Have a read through the below screenshots as it gives insights into areas of investigation, and the TYPES of genetic tests that could be done by a lab or research scientist to hopefully investigate further (despite normal androgen receptor binding).
From:
books.google.ca/books?id=bhP4XLB … #PPA384,M1
ok,thank you MEW…
FIRST: the clinic tests the genetic 5AR2 by blood and speaking with my doc he said that in blood i could find 5AR2 not alterated but i should test the 5AR2 from my penis skin or damaged area,cause just there the cells could show the mutation…is this right??? my question is,doesn’t the DNA be present in all my body’s cells and if it is alterated, it is everywhere in my body and not only in some areas ???
SECOND: I ve read the documents from you MEW,and i ve understand that the binding can be right but even with it,there can be the present of the androgens insensibility,so looking at CHAMS and AWOR posts,they already tested for DNA androgens receptors binding and it is working well,so i don’t know what other DNA test have to be done to get clear the situation…what i’m going to do is the 5AR2 (by what my doc said,i ll do it from cells from my penis) and what other DNA tests could I do ??? what are the name of more specific DNA tests that i ve to do to understand if all the process is right ? you guys were talk about MICROARRAY ??? so i ve to check DNA microarray to find what???..
I’m sorry to ask you this but i really dn t understand too much about genetic and second ,english is not my leanguage,so thank you MEW and everybody one more time for the help .
I wait an aswer, just tell me the list of genetic tests i ve to do and i ll do them sooner i can .
thank you
i’m willing to donate for Awor’s test. mew i hope you can find some arrangements so that we can donate for Awor’s test and for that site.
we are all in a dark tunnel,and if we do not gather efforts we will not find a possible way out. we are fighting this syndrome alone without any awareness of the medical community. no-one will help us if we won’t help ourselves.
Well said chams
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Thanks for your offers to financially support further scientific investigation. I promise you that I am working very hard in the background to get the right setup lined up to take our investigation to the next step. But I must also say that I cannot guarantee yet that I will succeed. So we can start talking about money once it first becomes clear exactly who is going to work on this and then what the exact scope of the investigation will be - and what it will cost. We aren’t there yet. It could also well be that another test is not enough and that it will take a full fledged research project instead. If this would be the case, we are talking at least 1 mio. USD. Unless Steve Jobs got so thin because of fin induced muscle wasting, and is on this forum, it probably will be pretty tough to get that amount of money together. On the other hand, perhaps some researchers somewhere on this planet are already working on something which is closely related to our problem. Perhaps then, they would be interested in including our “case” in their research efforts. That is precisely what I am working on, to identify and find these people.
I can’t stress enough how infinitly complex this subject matter is. We are not talking about off-the-shelf tests, where your doctor just needs to tick the right box on the lab form. This is not something you can just order from a lab. Scientists with a very specific and rare skillset need to design the exact study methodology before any lab work can even begin. You are likely to just waste your money at this point with what you are intending to do. And do further damage to your penis for that matter.
Yes, test the genital skin for reduced or absent 5AR2 activity, because that’s one area where 5AR2 is specifically located.
Other tests to be considered include the ones I pointed out with RED ARROWS in the screenshots above.
As for the gene expression microarray test, Awor has already discussed further above the current status (trying to find research scientists willing to undertake it)… so if your doctor is open to finding a scientific researcher(s) or molecular geneticist who specialises in androgen receptor function and gene expression that is willing to help setup such a test, do the test, and who can analyze the data… let me know by Private Message, so that Awor can be put in touch with them.
ok,thank you for the explication. i ve found a clinic testing for 5AR2 but anyway on monday i ll call a friend’s uncle that is a virus researcher and i ll ask him all the informations about where i could have these test done and at what doctors/researcher i could speak,cause that’s his area and he knows a lot of other researchers.i ll update.
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…shit I was re reading this post now that my mind is way cleared up … this theory ,about the receptors etc,makes a lot of sense !.. test for all this is a must !
We aren’t talking about DNA. Nobody has suggested that something happened to our DNA (23 chromosome pairs = genetic blueprint). AR ligand (hormone) binding tests with Chams and me have shown that DHT is “docking” correctly with the androgen receptor. So we are now basically asking the question: why then, nothing/not much happens? Studying gene expression is one suggested methodology of finding out what the “output” of the receptor is, given the “input” T/DHT. Upon ligand binding (activation), the receptor does what it is genetically programmed to do. It “expresses itself” so to speak. That is why it’s called “gene expression”. The androgen receptor is supposed to trigger some androgenic action by “expressing” itself. We are clearly missing that. How much action are we missing? This “amount” can be determined by comparing our AR gene expression to a control group (there are no standard ranges for this). And of course the six billion dollar question is why? Unfortunately, studying gene expression alone will not give us the answer for this.
I’ll send you a private message with a status update. I will not discuss what I am up to in the forum (for obvious reasons, you never know who is reading…). I am also glad to update anyone else that is interested via pm.
so to have a good answer after have done the gene expression test ,we need the gene expression test of other people without our symptoms ?..is this what you mean?
genetic is the reader of the dna …and chromosomes are 46 .
23 pairs = 46 chromosomes, that’s right 
that is also correct. We would need to study a sample of at least 20 sufferers and 20 healthy men to have statistically significant data.
From Dr. John’s recent post:
propeciahelp.com/forum/viewt … 3906#13906
Interesting that his experience administering high-dose TRT to post-Fin sufferers parallels that of the researchers here when it comes to treatment of men with androgen insensitivity:
I wonder what happened to the guy who had his dht receptors analysed and found to be downgraded, insights from such tests would obviously be very useful here. I wonder too why there’s been so many people permanently affected by this in the US in particular and yet there are relatively few active members here, I can appreciate some want to get on with their lives but a pretty big chunk of it has been ripped away and surely answers are sought? I wish someone in the States would get the ball rolling with a lawsuit too so this could be out in the open instead of limited to a web forum.
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like always i can t stay away from thinking wht is going on,so…
i was reading some studies(dn t have them now) about finasteride and receptors and it is clear thet fiasteride distruptes/reduces drammatically the AR receptors,so…no matter how much testosterone we have in our body(a normal body 'd need a small ammount to work) .
even if we have testosterone/dht,i think that our problem is a receptor problm;I know that there was a guy (CHAIM) who tested for the binding between hormones and receptors and it was fine,so it is what make me think that finasteride “burned up” many of our receptors,they don t work anymore and the hormone testosterone just binds with the small receptors left we have alive after finasteride…this is the reason we ve weak erections,weak orgasm ,brain fog,sleep problem etc…and more this is the reason testosterone cream doesn t work for us .
so what i think is that we have to restore our dead AR receptors and i think one/the only way to do this,it is a LONG LONG testosterone booster/TRT,we have to bring over the high ranges our testosterone so that receptors are stimulated again and can work again …
any thoughts?
I have many theories, unfortunatelly it is just speculation, no scientific evidence, just logic. Please correct me if i state something that doesn’t make sense biologically:
2nd theory: It is a combination of factors: Make an analogy between the body and and a car. We are low in fuel (DHT, eighter low level or not active as before, producing little NO- Nitric Oxide), the fuel pump is damaged (Prostate cells are killed by propecia), the driver doesn’t have the key to start the engine (low dopamine levels, chemical sex link in the spine broken (?), damage or lack of stimulation in the pituitary: lower levels of vasopressin, oxitocin, and endorfin). The alternator is damaged also (the adrenals).
3rd Theory: The drug is claimed to block 60 to 70% of DHT after administration. Maybe we are a small group that Propecia blocks close to 100% of the circulating amount of DHT.
4th Theory: Finasteride binds with the receptor for Dht so the receptor is blocked… Some of the drug is not eliminated because it is not circulating… just like a magnet stuck onto your refrigerator. The new dht produced doesn’t bind with the receptor, but still the binding test comes fine because fin is occupying this space. Basically, intoxication.
Honestly, it could be anything… nobody knows.
Our knowledge of the human body is still very limited, that is the truth. Just study about most medications, you will read there “the mechanism of action of NAME OF THE DRUG is not exactly known”… So it is basically trial and error. We were the first guinea pigs after the rats in laboratory… and came the error. And it has happened many times before in our society. In 1957 Thalidomide started being prescribed as the miracle sotlution against nausea for pregnant women. The result… 10000 to 20000 children were born with severe births defects. And these children are now adults who have lived a very hard life.
So, if we can do something, is lecture our loved ones (nephews, cousins, everybody), that a prescribed drug is to be used in case of disease or risk of death only. And they should choose drugs that are on the market for over 20 years.
