DHT/estradiol optimal ratio in men

[ak7802]

Hi, what's the optimal ratio of DHT to estradiol and testosterone? Testosterone and estradiol are within the upper limits of normal, while DHT is more than twice the normal range. Could this imbalance be causing erectile dysfunction and libido problems? If so, is it better to increase estradiol above the normal range or lower DHT levels to within the normal range?

 

[SS1LE]

yes longterm higher DHT can create issues for some, usually in the terms of displacing estradiol which in return gives you low E2 symptoms even though estradiol is in good range.

 

[FunkOdyssey]

Hi, what's the optimal ratio of DHT to estradiol and testosterone? Testosterone and estradiol are within the upper limits of normal, while DHT is more than twice the normal range. Could this imbalance be causing erectile dysfunction and libido problems? If so, is it better to increase estradiol above the normal range or lower DHT levels to within the normal range?

What protocol is producing these labs? Scrotal cream?

 

[WhiteMale]

IMHO the notion of a ratio of hormones is utter garbage.

You're not divulging enough to base an opinion off; labs and protocol.

 

[ak7802]

What protocol is producing these labs? Scrotal cream?

No scrotal cream, 35 mg testoterone enan Sub-Q every day, and 10 mg primobolan Sub-Q every day.

 

[ak7802]

yes longterm higher DHT can create issues for some, usually in the terms of displacing estradiol which in return gives you low E2 symptoms even though estradiol is in good range.

So, keeping estradiol higher than normal rage (about 70 pd/ml) might be a solution ?

 

[FunkOdyssey]

No scrotal cream, 35 mg testoterone enan Sub-Q every day, and 10 mg primobolan Sub-Q every day.

You're probably barking up the wrong tree with the ratio here. You're doing at least three things which are commonly associated with poor libido and erectile problems:

1. Daily injections of long esters
2. Use of primobolan at any dose
3. Massive doses of testosterone
4. (Controversial bonus) Subq injections

 

[Nelson Vergel]

T ng/dL x 0.04= E2 in ng/dL x 10= E2 in pg/mL (Estradiol is usually 0.2-0.4% of Total T)

T ng/dL x 0.1= DHT in ng/dL (DHT is near 10% of total T)


DHT/E2= 0.10/0.04= 2.5

 

[ParetoPEDGuy]

No scrotal cream, 35 mg testoterone enan Sub-Q every day, and 10 mg primobolan Sub-Q every day.

You're pulling too many levers at once, which makes this hard to diagnose cleanly.
DHT and E2 need to be in balance for optimal libido and erection quality. Most guys know you can raise E2 via HCG adjustments, less frequent/larger injections, or dropping AI-like ancillaries.

What fewer guys realize is that excessively high DHT acts as an aromatase inhibitor at the tissue level. Your labs can show "normal" E2 while your functional E2 is effectively suppressed. So you have two ways to fix the ratio: raise E2 or lower DHT.

Which is right for you depends entirely on your situation. Personally I had to lower DHT because 5 clicks of scrotal cream had me with bacne, oily skin and scalp pimples worse than puberty at 38. But if those sides weren't present I'd have just titrated HCG up instead, because I'm someone who needs higher E2 for maximum libido.

When I first got on Test Cyp 150mg/week plus 1000 IU HCG/week my E2 hit 61 and guys were telling me to take anastrozole immediately. Meanwhile my libido was absolutely unhinged, my wife was like "I can't do this anymore, this is worse than when you were a 21-year old sex addict, like I'd almost be relieved if you got a mistress at this point." lol

In contrast, some guys feel terrible above a certain E2 threshold regardless of DHT. Those guys need to lower DHT to fix the ratio because raising E2 simply isn't a lever available to them.

Now a few questions about your protocol:

-Why enanthate with daily injections? Long esters like enanthate aromatize less than cypionate even at once-weekly IM dosing, so daily subq with enanthate seems like an odd combination.

-Why primobolan?

-Have you tried testosterone cream? Scrotal application handles DHT reliably without excessive aromatization, and you can then dial in libido on an extremely granular basis purely by titrating HCG until you find your number. Much easier to optimize than managing injections.

 

[Nelson Vergel]

What fewer guys realize is that excessively high DHT acts as an aromatase inhibitor at the tissue level. Your labs can show "normal" E2 while your functional E2 is effectively suppressed. So you have two ways to fix the ratio: raise E2 or lower DHT.

Great comment.

When I first got on Test Cyp 150mg/week plus 1000 IU HCG/week my E2 hit 61 and guys were telling me to take anastrozole immediately. Meanwhile my libido was absolutely unhinged,

I am glad you are reporting this. E2 has been linked with libido, although I wish we had good data on T/E2 ratios and libido.

 

[FunkOdyssey]

Why enanthate with daily injections? Long esters like enanthate aromatize less than cypionate even at once-weekly IM dosing, so daily subq with enanthate seems like an odd combination..

I was with you, right up until this statement. Where did you get the idea that enanthate aromatizes less than cypionate?

 

[ParetoPEDGuy]

I was with you, right up until this statement. Where did you get the idea that enanthate aromatizes less than cypionate?

I can't post the PubMed link here bc I'm a new account but here is the article reference # on PubMed:

PMID: 34694927

Basically it was a comparison of IM Test Cypionate vs Sub-Q Test E

Some findings:

"However, subcutaneous TE was independently associated with lower post-therapy estradiol (p<0.001) and lower hematocrit (p<0.001) compared to IM-TC, after adjusting for covariates. Neither modality was associated with significant PSA elevation."

"At equal weekly dose (100 mg), IM-TC produces higher estradiol and higher hematocrit than SC TE. This is attributed to the higher Cmax from IM delivery driving more substrate available for aromatization at peak."

 

[FunkOdyssey]

"However, subcutaneous TE was independently associated with lower post-therapy estradiol (p<0.001) and lower hematocrit (p<0.001) compared to IM-TC, after adjusting for covariates. Neither modality was associated with significant PSA elevation."

"At equal weekly dose (100 mg), IM-TC produces higher estradiol and higher hematocrit than SC TE. This is attributed to the higher Cmax from IM delivery driving more substrate available for aromatization at peak."

As they said, the difference is attributed to subq vs IM injection, not the ester difference. There's another study out there from the manufacturer of Xyosted which shows the exact opposite though (AI summary to follow):

This is the Kaminetsky et al. 2015 Phase II study — the Antares Pharma-funded dose-finding study that became the basis for the Xyosted development program. The key data is in Table 2.

The study compared 50mg SC TE weekly, 100mg SC TE weekly, and a 200mg IM TE reference group already at steady state. They calculated E2/T ratios from the AUC₀₋₁₆₈ₕ values, and here's what they found:

The mean E2/T ratio (AUC-based) was 0.0063 for the 50mg SC group, 0.0055 for the 100mg SC group, and 0.0032 for the 200mg IM group. PubMed Central

So the SC groups had roughly 1.7–2× the E2/T ratio of the IM group — meaning for a given amount of testosterone exposure, significantly more was being aromatized to estradiol with subcutaneous delivery. That's the finding you were remembering.

What's interesting is that the absolute E2 levels were actually comparable between 100mg SC and 200mg IM (Cavg of ~48 vs ~50 pg/mL), but the IM group achieved that with nearly double the testosterone exposure. So the IM route was more "efficient" at delivering testosterone without proportional estradiol generation.

The full citation: Kaminetsky J, Jaffe JS, Swerdloff RS. "Pharmacokinetic Profile of Subcutaneous Testosterone Enanthate Delivered via a Novel, Prefilled Single-Use Autoinjector: A Phase II Study." Sexual Medicine 2015;3(4):269–279. It's open access on PMC: Pharmacokinetic Profile of Subcutaneous Testosterone Enanthate Delivered via a Novel, Prefilled Single‐Use Autoinjector: A Phase II Study - PMC

As an aside, the findings in this study reflect my personal experience with subq vs IM injection very faithfully.

 

[Cataceous]

...
What fewer guys realize is that excessively high DHT acts as an aromatase inhibitor at the tissue level. Your labs can show "normal" E2 while your functional E2 is effectively suppressed. ...

There are some nuances here. Systemic estradiol represents the sum of tissue-level aromatization. This hypothesis says that there can be local imbalances large enough to cause significant macroscopic effects, yet too small to noticeably affect serum estradiol. It's plausible, but I'd be interested in seeing specific evidence before fully accepting the idea.

In contrast, I believe DHT is also an antagonist of the estrogen receptor. Thus there is another mechanism for anti-estrogenic effects that is not reflected in serum estradiol levels.

...
As an aside, the findings in this study reflect my personal experience with subq vs IM injection very faithfully.

It's interesting to consider possible mechanisms for the pharmacokinetics of testosterone preparations to influence the average production rate of estradiol. One idea, which applies to higher doses of testosterone, is the saturation of aromatase. Considering that the effect becomes noticeable just above the normal range for serum testosterone, the saturation effect could in theory be a factor in reducing the rate of aromatization with forms of testosterone that result in higher/longer peak levels.

Alternatively, estradiol itself can influence the rate of aromatization. Some highlights when I asked grok:

Mechanisms Involving Aromatase Expression and Activity​

​

Aromatase expression is not static and can be regulated by sex steroids, including testosterone and its metabolite estradiol. Evidence indicates that exposure patterns could differentially affect this regulation:​

• Testosterone-Induced Upregulation via Estradiol: Testosterone itself does not directly upregulate aromatase in all tissues, but its conversion to estradiol can create a positive feedback loop. In male murine aortic endothelial cells, testosterone treatment increased aromatase expression and estradiol production in a dose-dependent manner (e.g., a 1 µM dose led to a 580% increase in aromatase expression and 350% in estradiol production). Critically, this effect was blocked by aromatase inhibitors (e.g., anastrozole), indicating that the produced estradiol mediates the upregulation. Non-aromatizable androgens like dihydrotestosterone (DHT) decreased aromatase expression, confirming the role of estradiol in this feedback. This mechanism is also mediated by estrogen receptor alpha (ERα), as ERα knockout reduced the response.
• Implications for Patterns: Sustained testosterone exposure (as with longer-acting esters) provides continuous substrate for initial aromatization, leading to prolonged estradiol production. This estradiol could then amplify aromatase expression over time, increasing overall conversion efficiency and estradiol AUC. In contrast, pulsatile patterns (higher peaks but troughs) might produce brief estradiol spikes insufficient for sustained upregulation, resulting in less cumulative aromatization despite the same average testosterone.
• Tissue-Specific Effects: In adipose tissue (a major site of aromatization in men), obesity-related increases in aromatase are linked to elevated estradiol, creating a vicious cycle where estradiol may contribute to further aromatase induction via inflammatory or receptor-mediated pathways. In the brain, aromatase expression is higher in males and regulated by estradiol, influencing behaviors and potentially amplifying local conversion during sustained exposure. However, direct comparisons of pulsatile vs. sustained patterns on aromatase induction are limited, with most evidence coming from dose-response or inhibition studies rather than temporal profiles.