Testosterone, dihydrotestosterone or 5ar2 antibodies.

I have personally felt much better from sleep deprivation. Numerous men with hormone problems on Meso RX and Crislers forum have also stated that there libido and/ or erections are better than usual when they are tired. It also seems common for normal men to get more erections when they are tired, so maybe the sleep deprivation benefits some us for a reason other than immune suppression?

edguider.com/forum/general-discussion/423-why-my-erections-better-when-im-tired.html
topix.com/forum/health/erectile-dysfunction/T8L61KV2EI6DM2SSO/p2
wiki.answers.com/Q/Any_connection_between_being_tired_and_instant_erection

When I took 1 gram of transdermal T which seems to be the normal dose for regular people. My total test dropped a couple of points and my free test dropped to 33.5 (43 - 138) and my estradiol also dropped a couple of points. My LH also became undetectable. There was some feedback loop telling my hypothalamis to stop producing testosterone even though my test levels were really low. Perhaps it was DHT. But if DHT was able to suppress my LH why wouldn;t it be acting upon my libido? If my testosterone was being taken out of action via antibodies not much of it would have been able to convert to DHT or Estrogen. If my DHT or 5ar was being taking out by antibodies it probably should not cause suppression.

I am still trying to figure out a logical way that these antibodies could work. If they took hormones out of action our LH should be high due to less feedback.

The only way to explain this partial feedback would be if the antibodies themselves had some kind of antagonistic effect on the hypothalamis but not on the cells. Does this seem like a tall order?

Does anyone know if we as a group need more testosterone to get into range than non pfs sufferers. A lot of us do have low testosterone but without elevated LH? This shows that something is telling our hypothalamas that we have enough hormones and not to produce any more.
Why is this happening?

“Cortisone may also be used to deliberately suppress immune response in persons with autoimmune diseases or following an organ transplant to prevent transplant rejection. The suppression of the immune system may also be important in the treatment of inflammatory conditions such as severe IgE-mediated allergies.[6]”

en.wikipedia.org/wiki/Cortisone

“Conclusion: The exam stress can result in a decrease in the IgE level and a significant increase in the cortisol
level. So, these changes may indicate the alterations of immunological status and presence of stress in an immunosuppressed
individual, affecting his/her health.”

sid.ir/en/VEWSSID/J_pdf/88120100424.pdf

So then can low cortisol lead to high IgE?


How many people here have low cortisol?

What could cause this high IgE?

Parasites? nutritionalmedicine.org.uk/phdi/p1.nsf/imgpages/franklin_TheRealCausesofIBS.pdf/$file/TheRealCausesofIBS.pdf

I know I have had digestion issues since around the time i stopped taking finasteride. But I don’t really think any of this could cause low 3adiolG. And total loss of libido.

Adrenal fatique? This diagnosis is not really recognized as valid. And could be just an easy answer to why people have low cortisol. When really this is not the root of the problem.

Chilln will say that thyroid hormones will increase the activity of some enzymes.

Is there any other way finasteride could have inhibited cortisol by down regulating an enzyme?


This site is great and I thank Mew for his efforts. But I am sure it can be improved. I think we need a weekly newsletter or notification which keeps everyone up to date. The process of gathering data is just too slow when we have to wait for people to find the threads and then decide to go tested.

If we had a weekly newsletter we could just post something like 4 out of 4 people tested have found that they have high IgE levels. We need to see if there is a pattern here. Please go to your doctor and test this week and post your results in this thread.

Same thing for body temps. Salivary cortisol and everything else. We need to increase the speed at which we can take action. I think we could easily double our rate of progress.

Excellent idea! I agree. We need more unity, better communication.

Our governments failed to protect us and refuse to help us. We’re all in this shit together–by ourselves.

/quick rant

Please use this thread to post about Testosterone, Dihydrotestosterone or 5ar2 antibodies ONLY.

This thread is not a general discussion about the immune system. This thread is not a general discussion about cortisol. This thread is not a general discussion about sleep times. This thread is not a general discussion about body temperature. This thread is not a general discussion about digestive issues. This thread is not a general discussion about parasites. This thread is not a general discussion about leaky gut. This thread is not a general discussion about adrenal fatigue. This thread is not a general discussion about any other random theory. If you want, you have the rest of the forum for all that.

I agree with the sentiments expressed above about better organisation. So, in order to save [Size=4]OUR FUCKING LIVES[/size] lets try and stay organised, focused and on-topic. OK?

/longer rant

You can not look at these things in isolation as they are very much interrelated

Says who?? You? Back up what you are saying with some evidence.

Discussing high IgE is only relevant if you can connect to to the topic of this thread. Discussing low cortisol is only relevant if you can connect to to the topic of this thread. Discussing digestion ‘issues’ is only relevant if you can connect to to the topic of this thread. Discussing adrenal fatigue is pointless and is only relevant if you can connect to to the topic of this thread. Discussing leaky gut is pointless and is only relevant if you can connect to to the topic of this thread. Discussing the immune system in general is only relevant if you can connect to to the topic of this thread. Etc Etc Etc.

Of course any real-world results are welcome.

The reason for this is so that useful information (a blood test result, a relevant study) is not lost in a sea of pointlessness.

How about this for some evidence? awor says he has this main problem figured out and that we should shut down the theories section so we don’t have to listen to bald impotent pricks like you.

Stop personal attacks and name calling.

Oscar has a good point with this statement:

The forum is getting bogged down by irrelevant posts. Regardless of the merit you think your posts have, make sure they connect to what’s being discussed in the thread and if it’s not apparent state the connection.

While the urgency is understood, we have a team of volunteers here struggling with their own finasteride induced problems working on this process. If you read Awor’s posts he spends a lot of time contacting researchers and studying instead of posting here. It would be great to increase the speed at which we can find a solution for persistent side effects caused by finasteride, however it’s not as easy as urging everyone to their doctor to get tested this week for something you personally deem important. I would venture a guess that quite a bit of damage has been done from the urgency of trying to treat PFS, arguably more damage than success. Look at the Greece prostatitis thread. How many who had taken finasteride came back better off than when they went over? Is there anyone other than Solonjk? If there’s evidence of success I haven’t seen please post it.

We need to mitigate damage at this point while we look for a solution, which means best-practices symptom management in the mean time. The only way to find this is to take the edge off the conversation, look at focused research, and work together.

The forum is open to new ideas and threads that are relevant to pursuit of knowledge about finasteride induced side effects and finding treatments for them. This thread was created with the purpose of discussing testosterone, dihydrotestosterone or 5ar2 antibodies. The very first posts states:

If you don’t like it start an alternative thread. We’re all in this to succeed.

I thought this thread was about antibodies… Dono how info directly related to antibodies a number of people have tested high for is not relevant.

I was also pondering exactly how these antibodies may work and result in the condition we are experiencing.

I did go of topic a little on a couple items. But worse things have happened.

Just wanted to put this here to keep the relevant info together.

onlineallergycenter.com/pdf/Hormone_Allergy_AJRI_3_10_06.pdf

Well, I am new here and in the same boat as everyone else. I really dont know how all this plays together, but I turely believe that are immune systems are at fault. When I first crashed I remember telling my wife that I think my body is destroying it’s self. I really know very little in reguards to this subject matter but I really think this is going to shed some light on the cause. below is a article that I found interesting. I just want to say thanks to everyone for there dedication and will power to strive to find a cure.

The immune system usually responds to some insult such as an allergen, a microbe, or a toxin, and then runs out of control. Finding and removing that trigger is essential. In a review in the New England Journal of Medicine, it was acknowledged that “even in a genetically predisposed person, some trigger, an environmental exposure, or change in the internal environment – is usually required for [autoimmunity].” (i)

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

lets thing our 5ar1 and 2 now underattack by our immune system, and as a result of it we all have autoimmunity why we choose to suppress the immune system iges?. in another words suppressing 5 ar and relieve the immume system and its random auto-attack mode?

our cure, if its possible, i think it has to include finasteride inside
and of course too much trt

and lastly finastrride may be our worst enemy and best friend at the same time.

1 Like

Has anyone given consideration to the role of the spleen might play in PFS?

Please present information as to why we would. Thanks

i ve applied testogel to my beard area for a while, after 7th day a hypopigentation, like "a vitiligo start sign " appeared. i could hardly seen in a low light but testogel changed the pigmntation, it has hard-shaped-borders between hypo and hyper pigmented areas with a little mole.

i am shocked, stressed , dont know what to do now.

my theory is now sometihngs attacking 5ar / and 5AR’s bitch friends /skin pigments ,5AR1 ,ETC. randomly

i am on the idea that re taking fin to kick these 5AR off and shut the autoimmune down simultaneously.

.have you guys experienced mole number increase?

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I don’t think 5 AR are not working. short lived recoveries after stopping fin or starting TRT should not be possible. Instead I am thinking antibodies are binding to DHT and this DHT when bind to our ARs, deactivates them. Each time we apply TRT it takes some time before ARs are deactivated and once ARs saturated T goes in Estorgen and we see rapid build up there.

Please don’t stop until you read all.

Our body’s immune system identified Fin/Dut as foriegn invadters and produced anti bodies against them but since these chemicals resemble our own natural DHT very much immune system keep attacking our own DHT even after we stop Fin/ Dut/SP.
Auto immune symptoms
look at the list of symptoms and see what symptoms we don’t have.
Muscle and joint pain, muscle loss,wieght loss, Candida, sleep problem, Anxiety depression, memory loss, digestive problems etc etc.
evenbetterhealth.com/autoimmune-disease-symptoms.php

Now read the following.

en.wikipedia.org/wiki/Autoimmunity
Molecular Mimicry - An exogenous antigen may share structural similarities with certain host antigens; thus, any antibody produced against this antigen (which mimics the self-antigens) can also, in theory, bind to the host antigens, and amplify the immune response. The idea of molecular mimicry arose in the context of Rheumatic Fever, which follows infection with Group A beta-haemolytic streptococci. Although rheumatic fever has been attributed to molecular mimicry for half a century no antigen has been formally identified (if anything too many have been proposed). Moreover, the complex tissue distribution of the disease (heart, joint, skin, basal ganglia) argues against a cardiac specific antigen. It remains entirely possible that the disease is due to e.g. an unusual interaction between immune complexes, complement components and endothelium.

here is my hypothesis and how events unfold in our system

-When we start using them, some sensitive souls’ immune systems kicks in and launches antibodies against these chemicals. As soon as We feel adverse effects we stop fin/Dut/SP etc cold turky. Now at this moment our body has high level of tosterone but low level of DHT . We feel better becaue DHT dependent tissues and not under fire.
-After discontinuation of finasteride or dutasteride etc our DHT returns and we feel better but only for a short time. Now body attacks our own DHT, and we start feeling bad and then worse and worse agian.

  • Some people restarted finasteride / Dutasteride and again felt better for a short time the reason antibodies were consumed by these chemicals and their concentration goes low and DHT gets a chance to work but again for a short time only , as soon as anti bodies increase these guys begin to feel worse again.

there are many many articles on autoimmune caused by mocular mimicry.
for example
drshrader.com/autoimmune_diseases.htm
this is very good article and highly recommend to read .

what is Molecular mimicry ?

Molecular mimicry is generally interpreted as the sharing of molecular structures (or their protein products) by portions of dissimilar genetic material (i.e. “resemblance” or cross-reactivity, most often between different organisms). This produces an “error in identification” by the host. The mimicking material is usually foreign (“non-self” e.g. bacteria) but the material contains components similar enough to certain host cells that the host then mounts an attack on “self.” In other words, a bacteria can trick the body into attacking normal cells that have a few characteristics of the bacteria. When you think a great deal about this, the prospect is frightening.

If a peptide bound by HLA-B27 were the result of molecular mimicry between host and organism, the receptor site would be considered by the host to be “foreign”. This could easily explain autoimmunity, or the breaking of self-tolerance, since autoreactive cytotoxic CD8 cells could then continue to attack the HLA-peptide reaction site and persist, despite the absence of any initial triggering agent, such as bacteria, virus, etc.

ncbi.nlm.nih.gov/pmc/articles/PMC1011230/
Molecular mimicry–hypothesis or reality?
A number of observations support molecular mimicry as a possible pathogenetic mechanism in diseases such as acute rheumatic fever, reactive arthritis after enteric infection or associated with Reiter’s syndrome, myasthenia gravis, or even in rheumatoid arthritis. Molecular mimicry can be defined as a sharing of epitopes in linear or 3-dimensional presentation on disparate proteins from entirely different sources–for instance, group A streptococcal membranes and human cardiac myosin. How exposure to or infection with organisms sharing molecular similarity with antigens of the human host can evade tolerance and actually induce a self-reacting humoral or cellular immune response is still not clear; however, a large body of evidence has now been accumulated that documents apparent molecular mimicry mechanisms in these disorders

Why I want to know about Accutan?
Accutane has totally different chemical structure.
I repeatedly asked bout accutane’s reaction with 5 ARs. and how it looks like after binding 5ARs with it?
if after binding 5 ARs Accutane looks like DHT? then my theory is right other wise we are having some thing else

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this sounds like something that could make sense, but what chemicals are similar to DHT in finasteride? i thought fin only changed 5AR2, not DHT, DHT is only the side effect of decreasing 5AR2?

this is very dumb question. Testosteron+5 AR----> DHT
finasteride+ 5 AR----> DH finasteride,

now Di hydro finasteride binds 5 AR irreversibly and attaches to AR receptors, kicking out DHT.

I have very high hopes.I am sure our right choice is immunologist not urologist, Endo or neurologist I have never been so optimistic in three years. I would have caught the flight to see this doctor but as you guys know I have lost the job and today was the last day of my insurance.

look at the list how many can be treated and most of these are auto immune disorder.

drshrader.com/ProblemsWeTreat.htm