enzymes in the gp it doesnt really fucking matter. the skeletal maturation effect is extremely real and studied. estrogen signalning in the growth plate is aggressive. "count of enzymes" is not particuarly important

 

[aac21]

tren and approved human use

hmm cancer drug that can make you blind vs two drugs that have been approved for human use and are commonly used in bodybuilding with decades of human data

stfu chatgpt warrior

 

[India lover 52]

im trying to tell you that letrozole even at its clinical dose wont affect igf-1 levels signifincatly. i am getting a bloodtest in 3 days so just wait gupps. i am on 2.5 letrozole and 14 gh

lets say even if there are low aromatase enzymes in the gp it doesnt really fucking matter. the skeletal maturation effect is extremely real and studied. estrogen signalning in the growth plate is aggressive. "count of enzymes" is not particuarly important

it doesn't effect ur systemic that much but it nukes ur local igf retard

yes... from high systemic e2 not the fucking trace 0.0000000001 mcg of e2 that is locally produced in the growthplate

tren and approved human use

parabolan retard literally everyone fucking knows this about tren


im not arguing with you anymore at least the other guy has obviously done his own research your just a retarded tiktokcel chatgpt warrior

and guess what bro, im taller than you will ever be or anyone in your bloodline has ever been and i've never done any hgh + ai retard stack jfl brutal genetic pill

 

[aac21]

nice bro! let me just take some advice from this retard jeet and stop taking my AI because muhh "local igf1 is nuked" super high iq

really retarded and idk if i have to drill it into your head or smth we dont give a fuck about "systemic e2" ideally we want high systemic e2, but low local e2 but letrozole is not selective. the e2 in your growth plate even with an AI still matures the plate semi rapidly. nigga thinks letrozole is a godfather.