EQ Aromatization

[gains4000]

I keep seeing “EQ is an aromatase inhibitor” around every single AAS forum.

Now to my understanding EQ converts to Estrone (E1).

When you Combine Testosterone and EQ the E2 levels can drop because both compounds are competing for the aromatase enzyme.

Now if someone was to use EQ only, they would still have Estrogen in their blood. It would be Estrone.

Do guys actually believe they are getting estrogen deficiency from using EQ with Testosterone?

If we dig back in old threads it’s common to see guys run 200 test 800 EQ and none of them were complaining.

I’d like to see the EQ AI conversation be settled!

 

[pickapeck]

i looked at the literature a while back when More Dates blatted this out. I recall that Estrone was 10x normal level so even if E2 is low I speculated that the estrone was fulfilling some of the function even if Estrone is considered a weaker estrogen. I didn't dig down deep to see what the kinetics look like at the estrogen receptors but that was my reasoning. When I was young a bottle of something was a cycle. A couple times that bottle was a bottle of EQ. i didn't have any problems. Weakish steroid but it was good for what i was doing back then.

 

[gains4000]

i looked at the literature a while back when More Dates blatted this out. I recall that Estrone was 10x normal level so even if E2 is low I speculated that the estrone was fulfilling some of the function even if Estrone is considered a weaker estrogen. I didn't dig down deep to see what the kinetics look like at the estrogen receptors but that was my reasoning. When I was young a bottle of something was a cycle. A couple times that bottle was a bottle of EQ. i didn't have any problems. Weakish steroid but it was good for what i was doing back then.

Agreed. Even if estrone is a weak estrogen it’s still a form of estrogen. And men don’t need a lot of estrogen.

besides yourself , I have seen guys in old threads use EQ only cycles and none were complaining about crashed Estrogen.

 

[Type-IIx]

EQ aromatizes to E1 & E2 (at 58% the rate of T). If it does lower systemic/circulating E2, it could plausibly be at least partly by saturation of Aromatase (though unlikely to be completely at the doses/concentrations at which this is reported given the Km value of T =[aromatase]=> E₂, [Κm = 1.83 nM], following Michaelis-Menten kinetics).

EQ is a potential inhibitor of 17β-HSD1. Inhibition of 17β-HSD1 => ↓E2 (though abolition would require inhibition of Aromatase & Sulfatase, also)

We know that DHT binds this enzyme (from Protein Databank, code: 3KLM) in two orientations, given the reduction of DHT into both (inactive) 3β-diol & 3α-diol by 17β-HSD1:



We also know that for DHT (or T, or 3β-diol, all substrates for it) to become a "good" ligand for this enzyme, they must more closely mimic the planar shape of the A-ring of E2 (which EQ does better than DHT) and provide a large hydrophobic core.

I tend to view EQ as a bit of an edge case for this action if it occurs, but certainly 1-Test ("DHB") & Primo (metenolone) seem to more closely meet these parameters given their saturated A-ring.

Practical difficult arises in sorting out AAS that might inhibit 17β-HSD1 just from the inherent dissociation of good ER ligands from the other groups within the nuclear receptor family. In a multivariate system, ER is most distal from the centroid (G) of the system... ER's value from this matrix (16.4) is distinguished from MR (3.56), GR (2.56), AR (1.38) & PR (0.48). ER is therefore the most atypical receptor as regard overall behavior of the 158 steroids tested & reacts differently from the other receptors which fall into an irregular stepwise progression (PR→AR→GR→MR) away from the center. ER is highly selective, GR & MR can be considered as a group, and AR & PR another group with respect to structure/activity, although there exist molecules that can distinguish between AR & PR and between MR & GR.

 

[gains4000]

EQ aromatizes to E1 & E2 (at 58% the rate of T). If it does lower systemic/circulating E2, it could plausibly be at least partly by saturation of Aromatase (though unlikely to be completely at the doses/concentrations at which this is reported given the Km value of T =[aromatase]=> E₂, [Κm = 1.83 nM], following Michaelis-Menten kinetics).

EQ is a potential inhibitor of 17β-HSD1. Inhibition of 17β-HSD1 => ↓E2 (though abolition would require inhibition of Aromatase & Sulfatase, also)

We know that DHT binds this enzyme (from Protein Databank, code: 3KLM) in two orientations, given the reduction of DHT into both (inactive) 3β-diol & 3α-diol by 17β-HSD1:

View attachment 170573

We also know that for DHT (or T, or 3β-diol, all substrates for it) to become a "good" ligand for this enzyme, they must more closely mimic the planar shape of the A-ring of E2 (which EQ does better than DHT) and provide a large hydrophobic core.

I tend to view EQ as a bit of an edge case for this action if it occurs, but certainly 1-Test ("DHB") & Primo (metenolone) seem to more closely meet these parameters given their saturated A-ring.

Practical difficult arises in sorting out AAS that might inhibit 17β-HSD1 just from the inherent dissociation of good ER ligands from the other groups within the nuclear receptor family. In a multivariate system, ER is most distal from the centroid (G) of the system... ER's value from this matrix (16.4) is distinguished from MR (3.56), GR (2.56), AR (1.38) & PR (0.48). ER is therefore the most atypical receptor as regard overall behavior of the 158 steroids tested & reacts differently from the other receptors which fall into an irregular stepwise progression (PR→AR→GR→MR) away from the center. ER is highly selective, GR & MR can be considered as a group, and AR & PR another group with respect to structure/activity, although there exist molecules that can distinguish between AR & PR and between MR & GR.

Do you believe that someone running EQ only would develop estrogen deficiency?

The drug aromatizes so I don’t see that happening.

To my knowledge even halotestin used for HRT doesn’t cause “crashed e2” like many complain about now a days.

 

[Type-IIx]

E1's potency to activate ERα is 2% that of E2 by the way so its concentrations would have to be upwards of 20 nmol/L or 20,000 pmol/L or 5 ng/mL to replace low-normal E2 levels in men.

 

[Type-IIx]

Do you believe that someone running EQ only would develop estrogen deficiency?

The drug aromatizes so I don’t see that happening.

To my knowledge even halotestin used for HRT doesn’t cause “crashed e2” like many complain about now a days.

I'm not the best to ask since I'm convinced this nouveaux ExcelMale "biohacker" type that have found their way to these forums to report low E2 symptoms while on TRT need a good doctor to sternly pose the question, "have you considered that you're faking it?"

Seriously. I think their symptoms are more related to training volume, underrecovering, and basically psychosomatic.

 

[gains4000]

E1's potency to activate ERα is 2% that of E2 by the way so its concentrations would have to be upwards of 20 nmol/L or 20,000 pmol/L or 5 ng/mL to replace low-normal E2 levels in men.

It’s safe to say EQ simply has Very Weak Estrogenic effects. It’s not a compound that causes excessive estrogen sides even at high dosages.

I don’t know if people claiming it’s a potent aromatase inhibitor that “crashes estrogen” Is the right way to describe EQ.