Testicle size is good, and I have tested the hcg.
I’m not concerned about general on cycle maintenance, but in particular resumption of fsh/lh without ceasing cycle.
E2 levels are clearly part of the cycle, or you couldn’t raise test using only an AI. It is not aromatase driven though, which I took to be the argument. E2 is not just generated by aromatisation.
What other pathways to E2 are there in males? It is my understanding that although conversion through aromatase can occur in different parts of the body, at all points it is aromatised from T.
From Sex hormone synthesis, regulation, and function | McMaster Pathophysiology Review :
The HPG axis and hormonal feedback in males
- The pulsatile release of GnRH from the hypothalamus causes the secretion of the gonadotropins LH and FSH (to a lesser extent) into the circulation.
- LH stimulates the release of testosterone from Leydig cells.
- Testosterone feeds back negatively on pituitary LH and hypothalamic GnRH.
- This effect may be mediated by estradiols generated by peripheral aromatisation of testosterone.
- FSH stimulates the release of inhibin from Sertoli cells.
- Inhibin feeds back only on anterior pituitary release of FSH.
- LH stimulates the release of testosterone from Leydig cells.
I don’t find anything that says that men produce E2 outside of aromatisation, so I appear to be wrong in that statement. I thought that it was produced differently in the adrenals but I’m not finding anything to back that up.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC179885/
Actually, it is more likely that Leydig cell derived estradiol would move toward the lymphatics, because the cells lie adjacent to endothelial cells of the lymphatic system and estrogens are reported to be in very high concentration within testicular lymphatics [47,88]. Because blood estrogens are in low concentrations in the male, we would assume that this source would provide limited endocrine activity in the reproductive tract. In the efferent ductules, the blood source would likely have even less effect than in the remainder of the reproductive tract, as these ductules are responsible for reabsorption of over 90% of the luminal fluids [91] and thus display an overwhelming luminal to basal orientation, which could limit the movement of substances from basement membrane into the cell cytoplasm. Although this hypothesis has not been tested directly, there are studies suggesting that this region of the male tract does not respond to exogenous androgens following castration
This seems to indicate that E2 doesn’t get around well enough to be a good signaller. That may be why the aromatase enzyme is so prevalent in the body, it needs to make it close to wherever it needs it.
Agreed. HCG just gets used much more due to the cost, and seems to be pretty efficient at maintaining fertility. If trying to conceive, HCG + FSH is the route to go, IMO.
Well all, quick update.
I dropped some pharma HMG into the stack just over a month ago and we found out the other day she is pregnant.
So 16 weeks in 400mg tren, 750mg test, 800mg EQ + 75iu HMG E2D and 500iu HCG E2D definitely effective at maintaining fertility.
Before the HMG I also chucked some ‘samples’ under the microscope around week 10-12 and there were definitely viable sperm present, just not too many, so HCG alone may be enough to maintain a low level of fertility, After the HMG a definite increase in both number and vigor of total sperm was noted starting around 2 weeks after first shot.
Hope this is helpful to those out there trying to conceive while remaining on cycle.
Wow congrats! I’ve read HMG is great but glad to hear first hand it works. Tagging @vonko1988 as he might be interested in this.
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I’m glad to see this thread because this question was also cycling in my head.
Theory looks good, it just wants some proof. styx123 haven’t posted his estradiol levels, just LH&FSH. Also Tamox is the worst AI one can use (judged by sides, efficiency and muscle loss).
Overall it’s very dangerous to use an AI, because estrogen is necessary for our health. But then there is Clomid which do not acts as Aromatize Inhibitor but as an estradiol antagonist. That means estradiol in our blood can be present but is not attached to the pituitary gland (hypothalamus) because estrogen receptors are occupied by Clomid. Clomid blocks them but do not activate them. Hypothalamus thinks we do not have any estradiol and produces FSH&LH.
Clomid can increase naturally produced testosterone. I just started taking it few days ago and I can see the effect.
Hopefully it can help us to fight sides of exogenous testosterone during the AS cycles.
I’m going to test that when I’ll be ON. I have my doubts though… Not only the dose would be high, I have to lower the estradiol with anastrozole to the lower normal values.
Fyi.
I was being a little aggressive with the prami which tanked my prolactin, and I ceased entirely after the panel.
Your E2 is in middle normal range. In theory your body should produce FSH&LH…
But it seems I’m missing something and pituitary glands are not working just by presence of estrogen… After a quick search, hypothalamus and pituitary gland are also stimulated by testosterone and progesterone - I do not know to what degree.
There are GnRH agonists on the market that could help, but they can desensitize GnRH receptors (do not know after what time at what dosages) that needs to be cleared later.
This looks like the end and I’m gonna stop to do bro science, I’m not gonna discover anything new. I’ll just stick with classic AS cycles and with clomid when I’m OFF cycle.
I think a lot. One could have high T due to injections, low E2 due to adex, and will most likely have close to 0 LH and FSH due to high T.
Thanks for opening the thread! I did a bit of research on that topic a few weeks ago and came to the same conclusion, there are androgen receptors in the hypothalamus. Would have been great if Clomid or Tamox worked for that application.
It would sure make cycling easy. Just stay on Nolva the whole cycle, come off, stay on a few weeks and good to go.
Wtf is the pink splatter all over those pages? Did you stab a unicorn in close proximity to that report?
Can we get @dextermorgan to do a quick analysis?
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SERMS will NOT maintain LH and FSH function. I have my own blood work to prove this.
I tried using 25mg Clomid daily with my 80mg Test per week TRT dose. That’s a very low TRT dose, let alone a cycle dose. LH and FSH came back near zero.
And no, I am not a primary before you ask. Once I dropped the Test dose and only kept the Clomid, my testosterone levels came back at 721 and LH and FSH in upper normal range.
There it is.
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This is consistent with my bloodwork, I was taking SERMs at the time for weeks prior with zero FSH and LH.
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Been on nolva 20 mg ED for 4 weeks while on a cycle. Nothing traceable as far as FSH and LH (<0.3). Id say doesn’t work while on cycle but I haven’t had very bad testicular atrophy as in previous cycles with good size loads (let go of 4 in ex last night). I am going to switch to clomid and rerun blood work to see if there are any changes in LH and FSH. Considering taking HCG also just to make sure the boys are being maintained during this experiment.
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this has been my experience using Nolva on TRT/AAS. Balls did shrink a little less, but no increase in LH/FSH. So there is something going on there, but I doubt it’s increasing fertility markers any.