Is this normal on ADT? Body hair gone

I’ve read some about BAT (bi-polar androgen therapy). Mostly being researched at John’s Hopkins. At this point, it is only employed in those who have become castration resistant. The idea is that the the cancer has adapted to a very low testosterone environment, in part, by developing many more androgen receptors. So what they do is leave you on ADT, but once a month give you a high dose injection of testosterone. As a result, your testosterone level is on a roller coaster. It goes from near zero to very high then back down to near zero, all in the course of a month. This variation supposedly gums up the cancer’s androgen receptors and can actually kill the cancer. The treatment also results in higher quality of life. The research is still in It’s still early days. I’m not castration resistant, but if i become so in the future, i will take a deeper dive into this possible treatment.

One of the main reasons they do BAT is to get back the ability of Zytiga or a ludamite to keep the PSA down.

Usually, they will do BAT for a few months and then put you back on the second drug.

Never heard of it having anything to do with killing the cancer it’s just an attempt to reset the resistance to the second drug.

Well, this was probably 3 years ago in Great Britain so never heard the follow up or if the treatment held the cancer at bay for good.
But the way they described was much more exaggerated than US BAT. They gave the patient a ‘massive’ dose of T - whatever that means - and all his metastases disappeared over time. Duke University is looking into this as we speak. There is a paradoxical reaction to T by aggressive cancer: it DIES from it, whereas less aggressive garden variety types thrive on it. It’s a paradox all right!

Well, this was probably 3 years ago in Great Britain so never heard the follow up or if the treatment held the cancer at bay for good.
But the way they described was much more exaggerated than US BAT. They gave the patient a ‘massive’ dose of T - whatever that means - and all his metastases disappeared over time. Duke University is looking into this as we speak. There is a paradoxical reaction to T by aggressive cancer: it DIES from it, whereas less aggressive garden variety types thrive on it. It’s a paradox all right!

Just found a study that discusses whether BAT does what you were talking about. In one study of 12 patients only one of them had tumor regression. Definitely something they could look into and maybe make it more widely available some day. They keep coming out with new treatments.

Here is a short synopsis of what they found

Given that tumor regression seems to occur in a minority of patients treated with BAT, identifying biomarkers that predict sensitivity could enhance the utility of this therapy.

My PSA went up to 67 and my cancer metastasised to my spine very aggressively when my testosterone was higher; in the three years since I started on ADT my testosterone has been extremely low, my PSA is undetectable, and there's been no new cancer progression.

One of the main reasons they do BAT is to get back the ability of Zytiga or a ludamite to keep the PSA down.

Usually, they will do BAT for a few months and then put you back on the second drug.

Never heard of it having anything to do with killing the cancer it’s just an attempt to reset the resistance to the second drug.

This is from “A Patient’s Guide to BAT”. When they refer to AR it means the androgen receptors.

One of the key things to emphasize is that BAT was developed to work against CRPC cells. These cells have adaptively fine‐tuned the AR to high levels in response to low testosterone produced by androgen deprivation. This high level of AR, paradoxically, makes the prostate cancer cell vulnerable to sudden exposure to high amounts of testosterone. In this case, “too much of a bad thing can be a good thing.” Flooding the prostate cancer cell with testosterone creates a problem for the cell. Now it has to suddenly deal with too much androgen bound to AR. This high level “gums up the works” so to speak. It disrupts the ability of the prostate cancer cell to divide as part of the growth cycle. In response, the prostate cancer cell either stops growing or dies.

It will be interesting to follow this research. I hope they discover biomarkers eventually to know who can/can't benefit.