E2 Levels on TRT

I haven't needed an AI on TRT or 'cycle' but my cycles are low - 250-300 mg per week max.
Look up cruciferous vegetables like broccoli and brussel sprouts and the reduction of hormone related cancers and issues. It has always been thought of the indole-3-cabinol content which I believe is part of it but those vegetables are loaded with DIM.
If you take 100-300 mg of DIM a day via supplement. Different supplements have different amounts but it is common to see 100 to 300 - recommended to take one a day.

One meal with 1/2 cup of brussel sprouts provides just over 100 mg. Broccoli/asparagus/brussel sprouts are like my desert - they are not filling and part of my regular diet. If you eat 4-6 meals a day, add in some cruciferous vegetables and you will be getting your DIM plus they taste good.

Just a thought for a second benefit of DIM - it is linked to lower cancer rates. I wouldn't put a person on AI just because regardless of what their far % is. I would get pre TRT hormone tests done and ask him how he feels with follow up bloods a month in and determine. Otherwise you could crash his estrogen or be wasting an AI and adding another drug that isn't needed. In the words of my good friend, don't throw shit at the wall and hope it sticks. Get the blood work done and then take the appropriate action.

Caveat - maybe someone like @Funnyman may know and can do it based on feel but the average person can't who doesn't have years of experience with blood work and symptoms.
 
Goldenrod said:
I haven't needed an AI on TRT or 'cycle' but my cycles are low - 250-300 mg per week max.
Look up cruciferous vegetables like broccoli and brussel sprouts and the reduction of hormone related cancers and issues. It has always been thought of the indole-3-cabinol content which I believe is part of it but those vegetables are loaded with DIM.
If you take 100-300 mg of DIM a day via supplement. Different supplements have different amounts but it is common to see 100 to 300 - recommended to take one a day.

One meal with 1/2 cup of brussel sprouts provides just over 100 mg. Broccoli/asparagus/brussel sprouts are like my desert - they are not filling and part of my regular diet. If you eat 4-6 meals a day, add in some cruciferous vegetables and you will be getting your DIM plus they taste good.

Just a thought for a second benefit of DIM - it is linked to lower cancer rates. I wouldn't put a person on AI just because regardless of what their far % is. I would get pre TRT hormone tests done and ask him how he feels with follow up bloods a month in and determine. Otherwise you could crash his estrogen or be wasting an AI and adding another drug that isn't needed. In the words of my good friend, don't throw shit at the wall and hope it sticks. Get the blood work done and then take the appropriate action.

Caveat - maybe someone like @Funnyman may know and can do it based on feel but the average person can't who doesn't have years of experience with blood work and symptoms.
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Veggies do taste good.

And yeah, its never a good idea to keep adding drugs to fix issues of other drugs.

Just like a hot tub of pool, sometimes you need to wait and let things balance out, instead of trying to chase things by adding in stuff to get perfect. There is no perfect.
 
Horror Cock said:
I think this is relevant enough to add my thoughts on another area.

Taking this for example: https://onlinelibrary.wiley.com/doi/abs/10.1002/jcp.22936

While winstrol is very drying, from the article above "we found that nandrolone and stanozolol caused a dose-dependent induction of aromatase expression and estradiol (E2) production. When used in combination with IGF-I they were more effective than single molecules in inducing aromatase expression."

So if you're concerned about longevity then don't just go about "if I don't get gyno I'm fine".

Sure overall you can't call any of the DHT derivatives "estrogenic" drugs, but in certain tissues the estrogenicity may be as potent as taking straight up estrogen. Everyone knows anadrol does it. Other studies also stated that anavar agonizes estrogen.

Which I theorize could be the reason why certain AAS cause testicular atrophy faster than others regardless of gonadotropin levels.
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Something else to be mindful of is that DHT has twice the binding affinity to androgen receptors as Testosterone. This is one of the reasons that adding a DHT compound can kill libido in some, or exacerbate E2 issues. Another curious point from some research in which oxandralone was used to aid in the healing of burn victims: The authors suggested that oxandrolone has an androgenic action and effect thus stimulating serum LH and testosterone.5 Both contribute to higher levels of circulating testosterone, higher dht, and higher E2. At least this is what I've garnered from the research I have done.
 
Goldenrod said:
I haven't needed an AI on TRT or 'cycle' but my cycles are low - 250-300 mg per week max.
Look up cruciferous vegetables like broccoli and brussel sprouts and the reduction of hormone related cancers and issues. It has always been thought of the indole-3-cabinol content which I believe is part of it but those vegetables are loaded with DIM.
If you take 100-300 mg of DIM a day via supplement. Different supplements have different amounts but it is common to see 100 to 300 - recommended to take one a day.

One meal with 1/2 cup of brussel sprouts provides just over 100 mg. Broccoli/asparagus/brussel sprouts are like my desert - they are not filling and part of my regular diet. If you eat 4-6 meals a day, add in some cruciferous vegetables and you will be getting your DIM plus they taste good.

Just a thought for a second benefit of DIM - it is linked to lower cancer rates. I wouldn't put a person on AI just because regardless of what their far % is. I would get pre TRT hormone tests done and ask him how he feels with follow up bloods a month in and determine. Otherwise you could crash his estrogen or be wasting an AI and adding another drug that isn't needed. In the words of my good friend, don't throw shit at the wall and hope it sticks. Get the blood work done and then take the appropriate action.

Caveat - maybe someone like @Funnyman may know and can do it based on feel but the average person can't who doesn't have years of experience with blood work and symptoms.
Click to expand...
I've seen that figure, and apparently Broccoli is even more potent, however, I don't believe it translates to a direct metabolized amount that is equivalent to 100mg of DIM. At least that was my understanding. I've taken DIM before, and there was an obvious and noticeable benefit, but I never noticed a similar benefit from regularly eating cruciferous vegetables.
 
resilient1 said:
Something else to be mindful of is that DHT has twice the binding affinity to androgen receptors as Testosterone. This is one of the reasons that adding a DHT compound can kill libido in some, or exacerbate E2 issues. Another curious point from some research in which oxandralone was used to aid in the healing of burn victims: The authors suggested that oxandrolone has an androgenic action and effect thus stimulating serum LH and testosterone.5 Both contribute to higher levels of circulating testosterone, higher dht, and higher E2. At least this is what I've garnered from the research I have done.
Click to expand...
Oxsndrolon will lower shbg as well
 
resilient1 said:
Something else to be mindful of is that DHT has twice the binding affinity to androgen receptors as Testosterone. This is one of the reasons that adding a DHT compound can kill libido in some, or exacerbate E2 issues. Another curious point from some research in which oxandralone was used to aid in the healing of burn victims: The authors suggested that oxandrolone has an androgenic action and effect thus stimulating serum LH and testosterone.5 Both contribute to higher levels of circulating testosterone, higher dht, and higher E2. At least this is what I've garnered from the research I have done.
Click to expand...
The action of DHT isn't linear with dose increases after all. Some studies concluded that it is more anabolic than testosterone - I believe it depends on which dosage range it is tested at.

I also believe endorphins are largely involved in suppressing LH, one rodent study feeding nandrolone saw some brain region increase endorphins 20 fold. Another rodent study showed enclomiphene lowers endorphins in hypothalamus. In that case, endorphin receptors are pretty adaptive, and when desensitized then LH suppression will happen less? But still there is a limit to the adaptiveness.

I still have not repeated my type of cycle with at least 3 bloodwork points. Trying to get bloodwork for free, I'm cheap. Where.... endorphins are the main focus.
 
Other non androgenic methods I'm looking out for include myokines, like irisin, and cannabinoid antagonists, which might become cheap enough and effective at some point, but for now every alternative I know of is expensive and not that effective.

Here are the studies mentioned in the recent reply above,


Europe PMC

Europe PMC is an archive of life sciences journal literature.
europepmc.org europepmc.org

It is possible that:

↑Sex steroid agonism → ↑Endorphin activity → ↓Gonadotropin secretion

If so, then a steroid cycle without being suppressed might be:

Exogenous testosterone + Naloxone coadministration = no suppression of gonadotropin secretion -> at the end, single dose of opioid agonist to desensitize

Two studies gave healthy men AAS, and separate group endorphin blockade with it, in whom LH did not get suppressed.



But then studies show in animals that after naloxone is ceased, testosterone goes below what was in control.

karger.com

Restraint Inhibits Luteinizing Hormone and Testosterone Secretion in Intact Male Rhesus Macaques: Effects of Concurrent Naloxone Administration

Abstract. The present study investigates how restraint affects the hypothalamo-hypophysial adrenocortical axis and the hypothalamo-hypophysial gonadal axis in intact, adult male rhesus macaques. Restraint was chosen because it is not physically painful or harmful to the animal, but rather serves...
karger.com karger.com

I myself felt overly high afterward, never did opioids but it definitely matched the description of mu-opioid agonists, when my endorphin receptors were hypersensitive.

This study shows that the rebound after opioids works in the opposite direction too, a dramatic increase in testosterone after a single opioid dose wears off and endorphin receptors are desensitized:

.... do not have the link right now, have screenshots 0fh5m1ctsvxc1.jpg e3x1ru5tsvxc1.jpg

Kratom is a legal mu opioid receptor, so, likely 3 days after the end a steroid cycle which included naloxone, a single dose of kratom might make you even more suppressed for a day or two, but then desensitize endorphin receptors enough that normal testosterone levels are swiftly restored without allowing the pituitary or balls to atrophy.

Additionally I included cyproheptadine during the cycle to offset potential cortisol spike from naloxone use, but I realise such a hypothetical cortisol spike wouldn't harm much if exogenous steroids are high enough. But the other benefit of it is, while the dopamine antagonism of cyproheptadine is made bearable with the steroids, the prolactin doesn't spike since cypro also blocks serotonin. And after the cycle, when cyproheptadine is ceased, prolactin stays low because the serotonin autoreceptor that is sensitive is not the one that causes prolactin secretion, but does regulate how much serotonin you make. While the dopamine receptor that got hypersensitive is the one that inhibits prolactin secretion. So, with overabundance of dopamine post-cycle, it is less problematic that the endorphin receptors are overly sensitive, prolactin won't really spike up.
 
Horror Cock said:
Oops. Original screenshot resolution: View attachment 63681View attachment 63680
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While it is true that in the exogenous DHT study, combining DHT with naltrexone elevated LH above baseline, the one with exogenous testosterone wasn't as straightforward.

There, I should correct that I read it wrong the first time, as the abstract did not clarify which number js the starting point, it said testosterone + naloxone caused the LH to go 6.9->7.3.

To clarify, administration of testosterone lowered LH from 7.6 to 6.9. Naloxone raised it back up to 7.3. Which means almost half of the suppression still happened.

That still keeps it open that naloxone coadministration might prevent the further suppression below 7.3 in this scenario, if dosing is repeated daily?
 
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