To be tested for something like this would require molecular testing at the genetic level, to evaluate the DNA of your Androgen Receptors and to check for mutations.
If you can find a lab, doctor, researcher or endocrinologist that would be willing to look this far into things, you may find some answers.
The following are just my own thoughts as to why:
The Androgen Receptor Gene Mutations Database
androgendb.mcgill.ca/
- See if you can find any info there… particularly regarding “Androgen Insensitivity Syndrome”…
“Syndromes of Androgen Resistance”
biolreprod.org/cgi/reprint/46/2/168
- Read about what happens when you have androgen receptor mutations/failure
“Androgen Receptor Gene and Hormonal Therapy Failure of Prostate Cancer”
pubmedcentral.nih.gov/picren … obtype=pdf
- This study mentions that "Androgen receptor (AR) binds androgens and mediates their effects on target cells.10 Much research activity has focused on the role of the AR in tumor recurrence and progression. The role of AR gene mutations in tumor progression has been studied in the vast majority of these studies. Such mutations can lead to impaired steroid binding specificity and to altered transactivational properties of the AR protein so that it retains its activity even when bound to other steroids than androgens.
Human Prostate Gene DataBase
ucsf.edu/pgdb/gene/87.html
"The androgen receptor gene is more than 90 kb long and codes for a protein that has 3 major functional domains: the N-terminal domain, DNA-binding domain, and androgen-binding domain. The protein functions as a steroid-hormone activated transcription factor. Upon binding the hormone ligand, the receptor dissociates from accessory proteins, translocates into the nucleus, dimerizes, and then stimulates transcription of androgen responsive genes. This gene contains 2 polymorphic trinucleotide repeat segments that encode polyglutamine and polyglycine tracts in the N-terminal transactivation domain of its protein. Expansion of the polyglutamine tract causes spinal bulbar muscular atrophy (Kennedy disease). Mutations in this gene are also associated with [u]complete androgen insensitivity /u."
Oligospermic infertility associated with an androgen receptor mutation that disrupts interdomain and coactivator (TIF2) interactions
jci.org/cgi/reprint/103/11/1517.pdf
"Infertility affects approximately 10–15% of all couples (1). Spermatogenesis is at fault in about half of them, but its cause is often covert. Androgens are required for normal spermatogenesis; however, most infertile men with impaired spermatogenesis have normal serum androgen levels. Therefore, attention has turned to the androgen
response apparatus, particularly the androgen receptor (AR). Mutation of the X-linked AR gene causes a wide range of clinical androgen insensitivity: complete, when the external genitalia are female; partial, when they are sufficiently ambiguous to require corrective surgery; and mild, when they are phenotypically male.
Three surveys of men with idiopathic infertility have yielded widely disparate frequencies of androgen-binding abnormalities in cultured genital skin fibroblasts (2–4). Genetic defects of the AR that cause mild androgen insensitivity with impaired or preserved spermatogenesis (5–7) are of particular interest because they may illuminate the fine structure-function attributes of the AR that permit differential regulation of androgen-inducible genes. To this end, we screened a large group of infertile men with defective spermatogenesis for abnormalities in the coding segments of their AR genes.
We found 3 unrelated subjects with the same missense substitution in the COOH-terminal portion of the ligand-binding domain (LBD) of the AR. One shaves infrequently; another has low-grade but persistent postpubertal gynecomastia. Unexpectedly, this novel mutation does not affect the ligand-binding characteristics of the AR; rather, it reduces the transactivational competence of the AR by impairing interactions
between the receptor domains, binding to androgen response elements (AREs), and function of the steroid receptor coactivator TIF2.
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however i was told the same when i called my drs offices to confirm my values. Then when i asked for the specific numbers and the ranges for them, turns out out i indeed have low T and of the range Free T. I even had a * next to my free T number on the lab report to indicate its out of range.