This give me an complete idea of what PFS could be.
When we when out of drug ( Finasteride ) there was an increase of 5α-reductase activity that was suppressed while in the drug .suggesting that the capacity to produce allopregnanolone is increased see #1
Then read the rest #s
1- 5α-reductase activity is increased in the hypothalamus in late pregnancy (Brunton et al., 2009), suggesting that the capacity to produce allopregnanolone is increased in pregnancy. Allopregnanolone may act locally to enhance GABA
2-Allopregnanolone may act locally to enhance GABA action in the PVN or on inputs to the CRH neurons to attenuate HPA axis responses to stress in late pregnancy.
3- The importance of allopregnanolone to inhibit HPA axis responses to stress in later pregnancy has been tested by blocking its production using a 5αR inhibitor, finasteride (FIN). Blocking allopregnanolone generation with finasteride (FIN) at a dose shown to reduce brain allopregnanolone content by up to 90% (Concas et al., 1998), substantially restores HPA axis responses to systemically administered IL-1β in late pregnant rats.
4- Patients with AD show an increased glucocorticoid production compared to healthy elderly control subjects. In addition, an increased 5α-reduction was seen in patients with AD. Thus an increased glucocorticoid production can be regarded as an early feature of AD since an enhanced production of 5α-reduced metabolites of cortisol was established (Rasmuson et al., 2001). 3α-OH-5α-reduced metabolites of cortisol interact with the GABAA-receptor and enhance the effect of GABA-steroids on the GABAA-receptor.
5- Chronic stress can impair memory (de Quervain et al., 1998). Memory impairment is permanent in persons with a chronically elevated adrenal production of GABA-steroids (Lupien et al., 2005). Memory impairment was also reported in chronic stress syndromes, so called “burn-out syndrome.” “Burn-out syndrome” occurs frequent in patients with AD.
6- The production of cortisol and GABA-steroids increased in parallel during stress (Purdy et al., 1991; Serra et al., 2003; Droogleever Fortuyn et al., 2004). During chronic stress, long-term exposure to GABAA-receptor agonist results in similar changes after prolonged exposure to benzodiazepine and alcohol.
7- Long-term and enhanced activation of the GABAA-receptor is an important factor in of memory impairment during stress. The response of cortisol and GABA-steroids to adrenal stimulation was similar in patients with AD as chronically stressed animals (Nasman et al., 1991, 1996). Patients with mild Alzheimer’s disease have a high and non-suppressible production of cortisol and GABA-steroids (Nasman et al., 1995).
8- After long-term exposure to GABA-steroids, down-regulation of the GABAA-receptor is expected (Yu and Ticku, 1995b; Barnes, 1996). A malfunctioned GABAA-receptor can be an important factor in the pathogenesis of stress-induced depression, “burn-out” syndrome and sex-steroid related depression (Drugan et al., 1989; Wihlback et al., 2006).
9-The down-regulation occurs at different levels in a time dependent manner: (i) desensitization; (ii) receptor internalization; (iii) receptor subunit degradation; (iv) altered expression of receptor mRNA (Barnes, 1996). Exposure to an agonist of the GABAA-receptor may cause changes in receptor mRNA and induce changes of the -receptor subunit composition (Smith et al., 1998.
This is my personal conclusion from what I read
After all seems that the receptor that is fuck is not 5-alpha-reluctance receptor or AR, it is he GABAa receptor the one that is FUCK, this is what I believe that in PFS occurred something similar to a “burn-out” syndrome, in other words a desensitization of GABAA receptors.
The second link explain down syndrome, as you can see guys there are different sub-types of GABAA receptors depending of the sub-type that is affected is the clinical pathology.
Seems that is why the androgen receptor wasn’t found as the problem at the Harvard study
Gamma-aminobutyric acid, or GABA , is the brain’s major inhibitory neurotransmitter to prevent overstimulation and therefore promote calm. GABA deficiency symptoms may include depression, anxiety , insomnia, and more…
Selective GABAergic treatment for panic? Investigations in experimental panic induction and panic disorder
Several studies have demonstrated that patients with panic disorder have a dysfunction of the GABA A receptors
Enhancing Orgasm with GABA . Orgasm release is controlled by the body’s levels of gamma-aminobutyric acid ( GABA ). … GABA helps inhibit excitatory neurotransmitters that can cause anxiety if the system is overstimulated. This is important, since chronic anxiety can lead to loss of sexual interest and sexual dysfunction.
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