Estradiol increases binding of DHT in prostate two fold in vivo
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Regulation of cytoplasmic dihydrotestosterone binding in dog prostate by 17 beta-estradiol.
"17 beta-estradiol enchances androgen-induced prostate growth in the castrate dog to a degree comparable to that seen in spontaneous prostatic hypertrophy. To investigate the mechanism of this synergism, cytosol androgen binding was measured by a density gradient technique in prostates of control and 17 beta-estradiol-treated castrate dogs. [3H]Dihydrotestosterone was bound principally to a moiety that averaged 8.6S in size. Approximately twofold enhancement of this binding by 17 beta-estradiol was demonstrable after 1 wk of treatment with 750 microgram/wk and after 3 wk with 75 microgram/wk. Under conditions in which binding in the 8S region was demonstrable with dihydrotestosterone and testosterone no binding of 3 alpha-androstanediol or progesterone was detectable. Thus, enhancement by 17 beta-estradiol of a prostate cytosol androgen-binding protein occurs under circumstances in which 17 beta-estradiol enhances androgen-mediated prostatic growth."
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@alfredoolivas this is exactly why you don't want to plummet E2 too low with an AI.
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@alfredoolivas this is exactly why you don't want to plummet E2 too low with an AI.
Really? So you can experience rapid prostrate growth to the point where it becomes problematic?
The whole point of this study was an attempt to replicate some of the conditions of BPH. The castrated dogs injected with estrogen may have seen tighter binding of DHT in the prostrate, but this isn't necessarily a good thing. The prostate may have been attempting to protect itself from a massive amount of stress hormone, and sucked up as much protective DHT as it could find.
Remember, these were freshly castrated dogs, and the all the dogs were sacrificed after six weeks, some much sooner. We don't know what would have happened had things progressed longer, but it's reasonable to to assume that DHT levels would have dropped and the effect of the supplemental estrogen would have been unopposed over a longer timeframe.
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I imagine it’s the elevated estradiol driving the binding of the DHT found in male pattern baldness as well, seeing that BDP and MPB have considerable overlap in diagnosis.
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I find this to be new-fangled "scientific" literature that introduces heavier nuance to play an old game. Here, the game is the blame-game of DHT as the driver of prostate issues. I am constantly looking for the exit out of these webs, of which there are plenty. My simple idea is DHT is a "hi-jack" victim, whilst responding in defense of the body. My point of view, or this general point of view is not difficult to grasp. It just takes a different angle, from a different height let's say to see it.
1. Estrogen Initiates the Aggression
The study proves that estrogen is the active, upstream instigator. It alters the tissue architecture by doubling the androgen binding sites. In the bioenergetic view, estrogen is a stress hormone that promotes water retention, tissue swelling (edema), and cellular proliferation. It createss a state of metabolic inflammation in the prostate.
2. DHT Arrives as the Defensive Shield
DHT is the body's most potent, non-aromatizable androgen. It is highly protective, anti-edematous, and supports oxidative metabolism. When estrogen creates a stressful, inflammatory, and structurally unstable environment in the prostate, the body increases DHT binding as a local defensive, adaptive response to counteract estrogen's destructive, proliferative effects.
3. The "Hijacking" and the Blame Shift
Because DHT is a powerful cell signaler, when it binds to a receptor site that has been artificially doubled and structurally altered by estrogen, the resulting growth is pathological or a hypertrophy. Mainstream medicine looks at the tissue, sees DHT bound to the receptors, and blames DHT.In reality, DHT tends to the site to defend the tissue, but because estrogen changed the rules of the game i.e. by altering receptor density and blocking protective steroids like progesterone, the DHT is "hijacked" into driving a corrupted growth process.
We should briefly look at how we would know this about DHT; being polar to estrogen...
1. DHT Downregulates the Anti-Apoptotic bcl-2 Gene
This is the cellular kill switch. One of the most profound pieces of evidence for the Estradiol-DHT model is how these two hormones control cell survival and death.
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The estrogen side: When 17β-estradiol binds to Estrogen Receptor Alpha, it upregulates a protein called bcl-2. bcl-2 is an anti-apoptotic protein, meaning it acts like a shield that prevents old, stressed, or damaged cells from dying. This is exactly how estrogen drives abnormal tissue accumulation and hypertrophy.
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DHT counters: When DHT binds to the intracellular androgen receptor it does the exact opposite: it downregulates bcl-2! By suppressing bcl-2, DHT attempts to strip away the protective shield estrogen gave to those damaged cells, allowing the body to clear out the excess, overgrown tissue
2. The 3beta-Adrostanediol Pathway
DHT does not just work through androgen pathways, and its metabolic breakdown products are highly active in opposing estrogen. Within the prostate, DHT is metabolized into 5alpha-androstane-3beta,17beta-diol.
- 3beta-adiol is the natural, primary ligand for Estrogen Receptor Beta. SO, in prostate tissue, ERalpha activated by estradiol promotes inflammation and rapid cell division. Conversely, ERbeta acts as the tissue's emergency brake and suppresses proliferation, lowers inflammation, and triggers tumor-suppressive actions. By flooding the tissue with DHT, the body ensures a steady supply of 3beta-adiol to activate ERbeta, attempting to shut down the aggressive growth signals driven by estradiol.
3. DHT and the Synthesis of Prostaglandin D2 (PGD2)
Now check this out, another fascinating mechanism involves local prostaglandin regulation. A metabolite of DHT has been shown to directly increase the transcription of prostaglandin D2 synthase via ERbeta activation. And as a side note I remember Peat talking about prostaglandin E as the negative, inflammtory mediator. Elevated levels of Prostaglandin D2 in the prostate serve a deeply protective function: to significantly decrease the risk of abnormal cellular proliferation and curtail the advancement of aggressive tissue growth. The body generates more DHT locally precisely to keep the defensive PGD2 pathway active!!
Suppression of Aromatase Activity
In our bioenergetic framework, one of the absolute worst-case scenario for a tissue is high aromatase activity, which converts circulating androgens into more tissue-destructive estrogen. DHT is a non-aromatizable androgen, meaning the body cannot convert it into estrogen. When DHT levels are robust, it exerts powerful negative feedback on local metabolic pathways, keeping cellular respiration functioning without providing fuel for the aromatase enzyme to create more estradiol.
Estrogen behaves as the true biochemical antagonist in the tissue, actively changing the receptor environment to force growth. DHT is pulled into the site to drop the cellular shields bcl-2 and pull the emergency brake ER-beta. Mainstream observations merely see DHT present at the crime scene and falsely accuse the defender. Hmm, sounds A LOT like the ole cholesterol BS blame game!
Now think about what typically happens!
What we see, typically, is clinical interloping, right? And from there, especially depending on "treatment," we are following a physiological cascade that actually can go in either direction, based fuirther on metabolic health. This means, there has been a medical hijacking of interpretation the whole time! I remember back in I early 2000s, Peat mentioned how they asked the best urologists in America what they would do based on PSA and prostate screening and they all said "watchful waiting" and NOT the surgeries and so-called meds they administer based on early assumptions.Fixing the bioenergy state of the individual would probably allow DHT to do its work and reverse things! As typical medical "treatments" can themselves be estrogenic, invasive, harmful, they could in theory propagate and encourage the estrogen profile or dominance of the situation! What one most likely witnesses is big med making matters worse, but walking away silently pointing at made-up villains. In "cancer treatment" in general is no different. The treatments end up destroying the patient and the conditions induced by treatment is labelled as cause in isolation i.e. organ failure, cardiac arrest, etc.
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@bio3nergetic said:What one most likely witnesses is big med making matters worse, but walking away silently pointing at made-up villains. >>
Sounds like Finasteride and Dutasteride
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