tyty
it cant are you dumb you litteraly said so youself
Where did I say so myself retard
why, doesn't mk increase test production tho through various pathways?
Nigga u think im rich im literally 15 cmon bro isnt just sarm + test base
to become mogger
Tf u mean it doesn't, mk triggers igf1 and gh release, those two also release test
its like anavar on steroids
son im crine
my phisque ain't work
so we are running dht derivitative, excuse spelling, nowadays
A nigga just asked if mk was a test base. You then went on to advise him to do slin,tren and dnp???? he would kill himself
slin and DNP are fine if ur smart and disciplined about it tho
Yesh because this nigga definitely seems smart.
yeah it will increase your trsticulars
I literally asked can it be used as a fucking test base because the pathology behind mk also increases test production like hop off my dick faggot none of you answered why no or why you disagree like atleast try to be helpful or kys, amen!
Please do not have children.
I literally asked can it be used as a fucking test base because the pathology behind mk also increases test production like hop off my dick faggot none of you answered why no or why you disagree like atleast try to be helpful or kys, amen!
are you retarded or mentally challenged
Your so fucking stupid you couldn't even process the question. MK increases test production by alot, if the test production is enough im asking if it can act as a test base. Are you this retarded that you lacked basic context on the thread and decided post "are you retarded or mentally challenged" like an iqlet
I've been laughing my ass off at this reply
omg you're actually such an ignoramus iqlet lol you dont even know basic endocrinology nor pharmacology so please leave this forumYour so fucking stupid you couldn't even process the question. MK increases test production by alot, if the test production is enough im asking if it can act as a test base. Are you this retarded that you lacked basic context on the thread and decided post "are you retarded or mentally challenged" like an iqlet
omg you're actually such an ignoramus iqlet lol you dont even know basic endocrinology nor pharmacology so please leave this forum
Pseudointellectual drivel, that study does not say what you think it does but you probably didn't even read itomg you're actually such an ignoramus iqlet lol you dont even know basic endocrinology nor pharmacology so please leave this forum
gh/igf1 can also be androgenic, thats why I stated constantly that it indirectly increase test production such an iqlet retard waste of grey autistic sperm
https://www.nature.com/articles/pr1986631
Natural selection at this point
Pseudointellectual drivel, it was showing the effects of IGF-1 increasing test production. Iqlet If you even understood the context behind it you'd know mk also increases IGF-1 which is why I says it increases test indirectly
. What you mean my theory, it was literally a simple question which asked can a compound which increases test indirectly, be used for a test base or temporarily holy iqlet im crine bro
mk677 does not increase testosterone by a lot you fat jewish retard and even if it caused a mild rise in eugonadal men thats irrelevant once sarms suppress FSH/LHomg you're actually such an ignoramus iqlet lol you dont even know basic endocrinology nor pharmacology so please leave this forum
gh/igf1 can also be androgenic, thats why I stated constantly that it indirectly increase test production such an iqlet retard waste of grey autistic sperm
https://www.nature.com/articles/pr1986631
Through increasing the sensitivity of Leydig Cells to LH by a mild degree, the production of which is almost completely shut down during AAS use rendering this information irrelevant you mongoloid greycel subhumanIqlet If you even understood the context behind it you'd know mk also increases IGF-1 which is why I says it increases test indirectly
please shut the fuck up you actual underdeveloped pre embryonic spermatozoon dont let me catch you posting retarded threads in this forumPseudointellectual drivel, it was showing the effects of IGF-1 increasing test production. Iqlet If you even understood the context behind it you'd know mk also increases IGF-1 which is why I says it increases test indirectly
"SmC/IGF1 increased both LH/hCG binding (x4-5), basal(x4) and hCG-stimulated (x15.5) testosterone" - and it doesnt by alot holy iqlet pls dnr ur sped germs on the forum pls dnr and spread them to ur kids instead kys and let future generations reap the benefits.
sure, u helped so much. You lack so much comprehension on the context dont even chat u sped fuck. MK indirectly increases test production the amplitude of that effect is what im questioning on where it can act as a test base or a temp one. If you need the context instead of going for insult retard holy grey kys
LMAO the paper you’re citing is in vitro using porcine immature sertoli cells in a serum free culture. increased lh/hcg receptor binding or steroidogenic responsiveness in isolated cells isnt same as increased circulating testosterone in vivo. that effect is entirely contingent on the presence of lh/hcg signaling. under sarm use lh/fsh are suppressed so the pathway youre appealing to is functionally inactive"SmC/IGF1 increased both LH/hCG binding (x4-5), basal(x4) and hCG-stimulated (x15.5) testosterone" - and it doesnt by alot holy iqlet pls dnr ur sped germs on the forum pls dnr and spread them to ur kids instead kys and let future generations reap the benefits.
"if it caused a mild rise in eugonadal men" the paper didn't even reference eugonadal men it was observing the effects of IGF in "the testis, porcine immature Sertoli cells cultured in a serum-free defined medium" you sped fuck kys lmfao, which if you even understood or could read the first sentence in the abstract you'd comprehend that it substantiated my claim iqlet
Wow, impressive how you managed to take an in vitro porcine Sertoli cell study and act like it singlehandedly predicts the entirety of human endocrine physiology. Congrats on that leap. Newsflash: Sertoli cells are not Leydig cells, and LH/hCG receptor priming in a serum-free dish is barely a whisper of what happens in a living human. You also seem to think SARMs slam LH/FSH to zero and render the testes completely brain-dead—reality check: suppression is rarely absolute, and Leydig cells can still respond to residual LH, paracrine signals, or even direct AR-mediated modulation. So yes, your “entirely inactive” pathway claim? Cute, but scientifically naive. Next time, maybe read a paper beyond the abstract before flexing your in vitro heroics.
The "amplitude" of this said effect is minimal and irrelevant if your going on sarms as it relies on LH/FSH which is entirely crashed via sarm usage.sure, u helped so much. You lack so much comprehension on the context dont even chat u sped fuck. MK indirectly increases test production the amplitude of that effect is what im questioning on where it can act as a test base or a temp one. If you need the context instead of going for insult retard holy grey kys
water, im not reading this israelGPT slopWow, impressive how you managed to take an in vitro porcine Sertoli cell study and act like it singlehandedly predicts the entirety of human endocrine physiology. Congrats on that leap. Newsflash: Sertoli cells are not Leydig cells, and LH/hCG receptor priming in a serum-free dish is barely a whisper of what happens in a living human. You also seem to think SARMs slam LH/FSH to zero and render the testes completely brain-dead—reality check: suppression is rarely absolute, and Leydig cells can still respond to residual LH, paracrine signals, or even direct AR-mediated modulation. So yes, your “entirely inactive” pathway claim? Cute, but scientifically naive. Next time, maybe read a paper beyond the abstract before flexing your in vitro heroics.
Ah, classic—“I’m not reading this IsraelGPT slop,” aka, ignoring facts because they hurt your fragile in vitro ego. Bold strategy, Cotton. Here’s the plot twist: dismissing evidence doesn’t make it disappear. That “slop” literally explains why your absolute claims about LH being totally dead under SARMs are laughably wrong. But sure, keep flexing your ignorance like it’s a personality trait—it’s working… for comedy, not science.
You also seem to think SARMs slam LH/FSH to zero and render the testes completely brain-dead—reality check: suppression is rarely absolute, and Leydig cells can still respond to residual LH, paracrine signals, or even direct AR-mediated modulation. So yes, your “entirely inactive” pathway claim? Cute, but scientifically naive. Next time, maybe read a paper beyond the abstract before flexing your in vitro heroics.
what the fuck nigga are you retarded? you think chatgpt insults make you smarter?
Ah, there it is—the classic “hur dur, insults = bad” defense. Adorable. Newsflash: I’m not trying to make you smarter; I’m just pointing out how confidently wrong you are while acting like a keyboard god. Insults aren’t the weapon here—your complete misunderstanding of endocrinology is. But sure, scream at your screen, maybe it’ll feel productive.
