your RAT study about adenoma and GoldFish both say the same thing. Therefore I trust them. Here are main points
ncbi.nlm.nih.gov/pubmed/7570607
1-Both your rat and Goldfish say damage to testicular cells.
2-Both say primary damage to testicles cause an increase in LH which agree with medical text books that primary damage cause an increase in LH. This is opposite to our condition. you (and no body in the world) can say how within hours LH can go high and then come back to ground? how withing hours an adenoma is formed.
3- Goldfish points at testicular damage but without creating any adenoma.
The bottom line from the link above are
1-Beta Sitosterol caused an increase in GnRH.Plasma GtH-II levels were elevated in male fish treated with beta-sitosterol on Day 4 and further increased in response to Ovaprim, suggesting that reduced plasma steroid levels were not due to effects on pituitary function
2-The damage to leydig cells was reconfirmed invitro
In other studies, testes pieces from beta-sitosterol-treated goldfish produced reduced levels of T and pregnenolone in vitro both basally and in response to the GtH-II agonist human chorionic gonadotropin (hCG) when compared to the testes from control fish. Basal and hCG-stimulated pregnenolone and hCG-stimulated T were reduced in follicles from beta-sitosterol-treated fish
So unless there are few cases of elevated LH,FSH I am not going to believe that our case is the same as that of rats or Goldfish.
To me looking at these two studies our issue is either brain damage or something else