I’d get it tested again. I’ve had many odd test results over the years. Errors happen all the time.
Why use a SERM to block estrogens when estrogens are the cause of gyno and lower E2 levels are easily achieved? Prolactin can be a component as well.
Crisler has said some regrettable things over the years.
Tren shows as estradiol on lab results. It’s been shown time and time again.
besides the fact that they are markedly better on your body than aromatase inhibitors? Lol.
Here is a good read for all you guys
Nothing really new there for me. But some of that material flies contrary to experience implying that higher E2 levels will lead to lower fat levels. The effects on composition are known be different from that. Many of the abstracts are troublesome as they do not fit TRT context. Just barfing everything can can be found into a forum thread is not useful. You can do better than sending people to that.
Actually you’re incorrect. Study after study shows low estrogen levels impede fat loss. There really is no point in going back and forth. You have your methods and I have mine. I would rather patients start on zero AI and add in zinc if anything. That’s plenty for
Also for instance in bodybuilding - arimidex is used pre contest to get rid of water. Not fat.
Just out of curiosity when you want to reduce water weight why would you take arimidex instead of the far faster and more effective furosemide? I have been but on both at one time or another. so I’m just curious.
The material that you linked to did not define “low estrogen levels” and you have not either. We have evidence here that E2=~22pg/ml does improve fat loss and proportioning around the belly and hips. Why are you not getting technical enough to present your own arguments clearly without asking guys to plow through someone else’s garbage dump of abstracts that also includes populations of near death males.
And stop referring to things with a body building context, most everything in body building forums is brain dead bro-science that is mostly wrong and harmful.
You go on and on about E2 levels and do not even point out that you are talking urine based levels when no one else here does such labs. While you may get urine info re ratios of E1:E2:E3, everything is subject to dehydration that concentrates urine so absolute levels are in doubt. You can get E1, E2 and E3 data from serum where things are more meaningful.
You are all unsubstantiated argument and lack precision and facts. Maybe you can up your game with better presentation.
As long as we are debating what kinds of hormone tests could/should be used, please see:
If your patients are using tamoxifen daily, does that mean they are not using HCG since HCG/Tamox should not be used together? (per KSman in PCT protocol)
I’ve wondered this too and haven’t been able to get a straight answer. I can state that from my experience, I don’t believe that nolva/tamoxifen maintains LH levels for those who are on TRT. I believe these individuals remain mostly shut down while receiving exogenous test, but the serm does its primary job of modulating specific estrogen receptors. This is anecdotal and not verified through labs though and is my belief because of testicular atrophy while only taking test cyp with 20 mg nolva daily did occur for me.
If the above is true, then technically taking hcg with nolva should be ok in this scenario, because there wouldn’t be LH released from the pituitary on top of hcg mimicking LH. The only thing stimulating leydig cells in the testes should be hcg.
Any thoughts on this would be great.
Joe normal-T guy takes SERM which hides estrogens from HPTA and LH/FSH increases as expected.
Bill low-T guy is on TRT with same T levels as Joe normal-T guy and suddenly one thinks that a SERM will not function under identical operating conditions?
SERMs do not work well if low-T cause was deep secondary hypogonadism, top end of HPTA needs to be somewhat functional.
Then why would testicular atrophy occur while on serm but not while on hcg for second scenario?
Because SERMs are not leading to adequate pituitary LH/FSH in your case. If you are hCG sensitive, you are LH sensitive. Atrophy is conclusive for low LH receptor activation. In this case, SERM is still blocking visibility of estrogens to the hypothalamus, downstream effects are inadequate.
Which of the two scenarios would be best?
Just increase serm nolvadex dose from 20 to 40 mg per day.
Keep serm nolvadex dose at 20 mg per day with low dose hcg 150 ius twice per week.
Both increase LH/FSH if top end of HPTA is working OK.
Both stimulate the testes but primary hypogonadism limits results.
One costs a lot more.
With more SERM, do labs LH/FSH to see if too high.
With both, watch that E2 does not get out of control from excessive LH receptor loading.
Do not see any big advantage to SERM+hCG.
Many times in medicine we go for trough levels
just before the next dose to determine that the lowest point is still in range.
Seems like Arimidex come in 1 mg tablets too.
Is anyone using this. What dose?
Hey everyone, I’m in Ontario (canada) and I read somewhere that our estradiol test isn’t effective … is this true? Im not sure if we even have a sensitive test here … According to this standard test my e2 is elevated… Is this a reliable number to go on or do I need a different specialised test here? thanks
Nope you can draw no conclusions from running the wrong E2 test designed for females, you can’t even make guess, those that do crash the E2.