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Wow. So, you saying you had no libido and "MAIS" at 21 before touching roids too? You've just told opposite here couple posts above. MAIS is congenital condition, whatever you have is endocrine system totaled by steroids.I think you are just a jealous fucker who has normal endocrine system after taking shitty dbol cycle and lost his fucking libido. Your hormones are 'normal'.
Your T is perfect and so is your LH you twat. I think you are a pussyhole who can't even handle a 4 week dbol cycle?
And yes, i concur with OP, I've had perfect levels for some time: T 600-700, E2 20-30, SHBG 24 and so on (now I've gained some weight and tested lowish on T), but was feeling shitty and with typical hypogonadal symptoms.
There's much more to health and libido than hormone levels and I don't have a freaking MAIS.
and thus a diagnosis of MAIS is not usually made without confirmation of an AR gene mutation.[5] The androgen sensitivity index (ASI), defined as the product of luteinizing hormone (LH) and testosterone (T), is frequently raised in individuals with all forms of AIS, including MAIS, although many individuals with MAIS have an ASI in the normal range.[5] Testosterone levels may be elevated despite normal levels of luteinizing hormone
I think you are just a jealous fucker who has normal endocrine system after taking shitty dbol cycle and lost his fucking libido. Your hormones are 'normal'.
Your T is perfect and so is your LH you twat. I think you are a pussyhole who can't even handle a 4 week dbol cycle?
SADE i am guessing you have done a lot of searching through the net about steroids causing MAIS? did you find many cases? is a simple test-e 10 week cycle gonna cause this shit?
If you had normal virilization levels and development as your peers in teens, no way you have MAIS.Mild Androgen Insensitivity Syndrome (MAIS)
MAIS is the phenotype at the other extreme to CAIS. Genitalia may be underdeveloped for a male or there may be simple coronal hypospadias or a prominent midline raphe of the scrotum.50 At puberty, MAIS takes two phenotypic forms, both presenting with various degrees of gynecomastia, high-pitched voice, sparse sexual hair and impotence. In one form of MAIS, spermatogenesis and fertility are impaired,53,54 while in another spermatogenesis is normal or sufficient to preserve fertility.52,55 Although experience with MAIS families is limited, they appear to harbor relatively little phenotypic disparity.
Subjects with MAIS AR mutations may have lower ejaculate volume, higher testosterone levels, higher oestradiol levels and higher androgen sensitivity index. However, the ranges for these variables are highly overlapping between men with and without AR gene mutations.56,57
If you had normal virilization levels and development as your peers in teens, no way you have MAIS.
His theory, I think, is that he had MAIS all the time, but taking roids lowered his natural T from normally supraphysiological to high normal. How much chances for all that to happen? I'd say near zero.MAIS (a congenital disorder typically manifested at puberty) being caused by AAS, utterly absurd (I've read they can also "cause blindness",lol) and a classic misapplication of sound medical literature, which has already been alluded to by Dr. S.
Understandably, I stopped following this post some time ago, nonetheless your steadfast resolve is appreciated Dr. S
Jim
technically you're right, he had the same chances of having undetected MAIS as everybody else in a room, how much is that 1:10,000 or something like this? And what were the chanced to be screwed by steroids? A LOT MORE THAN THAT, so that was the thing to start with.image with crap
sade said:Me, I started taking roids at age 21 a decade ago. Had no problems until I stayed on Test Enanthate for 9 months solid.
sade said:Yes, was diagnosed by an AIS specialist but my T is now low.
sade said:The weird thing is guys, I'm getting better wood now that my LH and T have dropped. T is now 290, 342 ngdl. When T and LH was elevated, libido was fucked, dead dick 100%.
Despite the return of supracastrate or normal levels of TT, there appears to be little return of potency, as measured by the IIEF, and little return of sexual desire.
In the entire cohort, only 10% of men regained the ability to have an erection sufficient for intercourse, and of men who were potent before any treatment, only two of 11 regained the ability to have an erection sufficient for intercourse.
My earlier post was in error having not read it completely, since your thoughts and commentary have, with few exceptions thus far have been pure conjecture. What literature directly supports your contentions?
What the heck is the statement; "the body was damaged and didn't restore it's responsiveness", based on?
What "deprivation theory" are you referring to?
Although someone may have a hypothesis and or theory they will remain nothing more, until confirmed or refuted based on sound medical judgement or literature! Otherwise it's utter nonsense, IMO.
The present study shows that men achieve supracastrate TT levels after LTAD, but there is a slow recovery of normal TT levels, and a significant proportion of men do not achieve supracastrate or normal levels of TT even several years after completing LTAD.
Despite the return of supracastrate or normal levels of TT, there appears to be little return of potency, as measured by the IIEF, and little return of sexual desire.
In the entire cohort, only 10% of men regained the ability to have an erection sufficient for intercourse, and of men who were potent before any treatment, only two of 11 regained the ability to have an erection sufficient for intercourse. The present study does not address the cause of ED in these patients, but factors other than TT levels appear to be important.
There are lots of folks post-AAS or propecia with normal T, E2, etc. levels suffering from hypogonadal symptoms. Seems it's some physical/mental changes leftovers that are hard to heal after body/mind was damaged by widely changing hormonal levels during/after course of drug. But it's not testosterone deficiency in common sense, all hormones may be within ranges.In conclusion, most men recover supracastrate TT levels after LTAD and external beam radiotherapy, but the time to recovery of ‘normal’ TT levels is prolonged. Few men recover potency and sexual desire. Patient age and the LH/TT ratio, may be predictive of the time to recovery of both supracastrate and normal serum TT levels.