I don't know which, if any, of these details might be pertinent, so I'll include everything I can think of.
I'm HSPC. T4 N1M0 G4+5. Diagnosed in 2018.
I've been using a modified BAT for 3 1/2 years.
Testosterone propionate. Olaparib starting two days prior to the first injection of a phase and continuing for a couple of days. A week prior to the end of the high T phase I start taking Orgovyx. After the main high T cycle ends I use darolutamide. I also am going to use some Zytiga.
After about a week I use gels or orals to get short T pulses. Hours or days. I've done them a dozen times and each time my PSA drops. Except for once. I had SBRT. My PSA went up a lot at first and then dropped. I "hope" that I killed a lot of the cancer (used Olaparib and aligned some of the sessions to high T pulses and some to low T). I know I didn't get it all because I still have PSA.
Anyway, those are the details of what I'm doing. Here is my question.
I was thinking of replacing half the Orgovyx cycles with High tE2 cycles. To get it done right I would probably have to overlap them by a few weeks (start estrogen patches a couple of weeks prior to the upcoming high T phase).
Comments? Suggestions? I'll graph it out and post a comment.
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PCaWarrior
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I plotted estrogen, orgovyx, and androgenic testosterone. The main reason that I would want to do this is to conserve orgovyx. I have enough for about a year and then will have to rely on my MO - or India.
How much does Orgovyx cost in the US? Here it is 170 EUR for 30 tablets (but free under universal insurance). I saw it was cheaper in the Uk than here.
High T for however long you determine then jump into ADT with daro and Orgo for whatever length you determine per PSA results and the last couple of weeks your going to use high dose E2 instead of Orgo and until you clear daro then jump bsck on high T?
That could work but have you been using low dose T during ADT cycles with success?
If so i would feel more comfortable using high dose E. But I queried ChatGPT
Question:
If i took high dose E2 instead 2 the last couple of weeks of ADT cycle instead of Orgovyx what would be my concerns with bad estrogen and or estrogen imbalance
Answer:
Concerns with High-Dose Estradiol (E2) Instead of Orgovyx in the Last Weeks of ADT
Switching from Orgovyx (Relugolix) to high-dose Estradiol (E2) during the last weeks of your ADT cycle presents several key concerns related to estrogen balance, androgen receptor (AR) modulation, and potential negative estrogen metabolites.
⸻
📌 Key Concerns: Estrogen Metabolism & Imbalance
1️⃣ Bad Estrogen Metabolites (E1 & 4-OH-E2)
• Estradiol (E2) metabolizes into different estrogens:
• Estrone (E1) – Can convert back to E2 but is less beneficial for AR modulation.
• 4-Hydroxyestradiol (4-OH-E2) – Potentially carcinogenic, forms DNA-damaging quinones.
• 16α-Hydroxyestrone (16α-OH-E1) – More potent than E2, linked to increased cancer risk in some tissues.
• Concern → If you’re pushing E2 high without supporting proper metabolism, you could accumulate harmful estrogen metabolites.
✅ Solution:
• Use DIM (Diindolylmethane) & Calcium-D-Glucarate to favor 2-hydroxyestrone (protective estrogen) over 4-OH and 16α-OH metabolites.
• Monitor E1/E2 ratio & estrogen metabolites with Urinary Estrogen Metabolite Testing (DUTCH Test or equivalent).
⸻
2️⃣ Estrogen Feedback on LH/FSH & Tumor Growth Risk
High androgens might enhance the effectiveness of radiation therapy by increasing DNA double-strand breaks (DSBs) or impairing DNA repair mechanisms in prostate cancer cells. This idea is being explored in research on androgen priming before radiation.
How High Androgens Affect DNA DSBs in Radiation Therapy:
1. Increased Cell Proliferation → More Radiation Sensitivity
o Androgens drive prostate cancer cell proliferation.
o Fast-dividing cells are more vulnerable to radiation-induced DNA DSBs because they have less time for repair before mitosis.
2. Androgen-Driven DNA Damage
o High androgen levels can increase replication stress, leading to spontaneous DNA DSBs.
o This may act synergistically with radiation, which also induces DSBs.
3. Androgen-Induced Defects in DNA Repair
o Some studies suggest that androgens can suppress homologous recombination (HR) repair, making cells rely more on error-prone NHEJ.
o This could make radiation-induced DSBs more lethal.
4. Androgen Receptor (AR) and DNA Repair Genes
o The androgen receptor (AR) regulates genes involved in DNA repair.
o High androgen signaling may alter the expression of key repair proteins, leading to inefficient DSB repair.
Clinical Implications:
• Androgen Priming: Some trials are testing whether giving high-dose androgens before radiation increases tumor cell kill.
• Bipolar Androgen Therapy (BAT): Alternating high and low androgen levels could make cancer cells more vulnerable to treatments like radiation or PARP inhibitors.
• PARP Inhibitors Synergy: If androgens impair HR repair, combining radiation with PARP inhibitors could further increase radiation sensitivity.
This is almost exactly what I did in 2023 when I had SBRT. I talked to my MO and the ASTRO president first. I aligned two SBRT sessions with high androgens and the remaining three with low androgens (we have clinical trial data backing ADT with RT). And I used a PARP inhibitor (olaparib).
In March 2024, I did SBRT to all visible (PSMA F18) oligomets (4 spine lesions) and added Pembrolizumab for the abscopal effect (SBRT increases the TILs count in and around the tumour, turning cold tumors "hot".)Same day I begun SBRT , I had the infusion of 1 cycle of pembro (Keytruda). As per several trials and documented experiences, I learned that for its efficiency Pembro must be infused on or a day or two before SBRT. I was going to have 5 days of radiation, so it seemed OK to do it on day 1.
And I did this while beeing on ADT and with ENZALUTAMIDE (sensitive to ENZA but not to ADT; 4 months in ENZA since PSA 8, had lowered -50% on ENZA already).
I didn't add high Testosterone because of pain and metastasis in the spine risking compression.
Then in August (5 months after SBRT) I begun BAT with PSA=0.9; spiked to 1.9 in high T, and my NADIR for now is 0.23 after the 1st full BAT cycle.
I had the prostate treated parcially with IRE in 2017 and NADIR was 0.7 then.
Next time, if necessary SBRT, I will add high TESTOSTERONE and again a PARP inhibitor. Will now also try to get Olaparib for high T BAT cycles.
I think Cabergoline is risky. I didn't like its side effects when.I read about it
Maybe DIM alone, or some Letrozole can control the E2 spike from Testosterone aromatization.
** some data suggests that high dose cabergoline could kill the CRPC cells when Enza does not work anymore. Seems that after beeing testosterone suppressed, the cells rely on prolactin somehow, and Cabergoline can kill them, beeing there.some literature about some anecdotal cures with that aggressive protocol.
In the PATCH trial, with 100 micrograms/24h E2 patches, E2 seemed to be safe, though some gynaecomastia ocurred. And PSA suppression was as effective as ADT. And serum E2 was around 70 (above the 50 normal top range value in men, but not too high).
I am using 50 micrograms/24 E2 Patch during all BAT except during high T. And might use 75 patch during ENZA.
Will use 200 to 400 mg DIM during High T to control serum E2 spike under 100.
I think that will suffice.
And control hipertensión with meds during high serum T.
And I add 100 to 200 mg aspirin daily to avoid blood clots due to E2 (and also to control the vitamin K2 effect).
We need to control red blood cell count also, but with short periods of Testosterone the proliferation has been mild. Just enough to get me out of the anemia range levels, thus recovering from fatigue and asthenia
BAT so far, seems to be working, and QOL improved. 🫡
Zinc ionophore plus cabergolin when nothing else is working. Suppressing prolactin when the tumor is androgen independent. (And maybe adding BAT to it?)(Dr Costello)
Thank you for mentioning the association between high E2 and prolactin. I found that, indeed, I had high prolactin levels when I was taking high-dose tE2. I've temporarily stopped taking E2 (gel), and will remeasure my prolactin soon.
• Prolactin (PRL) is a hormone that helps regulate metabolism, immunity, and hundreds of other processes.
• PRL is one of the stimulants for PCa when it is hormone resistant.
• PRL has been implicated in prostate cancer survival and resistance to hormone deprivation.
• Stat5 has been recently shown to promote human prostate cancer cell survival/proliferation and to be associated
with early prostate cancer recurrence. Stat5 is the main signaling pathway triggered by PRL.
• PRL is also expressed by prostate epithelial cells, and increased PRL expression
has been documented in high-grade prostate cancers.
• Estrogen stimulates the release of PRL.
• The structure of growth hormone and PRL are similar.
• PRL can be decreased by approximately 85% by using 0.25 mg of Cabergoline twice a week.
We don't have high quality evidence of the involvement of PRL in PCa. But I wouldn't want to take a chance.
1. The Suppression of Prolactin is required for the Treatment of Advanced Prostate Cancer – PMC ncbi.nlm.nih.gov/labs/pmc/a...
2. Frontiers - The Relevant Participation of Prolactin in the Genesis and Progression of Gynecological Cancers | Endocrinology Frontiers | The Relevant Participation of Prolactin in the Genesis and Progression of Gynecological Cancers (frontiersin.org)
3. Prolactin, stem cells and prostate cancer | ECE2011 | 13th European Congress of Endocrinology | Endocrine Abstracts endocrine-abstracts.org/ea/...
5. Low testosterone and low prolactin required for successful ADT: Testosterone, prolactin, and oncogenic regulation of the prostate gland. A new concept: Testosterone-independent malignancy is the development of prolactin-dependent malignancy! urotoday.com/recent-abstrac...
6. Prolactin receptor signaling: A novel target for cancer treatment - Exploring anti-PRLR signaling strategies – PMC ncbi.nlm.nih.gov/pmc/articl...
7. A Novel Patient Case Report to Show the Successful Termination of Untreatable Androgen-independent Prostate Cancer: Treatment with Cabergoline (Dopamine agonist). – PMC ncbi.nlm.nih.gov/pmc/articl...
8. A Proposed Efficacious Treatment with Clioquinol (Zinc Ionophore) and Cabergoline (Prolactin Dopamine Agonist) for the Treatment of Terminal Androgen-independent Prostate Cancer. Why and how? - PMC ncbi.nlm.nih.gov/labs/pmc/a...
9. Prolactin receptor targeting in breast and prostate cancers: new insights into an old challenge – PubMed pubmed.ncbi.nlm.nih.gov/285...
10. Local prolactin is a target to prevent expansion of basal/stem cells in prostate tumors - PubMed pubmed.ncbi.nlm.nih.gov/206...
11. Investigative Clinical Study on Prostate Cancer Part VIII: Prolactin Hormone and the Pituitary-Testicular-Prostate Axis at the Time of Initial Diagnosis and Subsequent Cluster Selection of the Patient Population after Radical Prostatectomy | Anticancer Research ar.iiarjournals.org/content...
12. Randomized Pilot Study of Cabergoline, a Dopamine Receptor Agonist: Effects on Body Weight and Glucose Tolerance in Obese Adults – PMC ncbi.nlm.nih.gov/labs/pmc/a...
13. A null study: Phase I Study of LFA102 in Patients with Advanced Breast Cancer or Castration-resistant Prostate Cancer | Anticancer Research ar.iiarjournals.org/content...
20. Development and Potential Clinical Uses of Human Prolactin Receptor Antagonists | Endocrine Reviews | Oxford Academic academic.oup.com/edrv/artic...
There is some evidence that using aspirin and darodarolutamide at the same time upregulates ARs by supressing cox-2.
If you are doing ADT with daro and/or other drugs, they are correct. You should only use NSAIDs with their approval. Usually it involves cardiac risk.
But for many reasons, this is not an issue with BAT. I can argue that theoretically that an NSAID with daro might be a good thing to do. There are at least 3 reasons to take them. One conventional and two theoretical.
My MO and I discussed this and decided to use aspirin.
Aspirin, a commonly used nonsteroidal anti-inflamatory drug (NSAID), has been studied for its potential role in preventing or delaying metastasis in prostate cancer. Here are some relevant findings:
* A large prospective cohort study found that regular aspirin use (>3 times/week) was associated with a significant reduction in the risk of lethal prostate cancer (distant metastases or prostate cancer death) compared to non-use.
* A meta-analysis of observational studies showed that aspirin use was associated with a decreased risk of prostate cancer incidence.
* The anti-metastatic effects of aspirin may be mediated through inhibition of platelet activation and aggregation, which can promote tumor cell dissemination and metastasis. Aspirin may also have direct anti-tumor effects through modulation of inflammatory pathways and inhibition of proliferation and angiogenesis.
* Potential synergists with aspirin in prostate cancer include other NSAIDs (e.g., celecoxib, a selective COX-2 inhibitor), metformin (an anti-diabetic drug with anti-cancer properties), and statins (cholesterol-lowering drugs that may have anti-metastatic effects). (Cancer Prevention Research, 2019)
* An ongoing phase 3 clinical trial (ADD-Aspirin, NCT02804815) is investigating whether regular aspirin use can prevent recurrence and improve survival in patients with non-metastatic prostate cancer and other solid tumors.
* Side effects of aspirin include increased risk of bleeding (especially gastrointestinal), stomach upset, and rarely, kidney toxicity. Regular use should be discussed with a healthcare provider, and caution is advised in patients with a history of peptic ulcers, bleeding disorders, or kidney disease.
But listen to your MO. They are right if you're on conventional ADT and/or ARSIs (daro for example).
Maybe but to my knowledge it hasn't been proven. I'd ask my MO and also my primary care physician for their opinions. Aspirin and other NSAIDs reduce some other health risks.
I get down to facts when I talk to my MO. I do not think dying of a heart attack is a good tradeoff for not dying of cancer.
Sure. There might be some that are of interest. If not let me know and I'll try to beef it up. I mostly focus on HSPC since that is what I am.
Aspirin
Aspirin, a commonly used nonsteroidal anti-inflamatory drug (NSAID), has been studied for its potential role in preventing or delaying metastasis in prostate cancer. Here are some relevant findings:
* A large prospective cohort study found that regular aspirin use (>3 times/week) was associated with a significant reduction in the risk of lethal prostate cancer (distant metastases or prostate cancer death) compared to non-use.
* A meta-analysis of observational studies showed that aspirin use was associated with a decreased risk of prostate cancer incidence.
* The anti-metastatic effects of aspirin may be mediated through inhibition of platelet activation and aggregation, which can promote tumor cell dissemination and metastasis. Aspirin may also have direct anti-tumor effects through modulation of inflammatory pathways and inhibition of proliferation and angiogenesis.
* Potential synergists with aspirin in prostate cancer include other NSAIDs (e.g., celecoxib, a selective COX-2 inhibitor), metformin (an anti-diabetic drug with anti-cancer properties), and statins (cholesterol-lowering drugs that may have anti-metastatic effects). (Cancer Prevention Research, 2019)
* An ongoing phase 3 clinical trial (ADD-Aspirin, NCT02804815) is investigating whether regular aspirin use can prevent recurrence and improve survival in patients with non-metastatic prostate cancer and other solid tumors.
* Side effects of aspirin include increased risk of bleeding (especially gastrointestinal), stomach upset, and rarely, kidney toxicity. Regular use should be discussed with a healthcare provider, and caution is advised in patients with a history of peptic ulcers, bleeding disorders, or kidney disease. The bleeding increase has been studied in ADD-Aspirin and for 100-300 mg/day is 0.03% (0.10% vs. 0.07% for non-users).
Aspirin has a short half-life. However, it acts on newly formed platelets and the platelets can’t create new COX enzymes so the effects of aspirin last for the duration of the platelets (approximately 10 days). As a result of platelet turnover, the recovery of COX enzymes is about 10% per day.
STAMPEDE shows that aspirin/NSAID use might be therapeutic. When combined with Zytiga/ADT the results are particularly promising. Abiraterone acetate and prednisolone with or without enzalutamide for high-risk non-metastatic prostate cancer: a meta-analysis of primary results from two randomised controlled phase 3 trials of the STAMPEDE platform protocol - PMC (nih.gov)
1. Inhibits angiogenesis, prostaglandins, inflammation, metastasis, cell cycle completion, and cell proliferation: The multiple effects of aspirin in prostate cancer patients – ScienceDirect sciencedirect.com/science/a...
2. Inhibits angiogenesis: Mechanisms of the antiangiogenic effects of aspirin in cancer – ScienceDirect sciencedirect.com/science/a...
3. Cohort study: Use of Low-Dose Aspirin and Mortality After Prostate Cancer Diagnosis: A Nationwide Cohort Study – PubMed pubmed.ncbi.nlm.nih.gov/308....
4. Association of Aspirin Use With Mortality Risk Among Older Adult Participants in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial | Cancer Screening, Prevention, Control | JAMA Network Open | JAMA Network jamanetwork.com/journals/ja...
5. NHANES: Aspirin Use and Lethal Prostate Cancer in the Health Professionals Follow-up Study – ScienceDirect sciencedirect.com/science/a...
7. Aspirin use might reduce prostate cancer mortality but only if used long term (>5 years): COX-2 inhibitors in prostate cancer treatment—hold your horses? – PMC ncbi.nlm.nih.gov/pmc/articl...
8. Aspirin use might reduce prostate cancer mortality but only if used long term (>5 years): Short-term effects of daily aspirin on cancer incidence, mortality, and non-vascular death: analysis of the time course of risks and benefits in 51 randomised controlled trials – PubMed pubmed.ncbi.nlm.nih.gov/224...
9. A large clinical trial showing that aspirin does not increase longevity and that it might increase cancer mortality: Effect of Aspirin on All-Cause Mortality in the Healthy Elderly | NEJM nejm.org/doi/full/10.1056/n...
10. Aspirin risk increases in those older than 70: Effect of Aspirin on All-Cause Mortality in the Healthy Elderly | NEJM nejm.org/doi/full/10.1056/N...
11. Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity | Nature nature.com/articles/s41586-...
13. Sci-Hub | COX-2 mediates pro-tumorigenic effects of PKCε in prostate cancer. Oncogene, 37(34), 4735–4749 | 10.1038/s41388-018-0318-9 sci-hub.st/10.1038/s41388-0...
14. Prospective cohort study: Aspirin and Non-Aspirin NSAID Use and Prostate Cancer Incidence, Mortality, and Case-Fatality in the Atherosclerosis Risk in Communities Study – PMC ncbi.nlm.nih.gov/pmc/articl...
I looked into celecoxib a few years ago. It seemed to me at that time that aspirin has a much better risk/reward ratio. I still have some celecoxib. Every once in a while I pop a pill.
I think one patient here wrote that celebrex is better because its only a Cox 2 inhibitor vs Aspirin, a Cox 1 & 2. Inhibiting Cox 1 effects lining of stomach, he said.
It is a more selective inhibitor. Only cox 2. Makes sense theoretically. Aspirin has data on it's side. In a nutshell, do you want to go with a theory or what works?
And he is correct. Has to do with the type of prostaglandins inhibited. The overall cardiac risk is rather high with celecoxib though (1-5% of people on celecoxib have a heart event any given year). The ADD-aspirin trial looked at the bleeding risk. They determined that your minor bleeding risk increases from 0.70% to 1%. I didn't have that data when I made my choice to take aspirin.
My heart is healthy though. I'm probably low risk. But my gut seems healthy also. So...?
Part of the choice for me boils down to data. Aspirin has it and is being tested in trials. Celecoxib doesn't have the data. Maybe that will change.
the one above yes. It is very fascinating and i also think this High T priming would work fantastic for chemo as chemo is more effective in fast growing cells.
Thanks. It detailed some risks. I'm aware of those. But what I was not aware of is that there is a possibility that estrogen makes olaparib therapy more effective. I'll look into that and might include tE2 once a year.
The potential synergy between estradiol (E2) and olaparib (a PARP inhibitor) is an emerging area of interest, particularly in hormone-sensitive cancers like prostate and breast cancer. While direct clinical evidence is limited, preclinical studies and biological mechanisms suggest a possible interaction.
Possible Mechanisms of Synergy
Estrogen Signaling & DNA Damage Response (DDR)
Estradiol can influence DNA repair pathways, particularly through BRCA1/2 regulation.
High E2 levels may impair homologous recombination (HR) repair, making cells more reliant on alternative DNA repair mechanisms (which PARP inhibitors like olaparib can block).
Androgen Receptor (AR) & DDR in Prostate Cancer
In prostate cancer, testosterone + estradiol (e.g., in Bipolar Androgen Therapy, BAT) has been shown to induce double-strand DNA breaks (DSBs).
If E2 further suppresses DNA repair, adding olaparib could exploit this vulnerability by blocking alternative repair pathways, leading to cancer cell death.
HR Deficiency & PARP Sensitivity
Cancers with HR defects (e.g., BRCA mutations, ATM loss) are more sensitive to olaparib.
If estradiol reduces HR efficiency, this could enhance olaparib’s efficacy even in tumors that are not inherently HR-deficient.
What I do when I ask chat bots for medical info is I ask them to cite references and grade the quality of evidence.
It takes weeks for T to go down in response to high E. It took me 5 weeks when I did it.
I think I would need to take my E2 high with just short breaks. But, my thought now is that I'm not going to go this route. I know that orgo works for me. I'll continue using it as needed until I run out. Might not ever happen.
Another way to get good info out of chat bots is to be very specific.
For example, I asked ChatGPT the following: “Please summarize the findings of the PATCH trial (estrogen vs. Lupron for ADT).”
Response was:
The PATCH trial investigated the efficacy and safety of transdermal estradiol (tE2) patches compared to luteinizing hormone-releasing hormone (LHRH) agonists, such as Lupron, for androgen deprivation therapy (ADT) in men with non-metastatic (M0) prostate cancer. The study included 1,360 men randomized to receive either tE2 patches or LHRH agonists.
urotoday.com
Key Findings:
• Efficacy: Transdermal estradiol was found to be non-inferior to LHRH agonists in terms of metastasis-free survival and overall survival.
urotoday.com
• Side Effects: Patients receiving tE2 experienced fewer hot flashes (44%) compared to those on LHRH agonists (89%). However, gynecomastia was more common in the tE2 group (85% vs. 42%).
urotoday.com
• Bone Health: Transdermal estradiol improved bone mineral density, whereas LHRH agonists are associated with bone loss.
pmc.ncbi.nlm.nih.gov
• Cardiovascular Safety: There was no excess cardiovascular toxicity observed with tE2 compared to LHRH agonists.
urotoday.com
• Quality of Life: Overall quality of life scores were improved in the tE2 group.
urotoday.com
These findings suggest that transdermal estradiol is an effective and potentially preferable alternative to LHRH agonists for ADT in men with non-metastatic prostate cancer, offering benefits in side effect profiles, bone health, and quality of life.
Pretty good summary. I wouldn't have thought to do this if you hadn't weighed in. Thanks.
I added the Patch summary to my book. I'm going to start using chat bots to do some of the grunt work.
I also pay the $20/month and i save the ChatGPT responses under different folders plus i have it create a word doc that is downloadable and email it to myself and save it on my phone and computer for further editing.
The other very cool thing is i also have it either read my medical reports or lab results in either pdf or any picture format and have it memorize it for future queries on my health options. Like how does this or that effect my gene mutations.
AIs are getting more and more useful. I wrote a math tutor for my son. And an essay writer and a language tutor. I wrote an AI doctor. Ask it something and it gives you what it thinks plus references and quality of evidence. Same for supplements. I should make a PCa specific ap. References, Quality of evidence, side effects if applicable, ease of insurance authorization if applicable. others?
May I ask what mutation you are using the oliparb for? I just finished up 6 rounds of doxecetal and looking at oliparb for bard1 mutation . I’m very interested in more info on BAT and E2 to help oliparb maintenance. Also any comments on the SE .
2. Several other studies testing olaparib in combination with DNA damaging therapies are underway or have recently completed. The results of these studies generally support combining PARP inhibitors with DNA damaging therapies.
3. Results of this study showed good response regardless of HRR status.
4. Testosterone enanthate or cypionate 400mg IM every 28 days. Olaparib 300 mg BID.
5. Excellent results for synergy with PARP inhibitor Olaparib. 47% of those who had an HRR mutation as well as 47% of those without an HRR mutation had a PSA50 response. 76% had a PSA drop. 26% had a PSA90 response. 61.5% had a radiographic complete or partial tumor response.
6. A control group was not included (Olaparib and injections of saline solution) but the radiographic response rate appears to be 1-2x what might be expected from Olaparib monotherapy.
And there are mouse and cell studies. Those and the trial and the mechanism of action convinced me to try Olaparib on a limited basis during most high T pulses. 2-3 days prior to a day or so after. I haven't noticed any side effects.
The strongest evidence is for BAT and olaparib. The E2 synergy is speculative.
Very little of what I do is SOC but most is backed by clinical trials and/or what I feel are solid theories. I can't recommend what I do to others. It's worked well for me but n of 1 is little to go on.
But if someone wanted to use tE2 for ADT that has lots of high quality evidence and large trials.
Good to see this discussion, as I have wondered with the resurgence of E2 for PCa control, if that it might have a place in BAT. I would guess the on-off cycles of two hormones might be doubly difficult to manage, but you guys with real world experience would have a much better Idea about that than me. In the case of you, PCaWarrior, it may turn out to be a case of necessity (Orgovyx shortage) will be the mother of invention (a new BAT treatment regime). With damn fine results expected to be outcome, of course.
The topic is prostrate cancer and modified hormones? Right?
My reply will not be able to be graphed out, but if you are working on your self, if its ok, I'd like to offer a brief piece of advice and insight.
First of all, All diseases have causes. It is when you learn how to properly, safely, and effectively approach these causes, that will you be able to reverse the conditions.
As just a couple examples of causes of diseases to consider:
Toxoplasmosis are conditions that are caused by the parasite Toxoplasma gondii. This particular infections is now beyond pandemic proportion worldwide, and is 'known' to alter the hormones of its host, and it "... encysts and induces chronic inflammation within the prostate of any species. ..." I suspect this microscopic pathogen could be causing part of your problems. I am placing sited article for you to view below.
There is also another infectious disease called trichomoniasis, caused by Trichomonas vaginalis. This one has been linked to prostrate cancer!
Lastly I will mention a tapeworm species, Taenia crassiceps. This infection will alter hormones, because it uses them to reproduce. If the hormones are altered, it is because something has altered them and using them to thrive.
I have 40+ years research, experience and skill working with people who suffer with chronic conditions caused parasites (bacteria, fungi, virus, helminth, protozoa ... etc.), and many cancers are included. I offer private interactive wellness services worldwide.
The common parasite Toxoplasma gondii induces prostatic inflammation and microglandular hyperplasia in a mouse model pmc.ncbi.nlm.nih.gov/articl...
Taenia crassiceps-Excreted/Secreted Products Induce a Defined MicroRNA Profile that Modulates Inflammatory Properties of Macrophages pmc.ncbi.nlm.nih.gov/articl...
Hi PCa could you possibly PM me about your BAT and oliparb. I have many questions not related to your ask, but this is looking like my next treatment routine. However the BAT therapy is difficult to find an MO willing to undertake the risks.
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Finally Undetectable PSA on BAT
3rd & 4th pBAT cycle results with daro question
