“How Hormone Receptors Affect Prostate Cancer”

“How Hormone Receptors Affect Prostate Cancer” (Ed Friedman) [#59] Frank Brancato, Russ Hollyer, and Brad Power May 21, 2023 “I look at their data, and their data tells me what's going on. So far, everything I've seen fits my model. But in some cases, the author of the paper will say these results are inexplicable or paradoxical.

And that's because they conflict with what they were taught in medical school.” – Ed Friedman “It turns out that in reality prostate cancer is caused by high local levels of estradiol, <not testosterone.>” - Ed Friedman Meeting Summary Does testosterone cause prostate cancer? Can hormones (testosterone) be used to treat advanced prostate cancer?

Conventional Wisdom : For decades, doctors were taught that testosterone causes prostate cancer. Their proof was that if rats were given high levels of testosterone, around two thirds of them would develop prostate cancer. Also, androgen deprivation kills prostate cancer.

A More Complex Model : However, in 2008 it was definitively proven that estradiol (a sex hormone, the most potent and abundant form of estrogen) acting on estrogen receptor-alpha (a chemical messenger that regulates the rate of transcription from DNA to RNA) is the primary cause of prostate cancer.

Testosterone doesn’t fuel prostate (and breast) cancer, it is a messenger on the pathway that tells the prostate cells to grow, divide, or die, along with other hormones. In this more complex model, estradiol, estrogen receptors, and aromatase (the enzyme that converts testosterone to estrogen), play key roles.

Testosterone, in fact, if administered in certain ways, can help control prostate cancer. Dr. Edward Friedman is uniquely qualified to describe this more complex model of the relationship between hormones, hormone receptors, and prostate (and breast) cancer. He has a Ph.D. in Biophysics and Theoretical Biology from the University of Chicago.

He has had four articles published about prostate cancer, two of which were peer reviewed. He has had eight letters to the editor about prostate cancer published in peer-reviewed journals. He has had one book published, "The New Testosterone Treatment: How You and Your Doctor Can Fight Breast Cancer, Prostate Cancer, and Alzheimer's" (2013).

What is a more complex model of how hormones cause prostate cancer? Prostate cancer is more immediately driven by estradiol, rather than testosterone, though testosterone is involved. Prostate cancer starts when prostate epithelial cells (cells which cover the inside and outside of surfaces) are exposed to high local (near the prostate) levels of estradiol, creating mutations.

Normally, prostate epithelial cells never divide, and prostate cells do not make estrogen.

“How Hormone Receptors Affect Prostate Cancer” (Ed Friedman) [#59] produced from testosterone inside prostate cells which have a mutation (in the 5AR gene) that starts convert

divide, and prostate cells do not make estrogen. But in the case of prostate cancer, high local levels of estradiol are

“How Hormone Receptors Affect Prostate Cancer” (Ed Friedman) [#59] produced from testosterone inside prostate cells which have a mutation (in the 5AR gene) that starts converting testosterone into estradiol. This activates the estrogen receptor alpha. When the estrogen (estradiol) triggers the estrogen receptor alpha, prostate cancer begins.

What are the practical implications of this more complex model for prostate cancer patients? ●The more advanced the prostate cancer, the more likely there are mutations that protect it from testosterone. Also, the more advanced the prostate cancer, the more estrogen receptor alpha present, which makes estradiol more deadly.

●If you still have your prostate, then it’s important to keep estradiol at low normal levels for good health and discourage additional cancer initiation. High levels of estradiol cause cell division and mutations in prostate epithelial cells, ultimately leading to cancer.

To monitor your estradiol and other hormones, you can get a hormone panel test, such as the Genova Diagnostics “One Day Hormone Check” . To keep your estradiol at low normal levels, you can take aromatase inhibitors or eat Brussel sprouts. ●If you don’t have a prostate, keep estradiol in normal range for good health. You should keep your estradiol at 13-20 pg/ml.

Sometimes it will become undetectable. It is a moving target if you introduce exogenous testosterone. ●High levels of testosterone act to prevent epithelial prostate cell division and can kill your cancer cells.

A better way to implement bipolar androgen therapy is to keep testosterone high and cycle DHT (dihydrotestosterone, the most potent hormone among the androgens, and considered a pure androgen as it cannot convert into estrogen.) What are possible future implications of this model? RU486, mifepristone, a drug which blocks progesterone, could be a game changer for prostate cancer.

How do key hormones contribute to prostate cancer and how can they be controlled? ●Testosterone: The main male sex hormone. A messenger that tells the prostate cells to grow, divide, or die. We can decrease it or increase it as desired. Receptor(s): Membrane androgen Receptor(s) (mAR), Intracellular androgen Receptor(s) (iAR).

●DHT: dihydrotestosterone, the most potent hormone among the androgens, and considered a pure androgen as it cannot convert into estrogen. Almost all of it is derived from testosterone via 5AR. If we want to block it we can use 5AR inhibitors (e.g., finasteride, dutasteride). We can decrease it or increase it as desired. Usually this will also involve increasing testosterone.

Receptor(s): Intracellular androgen Receptor(s) (iAR) ●Estrogen: Most of it is derived from testosterone via aromatase. If we want to block it we can use aromatase inhibitors (e.g., letrozole, anastrozole, exemestane).

d. Usually this will also involve increasing testosterone. Receptor(s): Intracellular androgen Receptor(s) (iAR) ●Estrogen: Most of it is derived from testosterone via aromatase. If we want to block it we can use aromatase inhibitors (e.g., letrozole, anastrozole, exemestane). If we want to increase it we can use estrogen patches, gels, or creams. Receptor(s): Estrogen receptor alpha (ERa) – usually bad. Estrogen receptor beta (ERb) – usually good

“How Hormone Receptors Affect Prostate Cancer” (Ed Friedman) [#59] ●Prolactin: This hormone could be used as fuel by some castrate resistant prostate cancer tumors. If we want to block it we can use prolactin inhibitors (e.g. cabergoline). Receptor(s): PRLE. ●Progesterone: One of its functions is to assist in testosterone production. Receptor(s): PRa – usually bad, PRb – usually good.

How can I learn more about Dr. Friedman’s theories? Please see his book and his website.

The information and opinions expressed on this website or platform, or during discussions and presentations (both verbal and written) are not intended as health care recommendations or medical advice by Cancer Patient Lab/Prostate Cancer Lab, its principals, presenters, participants, or representatives for any medical treatment, product, or course of action.

You should always consult a doctor about your specific situation before pursuing any health care program, treatment, product or other course of action that might affect your health.

“How Hormone Receptors Affect Prostate Cancer” (Ed Friedman) [#59] Meeting Notes The information and opinions expressed on this website or platform, or during discussions and presentations (both verbal and written) are not intended as health care recommendations or medical advice by Cancer Patient Lab/Prostate Cancer Lab, its principals, presenters, participants, or representatives for any medical treatment, product, or course of action.

You should always consult a doctor about your specific situation before pursuing any health care program, treatment, product or other course of action that might affect your health.

SUMMARY KEYWORDS receptor, testosterone, prostate cancer, cancer, intracellular, estriol, membrane, finasteride, cell, progesterone, estradiol, receptor alpha, showed, patients, give, amplified, paper, doctor, prostate, mutations SPEAKERS Ed Friedman (85%), Russ Hollyer (7%), Brian McCloskey (5%), John Sandiford (2%), Brad Power (<1%) Discussion Outline 1.Introduction to Dr. Ed Friedman. (0:00) 2.

Ed’s background and research. (1:39) 3.How prostate cancer originates and the role of estrogen. (5:32) 4.Hormone testing and prostate cancer. (13:07) 5.Good and bad androgen receptors. (21:10) 6.How to treat prostate cancer? (28:03) 7.How safe is estriol for men and women? (34:55) 8.Hormone sensitivity and prostate cancer. (42:29) 9.The problem with finding a doctor to treat prostate cancer.

(48:29) 10.The benefits of testosterone replacement therapy. (56:18) 11.

ors. (21:10) 6.How to treat prostate cancer? (28:03) 7.How safe is estriol for men and women? (34:55) 8.Hormone sensitivity and prostate cancer. (42:29) 9.The problem with finding a doctor to treat prostate cancer. (48:29) 10.The benefits of testosterone replacement therapy. (56:18) 11.Do you know if functional testing has been done?

(1:03:21) Russ Hollyer 1:03 We have today with us Edward Friedman, PhD. He's an expert on hormones. I was so excited when he agreed to present, even though it was on Sunday. I said any day, any time, I don't care if it's 2am, or 3am, at whatever the time, on whatever the day, I will be there. He is an expert.

He was the reason why I abandoned ADT and went to high testosterone, which worked for me for two years.

“How Hormone Receptors Affect Prostate Cancer” (Ed Friedman) [#59] Ed Friedman 1:54 Let me talk a little bit about my background. I've been researching hormone receptors since 2004. My first article was published in 2005. It was on prostate cancer and the properties of the androgen and estrogen receptors. After doing that article, some people I knew came down with breast cancer.

When I was doing the research for the article, there were so many papers talking about the receptors and saying that what they were seeing was exactly what they were seeing in breast cancer. So I started researching breast cancer as well. In 2007 I had my second article published, and I added progesterone receptors. Basically, all the receptors are almost identical in breast and prostate cancer.

The only exception is the membrane antigen receptor, which in women decreases BCL2, and in men increases it. I'm not going to go into all the details, but it's pretty close to being the same. Some people urged me to write a book. I had that published in 2013.

One of my fans happened to be a professional English teacher teaching people how to get a book published, and he volunteered his time and helped me to find a literary agent, and eventually became a co-author to make my book more readable in plain English. Since that time, I've had three more articles that I published in researchgate.

net, one of which was expanding on the role of estradiol in prostate cancer, and the latest one was looking at the BAT treatment in terms of what they're overlooking and what they're doing right. Everything I tell you is pure theory. It's based on what I'm seeing in the literature. It's not something that I'm making a guess at. “I think this.” It's like, “There are articles out there.

“How Hormone Receptors Affect Prostate Cancer” (Ed Friedman) [#59] You're a theoretician, a researcher, versus a clinician. A clinician looks at clinical results. I think they're both vitally important. You're looking at the theory, you're not looking necessarily at the practical applications. Ed Friedman 5:31 That's correct. And the other thing is that the clinicians will publish the results without giving a clear exp

tate Cancer” (Ed Friedman) [#59] You're a theoretician, a researcher, versus a clinician. A clinician looks at clinical results. I think they're both vitally important. You're looking at the theory, you're not looking necessarily at the practical applications. Ed Friedman 5:31 That's correct.

And the other thing is that the clinicians will publish the results without giving a clear explanation of why they have what they have. I'll give you an example. In fact, Dr. Denmeade says, it works because of the wind cap on a 402 cell line (?) and what that does, but in that paper he doesn't answer the question.

“Why do you have to have an amplified intracellular androgen receptor before high dose testosterone works?” “Why can't you just give even more testosterone if the only thing that matters is what's happening in the interest of the end of the receptor?” Those are the sorts of questions that I consider in theory, in which the clinicians are totally oblivious.

So with that in mind, I basically look at what people published and ask why. “Why is this the result?” Often I look at their data, and their data tells me what's going on. So far, everything I've seen fits my model. But in some cases, the author of the paper will say these results are inexplicable or paradoxical. And that's because they conflict with what they were taught in medical school.

I never went to medical school, so I never got indoctrinated in dogma, I just look at the actual data of what's been published, and work out logically what's going on. So let's start with how prostate cancer originates. To give you a quick background, for decades, doctors were convinced testosterone causes prostate cancer.

Their proof was that by giving the noble rat high levels of testosterone, they could get around two thirds of them to develop prostate cancer. So you assume they have the answer.

“How Hormone Receptors Affect Prostate Cancer” (Ed Friedman) [#59] deprivation kills prostate cancer, they thought testosterone was the villain. For decades, we taught them that in medical school. They were going on that assumption. It turns out that in reality prostate cancer is caused by high local levels of estradiol, which acts on estrogen receptor alpha.

They've shown that early prostate epithelial cells, which is where the cancer comes from, never divide. They're made from stem cells. They sit there. They die off. They get replaced. They never divide. The cancer is the dividing. They've shown you can take ordinary prostate epithelial cells, and with high local levels of estradiol, cause prostate cancer to arise.

In 2008 researcher Gail Risbridger from Australia, who's done wonderful work on estrogen and prostate cancer, proved beyond a shadow of a doubt that estrogen receptor alpha is what causes prostate cancer.