I have read some studies relating to low testosterone and aggressive PCa.

Keep in mind I am not a trained, educated, board certified or licensed medical person, just a fellow member of this club none of us asked to join, trying to make sense of it

The layman's version, our PCa is made up of heterogenic PCa cells, some die off in a low testosterone environment, others adapt, the old "selection" discussion. Thus the discussion about continuous versus intermittent and resistance, adding ARIs to stop those PCa cells wo are still around because they adapted to low T environments.

The selection discussion as I understand is behind the addition of ARIs. and at the heart of why we use combined versus monotherapy.

Some things to think about:

What was your starting T?
Once you started, has your T dropped to < 20?
Outcomes are different between radiation and ADT therapy in terms of PSA, with ADT my understanding is one wants PSA to be undetectable when on ADT, with radiation, you are looking for a "nadir."

A key prognostic indicator of treatment "success" and prognostic for terms such as progression free survival, overall survival, radiographic free survival, is one's PSA reaching undetectable within the first six to nine months when using ADT.

The clinical data you describe indicates a reasonable degree of success at this point, as others have said, stay the course, assess and then decide based on the clinical data, what's next.