You see some of this regarding vitamin k having a chance to be bacterial based. Could there be a chance for hypercoagulability?
Vitamin K2, a Naturally Occurring Menaquinone, Exerts Therapeutic Effects on Both Hormone-Dependent and Hormone-Independent Prostate Cancer Cells
VK2 treatment reduces androgen receptor expression
Testosterone 5 alpha-reductase inhibitors, menaquinone 7 produced by a Bacillus and phenazine methosulfate.
Then on the opposite side of things,
Vitamin K epoxide reductase regulation of androgen receptor activity
“Previously, we identified warfarin and other vitamin K antagonists as AR inhibitors”
then back to Fin,
In this study, finasteride decreased the expression of epithelial androgen receptor in a tissue specific manner. The correlation between epithelial androgen receptor and the extent of luminal epithelial atrophy suggests that epithelial androgen receptor may be directly regulating the atrophic effects observed with finasteride treatment.
The moral of the story would be is there any abnormal vitamin k involvement with what we got going on that could be bacterial driven. Just something to be aware of, just in case.