Pretty much what I had. I will post my before results and after next few days.
I beleive the source of libido is FSH, if its low thats one main reason your stuck with the feelong of low libido.
Yes please do, and Iām sorry I got it flipped really low fsh and losing lh, but interestingly enough I donāt have major problems libido wise. Itās in all other aspects that Iām struggling, physical and mental.
Interesting point
Over the years I have always seen LH increasing more so then FSH for me .
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Interestingā¦look at this article.
Shows Testosterone does not really reflect libido rating, where as interesting and I can confirm in my case with results I will post. Before Mifepristone I had high prolactin. After Mifepristone my last test shows my prolactin is now within range.
So based on the study showing prolactin levels could influence libido is high and also based on the results I will post before and after.
Please have a read below. Good study. Also I believe the core of our problem is in the hypothalamus and pituarty glandā¦.what caused the dysfunction ? I would say the dysfunction in the glucorticoid system. The glucorticoid system is very undervalued here.
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I wish they asked those 100 in the study how many took finasteride.
Based on the study it doesnāt really matter, as weāre trying to distinguish can FSH be one of the main reasons for libido, the study states that prolactin variances and FSH caused libido movements in the patients
Can you quote that about FSH?
All I can see is that prolactin and fT was of value.
Makes sense, because the prolactin release causes the refractory period between orgasms in men.
Also Cabergoline seems to decrease it, and increase libido https ://pubmed.ncbi.nlm.nih.gov/14656205/
EDIT: Also relevant, from the abstract: āThe antiprogesterone mifepristone facilitates prolactin release, an effect enhanced by administration of the opioid antagonist naloxone. The present study explores ultrastructural changes in lactotropes after mifepristone and naloxone administration, correlating them with the expression of pituitary prolactin.ā https://pubmed.ncbi.nlm.nih.gov/18832805/
@Cbrandel If you want to take a milder progesterone antagonist, you could research Astragalus, it promotes healthy kidney function as well, and also raised FSH and LH in mice: āAstragalus. fascicolifolius extract caused a significant increase abortion in mice. The levels of progesterone, FSH and LH were significantly different among the groups such that mean progesterone level was lower and mean LH and FSH levels were higher in the Astragalus. fascicolifolius extract-treated groups than the pregnant, untreated group.ā https://pubmed.ncbi.nlm.nih.gov/33854929/
EDIT2 15-11-2021: Iāll respond in my reply again. @Ronnie99
yes but does it eaise LH and FSH permanently or just while on the tretment ?
It does also function as a very mild pct. But itās never used that way. Could be that the restoration in LH and FSH stay restored because of it, like with pct. Not sure. Study is specifically talking about the treatment, not after. Thanks a lot for posting your bloods by the way 
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Wow didnt know that, thanks for the info here.
Its in the discussion at the end.
ā Although it seems more likely that decreased libido is a secondary phenomenon related to a defence mechanism in men with ED, in the present study, no statistically significant relation was found between ED and libido. PL levels were found to have a significant relation with decreased libido. Govier et al found a 16% incidence of hypogonadism and 57% of this group had neither decreased libido nor testicular atrophy.ā
PL - Prolactin Levels
?? I asked about FSH not prolactin.
You said this but itās not in the study thatās why I asked where you got it from.
yes your rite I meant to say to distinguish between fsh and prolactin (apolagise for confusion) , and prolactin seems to be a very important factor in determing the level of libido.
so if you guys reduce your prolactin there should be a very noticeably difference in libido levels.
though I believe the best way to treat this is to treat the root cause which is I believe is the hypothalamus or hippocamlus and i beleive it was the reason why i beleive the problem is with the dysfunction of our glucorticoid system becuase the negative feedback in the HPA goes back to the hypothalamus and even the hippocampus. so it makes sense that the problem is not finasteride or retinoic acid accessing those 2 brain areas, the problem is somehow the finasteride and retinoc acid dysfunction the glucorticoid system, particularly the negative feedback with goes into the hypothalamus and hippocampus therefore now causing the dysfunction and the downward spiral of hormones dysfunction within the HPA axis.
Mifepristone provides a pause in the HPA loop, therefore practically providing a reset rather than using supplements to temporairly pump up hormones.
Anyone who has tried mifepristone in Denmark?
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yes but does it eaise LH and FSH permanently or just while on the tretment ?
how you doing brother ?
Hi Guys,
Below is some of my tests before Mifepristone and after Mifepristone just for referance.
Before Mifepristone
After Mifepristone
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What you did was surpress the immune response, see study āmifepristone challengeā - thats why you got better in REBOUND also, not on the drug itself.
youād get the same results with dexmethasone or infliximab basically
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Good catch.
The reset of stress system activity by MIF could be due to the following factors:
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(1) The detrimental effects of high corticosteroid concentrations via GR activation are prevented by GR antagonism. This approach has obvious benefit during continuous or high-frequency blockade of the GR.
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(2) The high circulating corticosterone concentrations may have caused a long-lasting rebound suppression of HPA-axis activity, particularly since MIF is rapidly cleared.
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(3) MIF may become an agonist in transrepression and promote cell- and context-dependent recruitment of coactivators and co-repressors in a cell-specific fashion in brain stress circuitry
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(4) Enhanced brain MR activation may become prominent relative to the MIF-modulated GR. The altered MR:GR balance could be part of a compensatory mechanism producing altered patterns of inhibitory and excitatory circuits underlying reset of stress system activity. This includes the role of MR and GR as homo- or heterodimers in binding to GREās, transcription factors, and co-regulators as well as their rapid non-genomic actions.
Interesting, but quite complex.
Case study about a man who couldnāt tolerate mifepristone more than a few weeks due to sides.
- but 2 weeks later the patient discontinued therapy as he could not tolerate side effects related to adrenal insufficiency associated with mifepristone, such as weakness, fatigue, and dependence of potassium supplementation due to hypokalemia.
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You cant be sure you will get the same results with those two options.
Yes seems it was the Rebound that got the balance again.