Is this "No AI" Thing Really for Everyone?

Pharma / TRT Testosterone Replacement
62

Here’s my current stance on AI’s. Estrogens are important for a myriad of differing functions within the human body. From nitric oxide mediated vasodilation to glucose/lipid metabolism to neurological homeostasis and more.

That being said, there is no literature as to what quantifies an adequate estrogen to androgen ratio, there is no literature as to what concentration of estrogen in healthy men constitutes as healthy.

Like testosterone/dihydrotestosterone, you CAN have too much estrogen, and risks are associated with excess estrogen. If you go to mims and look at the side effect profile for estradiol an increased risk for “stroke, myocardial infarction, deep vein thrombosis” are all included within postmarketing reports.

AI’s aren’t poison… And side effects mediated from AI’s likely aren’t a byproduct regarding the chemical composition of the medications themselves, rather side effects would be related to a reduction in circulating estradiol.

A few months ago out of sheer curiousity I tried a minute dose of anastrazole with my TRT. The sky didn’t intrinsically fall, a slight drop in water retention was noted. Aside from that libido, sense of well-being, health parameters were relatively unchanged. This isn’t to state long term implications wouldn’t become apparent, however the hysteria over AI seems a little bit overdone. We were all duped through physiolojik at one point in time.

Take it… Don’t take it, it’s almost certainly healthier if you don’t; but that’s your perogative/benefit risk assessment to make.

It should be noted androgen mediated water retention can be initiated through a multitude of mechanisms. Androgens increase 20-hete production. In laymen’s terms more 20-HETE→+ angiotensin II →+ aldosterone → increased water retention.

Estrogen also covers a role regarding fluid balance, so if you’re taking 1000mg test/wk, noticing significant water retention/hypertension and an AI somewhat cancelles this out it would only appear logical to use one for a short period of time as opposed to dealing with hypertension of which can induce a myriad of pathological conditions. That being said using 1000mg test/wk for a prolonged period of time will probably fuck you up regardless :rofl:

I’m not a doctor/expert, rather this is my opinion. If you need an AI on a pure replacement dose of test (not a cruise/grey area dosing) and you don’t have any type of hepatic pathology, aromatase enzyme defect/abundance (i.e klinefelters syndrome, aromatase excess syndrome or something), you aren’t overweight/obese etc there’s a decent possibility T dose is too high. I have to deal with significant water retention above 125mg/wk, the simple solution is

A: don’t go above 125mg/wk for trt, my bloods/sense of well-being are fine on 125mg/wk
B: use a smidge of anastrazole and increase the dose because I’m vein and don’t like dealing with water retention around my face.

90% of the time I’ll root for option A.

Aromatase inhibitors aren’t classified as poisons btw, ethyl alcohol is classified as a poison… But not aromatase inhibitors.

Back to making random jokes and talking about random stuff on the politics/off topic section for me.

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Isn’t this meme the best? Look at the guys face… It’s all flat!!

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63

Blasphemy. Reasonable statements like that won’t be tolerated here.

64

Well said.

65

Maybe you need to be a bit more CLEAR in what you write then, as I wasn’t the only one not understanding what you’re trying to convey.

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66

Amen

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67

No. Reread my posts in this discussion. Literally every post mentions an AI. Every post.

68

Test can be poison, HCG can be poison, E2 can be poison. It all depends on the dose / level. If E2 is high enough, then pick your poison.

69

All studies by association. Association does not prove causation. When they raise T/E2 in men they improve. Literally in every study. I’m still waiting for someone to send me an interventional study where they raised T/E2 in a man and it caused harm. Every time I ask for one of these I’m left with the sound of crickets. There are lots of studies where one thing was associated with another which becomes a moot point when you actually perform the exercise and compare the before and after. I still have no idea why men not on TRT with either low, mid-range, or high T levels ever felt compelled to block estradiol. Yet the second they replace T with an exogenous source suddenly E2 becomes the devil. It still blows my mind. I always ask TRT guys how many non-TRT guys they know that are on aromatase inhibitors simply to block E2 yet AIs are prescribed almost by default even by docs prescribing 80mg a week. You can’t get more ridiculous than that if you tried.

70

You’re referring to replacement right? This theory goes right out the window when you start looking at supraphysiologic dosing, which appears to begin around the 200mg/wk range wherein lipids begin to take a hit. Then you have biomarkers indicative of oxidative stress becoming elevated starting around the 300mg/wk mark, the threshold is even lower within rodent models.

I can quote one study wherein elevate E2 out of proportion in relation to androgen index was purportedly culpable for low libido, wherein the administration of anastrazole ameliorated symptomatology. I’m not on any particular side here and don’t feel like going down this rabbit hole.

I’m not solely referring to TRT. For TRT an AI GENERALLY (almost always) isn’t required, for “grey area” dosing and/or dosing associated with bodybuilding regimes some men may require an AI, in which case the benefits may outweigh the risk of having a BP of 150/95 due to significant water retention/bloating. In terms of aesthetics, if dosing high I’d rather take the risk of using an AI than look like a marshmallow man… But that’s just me.

No, estrogen isn’t the only factor culpable for T mediated fluid retention, but it does play a role. There’s no data indicative vastly supraphysiologic E is safe for long durations of time. Stating you have patients doing fine means nil in the grand scheme of things. Give me placebo controlled, quantitative data forty years down the line covering health outcomes.

In terms of data we have covering AI use and cardiovascular risk, we are primarily confined to breast cancer subjects and/or men with hypogonadism.

Results are generally somewhat inconclusive and/or contradictory

Perhaps subjective long term risk differs when simultaneously and exogenously altering androgen index.

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71

You’re disappointing me here. You know better than this. Dose is irrelevant. I get a total T of 700 or so with 200mg a week. Not supra. Other men may get 2000 total. Dose is irrelevant. There are TONS of docs who target the mid range and still prescribe an AI.

I don’t need to explain this to you. You know this already.

72

I do, but I’m not referring to outliers. Let’s make a blanket generalisation. Take 1500 men, give them 250mg/wk, the cavg on a box plot will be say… 1700ng/dl, HDL takes a dip, HCT/RBC climbs up, diastolic/systolic BP sub-clinically climbs, homocysteine goes up, as does CRP.

For some this effect will only become apparent at 500mg, for others 100mg. But as a blanket generalisation the negative effects begin at around 200mg/wk for most.

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73

Agreed, and at THIS point it isn’t necessary for say… 99.9% of men. Climb into bodybuilding/grey zone territory and the story starts to change though.

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74

Also the study in question indicates an androgen deficiency with high estradiol so they automatically blame the estradiol. When they give the man an aromatase inhibitor he winds up converting less testosterone to estrogen which leaves him with more testosterone. Instead they could have simply raised testosterone without the need to alter estradiol levels by any stretch of the imagination and he would have improved just like every other study out there that goes through that exercise.

75

Why do these discussions always need to go towards bodybuilders taking 15 different synthetic compounds? I only talk about men on trt. I don’t discuss bodybuilders. Bodybuilders don’t take only testosterone. As soon as you’re taking all these compounds that ridiculous doses all the rules go out the window. My focus is getting men healthy with trt and that’s where it ends.

76

My current TT is likely <200 at this point. My DHT is likely as close to 0 as it’s ever been. My E2 is probably in the 50’s (will find out in February). Libido is uncontrollable and I can drill through 3/4” OSB at a moment’s notice. My wife is unable to keep up and I’m 15 years her senior. I have zero bloat. My BP is steady at 120/80. I retain no additional water anywhere that is visible and obvious. My mental health has never been better. Maybe E2 isn’t the devil, guys?

77

Plenty of recreational bodybuilders/powerlifters/strongmen primarily stick it testosterone. Despite being touted as the elixir to longevity, dose testosterone high enough and it carries virtually identical risks in comparison to synthetic compounds. Just because something isn’t synthetic doesn’t equate to it being fantastic/superior, though I’d argue testosterone is optimal when it comes to replacement. Cannabis, opium and the cocoa plant are also naturally produced, all have medicinal properties but are prone to misuse.

You off trt? Why?

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78

Last test shot was 50mg 11 days ago.

Go find my log on Pharma. You in particular would be interested in my experiment.

79

That’s right… You’re on ment right? Perhaps I’ll try that one day far down the line.

80

Funny how that works, right?

I’ve helped more men than I can count. I just want everyone to feel better. I’ll offer any help I can to get them there. I still don’t understand why there is so much argument and resistance when I have physician after physician reporting the exact same thing. I am organizing a doctor’s round table on February 6th which will likely be a live event on that YouTube channel where I will have a number of Physicians involved going over everything. Hopefully that will be the end of it!

81

Look, I don’t agree with the use of an aromatase inhibitor to treat hypogonadism. If one wanted to attempt an HPTA restart SERMS would be a superior choice imo (though I’m not a doctor).

What I was going by is

  • the use didn’t acutely seem to alter parameters associated with an increased risk for CVD

That’s all. I’m not for or against the use, I believe it ought to be an individualistic decision based upon the patients desires/requirements.