Happy coincidence. My BP was running high and has since calmed down with a reduced dose of MENT and the valsartan. After I got on it I read everything I could find and learned that ARBs are miracle drugs.
Still scratching my head on what MENT is?
I have a favorite blood pressure medication 2 mg Doxazosin because its secondary application is reducing BPH which I get from Blasting. Also 2mg Dox plus 5mg cialas is a know combo for improving Vascularity.
Love your post. I don’t know if I’d agree here though. Other AAS have the ability to interfere with GC function too, Tren does it the best though (the recomp effect people are reporting could be explained by that). Also, chemically Tren is a steroid, but it has some SARM like activity. I don’t agree with some of the reasoning the researchers use though (calling it SARM like only because it doesn’t get 5a reduced).
Yeah, I think it’s fair to argue that it is both a SARM and not a SARM. There’s a decent enough argument for both. Schrödinger’s Tren would perhaps be the best description.
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7a-methyl-19nortestosterone.
Thank you. The AAS Trestolone
You don’t need to use Bitcoin. All cryptocurrencies are quite volatile ATM, but if you use a crypto worth less per coin the fluctuations shouldn’t be that great
To note, I don’t buy crypto for “purchases” these days, it’s more for perhaps a long term investment. Try find a vendor that accepts monero. Transactions with monero are arguably more secure anyway.
I’ve been getting into cryptocurrency and to a degree stocks.
It just depends on which side of this curve you bought in. When I started buying bitcoin they were 18K and when I was buying my hobby drugs of choice Bitcoin was 60K. So TE/HGH/Anavar/Anastrozole was basically free.
My father also got lucky with btc, purchased a full bitcoin when it was like 10k
The only one I made a decent profit from was dogecoin and to a smaller degree, etherum classic and ripple.
Interesting I only use coinbase and you can’t buy dogecoins from them.
Supposedly they’re are going to be integrating that in the next month or two.
Sorry I’m late to the party. Good topic and that’s why I made this topic:
Problem with answering this question is no one really knows how T:SHBG interaction really works and there’s no harmonized methods for measuring free T. You’ve got a lot of people throwing out their fT numbers and have no idea the inherent limitations on the test. Their Doc doesn’t really get it either.
Free Hormone Hypothesis still very much an active area of research and I sure can’t answer your question. What drives adrenergic effect of T on the heart? TT or fT.
Is T bound to SHBG biologically active? I believe the answer is yes.
Is TT or fT concentration the driver for conversion to E2?
How many guys go to the trouble of collecting time based data points to estimate their effective clearance rate for TT or know their peak/trough on a particular dosing regimen?
Plot my cycle or whatever other website guys use now ain’t going to give you the plot above.
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It definitely is; SHBG has its own cell receptors. Here is a semi-recent paper about its various effects:
Here’s a couple of nuggets of wisdom from the paper (they’re using Te as an abbreviation for testosterone):
“It is well known that SHBG reduces cellular uptake of Te; however we have demonstrated that SHBG may also maintain stable levels of biofunctional Te and physiologically relevant intracellular Te levels by reducing Te glucuronidation and efflux.”
“When SHBG is reduced or absent, excess free Te may enter cells and oversaturate the ARs since it has been reported that AR saturation occurs at approximately 2-3 nM in prostate [26]. The LNCaP cells may respond to this by rapidly glucuronidating and effluxing the excess Te.”
For those who are not nerds, glucuronidation is the body’s way of “tagging” a molecule for excretion by the liver or kidneys. Glucuronidated testosterone is, for our purposes, worthless.
TL,DR: SHBG is very important - don’t intentionally try to lower it unless you are an outlier who has ridiculous amounts of the stuff.
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Thank you for sharing this article. Since most are TLDR, wrap your head around the conclusions wrt the Prostate cancer cells:
Here’s recent review of free hormone hypothesis for various hormone groups. Notice the punt when it comes to definitive conclusions wrt to sex steroids as there so much to learn and appears very tissue dependent.
https://asbmr.onlinelibrary.wiley.com/doi/full/10.1002/jbm4.10418
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Nice read:
[URL unfurl=“true”]https://academic.oup.com/edrv/article/38/4/297/4071740?login=true[/URL]
Excerpts:
As I wagered with “madman” in the past on ExcelMale, I’m betting we still have a ways to go before harmonized fT levels make their way into mainstream clinical decision making.
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I guess my questions would be:
Can T+SHBG attach to the AR?
Can T+SHBG be aromatized into e2?
How does T separate from SHBG (or does it)?
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Answer here depends on what scheme you buy in Fig 4? What ratio of mechanism 4a vs 4b may be tissue dependent and if could very well be that both fT and SHBG-bound T both contribute to overall intracellular aromatization.
Excellent questions and fun to ponder. Thank you! Quickly you find that many of the simple constructs used to discuss TRT (e.g., free up that T dude!) quickly become murky.
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That is for sure lol. I’ll read these when I get home