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My hgh run

Startingover said:
70 was my estridol
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At 2.5 ius I think you said.

More than one factor involved like @Glycomann mentioned. The dose, the test timing, individual genetics, condition of a persons liver, metabolism is gonna differ, quality of the gh... A lot going on. Right now I'd get e2 back in range and retest. It'll give you a lot better idea for you individually.
 
1 mg arimidex or 25 mg aromisin per week will or should bring your e2 down to reference range


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Startingover said:
Best way to get in range?
Last question I promise..lol
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H2o1 said:
1 mg arimidex or 25 mg aromisin per week will or should bring your e2 down to reference range


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This ☝️
But split the dose. i.e. 1/2mg Adex twice a week or 12.5 Aromasin the same way. Just don't overdo it and crash your e2.
 
It'll be, once again, individual with that as well. Just keep up with your labs and you'll figure it out. 👍
 
SB Labs
OlePhart said:
Slightly low to in range from what I've read is best. Out of range on the high end is where it starts to drop off the higher it goes.
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Novadex crushes IGF-1. So blocking estrogen with nolva has the opposite effect. I recall AIs also have that effect. so maybe to low and to high is an issue.
 
Glycomann said:
Novadex crushes IGF-1. So blocking estrogen with nolva has the opposite effect. I recall AIs also have that effect. so maybe to low and to high is an issue.
Click to expand...
As long as e2 stays in range it's not detrimental. It's over use that has a bad effect.

Quote:
"Based on available research, aromatase inhibitors (AIs) do not appear to significantly affect insulin-like growth factor-1 (IGF-1) levels in men when estradiol (E2) is maintained in the normal physiological range.
Here's a detailed breakdown of the relationship between AIs, E2, and IGF-1 in men:
AIs impact E2, not IGF-1: Studies in men who have been treated with AIs show that when E2 levels are not significantly lowered (for example, in combination with testosterone or growth hormone), their IGF-1 levels remain stable. This suggests that the primary effect of an AI is on E2, and not directly on IGF-1.
E2 influences IGF-1: In men, E2 appears to influence the growth hormone (GH) and IGF-1 axis. However, research indicates that E2 primarily inhibits IGF-1 production in the liver in a dose-dependent manner. When E2 is sufficiently suppressed, IGF-1 levels tend to increase. If E2 is kept in the normal range, this inhibitory effect is unlikely to be fully removed, so IGF-1 should remain steady.
Correlation vs. Causation: Some studies in conditions like aromatase deficiency, where E2 is very low, have shown a correlation between low E2 and low IGF-1. However, this does not mean that AI use will automatically lower IGF-1. The primary cause of low IGF-1 in aromatase deficiency is the lack of E2, which the body relies on for various processes related to the GH-IGF-1 axis. AI use, if E2 levels stay normal, does not create this same deficiency."
 
OlePhart said:
As long as e2 stays in range it's not detrimental. It's over use that has a bad effect.

Quote:
"Based on available research, aromatase inhibitors (AIs) do not appear to significantly affect insulin-like growth factor-1 (IGF-1) levels in men when estradiol (E2) is maintained in the normal physiological range.
Here's a detailed breakdown of the relationship between AIs, E2, and IGF-1 in men:
AIs impact E2, not IGF-1: Studies in men who have been treated with AIs show that when E2 levels are not significantly lowered (for example, in combination with testosterone or growth hormone), their IGF-1 levels remain stable. This suggests that the primary effect of an AI is on E2, and not directly on IGF-1.
E2 influences IGF-1: In men, E2 appears to influence the growth hormone (GH) and IGF-1 axis. However, research indicates that E2 primarily inhibits IGF-1 production in the liver in a dose-dependent manner. When E2 is sufficiently suppressed, IGF-1 levels tend to increase. If E2 is kept in the normal range, this inhibitory effect is unlikely to be fully removed, so IGF-1 should remain steady.
Correlation vs. Causation: Some studies in conditions like aromatase deficiency, where E2 is very low, have shown a correlation between low E2 and low IGF-1. However, this does not mean that AI use will automatically lower IGF-1. The primary cause of low IGF-1 in aromatase deficiency is the lack of E2, which the body relies on for various processes related to the GH-IGF-1 axis. AI use, if E2 levels stay normal, does not create this same deficiency."
Click to expand...
I wonder where the cut-off E2 is. ERalpha activity is required for IGF-1 production to some degree but STAT is also. I think it's complicated and different in men and women. Women on birth control have varying impact on IGF-1 production, which can be up or down depending on the drug combo of synth estrogen and progesterone and dose. DEfinitely IGF-1 is effected in women and it modulates with their menstral cycle being highest iGF-1 and GH with the higher points of estrogen concentration. I'm not sure how that breaks down across tissues but mostly describing liver production.

That proper AI treatment where E2 is in normal range is reflected in normal IGF-1 levels doesn't surprise. If this is an AI generated analysis we might take caution. Maybe ask it to review and summarize all information related to estrogen levels related to igf-1 production in men. Cochrane may have already done their meta analysis.
 
I did the ChatGPT on it. Here are the results.

Summary — how​


Below is a focused, reader-friendly summary of the mechanisms, human & animal evidence, and clinical implications linking estrogen to hepatic IGF-1 in men — with the key supporting citations.



Short answer​


Estrogens (especially 17β-estradiol acting through hepatic estrogen receptor-α) increase hepatic IGF-1 production in men both by (1) modulating the hypothalamic/pituitary GH axis (increasing GH pulse/activity that stimulates IGF-1) and (2) directly stimulating IGF-1 transcription in the liver (GH-independent pathway). Loss of estrogen signaling (aromatase deficiency, aromatase inhibitors, or some SERM effects) is associated with lower IGF-1 in men. Cell+2PMC+2



Mechanisms (what the biology shows)​


  • Direct hepatic action via ERα: Liver expresses estrogen receptor-α (ERα). Activation of hepatic ERα increases IGF-1 mRNA and circulating IGF-1; conversely hepatic ERα loss or caloric restriction reduces IGF-1 expression. This is a direct transcriptional/regulatory effect in hepatocytes. Cell+1
  • Modulation of GH secretion (central effect): Estrogens amplify growth-hormone (GH) secretion/pulsatility during puberty and in adults; increased GH then stimulates hepatic IGF-1 production. Some testosterone effects on IGF-1 require aromatization to estradiol. PMC+1
  • GH-independent pathway: Experimental work shows estradiol can raise hepatic IGF-1 even when GH receptor signaling is disrupted, indicating an additional GH-independent mechanism. Wiley Online Library+1


Human evidence & clinical observations​


  • Aromatase deficiency (human cases): Men with congenital aromatase deficiency (cannot convert androgens → estrogens) exhibit impaired GH secretion and low serum IGF-1, illustrating estrogen’s necessity for normal GH/IGF-1 axis in men. Estrogen replacement restores many functions. New England Journal of Medicine+1
  • Aromatase inhibition / aromatase inhibitors (AIs): Studies in men show that blocking aromatase reduces estrogen levels and can reduce GH–IGF-1 axis activity (some studies report lower IGF-1 after aromatase inhibition). Conversely, testosterone treatment that is aromatizable raises IGF-1, and non-aromatizable androgens have less effect. PMC+1
  • SERMs and other agents: Some agents that alter estrogen signaling can change IGF-1; for example, recent clinical reporting shows that clomiphene (a SERM used in hypogonadal men) may reduce serum IGF-1 in some patients — suggesting clinical therapy that changes estrogen action can affect IGF-1. (This is an area where monitoring may be warranted.) OUP Academic


Animal & mechanistic studies (support)​


  • Multiple mouse studies and detailed mechanistic papers show estradiol (including 17α- and 17β-forms) increases hepatic IGF-1 and that liver ERα is a critical mediator integrating nutrient and reproductive signals to control IGF-1. These provide the mechanistic basis for human observations. PMC+1


Important nuances & modifiers​


  • Route and context matter: In women, oral estrogens (first-pass hepatic exposure) can lower IGF-1 by altering GH action in the liver — route-dependent pharmacology matters. In men this specific route effect is less commonly used, but it illustrates that how estrogen is delivered/produced (endogenous aromatization vs oral pills vs transdermal) can change hepatic outcomes. OUP Academic
  • Dose & timing: Physiological (pubertal/adult) estradiol levels support normal GH/IGF-1. Very high pharmacologic estrogens or different estrogenic compounds may have variable effects.
  • Nutrition, liver health, and age: IGF-1 is also strongly affected by nutrition, hepatic function, and age; estrogen is an important regulator but not the only determinant. BioMed Central


Clinical implications (practical)​


  • If you alter estrogen levels or signaling in men (using aromatase inhibitors, SERMs, exogenous testosterone that is non-aromatizable, or giving estrogen), expect possible changes in GH/IGF-1: usually a reduction of estrogen → lower IGF-1, and restoration of estrogen → IGF-1 recovery. PMC+1
  • Monitoring: When treating men with aromatase inhibitors, SERMs (e.g., clomiphene), or unusual androgen regimens, clinicians sometimes monitor serum IGF-1 (and clinical signs of GH deficiency/changes in body composition) because changes can be clinically meaningful. Recent reports recommend interval monitoring in some contexts (e.g., clomiphene therapy in hypogonadal men). OUP Academic
  • Bone and metabolic health: Because IGF-1 and estrogen both affect bone and body composition, disrupting estrogen → IGF-1 signaling can have downstream effects on bone density, muscle mass, and metabolism. World Journal of Men's Health+1


Bottom line (one-liner)​


In men, estradiol — primarily via hepatic ERα and by shaping GH secretion — supports normal hepatic IGF-1 production; reducing estrogen signaling (aromatase deficiency or pharmacologic aromatase inhibition / some SERM therapies) is associated with lower IGF-1, while restoring estrogen signaling raises IGF-1. Cell+2
 
Bibliography

Short annotated bibliography — estrogen and IGF-1 in men (key human case reports/trials + mechanistic papers)​


Below are concise entries (citation = clickable link). Each entry has a 1–2 sentence summary and a single-line clinical/mechanistic takeaway.



  1. Della Torre S., et al., Cell Metabolism 2011 — “Amino acid-dependent activation of liver estrogen receptor α.”
    Summary: Demonstrates that dietary amino acids activate hepatic ERα via mTOR signaling, increasing hepatic IGF-1 mRNA and circulating IGF-1 in mice; describes a direct nutrient–ERα–IGF-1 transcriptional pathway in liver. PubMed
    Takeaway: Hepatic ERα is a direct regulator of IGF-1 expression and integrates nutritional signals with estrogen signaling. PubMed
  2. Rochira V., et al., Journal of Clinical Endocrinology & Metabolism 2010 — “Tall stature without growth hormone: Four male patients with aromatase deficiency.”
    Summary: Case series of aromatase-deficient men showing impaired GH/IGF-1 axis and low serum IGF-1; assesses effects of estrogen replacement. OUP Academic
    Takeaway: Human aromatase deficiency illustrates that lack of estrogen reduces IGF-1 (and perturbs GH function) — clinical proof that aromatization matters for normal IGF-1. OUP Academic
  3. Baykan EK., et al., JCRPE (case report review) 2013 — “Aromatase deficiency: a rare syndrome” (adult male case & review).
    Summary: Describes features of adult male aromatase deficiency and reviews previously reported cases including effects on puberty, bone, and IGF-1/GH axis. J Clin Res Pediatr Endocrinol
    Takeaway: Multiple case reports consistently show lower IGF-1 in aromatase-deficient males and improvement with estrogen therapy. J Clin Res Pediatr Endocrinol
  4. Sidhom S., et al., Aging (or PMC) / preclinical 2020 — “17α-Estradiol modulates IGF-1 and hepatic gene expression.”
    Summary: In male mice, 17α-estradiol increased hepatic IGF-1 production without altering GH pulsatility, supporting a GH-independent hepatic effect of estrogens. (Open-access PMC). PMC
    Takeaway: Estrogen can raise hepatic IGF-1 through liver-intrinsic mechanisms separate from changes in GH secretion. PMC
  5. Qiu S., et al., Scientific Reports 2017 — “Hepatic estrogen receptor α is critical for regulation of …”
    Summary: Conditional liver ESR1 (ERα) knockout mouse studies show hepatic ERα influences metabolism and IGF-1 regulation; adds genetic evidence that liver ERα contributes to systemic IGF-1 levels. Nature
    Takeaway: Genetic loss of hepatic ERα alters IGF-1 regulation in vivo — supporting liver ERα as a necessary mediator. Nature
  6. de Ronde W., et al., Endocrine Reviews / Review 2011 — “Aromatase inhibitors in men: effects and therapeutic options.”
    Summary: Comprehensive clinical review describing how aromatase inhibitors affect sex steroid balance, GH/IGF-1 axis, growth/height outcomes, and metabolic consequences in males (children and adults). PMC
    Takeaway: Pharmacologic reduction of estrogen via AIs commonly changes GH/IGF-1 dynamics — clinicians should expect and monitor such effects. PMC
  7. Dias JP., et al., Clinical Endocrinology (or similar) 2017 — testosterone aromatization and IGF-1 in older men.
    Summary: Studies in older men receiving transdermal testosterone vs non-aromatizable androgens show that increases in IGF-1 relate to aromatization to estradiol. ScienceDirect
    Takeaway: Testosterone’s effect on IGF-1 in men is at least partly mediated by its conversion to estradiol. ScienceDirect
  8. Zhang KW., et al., 2019 — “Estradiol-17β regulates expression of IGF family (mechanistic review/experimental).”
    Summary: Mechanistic paper summarizing estrogen regulation of IGF family members in liver and other tissues and describing ER-dependent transcriptional regulation of IGF1. ScienceDirect
    Takeaway: Molecular data support estrogen (via ERs) as a transcriptional regulator of IGF-1 expression across species. ScienceDirect
  9. Mogar N., et al., Journal of Endocrinology and Surgery (J Endo Surg/JE S?) 2025 — “Reduced IGF-1 Levels Following Clomiphene Treatment for Hypogonadism.”
    Summary: Recent clinical report/series (2025) documenting significant decreases in serum IGF-1 in some hypogonadal men treated with clomiphene citrate (a SERM that alters estrogen signaling), recommending interval IGF-1 monitoring. OUP Academic+1
    Takeaway: Clinical manipulation of estrogen signaling with SERMs (e.g., clomiphene) can reduce IGF-1 — an actionable clinical observation with monitoring implications. OUP Academic


Quick methodological note​


  • The list mixes human clinical case reports/trials (Rochira 2010; Baykan 2013; de Ronde 2011; Mogar 2025; Dias 2017) and mechanistic/animal studies (Della Torre 2011; Sidhom 2020; Qiu 2017; Zhang 2019) because the strongest mechanistic support comes from liver-focused animal/genetic work while human evidence is largely case-based, small trials, or therapeutic perturbation studies. PubMed+2
 
Glycomann said:
I wonder where the cut-off E2 is. ERalpha activity is required for IGF-1 production to some degree but STAT is also. I think it's complicated and different in men and women. Women on birth control have varying impact on IGF-1 production, which can be up or down depending on the drug combo of synth estrogen and progesterone and dose. DEfinitely IGF-1 is effected in women and it modulates with their menstral cycle being highest iGF-1 and GH with the higher points of estrogen concentration. I'm not sure how that breaks down across tissues but mostly describing liver production.

That proper AI treatment where E2 is in normal range is reflected in normal IGF-1 levels doesn't surprise. If this is an AI generated analysis we might take caution. Maybe ask it to review and summarize all information related to estrogen levels related to igf-1 production in men. Cochrane may have already done their meta analysis.
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Definitely different in men and women by a mile. Everything I've read so far i look for in men. The one I posted is specific to men. I'll keep reading about it but so far everything I've seen points to stable e2 levels being the common factor. I'll look for pubmed stuff as well.
 
Startingover said:
I'm gonna go with glycoman!!
Answer is 7!!
my heads spinning. Lol
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Pretty much the other oldfart and I are in agreement and learning from one another. Many of us older men discuss, debate and learn from one another. I like that better than the newboy 14-25 year old bitchy squabble "post a pic" mentality, not that all of them are like that. We can send them to Meso.
 
Glycomann said:
Pretty much the other oldfart and I are in agreement and learning from one another. Many of us older men discuss, debate and learn from one another. I like that better than the newboy 14-25 year old bitchy squabble "post a pic" mentality, not that all of them are like that. We can send them to Meso.
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Exactly. And finding a pubmed study on this specifically looks like it might be a pain but I'll keep digging.
 
3rd day into lil gig running..
Forgot why I like tbol so much..
This 9/10 weeker should be interesting for sure man..
 
Still chugging along.
Hovering slightly below 225 morning weight consistently.
pumps are great!
Overall feeling fantastic!
Sleep has improved.
From very broken sleep to 1 bathroom run and good 7hrs..
Which is phenomenal for me.
Also been making it thru the day nap free.
I've also added 50 mgs nad+ which always has given me increased vasularity.
Also some hrt research shows tjey are prescribing it along side hgh therapy now.
Have it on hand figured why not see how they work together?
 
This is off topic, but if you only had 50iu’s of gh would you run it or buy more to run it longer? I got a free kit last year, but I’m not sure when I will be able to stock up on the stuff. I just wonder if I run 50iu’s, say, 2iu’s a day until it runs out, I f I will get any benefits from it?


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Darkhrse99 said:
This is off topic, but if you only had 50iu’s of gh would you run it or buy more to run it longer? I got a free kit last year, but I’m not sure when I will be able to stock up on the stuff. I just wonder if I run 50iu’s, say, 2iu’s a day until it runs out, I f I will get any benefits from it?


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I'd just hold onto it until you can get more, 25 days isn't going to do nothing.
 

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