Apparently, the article discusses a study that solves the paradoxical effects of testosterone in prostate cancer. The study found that prostate cancer cells are hardwired to proliferate when testosterone levels are very low and differentiate when hormone levels are elevated. The study also provides insights into how bi-polar androgen therapy works and could help physicians select patients who are most likely to respond to this intervention.
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Jpburns
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No T (through ADT) which helps stop cancer, at least for some time before it mutates/adapts
Low T that helps cancer spread, which is likely the relative low T levels that we might have had when we got older and developed cancer
High T that kept cancer at bay when we were younger and that could possibly help get it back under control once its mutated, provided we don't already have active tumors in our bones.
I am not saying that I am right, just that this is how I understand this.
This is interesting to me. I just started ADT but will be on it for at least 2 years. I have naturally high levels of testosterone (900+ at beginning of ADT) and think that, since I’m on Orgovyx which has a much higher T response at end of therapy compared to Lupron, I would be very interested in testing BAT down the road as I transition off my every day ADT. I am concerned about CRPC and I am open-minded about learning more about BAT as more trials and studies come to light.
Interesting...Over the course of my 10+ years I have wondered about the lifetime ban on T that seems to pervade the medical community (and patients).
I did not have my T checked when I was diagnosed in January 2014 ( I knew so little...). The first time was in January 17 when Mayo checked it at the start of triplet therapy, just under 300, so, low.
When I completed triplet therapy in May 18. my T over the next 4+ years rose first to 135, then 400+ and finally 600+ when I went back on treatment for a year.
If the prevailing theory that T is bad were "correct," my PCa should have long reared its ugly head before roughly 2022. Why didn't it, my oncologist had no explanation, nor have I found one.
This time around T has recovered to 400+ in the first six months. There is some evidence that there is PCa activity, labs showed .01 in July and .03 in October rather than the <.04 while on treatment. So, as I've said before, the analogy is akin to seeing the headlight of a train in the far distance, I know it coming my way, when it will get here, I don't know but we have decision criteria in place to define when that is and deal with it.
The Nature Comms study the Duke Health news refers to is worth reading by those with some biochem background although it is very technical. I have read it through once but it needs a couple of reads.
I have often wondered why it is that as androgen levels fall with age PCa risk rises, and that androgen levels are lower and FSH higher in those with PCa compared with those who do not have PCa.
This Nature Comms report referred to may offer an explanation for this observation. The Nature paper is not clinical and reports work in cell and animal models of PCa and shows that high dose testosterone inhibits PCa proliferation while low doses promote it . The paper identifies the biochemical mechanisms.
The paper, although entirely laboratory based, raises some serious questions about the whole model of PCa therapy which is entirely geared to androgen deprivation and blockade which leads, in many patients, inexorably to resistance and to a raised risk of neuroendocrine tumours.
Perhaps raising testosterone levels would be better for patients with early and not just those with late disease?
I had never seen the acronym FSH (Follicle-stimulating hormone) before reading your reply so I just researched it. There is more info at drsudhirbhola.com/post/unde... but here is a little bit from that site that I've copied below the ***.
You wrote: "I have often wondered why it is that as androgen levels fall with age PCa risk rises, and that androgen levels are lower and FSH higher in those with PCa compared with those who do not have PCa."
When you say that FSH is higher in those with PCa, do you mean before or after they've been diagnosed/treated? I ask because FSH being higher in those treated with ADT makes perfect sense since the ADT stops our production of sperm and testosterone so FSH goes up to compensate.
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What is FSH?
Follicle-stimulating hormone (FSH) is a glycoprotein hormone produced by the anterior pituitary gland. In men, FSH is essential for spermatogenesis, the process by which sperm are produced by the testes. FSH stimulates the Sertoli cells in the testes, which support the maturation of sperm cells. The hormone's production and release are regulated by the hypothalamic-pituitary-gonadal (HPG) axis, a complex system involving the hypothalamus, pituitary gland, and gonads.
Causes of Elevated FSH Levels in Men
High levels of FSH in men can be indicative of underlying health issues, often related to the testes' function. The most common causes include:
* Primary Testicular Failure: This occurs when the testes are unable to produce sufficient levels of sperm or testosterone. Causes of primary testicular failure can include:
* Genetic conditions such as Klinefelter syndrome.
* Physical damage to the testes from trauma, surgery, or radiation.
* Infections like mumps orchitis.
* Autoimmune diseases.
* Androgen Insensitivity Syndrome (AIS): This is a condition where the body's cells are insensitive to androgens (male sex hormones), leading to higher levels of FSH as the body attempts to compensate.
* Chemotherapy and Radiation Therapy: Treatments for cancer can damage the testes, leading to reduced sperm production and elevated FSH levels.
* Aging: As men age, there can be a natural decline in testicular function, which may result in increased FSH levels.
* Idiopathic: In some cases, no specific cause for elevated FSH levels can be identified.
As we age androgen production falls and in response pituitary FSH rises. It’s simply a feedback mechanism between pituitary gland and peripheral organs - testes, adrenals etc.
There’s a MedOnc at Fred Hutch in Seattle who has been quite involved with BAP studies for several years: Michael Schweizer. He speaks annually at the Pacific Northwest PC conference. Here is the 2023 video (skip to 2:44:30): ubc.ca.panopto.com/Panopto/...
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Is there a connection between testosterone level and severity of prostate cancer at diagnosis?
