Androgen Insensitivity Test

I live in Tampa, FL about 30 mins north of the All Children’s Hospital in St. Petersburg. Their Molecular Genetics Lab tests for androgen insensitivity (Complete, Mild, & Partial). I’m going to find a way to get this test done somehow. Hopefully I can convince my PCP, or Dr. Jacobs (When they confirm my appointment) to approve it.

http://www.ncbi.nlm.nih.gov/sites/GeneTests?Db=genetests&Cmd=ShowDetailView&TermToSearch=3117&ordinalpos=2&itool=GeneTests_EntrezSystem2.GeneTests_PEntrez.GeneTests.GeneTests_ResultsPanel.GeneTests_RVDocSum&disease_id=2575&test_type=clinical

Maybe this can help shed some light on this, and say once and for all if there is really a mutation or just an effed up HPTA.

Very interesting. Keep us posted. I have a feeling most of us are gonna come back partial androgen insensitive. My Testosterone is almost 700 , 200-1200 reference and I’m still not better.

If they test for this there do they also treat androgen insensitivity?

I’m still trying to research treatments. Most sources have stated that the outcomes of those treatments as “generally disappointing”. But that is using the method of supplemental androgens as a method of treatment. I assume that means HRT/TRT.

Here is an Androgen Receptor Gene Mutations Database I found a little interesting as well:

http://androgendb.mcgill.ca/

BTW I highly doubt raising test levels are going to fix anything long term. 5AR is responsible for alot of chemical process other than T to DHT. What we need is to somehow raise expression (affinity?) of that enzyme somehow.

For instance, I noticed people saying progesterone was high in alot of their labworks, blaming high progesterone as one of the reasons for sexual sides and brain fog. I say the progesterone is high because it’s not being converted to dihydroprogesterone via 5AR and then onto allopregnanolone properly. Similarly how high Test doesn’t correlate into high DHT.

The three chemicals bolded below are the directly affected by suppression of 5AR that I know of:

Test -> DHT (manliness, estrogen suppression, libido, CNS functions)

Progesterone -> Dihydroprogesterone -> Allopregnanolone (involved in GABA receptor activity, neurogenesis)

11-Deoxycorticosterone -> Tetrahydrodeoxycorticosterone (THDOC) (controls stress, anxiety, & depression)

Hey Merk, I didn’t read that in the effing literature…

On a side note, I have noticed that 5AR Type II is involved in 5-Alpha-reductase deficiency (5-ARD) but not 5AR Type I. And I can only find literature supporting Type II in relation to sexual problems. Never a mention of Type I. There might be, but I haven’t come across it yet.

Bradwaggoner, only two other people have had a similar genetic test… viewtopic.php?f=27&t=2216

Of course AIS/PAIS is an inherited disorder. This is not the same as suffering from the effects of a drug that may have induced sever side effects through epegenetic changes (see above) or more than likely cell death viewtopic.php?f=27&t=4327 .

[It is unlikely there is a problem with the 5ar2 enzyme. If something was wrong with 5ar2 people would not have normal DHT levels. 5ar1 does not compensate for 5ar2 otherwise finasteride wouldnt work. Also 5ar1 occurs in a different part of the body. Simple as that.]

ok, i did a search but didn’t see that come up when I did. Noted.

I do see what you are saying about DHT, and I think you are right for the most part, but I still think there may be 5AR issues possibly going on in some of us. Honestly, I really don’t believe that is my issue. But for the ones who have low allopregnanolone and high progesterone along with low DHT, this could be the case.

Apologies if im late as I only check in once in a while.

I had no Idea Fin was classed as an anti-androgen drug.

en.wikipedia.org/wiki/Antiandrogen

To Oscar:

Taken from http://blog.alanjacobsmd.com/alan-jacobs-mds-blog/2010/06/a-proposed-mechanism-for-prolonged-sexual-side-effects-from-finasteride.html

“Several young men seen for hypogonadism (low libido, erectile dysfunction, low energy, etc) after using finasteride have been found to have low-normal levels of bio-available testosterone and LH. This leads to the question of whether partial androgen resistance is at play. It has been shown that androgen insensitivity can occur even without mutations in the genes coding for the androgen receptor1. How then to connect finasteride use to the development of partial androgen resistance, especially outlasting the use of the drug?”

So you are right, and that would make the test I was going to do basically useless.

Does anyone have any idea if we could test for Androgen Resistance?If such a test even exists outside of a research lab environment?