Ye
Yes 100% forgot TUDCA cuz I only use with orals and NAC I also take liposomal glutathione daily.
MESO-Rx
Anabolic Steroids
Aromatase Inhibitors Fix the Number but Break the System, open discussion.
- Thread starter BALLISTIC
- Start date
bananafeet
Member
A lot of this is personal taste. Type2x has some firm opinions that other people don't share. If it's working for you don't change it!
Do Anastrozole or Aromasin reduce gyno?
“Anastrozole is generally ineffective for clinically meaningful prevention/treatment of gynecomastia, and there is no high-quality evidence that exemestane (Aromasin) reduces gynecomastia.
“Anastrozole is generally ineffective for clinically meaningful prevention/treatment of gynecomastia, and there is no high-quality evidence that exemestane (Aromasin) reduces gynecomastia.
- Bicalutamide-induced gynecomastia (best human RCT data): In a double-blind placebo-controlled RCT (n=114, 48 weeks), gynecomastia occurred in 73% with bicalutamide alone vs 51% with anastrozole 1 mg daily (not a clinically adequate reduction), while tamoxifen 20 mg daily reduced it to 10% (P<.001) 1O. This directly addresses Al efficacy in a common drug-induced gynecomastia model.
- Meta-analysis in the same setting:
Systematic review/meta-analysis of 9 RCTs found anastrozole did not show significant benefit, whereas tamoxifen reduced gynecomastia risk by 82% (RR 0.18) 2 U This synthesizes the total randomized evidence for prevention of antiandrogen-related breast events. - Pubertal gynecomastia: A randomized double-blind placebo-controlled trial (n= 80, 6 months) showed response (≥50% US volume reduction) 38.5% with anastrozole vs 31.4% placebo (P=0.47), i.e., no significant benefit.
- Exemestane (Aromasin): The provided evidence shows endocrine effects in males (estradiol suppression and testosterone increase) but does not establish gynecomastia reduction in controlled trials 4 (V. So, you cannot assume clinical efficacy for gynecomastia from mechanism/ PD alone.
BALLISTIC
Member
That's the burden, of these meds outside the well documented health detriment of continuous use. Do you aromatize moderate or heavily. Face value of what you're current running I think (opinion) you could get away without. 600T is enough for signaling of aromatization in most and if keeping levels consistent (daily dosing) with natural biology, absent negative side effects you could be fine. Adding 100mg mast gives you the DHT antagonism to breast tissue, and primo effectively dulling E2 signal. On labs your numbers could appear wrong (high/low) but overall you feel great. Have you experimented with this by chance? If so was it determined you needed AI?
Just mine above, most will be remedy by frequent dosing and daily being best. It takes time for the body to reach homeostasis. Most give up before showing this to occur. Also diet my man, along with various other factors dependant on what you're currently running.
Absolutely bro, and honestly, thanks for that FUBAR thread. I was already deep into research when I came across it and had a full on “holy shit” moment. You were describing the exact issues I’d just started resolving personally, and it forced me to stop and really reassess how we frame estrogen in this context.
BALLISTIC
Member
@adrenalytic
There’s pretty strong mechanistic and clinical support for not aggressively suppressing estradiol when running supraphysiologic androgens. Estradiol plays a direct role in CNS stability, serotonergic tone, endothelial nitric oxide signaling, lipid handling, and cartilage hydration. That’s why higher E2 often correlates with better joint integrity, improved mood, and reduced sympathetic overdrive, even when total testosterone is high. I’m genuinely curious how you’re feeling now and whether you’ve noticed tangible improvements since FUBAR. Haha
The issue isn’t high vs low E2 in isolation as I’ve said before, it’s estradiol that’s disproportionate to androgen signaling or poorly metabolized, often due to compound interactions or hepatic handling issues. With that I still read so many folks reciting what they were told rather than actually evaluating, so thank you for engaging and I thoroughly look forward to your feedback when you can.
I don't pretend to know things I don't and so you sent me on a search quest. Knowledge is ultimately what I was seeking, and this is what I came across.
Compounds like DIM and calcium D glucarate may have a role without undermining estradiol’s protective functions. I’m not claiming certainty here, just what I read...but the mechanism is interesting.
From what I’ve been digging into, DIM doesn’t meaningfully suppress aromatase in vivo, but it does bias estrogen metabolism toward less proliferative hydroxylation pathways. Importantly, this happens without collapsing serum estradiol, preserving CNS, joint, and vascular benefits. CalciumD glucarate, on the other hand, reduces recycling of estrogens potentially smoothing peaks and improving clearance without forcing E2 into subphysiologic ranges. That distinction alone makes this approach worth discussing. Thanks again for educating me.
So these aren’t estrogen suppressors they’re better viewed as estrogen QC (quality control) tools? At least that's what I'm understanding. If I'm wrong throw rocks at me.
In contrast, chronic AI use produces a very different physiologic state, one we’re all familiar with...reduced endothelial function, worsened lipid profiles (often requiring another medication to fix) we all see this stated daily in Meso, increased joint dryness and connective tissue complaints, and the ironic addition of omega oils and joint supplements like glucosamine /chondroitin/MSM that rarely solve the underlying issue. CNS irritability and that “neuro electric” feeling you mentioned are also classic statements.
All of this lines up with what we see clinically when estradiol is pushed too low relative to androgen load. In your case, an E2 around 60 on moderate injectables plus recent Dbol isn’t inherently a problem, I’d argue it’s protective, assuming hematocrit, blood pressure, lipids, and inflammatory markers are in range. So the real question is, how are you actually feeling overall? Currently?
If anything, the smarter outlook here isn’t “how do I lower E2?”, it’s can estrogen handling be improved while preserving signaling? Running DIM or calcium D glucarate shortterm and pulling labs isn’t about chasing a lower number it’s about confirming that estrogen remains functional rather than excessive. Balanced, permissive estradiol tends to be far less harmful longterm than repeatedly suppressing aromatase in a system already dependent on estrogen for homeostasis under high androgen exposure.
There’s pretty strong mechanistic and clinical support for not aggressively suppressing estradiol when running supraphysiologic androgens. Estradiol plays a direct role in CNS stability, serotonergic tone, endothelial nitric oxide signaling, lipid handling, and cartilage hydration. That’s why higher E2 often correlates with better joint integrity, improved mood, and reduced sympathetic overdrive, even when total testosterone is high. I’m genuinely curious how you’re feeling now and whether you’ve noticed tangible improvements since FUBAR. Haha
The issue isn’t high vs low E2 in isolation as I’ve said before, it’s estradiol that’s disproportionate to androgen signaling or poorly metabolized, often due to compound interactions or hepatic handling issues. With that I still read so many folks reciting what they were told rather than actually evaluating, so thank you for engaging and I thoroughly look forward to your feedback when you can.
I don't pretend to know things I don't and so you sent me on a search quest. Knowledge is ultimately what I was seeking, and this is what I came across.
Compounds like DIM and calcium D glucarate may have a role without undermining estradiol’s protective functions. I’m not claiming certainty here, just what I read...but the mechanism is interesting.
From what I’ve been digging into, DIM doesn’t meaningfully suppress aromatase in vivo, but it does bias estrogen metabolism toward less proliferative hydroxylation pathways. Importantly, this happens without collapsing serum estradiol, preserving CNS, joint, and vascular benefits. CalciumD glucarate, on the other hand, reduces recycling of estrogens potentially smoothing peaks and improving clearance without forcing E2 into subphysiologic ranges. That distinction alone makes this approach worth discussing. Thanks again for educating me.
So these aren’t estrogen suppressors they’re better viewed as estrogen QC (quality control) tools? At least that's what I'm understanding. If I'm wrong throw rocks at me.
In contrast, chronic AI use produces a very different physiologic state, one we’re all familiar with...reduced endothelial function, worsened lipid profiles (often requiring another medication to fix) we all see this stated daily in Meso, increased joint dryness and connective tissue complaints, and the ironic addition of omega oils and joint supplements like glucosamine /chondroitin/MSM that rarely solve the underlying issue. CNS irritability and that “neuro electric” feeling you mentioned are also classic statements.
All of this lines up with what we see clinically when estradiol is pushed too low relative to androgen load. In your case, an E2 around 60 on moderate injectables plus recent Dbol isn’t inherently a problem, I’d argue it’s protective, assuming hematocrit, blood pressure, lipids, and inflammatory markers are in range. So the real question is, how are you actually feeling overall? Currently?
If anything, the smarter outlook here isn’t “how do I lower E2?”, it’s can estrogen handling be improved while preserving signaling? Running DIM or calcium D glucarate shortterm and pulling labs isn’t about chasing a lower number it’s about confirming that estrogen remains functional rather than excessive. Balanced, permissive estradiol tends to be far less harmful longterm than repeatedly suppressing aromatase in a system already dependent on estrogen for homeostasis under high androgen exposure.
lukiss96
Member
Anyone noticed that taking Test like for years with no come off, you need less AI than initially?
BALLISTIC
Member
Absolutely, you blunt receptor sensitivity. Over time many report needing higher doses to receive the same benefits. This is not considering overall size and potentially requiring more to support retaining said tissue.
BALLISTIC
Member
SERDS
I was asked about SERDs VS SERMs in an outside conversation. I'm sure most are aware of SERMs so I'll just cover why SERDs Is an absolute NO. Simple basics and you can read more if you feel the need.
Not that anyone I'm aware of is using SERDs.
They do NOT support the higher E2 with higher androgen load model.
SERDs are NOT an AI and it doesn’t manage estrogen. It’s a SERD, it destroys estrogen receptors outright. That means even if blood E2 looks normal or high, estrogen signaling is effectively zero.
The whole reason many of us feel better letting E2 rise with higher androgen load is because estrogen is protective in these ways.
CNS stability & mood
Endothelial / vascular function
Lipids
Joints & connective tissue
Autonomic balance
SERD eliminates those benefits entirely. Labs may look fine, but functionally you’re estrogen deficient. If the goal is balance not suppression SERD is the opposite direction. It’s more extreme than an AI. Estrogen isn’t the problem. Broken estrogen signaling is.
I was asked about SERDs VS SERMs in an outside conversation. I'm sure most are aware of SERMs so I'll just cover why SERDs Is an absolute NO. Simple basics and you can read more if you feel the need.
Not that anyone I'm aware of is using SERDs.
They do NOT support the higher E2 with higher androgen load model.
SERDs are NOT an AI and it doesn’t manage estrogen. It’s a SERD, it destroys estrogen receptors outright. That means even if blood E2 looks normal or high, estrogen signaling is effectively zero.
The whole reason many of us feel better letting E2 rise with higher androgen load is because estrogen is protective in these ways.
CNS stability & mood
Endothelial / vascular function
Lipids
Joints & connective tissue
Autonomic balance
SERD eliminates those benefits entirely. Labs may look fine, but functionally you’re estrogen deficient. If the goal is balance not suppression SERD is the opposite direction. It’s more extreme than an AI. Estrogen isn’t the problem. Broken estrogen signaling is.
lukiss96
Member
Interesting, I hear that. From my experience, I feel like I can do great with 375mg (1.5ccs) now and back then I needed like 500mg to achieve the same effects.
Granted my goal is not to exactly gain more size than I already have, but make muscles more mature, quality and dense, while retaining & improving my athletic ability (gymnastic rings, bars, cardio in combination with heavy lifting) keeps me in good condition and not too heavy.
BALLISTIC
Member
That makes sense, especially given your goals and training style. Early on, higher doses feel necessary because a lot of what you’re sensing is CNS stimulation, glycogen, water, and novelty (feelings).
After years on, androgen signaling is more efficient in several ways also...neuromuscular coordination is better, and you’re no longer chasing that initial dopamine and strength surge. When the goal shifts from adding mass to density, maturity, and athletic output, lower doses often work better. You’re getting better tissue quality, less systemic stress, better recovery, and you’re not fighting excess water, BP, or cardio suppression.
Rings, bars, and conditioning expose inefficiencies fast, being lighter, tighter, and hormonally stable beats brute force dosing every time. Especially in harm reduction and longevity. I have huge respect because that training is paramount and harmony of core strength. Endurance against fatigue.
I should clarify, because I stated that previous post in a non-informative mentality. I don’t think it’s true AR desensitization. Muscle androgen receptors don’t really blunt in a way that forces dose escalation. What changes over time is CNS response, water/glycogen effects, and overall hormonal background. Once you’re past the growth phase and focused on tissue quality and performance, lower doses often express better, not worse. I'm personally looking to focus my attention this way.
If AR desensitization were the main driver, longterm TRT would stop working, and it clearly doesn’t. Most adaptation people feel is neural and systemic, not receptor level failure in muscle. But it does occur much like any drug needing stronger exposure to receive the felt aspect.
Edit: I should have initially elaborated further. My apology dude, as I was reading about the SERD context above.
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bananafeet
Member
Chronically lower estrodial could be due to a lack of FSH in a suppressed male (no gonadotropins):
"Circulating levels of estradiol in women are controlled by follicle-stimulating hormone (FSH), which regulates transcription of the aromatase gene (CYP19A1) in ovarian granulosa cells."
Follicle-stimulating hormone/cAMP regulation of aromatase gene expression requires β-catenin.
I wonder if using HMG could work in men to make aromatase in the testies again and increase estrodial? HMG is an anolog of both LH/FSH while HCG is only a LH analog.
HCG does reliably increase estrodial in men, but I suppose that would only be the case if there was still aromatase in the testies.
I keep coming back to menopause and PCOS because there are a lot of parallels to steroid users and these conditions. (Lack of estrodial, esterone dominance, androgen dominance, lack of aromatase expression etc).
Anyway maybe someone else can have a look at it. Or run some HMG and see if it brings up E2 when HCG won't.
In women peripheral aromatisation mainly increases estrone not estrodial. I don't fully understand how one could have low estrodial in the presence of a large amount of testosterone. But maybe that can be downregulated as well?
Edit: I add this because menopause and PCOS are mainly androgen dominant, and if women made estrodial instead of esterone in peripheral tissues (outside the ovaries) then half of the problems wouldn't exist.
"Circulating levels of estradiol in women are controlled by follicle-stimulating hormone (FSH), which regulates transcription of the aromatase gene (CYP19A1) in ovarian granulosa cells."
Follicle-stimulating hormone/cAMP regulation of aromatase gene expression requires β-catenin.
I wonder if using HMG could work in men to make aromatase in the testies again and increase estrodial? HMG is an anolog of both LH/FSH while HCG is only a LH analog.
HCG does reliably increase estrodial in men, but I suppose that would only be the case if there was still aromatase in the testies.
I keep coming back to menopause and PCOS because there are a lot of parallels to steroid users and these conditions. (Lack of estrodial, esterone dominance, androgen dominance, lack of aromatase expression etc).
Anyway maybe someone else can have a look at it. Or run some HMG and see if it brings up E2 when HCG won't.
In women peripheral aromatisation mainly increases estrone not estrodial. I don't fully understand how one could have low estrodial in the presence of a large amount of testosterone. But maybe that can be downregulated as well?
Edit: I add this because menopause and PCOS are mainly androgen dominant, and if women made estrodial instead of esterone in peripheral tissues (outside the ovaries) then half of the problems wouldn't exist.
SnowyMiami
Member
Wanted to weigh in on Asin vs Adex for TRT. I started a quarter pil Asin (6.25mg) E3D. Low grade anxiety improved, that weird disconnected feeling of high E2 went away and interest in sex returned. Joints feel fine. All around just a smoother experience than Adex.
I think Adex has its place for big cycles but is just too potent for the average home gamer.
I think Adex has its place for big cycles but is just too potent for the average home gamer.
BALLISTIC
Member
People think high E2 water, but low E2 creates a different, uglier kind of water.
RAAS/aldosterone disinhibition, estradiol normally suppresses RAAS. When E2 drops too low, aldosterone rises, and kidneys retain sodium/water. This results in smooth, stubborn, puffy water that doesn’t respond well to treatment other than a remedy for E2.
This is very common in AI overuse, high androgen load with suppressed aromatization also Tren/DHT heavy stacks. Loss of endothelial nitric oxide, E2 up regulates eNOS, Low E2 vasoconstriction, poor capillary flow with interstitial fluid leakage. Water sits outside the muscle SubQ(subcutaneous). You look plump all over. But mostly develope distinct areas of edema.
Cortisol & sympathetic dominance, estradiol buffers cortisol, low E2 higher cortisol push. Cortisol also retains sodium while it adds to BP volatility and water. Kidney perfusion changes estradiol improves renal blood flow, low E2 reduces glomerular perfusion efficiency, then your kidney responds by holding fluid. Not kidney damage kidney compensation for not holding a balance.
adrenalytic
Member
Yes, that is my understanding of them as well. They essentially help E2 metabolize more efficiently. That's an interesting tidbit about CDG. I didn't know it functioned like that.
Regarding blood markers, I recently posted this. Didn't get any traction but I don't think many people visit the Blood Serum Testing subforum.
You'll find all pertinent markers in the table there. The biggest issue you'll see is my CRP is not good right now (6) but I suspect that is due to an infection I had been fighting earlier in the month (WBC is elevated slightly) as well as a shoulder injury and your typical enhanced training inflammation. But I otherwise feel fine. Mood is normal and even optimistic at times, sleep is great (I never had sleep issues anyway) and my training is productive even though I'm in a deficit.
Unfortunately, the shoulder injury (strained my supraspinatus doing side raises of all things
) has kept me off pressing movements for the better part of the past 3 weeks so I couldn't tell you if I am still experiencing the neural current as that was only happening on heavy bench.I'm probably 2 more weeks out from being able to press again. Shoulder injuries suck. But I will be sure to update when I'm back at it.
Cheers, bud.
Interestingly, I find the opposite with high estrogen. My mood often plummets and that sympathetic drive kicks into high gear. I become more reactive, irritable, and defensive. I also don't get nearly as good pumps and I get ED. The sympathetic tone seems to override any of those other perceived benefits. Anecdotal of course.
I find that I have a bit more wiggle room when my test levels are very high but when they are around that 1200ng/dl or lower, that window becomes much more narrow for estrogen balance. I know you cover that scenario a bit with the ratio discussion.
This conversation is very interesting to me as estrogen levels have always been the bane of my PED use. Too high or too low and always struggled to find that sweet spot. Then the factor of DHT impact even when estrogen appears in a 'good spot' on blood work.
BALLISTIC
Member
It gets interesting is exactly with what you mentioned. The window changes depending on testosterone levels. When total androgen load is very high, most seem to tolerate a wider estrogen range without symptoms. But once testosterone is closer to low or below acceptable levels, that acceptable estrogen window tightens dramatically. Small deviations in either direction suddenly become symptomatic. That’s where the ratio discussion becomes far more useful than chasing a static E2 number.
I also think this is where blood work alone can misleads people, especially once DHTs or 19nors enter the picture. You can have estrogen sitting in what looks like a good range on paper, yet still feel off because DHT signaling, CNS stimulation, or altered AR/E2 balance is shifting how that estrogen is actually perceived physiologically.
Your point about estrogen being the recurring pain point in PED use really resonates. Too high or too low is obvious, but the frustrating part is when labs say things are fine and the body clearly disagrees. That’s usually when I suspect the issue isn’t estrogen quantity, but estrogen relative to total androgenic and CNS load, plus whatever masking effects certain compounds like nandrolone on joints introduce.
This is exactly why I think these discussions need to move away from fixed targets and toward contextual balance, how estrogen behaves within a given androgen environment, not independent of it.
