You guys have empowered me to ask the right questions...
I met with my MO today and he agreed to start measuring DHT , Estradiol and free Testosterone as well and PSA and T going forward.
PSA was stable at 0.03 only blood # out of ordinary was ALT = 99 normal range 16-61. Dr. says "liver enzymes were elevated and your potassium levels were low."
We had a discussion about Avodart and he said he would consider a prescription if I could show him persuasive studies.
The following 5 are the best I could find. Does anyone have a favorite study that helped them convince their MD to prescribe Avodart?
TIA
ncbi.nlm.nih.gov/pmc/articl...
Progression-free survival
Multivariable adjusted HR of 5ARI treatment in predicting progression-free survival
was available in five studies. Our results demonstrated 5ARIs could significantly prolonged
the progression-free survival time in PCa patients (HR = 0.57, 95% CI [0.34–0.96],
P = 0.04), with moderate heterogeneity (I
2 = 69%, P = 0.01) (Fig. 6). The inverted funnel
plot did not find any publication bias.
ncbi.nlm.nih.gov/pmc/articl...
Dutasteride is known to be effective in preventing prostate cancer and treating low-risk prostate cancer. However, the role of SRD5A inhibitors in the progression of prostate cancer to CRPC has not been well studied (18). The development of CRPC is still dependent on DHT, and some next-generation drugs targeting the androgen signaling pathway were reportedly effective (11-13). We therefore assessed the effects of dutasteride in patients with CRPC by assessing changes in PSA levels. The present study showed that 41% of patients with progressive CRPC showed a decrease in their PSA level, with 17% showing a decrease greater than 50%.
Avodart blocks DHT
urotoday.com/center-of-exce...
In a paper published in June of 2018, a team led by Nima Sharifi from the Cleveland Clinic identified that certain metabolites of abiraterone are AR agonists. As such, abiraterone metabolism creates its own competitor, in a manner of speaking... [by producing] 3-keto-5-beta abira abiraterone [which] ends up as an androgen agonist, thus potentially mitigating the antitumor potency.
The enzyme that catalyzes the conversion of D4 abiraterone to 3-keto-5-alpha abiraterone is 5 alpha reductase, the very enzyme that could be catabolized by the addition of a 5 alpha-reductase inhibitor such as finasteride or dutasteride. Although such treatments have not resulted in substantial antitumor activity, they have not been studied in this context.
One possibility is that we could combine abiraterone with 5 alpha reductase inhibitors. This has been done on a small scale but not based on the genetics of polymorphisms."
Do you take many supplements/drugs? I used to take too many and my liver enzymes started going up and my kidney function deteriorated. I stopped them for a couple of weeks, retested, and everything was going back to normal. So I reduced them other than the ones that my MO suggested and the ones that have some RCT backing.
If you aren't doing high T or BAT I think that dutasteride is a great option. It's going to take whatever DHT you have lower. I haven't noticed many sides so I take some finasteride (short half-life) during the low T phase of BAT.
In general, I'm not sure if the drug sides are worth it for the small decrease in DHT if you are on ADT (particularly if you are concurrently using a cyp17 inhibitor such as Zytiga). But that probably depends on the individual and how they react. If the sides are palatable, I would opt for it. I did both fina and duta when I did ADT.