What do people think of this? Yes it's only a single "novel" patient case. I could swear I've seen posts elsewhere about people concerned with having too low of a level of Prolactin but this asserts that reducing/eliminating it is therapeutic once the cancer switches over to being castration resistant?
Cabergoline Reduces Prolactin To Cure... - Advanced Prostate...
Advanced Prostate Cancer
I have reported on a natural way to control Prolactin--->usually for Hormone Sensitive men.It is the use of Mucuna L-Dopa. I check my Prolactin 2 times a year--and if I see it in the middle of the range, I use this supplement to bring the Prolactin towards the low end of the range.
Thanks. I think I saw you mentioned that. I'm actually struggling with low energy and lack of motivation even with exercise and good diet. Having trouble staying "on task", lots of procrastination, no drive - classic indications of low dopamine levels. I think PCa diagnosis and everything that comes with it and after that has definitely contributed. Artificially bumping dopamine up (unless you have Parkinsons) is not the best idea as my understanding is creating a surge makes the baseline drop down to lower than it was before then very gradually comes back up. Maybe a moderate dose Mucuna L-Dopa would be something safe for me to try. I hate to resort to caffeine.
There are many positive papers on the use of Dark Coffee--->which has over 400 compounds and Caffeine is not the only Compound that gives you a lift. There are many dozens of Polyphenols, where some are considered anti-cancer.
For a Boost---to get you going for your day--why not look at using Panax Red Korean Ginseng. This does give a kick---do not ask me about doses---you would have to find your own dosage, if you use this.
On my (decrepit) memory, Siberian ginseng is considerably more potent than the Korean variety. I used it extensively in high pressure jobs long ago and yes, it does have a kick.
Dr Leslie Castello has papers about Use of prolactin lowering and use of Zinc and zinc ionophores. Lately I have not seen any new info in this area. I do use VITEX FRUIT caps intermittently to keep serum Prolactin level low.
LearnAll, any particular reason why you take Vitex intermittently? I take one cap daily, except when I am away, which means about 70 % of all days.
Thanks. Seems to be a controversial area. There's nothing there beyond 2010 and I can find very little in the way of more recent RCTs regarding Prolactin suppresion in treating PCa except this (which refers to the related actual study). Is there other newer info out there with a more conclusive result regarding efficacy of Prolactin suppression?
To anybody interest here are my numbers:
Two hears ago my Prolactin was at the lowest end of the normal range @3 ng/ml (NR: 2.6-18).
Six months ago, when Nal posted regarding Mucuna L-Dopa, I tested again and this time it had climbed to 5.5 ng/ml. For two months I took Mucuna L-Dopa and it dropped to 5.0 ng/ml. Not a big deal, actually within the tolerances of the test. At this point in time I switched to Learnall's Vitex fruit. Two months later it had climbed to 6.6 ng/ml. At first glance, the latter doesn't do any good. But, it may not be so, according to my particular history which accounts that between the 3 and the 5.5 I had started my Bicalutamide maneuvers. Bicalutamide, even at a fairly low dose, pushed upwards all my hormones. In order to somewhat normalize things I devised the ratio Prolactin/tTestosterone.
This ratio as a percentage (%) was 0.262 two years ago, rose to 0.333 before starting Mucuna L-Dopa, dropped to 0.294 before starting Vitex fruit and plunged to 0.176 during the latest reading of 6.6 as my tT skyrocketed to 3755! (all endogenous, if you please). I keep taking Vitex fruit until the bottle empties and then I will let some time to pass before a new "clean" test.
as my tT skyrocketed to 3755! (all endogenous, if you please).
Now don't leave me hanging, please elaborate
Nothing to elaborate, every hormone went UP.
My endogenous hormone factory worked overtime, or the lab's analyzer has been broken!
Latest test results were:
Total Testosterone: 3755 ng/dl (past average 1400)
Free Testosterone calc.: 38.7 ng/dl or 1.03% of tT (past average 0.79%)
DHT: 0.92 ng/ml (past average 0.586)
E2: 61.1 pg/ml (past average 52.4)
SHBG: 176.6 nmol/l (past average 141.7)
According to your Bio., last entry was starting Bicalutamide in '21, is this still your current and only therapy?
Total Testosterone: 3755 ng/dl (past average 1400)
Any thoughts on why this is occurring, you must feel like a 17 year old??
The graph shows my response from the day I started Bicalutamide until 25 days ago.
My own devised strategy is the next step to BAT. BAT is a saw tooth control loop like your heating/cooling thermostat. I have upgraded it to a proportional control drive mechanism like the governor of a genset (feed as much fuel as to keep the frequency within nominal range under a varying electrical load). Bottom line is that the surge in my hormones may be an indication that my scheme works. 1/7 of the usually prescribed dose is enough to impede the hormone supply to the cancerous cells which in return desperately ask for more and more. I hope that by keeping the equilibrium, i.e. equal number of cancer cells killed to those divided, I make more difficult the proliferation of hormone insensitive cells. We will see how it will go.
This is a subject I'm trying to get more educated on so forgive me if this is a "Duh" question. Has anyone individually or any study been done that taking prolactin to extremely low levels BEFORE castration resistance has developed (such as throughout ADT) effectively provides a very significant lengthening to the time the PCa becomes castration resistant? If there's little to no prolactin present for the PCa to switch over from testosterone as a fuel, it seems to me theoretically the switch might take much longer or possibly never even happen? I know the substances that reduce prolactin increase testosterone but to a much lesser degree it sounds like so I would assume the ADT would still overcome it and get the Testosterone down low enough? Or maybe the timing would be to start Cabergoline after X months of ADT when the PCa is begun to start to adapt?
I see that Dr. Snuffy Myers also was saying Cabergoline can help with sexual side effects of Avodart (traditional ADT too?)
I used estrogen patches for ADT. Coupled with Zytiga I had unmeasurable levels of T. I was doing cabergoline at the time and my PRL was 1.0.
I switched to Lupron. Coupled with Zytiga my T is 15-25. I haven't stopped the cabergoline.
I have used Zytiga for the last 4 years so I'm on the higher end of efficacy. Most men have to stop.
Seems like the estrogen patches/Zytiga combo isn't affected much, if at all, by cabergoline.
When I do ADT my libido is there but very rarely. Maybe once or twice a month.
Cabergoline 0.25 mg 2x/week has been very effective for me. My PRL was 4.0+ and has dropped to around 1.0 and has been holding there for 4 years. 2019: ncbi.nlm.nih.gov/pmc/articl...
2020 null: ar.iiarjournals.org/content...
Dr. Kwon at Mayo thinks PRL is the #2 driver of PCa.
@smurtaw What stage are you at (initial biochemical failure, metastatic disease, castration resistant metastatic disease?) Have you already done or are concurrently doing treatment with the traditional ADT drugs or are you using Caborgoline as a monotherapy at an early stage? Apparently once the Prostate Cancer becomes castration resistant, PRL is the #1 driver. It is unclear to me if Dr. Snuffy Myers was putting people on Avodart without ADT upon initial recurrence to delay use of ADT or was he combining it with ADT drugs right away?
That 2019 report sort of summed up things:
"However this relationship has been largely unrecognized and ignored by contemporary clinicians and biomedical investigators; including urologists and oncologists. This is apparent from a PubMed search of “prolactin and androgen-independent prostate cancer” that reveals only 12 citations; of which 5 were published within the recent 10 years (including Costello and Franklin ). The PubMed search with “prolactin and castration resistant prostate cancer” produced only 6 citations; 3 being published in the recent 10 years. Also notable is that the 2016 extensive review of prostate cancer with over 300 references makes no mention of prolactin ."
I was diagnosed in 2017. Gleason 9, T3c, local lymph node involvement, organs, no mets.
I had RP in 2018. Followed by estrogen patch ADT for 6 months. Then high testosterone and now BAT.
I have done zytiga and cabergoline throughout. Also statins for the last 3 1/2 years.
Still not CRPC and as far as I know no mets. I am trying to get some scans to check but I'm having a hard time finding a pylarify location that is covered by Aetna. I'd fly if one is available so I'll look around. If anyone knows of one, let me know. Seems like if you have medicare it's really simple. If you have commercial insurance it isn't.
How are the side effects on zytiga + cabergoline? Much of a hit to quality of life? I'm on Regence Blue Shield and Virginia Mason (Seattle) had no issue get approval on the Pylarify PSMA scan but not sure about Aetna.
I had some fatigue from Zytiga early on and my MO dropped the dose. Seems to have gone away (body habituated to the stress?). So now I am on the full dose.
I never noticed anything different when I started cabergoline. Maybe some swelling but there are so many causes for that I don't know if I can single out the cabergoline. I'd stop to see if it's that but I don't have much of an issue with the swelling.
I can't answer the specific questions from jazj, but judging by the reports provided by Patrick/pjoshea13 as a whole, it indeed seems that keeping prolactin low is probably good.
I am taking prescription-free Vitex, but assumed it was inferior to prescription-only cabergoline/Dostinex. However, stimulated by the post of jazj, , I found a study indicating that the prolactin-lowering effects of Vitex are quite similar to cabergoline, at least for women.
A big thanks to LearnAll for pointing me to Vitex, I would probably not have tried the prescription hassle.
See table 2 in "The Effect of Vitex Agnus Castus Extract on the Blood Level
of Prolactin ....... in Hyperprolactinemic
Women", Crescent Journal of Mediccal and Biological Sciences, October 2020.
The study also indicates Vitex ups serum estradiol greatly, considerably more than cabergoline/Dostinex, table 5. I am not sure this is good, at least for someone BRCA2+ like me , but I will let the prolactin effect override that unless I learn something to the contrary here.
Frustratingly, no dosage was given, only that Vitex was "prescribed in an almost side-effect free dosage". One tab a day?
So is sort of the overall consensus that you should ask to have your prolactin level checked when you have your PSA checked and no matter what stage of the disease you should try to keep it at what < 5? It appears there is not yet sufficient evidence to make it SOC for most MOs at this point which begs the question if there is any evidence of a potentially significant downside, especially early on right after initial biochemical recurrence?
Perhaps considerably lower than 5 is better.
I keep mine below 1.5. I've read that it can cause sexual side effects.
I don't really notice that but perhaps it tames my crazy high libido when I am using the high testosterone phase of BAT+.
I'd try out some of the natural alternatives to cabergoline but it works so well and is FDA regulated and cheap through goodrx.
Reluctantly, I am planning to drop the vitex for cabergoline. The former raises estrogen much more, per table 5 in that study I posted, and this is probably not good for those of us who are BRCA2+, according to Richard Wassersug, a doctor and member on this forum, whom I just contacted. Will check my prolactin and estrogen levels first.
Thanks. Please post the results. Most of the guys on alternative supplements to lower prolactin don't really go very low. Caber is a drug but you could get your PRL where you wanted it and titrate down if desired. I did that for a while since my PRL was undetectable. In the last lab, it was barely detectable.
Does anyone know what Dr. Snuffy's "official" target was? I may have seen a video where he mentioned it but can't remember. It sounds like < 3 or < 2 then might be the better target. I think Dr. Myers tested constantly to dial in the dose to minimize side effects. Just not sure what the level target was for dose adjustments.