That paper is from 1985
Oscar, it is a fact for you, you have ige antibodies. The question is what are they against, i am testing myself tomorrow for this(ige) down at the lab to see if it is common among pfs men.
so?
unfortunately the link I posted doesnât talk about the symptoms of Anti DHT anti bodies.
Oscar what does make you think that we have anti 5 AR anti bodies. We did not mess up with 5 ARs we messed up with DHT. when we are using DHT we are bypassing 5 ARs. If there are 5 AR anti bodies then not body should get any benefit after stopping fin or after starting TRT. Most of the PFS sufferers get initially well and then they get worse.
I have posted this paper already and quoted from it extensively in this thread. At the moment im thinking a reaction towards 5alpha-reductase, but it could be something else. Other autoimmune endocrine diseases exist that are directed against hormones or hormone receptors (hence the title of this thread) none of which have been ruled out.
5alpha-reductase regenerates after stopping Finasteride, that seems one good explanation for a âtriggerâ of an autoimmune reaction of this sort, hence the âCrashâ. Sps, I just explained to you why I think T and DHT does not work.
I dont know how relevant IgE by itself is, I really need to ask a specialist. I do know is testing is important, and everything discussed in this thread can be tested for quite easily by someone that knows what they are doing; but it would require a pathology laboratory at a hospital to run some specialised tests.
This could also explain Mariaâs symptoms. She was injected with sex hormones and that couldâve triggered an autoimmune response similiar to ours.
Dht is a very aggressive androgen. The immune system could have taken great offense to it returning.
I was thinking a similar thing, but instead of androgens mediated her symptoms, somehow she is having a reaction against estrogens as her symptoms are virtually identical to hypoestrogenism/postmenopause. But i dont want to waste any time on maria trying to connect her problems to ours.
Ok Guys today I sent email to CUhospital about auto immune anti Androgen receptor anti bodies. I urge every body here to please look for any resource who can help us with auto immune anti bodies. I really want to sort it out.
So is there one androgen receptor for all androgens? Does the cell uptake testosterone and then convert it by 5ar to DHT inside the cell? What about free form DHT, this binds to the receptor and then activates the gene transcription?
If DHT was bound by an antibody would it still measure as DHT in the blood? Do we have some kind of antibody which is a receptor agonist which binds to the receptor blocking other androgens from binding?
Are we responding to the anabolic effects of testosterone? Or are these suffering too?
If we had a antibody to 5a this would be visible on urinary hormone profiles right? I think I have seen low 5a activity on some peoples profile.
How is 5-adiol-g implicated in this thread? Does the t bind to the cell, the cell then reduces it to DHT > and then 5-adiol-g?
I had an almost 100 percent recovery for a few days on arimidex. I wonder how I would explain this? Before I took the arimidex I took loads of testosterone, proviron and also some andro hard my libido did not recover on any of these. But I had a full recovery on just arimidex. This only lasted a couple of days.
Yes. Yes. Yes.
Yes. Maybe, there are other illnesses that do, such as Gravesâ disease and Myasthenia Gravis. I mention anti-AR antibodies earlier in this thread.
It depends on the symptoms and whats causing them I suppose. This thread brings 3 new viable ideas as to why muscle loss can occur (5a-R is also found in muscle).
Of course, the question is then: Why doesnt everyone have muscle loss?
Well, these ideas also include lots of variables. For example, the strength of autoimmune reaction, the enzymes involved (5a-R 1,2,3) the levels of enzymes in each person, different effects on different tissue. Maybe this reaction only happens transiently for some or only occurs in a certain %.
Dont know. I agree.
Dont know. Yes, although the âgâ part is actually added in the liver.
Dont know. Try and get tested for an immune reaction against the hormones, enzymes and receptors effected by finasteride and you might find out!
I found this interesting, that body temperature can be reduced by a mechinism that is semi-related to the antibody idea and has nothing to do with thyroid and adrenals.
.
Vincentv refer to this study as an example of how antibodies can deactivate hormones, whilst still showing up normal on blood tests.
for example an injectable dht derivative - masteron could be deactivated by a specific antibody?
Sanane i pulled this quote from the paper that is in the thread âhormone allergyâ maybe it helps?
So if we had a androgen receptor blocker type antibody that was not an agonist in some way wouldnât this result in High LH? If the antibody attached to the hormones disabling them wouldn;t LH also be high as there would be little feedback on the hypothalamus.
So LH would only be low if the receptor blocker or antibody was partially stimulating to the receptor? I wonder if having any form of hormone in the androgen receptor in the brain/hypothalamis cause it to be satisfied and stop asking the pituitary to produce more LH. Or is it the amount of âandrogenicityâ of the hormone that controls LH. There are multiple factors to consider like estrogen and progesterone and so fourth. hmmmm.
I am sure I grew more hair body hair on testosterone. I also lost more hair from my head. It was clogging up the drain.
Would be interesting to have a list of which hormones have the most powerful negative feedback on LH secretion.
With those thyroid patients, they respond fine when they are give more t4/t3?
If we had an antibody attaching itself to just DHT, what would happen? Testosterone or estrogen would go up to a point where they were creating creating negative feedback on the hypothalamus?
As far as effects on LH/FSH go;
anti-AR antibodies: Receptor antibodies do not âblockâ receptors but they can âdownregulateâ receptors. For example here: ââŚTSH receptor autoantibodies can directly suppress TSH levels independently of circulating thyroid hormone levelsâŚâ (see jcem.endojournals.org/content/86/10/4814.full). Therefore high levels of anti-AR could lead to hypogonadism-like symptoms without raising LH/FSH. Remember, anti-AR antibodies are naturally occuring, but in low amounts.
anti-DHT antibodies: Dont see why these should have a significant effect on FSH/LH if Fin didnt.
anti-5a-R antibodies: Dont see why these should have a significant effect on FSH/LH either. Like anti-AR antibodies these have already been discovered in patients blood, but no proper studies have ever been conducted.
As i said before, these ideas are seperate, and a reaction against 5alpha-reductase is currently my favourite as it has the least problems.
Of course during the âcrashâ LH lowers along with T. These ideas dont explain why that happens. Maybe its linked to the autoimmune response/stress. It has been described as tertiary hypogonadism. A rare cause of this is Autoimmune hypophysitis (see jcem.endojournals.org/content/92/6/2038.long) which is linked to thyroid antibodies and can occur as a result of adverse drug reactions. Maybe its also commonly found in one of the above three scenarios in the same way TSH is raised during the crash. Just a thought.
âAs i said before, these ideas are separate, and a reaction against 5alpha-reductase is currently my favorite as it has the least problems.â
When people supplement with androgen arenât a lot of them loosing hair? As I said I grew more body hair on 200+mg Test e per week and also lost some hair on my temples. I did not really notice any change in strength. I probably went up to about 350mg per week. I was on the testosterone for a couple of months.
Does directly ingesting DHT work around the lack of 5AR?
I am pretty sure I did not lose my libido straight away when taking finasteride. From what I remember it occurred after a couple of weeks. I also clearly remember one specific time in which I was more turned on by some porn than I had ever been while on finasteride. But this was only one time.
The link with DHT and libido seems to be very strong. But as we age does our DHT and E go up naturally? and our free T goes down. This correlates to a declining libido right?
I have always been going to the gym regularly for 9 years. I remember that after I stopped finasteride I tried to bulk up a bit. But the only bulking I could do was to increase the size of my love handles. I never had any signs of love handles pre finasteride. I assumed this is because of low T. But when I was on T for a number of months I should have noticed a significant boost in strength⌠but I did not. My free T is below range.
I also remember when I took my first andriol capsule I felt the desire to masturbate. That was the first time I had felt this post fin. This also happend with arimidex in August. But the effects never lasted.
Do you think finasteride drove out testosterone levels way up to a dangerous level causing our body to create some kind of testosterone antibodies or AR antibodies?
I would have to say I never experienced much of a crash. I basically lost my libido after a number of weeks and it never really came back after that.
So if finasteride caused antibodies to T, most of us should not experience the anabolic effect when taking testosterone. But I guess if all testosterone was being blocked we would probably not see the androgenic effects too as there would not be much T available for conversion to DHT.
I am saying this because I grew body hair and lost hair on my head while on T but did not notice much at all in terms of muscle growth or body composition changes. I also felt very horny at one point while on Finasteride when my DHT should have been partially inhibited. I think I have seen this elsewhere too.