what about the progesterone cream, are u still using it? How long and what about your feeling?
what about the progesterone cream, are u still using it? How long and what about your feeling?
Legendary. I have read a whole bunch of stuff about fat cells I am still not too sure about it but some studies indicate fat cells have propensity to create estrone not estriol and estradiol. I am not 100 percent sure about is and it seems complicated. But as I said when on a very low dose of trt 28.5mg E3d my free t was only mid range and my siliva Estriol and Estradiol were over range. Maybe this could be a good indicator. I sugggest you look into testing these things ASAP. Oh yeah despite estradiol and estriol being over range estrone was just above the bottom of the range!
I also got the best woods in my life on anti estrogens but for me and everyone here the results are not stable. Also even when I take a small dose of anti estrogens I get pains in my sholder joint within 1 hour and then sometimes in the joints in my foot. I worry that it is lowering estrogen way too much in some areas.
Your experements are good and please keep them up and keep logging what happens it is useful to all of us. If you could do some blood tests on letro only that would be great too test when you are feeling good if you can. I know your in South Africa maybe there are no siliva tesing places there?
There is debate over whether phytoestrogens block the Estrogen receptor maybe you could give them a go. Like soy and pommigranite, flax , red clover.
Pirston: I’ve never tried progesterone cream
Vincentv: Thanks for the thoughts, I’ll be running this info past my endo when I see him. I’m not sure about saliva testing over here but will definitely look into it. Presumably cheaper? These tests and doctor visits are really setting me back…thanks again, will revert when I have more info
I’ve put this in my thread but I’ll put it here as well cos I’d love some feedback on it
Spanked the monkey today. No desire to do so, just a test!
Very difficult to reach orgasm. Not particularly pleasurable and no force or quantity.
Libido is worse now than ever I would say. I’m at zero libido right now!
I have read along the lines that clomid being a week estrogen is in itself potentially suppressive. The letrozole would reduce aromatisation of natural testosterone that was being stimulated by the clomid but not combat the effects of the clomid itself. Not sure if my understanding of this is correct. Hoping that I start to feel better after PCT has ended.
would love some feedback on this!
Oh can I just ask as well please can you confirm that your endo recommended continuing with the letrozole continuously throughout or stop when you are not taking clomid. I thought you said continually but I want to be sure.
Yeah Letrazole continuously thoughout. I’m actually only on Letrazole now, no Clomid…
How are you doing now ?
Quick update, did my 4 weeks on just letrazole, it felt great. The last week in particular was sexually the best I’ve felt since this started. I suspected something was different. Sure enough, did my follow up tests and not only did my T rise again, but my E plummeted which hadn’t happened before.
Oestradiol: <37 pmol/L (Low)
Total T: 33.7 nmol/L
Free T: 1064 pmol/L (High)
FSH: 7.3 U/L
LH: 12 U/L
Have a follow-up with my Endo next week to chat about the way forward. If you guys have any PFS / Hypo questions you’d like me to ask him, let me know. The guy is a genius. I know a couple of you were curious about remote consultations with him, so I’ll ask him about that too. Chat soon
legendary are you still taking letrazole or clomid ? I found that any benefit I got from either drug was just temporary.
I’m on and off at the moment. My levels do drop when I go off, not quite to baseline though. So at the moment it’s acting more as an effective treatment than a cure. Will be chatting more to my endo about this next week…
I also believe it just treats the symptoms but does not get to the root of the problem.
I’d be more than happy to take it forever if it made me even close to normal again.
Clomid is quite toxic its not a good idea to be taken it indefinitely.
I meant the letrazole, though that could be toxic too for all I know.
Have a very interesting update.
My suspicions about my response to Letrazol alone vs Let + Clomid seem to be correct.
Recap: my T spiralled out of control and in my most recent test, my E was undetectable - just by using an AI - Letrozole. No Clomid, HCG or other stimulants involved. I suspected this was an abnormally high T response to just using an AI alone.
Basically, my Endo’s theory is that I have both abnormal aromatase activity resulting in higher E levels, and an abnormally high denisty of E receptor sites. A “double whammy” in his words. But the good news is, my body is producing shitloads of testosterone and requires no stimulation whatsoever when E is under control.
I recorded our conversation and did a basic transcription. It’s an absolutely fascinating read for anyone effected by PFS.
Bottom line is I’ve decided on half a tab (1.25) of Let per day at the moment, and feel really, really good. Libido and dick in general feel almost back to pre-PFS levels. I am horny again and tugging a couple times a day to relieve sexual tensions. Dick is hanging well at the moment, minimal shrinkage. Feel very positive.
Read the transcript and let me know what you think. Will respond for the next week or so and then will be taking a leave of absence from the forum. Will check in again in a few months.
All the best…
[Start rough transcript]
Doc (actually laughing).
"Very unusual problem.
If E is too low it increases cardiovascular mortality, too high, it does the same. E was probably initially responsible for you running into the trouble in the first place. Finasteride was the catalyst, but driving the underlying problem is E.
You have a thumpingly high level of testosterone without getting stimulated whatsoever, which is unusual to this extent, even when blocking E.
This is so bloody rare that we don’t have any data to decide what is optimal E level for you.
We need to play around and see where your sweet spot is.
We need to find a balance between adjusting AI dosage, watching T levels, see how you feel and marry the 3.
Studies suggest serum E should be 60-90. Your E is undetectable after Let protocol. <37 means it could be 36.5 or 0.
We need to proceed more cautiously. Do a month of Let, 5 days on, 2 days off. See how you fee. The next month do every other day. Do a blood panel end of second month and see where E is and if there’s a detrimental affect on T.
Suspect that even your E reading is not accurate or telling the full story. Suspect you sensitivity to E is substantially higher than normal.
If a normal guy has E of 60, he may have no problem since his receptor density is not high enough. In your case it may be a problem since I suspect you have much higher receptor density. We have no test that can measure receptor density. So we have to use clinical symptoms to see where the sweet spot is.
See what the happy marriage is between functionality, cardio vascular protection and T. Only reason for doing the future tests is to see that the E has not gone high enough to switch off your T production.
Very little in the way of medical literature that will guide us in this unique problem. Might think that the lower the E the better, but studies show that is should not be too low and also has implications in terms of bone mass.
My Q: Why is E higher in the first place? Even if I have greater number of receptor sites and that’s the one problem, why is it high to start off with?
A: The activity of the aromatase enzyme is higher in your case. Why this is we do not know, the tech to evaluate this is still being evaluated. We should have the ability within the next two years to give you that answer. We will then be able to map the gene that transcribes aromatase. If you have a point mutation (sic?) that gives you advantage in terms of activity then that will be the reason. Suspect the problem is at the genetic level. The interesting thing is not everyone with the genetic mutation gets the same physical features. How the body expresses the genes is different. The 5 alpha reductase inhibitor in your case was probably a catalyst to expose the genetic mutation. It may have happened anyway, but probably happened sooner than it may have. This is all speculative. Don’t have a test to prove this theory conclusively.
Q: I obviously don’t need the clomid anymore since I don’t need to get stimulated to produce T correct?
A: Correct. Your body weight, muscle mass and body fat will determine what your maintenance dose of Let will be. Need to keep working out and losing as much fat as possible. Keep on with DHEA dose.
Q: Long terms affects / dangers of being on Letrozole and DHEA?
A: Long term affects of AI - studies on men show no real substantial detriment. Studies on woman however show it accelerates osteoporosis. For some reason men don’t get that. Side effects - if there were bone issues you’d be having excruciating pain right now. Don’t have long-term safety data because as you can appreciate, most men don’t use this medication. The limited data we do have suggests that at least at the 5 year mark it’s well tolerated.
Q: And the DHEA?
A: There’s controversy regarding safety especially re: the prostate. Studies show that in the presence of high E, DHEA is actually not advised. As long as you can regulate E, you shouldn’t have issues with DHEA supplementation. You’re not using massive doses (currently on 50mg per day). When you start looking at over 300mg per day then it does affect the heart muscles causing difficultly for them to relax, and affects electro rhythms of the heart. You’re not using anything close to that. Studies show problems with heart really are at about 1000mg per day.
Q: Why is my DHEA low in the first place and will taking supps long term affect my bodies ability to produce its own?
A: Don’t have detailed answers for you, but if you look at the production of DHEA from the gland, it is produced by a precursor called 17-Hydroxypregnenolone which requires an enzyme called 17,20 lyase. We think that from a genetic perspective, in your case that enzyme doesn’t work well. As for supplementing turning off your own production, good question, but evidence suggests this is not the case. Unlike thyroid, where if you supplement, it switches off natural production, when we measure adrenal glands and measure DHEA, it doesn’t. Why this is different is that if you look at the (denol? sic?) synthesis of hormones in the adrenal gland, there’s 17. (Denol? sic? )synthesis in Thyroid is 1. I don’t believe there is negative feedback established with DHEA supplementation. There are some issues with other hormones e.g. pregnenolone, but not yet with DHEA. But watch this space.
A: My biggest stress is still shrinkage, what could be causing this?
Q: Could be a local problem. Not necessarily just blood flow, but could be a spasm of the muscle that causes testicles to ascend as well. Neuro vascular sheath runs through the muscle, called cremaster muscle. Unusual spasms with cremaster will create problems getting bloodflow to genital region. Have you tried L Arginine?
A: Did take for a while. Didn’t notice much improvement.
Q: Should take it two hours after last meal just before going to sleep. Physiologically you wake up in the morning with an erection because blood flow increases to the testicles significantly. this increases the circadian rhythm of T, the idea here is to mimic that process as much as you can. So take L-Arginine as late as possible.
The question is, is it not working because it won’t work for you, or not working because you have taken enough. How you know: trick is to go up on dose until you wake feeling like you have a hangover, head throbbing, then you know you’ve taken too much. Then drop dose. If it doesn’t improve your situation then stop taking altogether.
Q: Has finasteride damaged my dick or receptor sites in my dick?
A: Theoretically it’s possible, perhaps not receptor, since it’s a 5-Alpha reductase inhibitor, it doesn’t really work at the level of the receptor per se, but what it does is influence your own DHT and DHT is responsible for fluctuation in penis size. It could be possible this is attributed to that. It is physically possible.
Q: Is it worth testing DHT since we aren’t seeing whats happening inside the cell?
A; You could test, but if it comes back normal then what do you do? And if it comes back high then what do you do?
Q: Should I be taking topical DHT? Proviron?
A: Proviron - effect on DHT is actually not great. Has a greater effect on SHBG, increasing free T. Wouldn’t recommend something as hectic as Provrion, rather use Tribulus or (main ingredient in: stinging nettle extract). I don’t know much more about topical other than some guys use it cosmetically to increase the size of their dick.
Whether or not you get systemic absorption is unknown. You’re not injecting it like we used to do.
Q: Vitamin D supplementation? (mine was low)
A: Target serum is about 50, but controversial. Nothing off the shelf will get you there. Need 50 000IU. Calciferol is available on prescription. To get your level up to 50 need to take it twice a week. But remember that serum is just the tip of the iceberg. VD is a fat soluble vitamin, stored in fat tissue, liver, brain, muscle, by the time its in the blood very little left in tissues as well. Other benefits of keeping it high is affect on serotonin. Could affect your anxiety.
The way you take it is important. After a meal because its fat soluble. After biggest meal, twice a week.
Overall, your testosterone is functioning normally, the issue is the E.
Double whammy is super sensitivity plus high levels.
Advise on DHEA is to stock up on DHEA before government clamps down on the importing / OTC loophole.
Q: Alprazolam or Bromazepam for shrinkage?
A: Stay away from those.
Q: Will you consult with people overseas / guys I’ve chatted to on forums?
A: They have to come see me for a physical exam, I never just treat results.
Q: What is your take on PFS in general?
A: Response is very idiosyncratic. There are guys who take 5mg and no issues. Guys who take things topically in the hair yet have huge issues.
We think it is actually regarding epigenetics of how T is expressed in the body. The T response element. Something to do with the colons in between the active gene sequences, it’s analogous to a condition called Foster Kennedy Syndrome. You have a problem with polyglutamine type testosterone where guys have normal T but grow breasts and have shit libidos. The DHT levels in these individual are high. How does that work?
I believe Finasteride is a catalyst. If you have the right ingredients, its an explosion. If you don’t, you tolerate it perfectly well. We don’t know enough yet.
You managed to get things rebooted and produce T pretty quickly, lets hope long term you don’t need letrozole.
After 2 months test E. After 4 months test Vitamin D. Chew into VD tablet for better absorption.
Important - with AI’s, your body composition is critical, at the risk of sounding vain you have to look like a super model. Low fat, high muscle mass.
At least he took the problem (PFS) seriously. He doesn’t think “it’s all in your head”.
I hope this protocol works for you, buddy. Let us know after a few months.
Question: is this doctor from South Africa as well?
I wish your Dr would write up an exceptionally detailed (anonymous) case study of treatment chronology so we could take it in to other MD’s. What you’ve documented is great, but as I’ve said many times, Drs believe other doctors.
I’d like to get a pool together here to fund paying his Dr a couple grand to do it.
Interesting he thinks estrogen receptors have upregulated/oversensitized. This year’s research should verify this or not.
Also, could it be that if you block 5 ar, aromatase becomes up-regulated because you cannot convert T to DHT, so it must become estrogen?
Glad you are feeling better. I feel like I have the worst condition ever. I have zero sex drive or erections. All my memories of past relationships were erased after the crash. My hair has regrown over the last 10 months even though I am not taking propecia. How fucked up is that?
You all know my feelings why there is an imbalance of estrogen at the receptor site.