No it shouldn’t, there’s the facet of androgen to oestrogen ratio. There are various benefits that keeping E2 in range with T has (neurological regulation, optimal glucose/lipid metabolism etc). To expect (when fiddling with hormonal balance) E to stay at physiologic ranges while T skyrockets is an unrealistic and stupid expectations. All T metabolites play pivotal roles within regard to bodily homeostasis, and interfering with them can have profound implications regarding downstream pathways fo which can unleash a cascade of consequences.
Think about DHT, why don’t we block the fuck out of DHT when we blast? With you’re rhetoric, clearly we all need to take finasteride to crush DHT because T converts to DHT. Estrogen gets a bad rap, is needlessly demonised by all the gym bros etc when half the shit you’re blocking it for has nothing to do with oestrogen to begin with. Fluid balance is mediated by aldosterone, blood pressure and whatnot tends to be mediated by RAAS functioning. Estrogen favourably modulates the RAAS, lessens Angiotensin II mediated aldosterone secretion and favourably modulates adrenal functioning… AAS induced water retention (while partially oestrogen mediated) is typically stemming from a myriad of other factors (impact on RAAS/adrenals relatively independent of E)… not “oestrogen, crush the fuck out of that”.
It’s been noted in literature that T alone in supra doses has minimal impact on cholesterol, when combined with an AI (I think it was like 300mg + AI) HDL drops by like 40-50%. As messing with T-E balance aggravates endothelial dysfunction moreso than AAS alone, telling someone “take an AI regardless of symptomatology” is dangerous advice. Furthermore, oestrogen is pivotal for nitric oxide release (vasodilatation effect, needed for erections), maintenance of bone mineral density (though with adequate androgen this isn’t as much an issue… though it still pertains significance), joint/connective tissue health is also somewhat dependent on oestrogen.
So to sum it up, why advice someone to potentially throw off
- lipid pannel
- glucose tolerance
- adequate vascular healht
- bone, joint and connective tissue health
- erectile function
If you’re going by the rhetoric “because levels are supraphysiologic”, then we need to crush DHT too, and… what about testosterone, that’s also very high… there are negative outcomes associated with supraphysiologic concentrations of all these hormones, particularly testosterone/DHT moreso than E.
The notion of prostate enlargement is somewhat flawed though, if you don’t get it from 100mg test you probably won’t get it from 500mg. Unlike skeletal muscle the prostate is rather stagnant in that no more AR appear to be synthesised in response to increased androgen concentration, AR in skeletal muscle can be upregulated (more synthesised etc)… the prostate appears to have a finite amount of receptors, of which no plasticity is present… hence why prostatic enlargement tends to be so dependent upon genetic predisposition. DHT however is responsible for hairloss, body hair growth… but blocking DHT has MANY consequences (metabolites act as neurosteroids) and the same can be said about blocking oestrogen, our body is meant to function within adequate ratio, don’t throw off/block natural conversion pathways regarding hormones unless it’s absolutely required
That being said, if you’re on a very high dose (say 1000mg test) there is legitimate possibility for oestrogen alone to cause side effects (severe bloating can be induced if levels are high ENOUGH… like really high), tamoxifen would be first line treatment (for say gyno or something), then non suicidal aromatase inhibitors… at a low dose, not so high you crush E2 back into physiologic ranges whilst T is 10x ref range