Just had another round of blood tests. First, and most importantly, PSA dropped to 0.02 (Ulta Lab test lowest limit, but not >0.02) from 0.06 at 6-month post-SRT. Am now at 10-month post-SRT and will have UC lab test again at 12 months.
However, here are hormone related results. First number is from Nov 21, second from Apr 22 and third is Range per test cite.
-T Free28.7/ 20.3/ 35-15 (out of range)
-T total288/ 242/ 250-1100 (out of range)
-SHBG58/ 65/ 22-77
-DHT15/ 13/ 12-65
-DHEA47/ 34/ 24-244
-E2<15/ <15/ <39
-FSH13.8/ 1.6-8.0 (out of range)
-LH6.2/ 1.6-15.2
-Homocysteine10.3/ 11.1/ <11.4 (trending up)
I don’t and never have functioned well with low T. Had done T shots for many years prior to PC (Doc did follow E2 but maybe not good enough and I did not know). One year after RP and PSA <0.01, Uro let me start up with gel and 6 months later, PSA at 0.1 and started my BCR path to SRT. I have tried all I can think of to get T up naturally but going in wrong direction. I am doing well keeping E2 low and DHT low, but not so much at increasing T. Here is what I take both to increate T and keep E2 low: Keep E2 low-Zinc 30mg, Boron 9mg, Dimm 300mg. Increase T-Avina Sativa 1500mg, Nettle Root 2000mg, Tongkat Ali 1200mg and Ashwagandha 500mg. I also wonder if my high level of Melatonin is hurting T. I take 180mg at night for prooxidant.
I am reluctant to start HRT again after issue last time I started it, but low T really effects QOL and relationship. I have read Freedman’s book and other items so I understand that should not be issue as long as E2 and DHT kept low. I will be taking to my URO about this but looking for any words of wisdom. And is a URO (U Chicago who did RP) the correct doc to talk to? Maybe Block Center for Integrative Cancer Treatment in Skokie (they don’t take my company BCBS so have to wait until August when I have Medicare and Supplement)? Should aim be T at 500 or T at 1500?
Any helpful input is appreciated.
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What is the advantage of stimulating or simulating LH/FSH rather than add exogenous T temporarily? Does stimulation/simulation of the base hormones cause them to regain natural activity over time without continual use of drugs? And is this faster than having your natural T recover (if it ever does)?
I have always thought that HCG and Clomid have certain risks that I don't want to entertain unless I have to. I have never looked into either of them since bio-identical T did not seem as risky.
Just to be clear: if you have hypogonadism then Clomid and/or HCG might be used for a short time to get your T engine going? How about a low-dose TRT (getting you to say 300 ng/dl). Do you think that the low dose would keep your endogenous down?
I think the consensus is supplement to increase T is unrealistic. I started the androgel on one year anniversary of RP when PSA was <0.01. In 6 months went to 0.1 and I stopped. PSA kept going, leading to SRT. This is why I am reluctant to start that again even though I know so much more now re T, E2, DHT, etc.
If you’ve taken supplemental T shots ‘for many years’ I would think it unlikely you are going to recover it naturally in your ‘60’s. I assume you are not on ADT?
Not on ADT. Work out 4-5 days/wk. I do a cardio day which is bike, outdoor when I can (in Chicago area and woke up today with new snow outside) about 12 miles tracked with MapMyRide. Indoor have Wahoo Kickr and do HIIT 30 min. Then do lift day, bench, bent over row, upright rows, incline dumbbell curls, wrist curls, inverted wrist curls, tricep press, squats and toe raises. Then I take day off and repeat. I have my own power cage in basement so all with free weights.
You may be right, May be unrealistic in my supplement hope. Thanks.
Yes, that looks like my choices, other than the items mentioned by TallAllen. Time to email my old URO who recently retired for his personal thoughts also.
But if your testosterone is lowish, but still enough for "saturation", wouldn't additonal testosterone not affect it unless there was residual cancer? I read an article about a testosterone challenge. Its sort of an early way to see if you have residual cancer.
And I don't think just one .1 would be enough to make that determination in any respect. I'm kind of in the same boat with you, I have a very low PSA but I am going to wait for it to rise. I rather doubt it will ever get over 300, since I did take Androgel for a number of years. I didn't have an RP, so the PSA numbers would be off for me a little if I took the challenge.
So the bottom line of that article basically says that after RP, you either have cancer cells still in there or you dont. If you do, with the PSA still low they could grow to the point of a problem without you knowing it, so better to find out now when still small and deal with it. I see the logic, but I also see so many flaws with the reasoning. What if current T is not enough to ignite it and if it stays low your whole life you may never have a problem. Maybe stays dormant. Maybe over the dormant period they come up with a cure or better this or that. And how does this square with Edward Freidman's concept? Was E2 or DHT high causing this so no issue if those are controlled? This is why I was hoping for more natural increase but may not be possible. Thanks for sending that. Definitely keeping that article.
Maybe, but If I remember right, Morgenthaler, the Godfather of T in PCa patients, says your T is high enough for "saturation." I think. Meaning any more isn't going to make a difference. As easily as more T might increase it, the opposite may be true also. It may stay at .1 regardless. In which case, I think I know how you would want to go.
I will have to look into this further, but how does one know if their T is at "saturation"? I guess the concept that if I have saturation and all is well and cancer not growing, then saturation+ should not make any difference re cancer. I feel the key is knowing if I am at saturation or not.
Great. Your dedication to strength and fitness gives you the greatest possible advantage whatever path you take.
You will note the lengths that guys will go to avoid testosterone suppression. It’s a solid choice for some, a terrible one for others. Disease stage, PSADT, scan results, many things we can try to use as a guide, but it’s all a educated crapshoot at the end of the day. The disease is just too heterogeneous to know.
BAT is naturally also a very attractive option, but unfortunately not effective for everyone, and usually not for long. It’s also often misunderstood as providing the kind of relief that men seek from supplemental T. Not true for most. Yet certainly worth looking into.
A return to supplemental T may be worth a shot, no pun intended. Not sure I would try it myself.
There is one other possibility but it has dangers. I use selective androgen receptor modulators (SARMs) on the low T phase of BAT. SARMs do not appear to cause any liver damage to me. But they do cut my HDLs in half. They do not appear to affect my PSA levels or the ADT effectiveness. My MO reviewed my research and test results and she is all for them (even with the HDL decrease). Even with her blessing I only use them in cycles and at fairly low doses.
So, this BAT program goes from a very anabolic, high-energy environment to a somewhat anabolic, okay energy environment. But SPT was the best! For those two years, I felt like a 30 year old.
SARMs are experimental stuff though and I have only found one doctor who could prescribe them.
1. Selective androgen receptor modulators: in pursuit of tissue-selective androgens - PubMed
5. SciHub | Comparison of the three SARMs RAD140, GLPG0492 and GSK2881078 in two different in vitro bioassays, and in an in-silico androgen receptor binding assay. The Journal of Steroid Biochemistry and Molecular Biology | 10.1016/j.jsbmb.2019.02.014
11. Study to Evaluate the Safety and Efficacy of 13 Weeks of the Selective Androgen Receptor Modulator (SARM) GSK2881078 in Chronic Obstructive Pulmonary Disease (COPD) Study Results ClinicalTrials.gov
12. A Novel Selective Androgen Receptor Modulator (SARM) MK4541 Exerts Antiandrogenic Activity in the Prostate Cancer Xenograft R3327G and Anabolic Activity on Skeletal Muscle Mass & Function in Castrated Mice | Request PDF
17. Very large amounts used: JCI Selective androgen receptor modulators activate the canonical prostate cancer androgen receptor program and repress cancer growth
I wouldnt mind feeling like 50 again. I am thinking of adding DHEA to see what it does per one RCT study I just came across and numerous articles. My DHEA is really low. Thoughts?
Semper Fi Devil-dog. Your workout regimen is inspiring. Hope you can read all of RSH1's linked articles and give us your summary analysis! I'm on a similar modified (longer cycle) BAT.
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