Testosterone, dihydrotestosterone or 5ar2 antibodies.

Im starting to contact universities, fuck it im sick of this pfs shit, i want out.

But dgreen to find a suitable treatment we need to nail the problem first.

3 things need to be tested, 5ar2, dht and ar antibodies. Oscar found some studies showing that ar antibodies do exist, but i cant work out why the immune system would attack the ar for us. Possibly it could look like there is a problem at the ar level because the hormone(dht) is not binding because the immune system has “deactivated” it
Awor did say it was highly unlikely that we have a problem with 5ar2, he said not to speculate aswell so i will stop there.

Jn is on cortisol and t and says hes recovered(who knows with him though), some have claimed benifits off cortisol or things that increase cortisol, others have claimed benifits off alcohol, weed and ghb, all immunosuppressive, so there is substacial evidence there that symptons can be reduced, no matter what the root problem ends up being.

I still think we can get some clues from vasectomised males. They get IgG anti bodies and become hypogonadals. Their total T, DHT, LH and FSH are also low just like us.
There are so many companies making anti DHT,testosterone and 5 AR anti bodies. Can we contact them and ask them if they can test our blood for the presence of these anti bodies?

Yes contact them, you have nothing to loose, although it may take some sort of lab based investigation.
Also at this stage lets not compare us (people who took 5ari) to those who didnt, we are in different boats.

here we are discussing anti bodies.
have you read vasectomized males’ stories?
I have contacted some companies but not response so far.

Sure sps it looks good for this theory that antibodies can cause these sides. But it is two different ball parks. (finasteride and vasectomy)

sps you sent me a link about a few of these guys and as I told you those who ended up with low T recovered via TRT. Clearly we are different.

Yes its quite common for the body to reject something after an operation. Here we are talking about a returning hormone and/or enzyme.

Yeah the next thing to do is get tested for this. Although not sure what exactly they would be looking for other than some sort of anti-androgen or anti-AR autoantibody. But the good thing about this ‘theory’ is that current blood tests do not exclude the possibility of such a thing being present - we know from the research papers that anti-androgen antibodies are present without inflammation.

But there are still problems with the theory: For example, after stopping Fin, LH/FSH drops. With anti-androgens such as Flutamide, LH spikes in response to no negative feedback on the pituitary. In the research paper with anti-testosterone auto-antibodies, the same thing happens.

Although there are hardly any papers on anti-AR autoantibodies, there are a few on anti-Estrogen Receptor (ER) antibodies. Studies show anti-ER actually interacts with the ER receptor “Like E2 but unlike antiestrogens, this biological effect corresponded to down-regulation of the receptor protein” [1] and actually competes with Estrogen [2]. How and why this happens (as discussed in this paper[3]) may be due to a natural mimcary “attributed to their molecular resemblance to the hormones” or effecting the ER in another way. This would cause low LH.

Dont know if continued hairloss/other wierd hair problems are caused by the same thing, or how/why anti-AR antibodies can develop (or even if its different to anti-androgen antibodies???).

[1] ncbi.nlm.nih.gov/pubmed/2036991
[2] ncbi.nlm.nih.gov/pubmed/2947910
[3] jcem.endojournals.org/content/82/10/3464.long

Would lowered growth hormones suggest the problem is at the enzyme level? I dont know does anyone have an opinion on this?

What would you consider to be low GH?

Well just about everyone here has a fsh at the bottom of the range, lh in my opinion looks normal in general.

I guess the point is that we dont have high growth hormones, but we are not taking an anti-androgen (flutamide) or the antibodies dont neccessarily have to be against testosterone, ala the studies provided.

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Well I guess the main point is that there seems to be a naturally produced anti-androgen that does not lead to raised LH/FSH – in fact it may lower LH/FSH in high enough doses (such as the acute phase/‘crash’). Though i would argue for most the problem is at a local level, it may still effect the HPTA.

I think that due to the nature of my symptoms the ‘autoimmune reaction’ would have to stop androgenic activity.

Also, I see no reason why we couldnt have anti-AR and anti-androgen autoantibodies active at the same time. And lets not forget Finasteride (along with its 5aR reduced metabolite Dihydrofinasteride) is also a synthetic androgen.

This is a good point.the reason for high LH in case of Flutamide is that it blocks Androgen receptors in all parts of the body including brain.
ncbi.nlm.nih.gov/pubmed/2674764

saw palmetto binds to androgen receptors but finasteride does not but in both cases LH and FSH are low. So we should conclude from flutamide effects that our Androgen receptors fine?
observations from TRT and DHT(proviron) also points in this direction. Almost all of users(Awor,kazman, ehh etc) report that TRT stops working after some time.
Clearly 5ARs are not the cause as DHT is bypassing them.
the only possibility remains is Anti bodies(my assumption).
The reason I cited Vasectomized males is that anti bodies dont alway cause high testosterone or hig LH and FHS as Oscar thinks.

There could be a whole nother mechinism at play here, i dont know how to explain it scientifically, but lets say for example the body is fighting of dht then why would it want to increase testosterone, it would just make the job harder, wouldnt it want to decrease t, we do all generally have low free t, most without high shbg, perhaps this is the reason and eveidence for a testosterone antibody.
This also brings into play the whole thing as why some feel worse when androgens are increased, the immune system has to work harder.

On another train of thought, is there such a thing as free dht and is there testing available, and has anyone had it if there is.
This could be one potential way that the body is doing it, going off of the thyroid hormone study, of course there could be other ways.

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Thats the reason I posted about this originally.

The way I see it, anti-AR/ant-Androgen autoantibodies would only be produced locally in sex-steroid dependent tissue (where Finasteride has acted upon 5aR) which will now stop both DHT and Testosterone activating the AR.

Therefore you can add Testosterone, and build muscle, but negatively effect your penis due to increase 5aR/DHT production and the resulting antibodies. A bit of a catch-22 situation! So the same mechanism, but to a lesser extent, prevents Testosterone from working at all, or only transiently.

Muscle loss would be caused by these antiandrogens being present in circulating blood (though starting off in a few local locations)and partially blocking the activities of T elsewhere. This is why why increased T is needed to counter this. (Though 5aR2 is found throughout the body viewtopic.php?f=8&t=5168).

oscar - perhaps you should contact one of the authors of the ER antibody papers and see if their is possible testing for AR antibodies? Also, my LH and FSH was quite high after stopping fin, not low.

OK guys suppose we have developed Anti-bodies then what is the solution to this?I think anti-bodies related problems are not easy to treat.
golf you say your LH and FSH were very high after stopping fin. how are these now?still high?
I think I have seen a post on this forum made by a lady. She mentioned that after finasteride use her husband developted anti-sperm anti bodies, which were clinging to the tail of the sperm.I am trying to find it, can some body help to find this post?
so far my emails to companies which develop anti-DHT,testosteron etc anti bodies are unsuccessful. They are telling me that they don’t have any tests for us.I have contacted so far two companies.one in US and the other in UK.

My LH is in the upper end too. Maybe Im developing (or had, judging by my low test) gonadol failure on top of everything else.

I have contacted the only lab that I can find that will even test for this (its in the US). Whether or not this lab even does ‘requests’ for private individuals or if ive phrased exactly what im asking for correctly, i dont know.

A large number of endocrine diseases actually involve antibodies so testing for the things mentioned in this thread is actually very easy, but without a bespoke research project with knowledgeble people involved (like awor set up) it may never happen.

Another qusetion i want to throw into this thread, and hopefully it wont derail it to far, is why can i only get 2 days out of 1 type of pde5i.
On the 3rd day i have no reaction, like my body has worked out how to deactivate it and is just doing it for the hell of it, i have to cycle. My doctor said this is not normal, that he has never seen a tolerance built up so quick.
Alot of people have experience’s like this with all sorts of supplements, is the immune system involved here?
Im bumping the free dht thought aswell, wouldnt this be quiet interesting to see what a pfs sufferer turned up here, although the dht we are talking about is very localised.

Also i have contacted two universities, no reply from one and a whole load of “our funding doesnt cover this” yap from another, its depressing.

I find the theory of an autoimmune reaction to be the most interesting, check out this article:

huffingtonpost.com/dr-mark-hyman/is-there-a-cure-for-autoi_b_756937.html

If propecia triggered an autoimmune reaction, it would explain why some of the recoveries have been natural recoveries by living a healthy lifestyle (thus eliminating triggers that exacerbate an autoimmune response), and also recoveries attributed to dexa and other immuno-suppresant drugs. It seems to be a plausible explanation for both types of recoveries.

Dr. Hyman (author of the article above) is not taking new patients and his office didn’t seem familiar with PFS, but I’m looking into making an appointment with one of his colleagues nonetheless…