I believe tribulus has cured me!

If that is the case that we do not respond to adrogens, What about AR coactivators ?
There are also AR activator as : protein arginine methyltrasferase 5

Can you describe the head feeling a bit?

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It is weird, my like maybe what is called brain fog.
Any body knows about SARMs, in particular Ostarine?

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Getting better again, I am getting out the crash, this is fucking weird, yesterday my penis still numb from the crash, today in the morning was a littler better compare with yesterday, now in the afternoon very sensitive again.
I never been like that with so many consecutive ups and downs, I will not touch creatine again until I feel confident.
There is another interesting supplement that maybe I will try to see what happen
D-Aspartate, I will stop for Iwhile dopa and combine D-Aspartate + Tribulus.
Let you know guys

Gadd45b and N -methyl-D-aspartate induced DNA demethylation in postmitotic neurons

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I think that we all are looking for a solution with the wrong doctors, urologist, endocrinologist, neurologist general doctors,
The only doctors that can go deeper to the problem are Neurophysiologist .

Better to fight this condition with this kind of doctors that by alone.

I will make an appointment soon,

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WILD THEORY AHEAD:

Iā€™ve been taking some things like Vitamin D and Mucuna recently (that should increase testosterone). And as expected, I feel more androgenic and have energy overall (I have done some light jogging recently) but my brain fog seems worsened.

Iā€™ve been thinking about it (as much as I could) remembering that my first Tribulus cycle helped with my brain fog permanently, and we know that trib is supposed to increase androgen receptor density in the brain.

We also know that 5-AR in the brain is negatively regulated by androgens (opposite to the one in the periphery). I believe this has to somehow happen through the androgen receptors in the brain. We know that increasing androgens makes many people worse, and that increasing AR density seems to help. Given those things, I believe that the important factor here are the amount of FREE androgen receptors in the brain (ARā€™s without any testosterone or DHT attached to them).

I believe it is the amount of saturated AR in the brain that regulates 5-AR activity there, in other words the less free available androgen receptors in the brain the more it downregulates 5-AR1 activity. This would explain why people get better lowering androgens (more free ARā€™s) and the plausible explanation for this is that during Finasteride usage, the amount of ARā€™s that each cell expresses becomes drastically lowered to match the low androgen levels, which why you donā€™t experience the brain fog symptoms while youā€™re on Fin. Once you get off, the DHT levels return to normal, now oversaturating the small amount of ARā€™s you have available leaving you with low amounts of free AR, your brain detects this as ā€œWay too many androgens, shut it down!ā€ and as a result downregulates 5AR1 in the brain leaving you with brain fog and all these other cognitive symptoms. What I think we need to achieve is to increase our AR density to the point that our hypothalamus (or whoever regulates this) can once again deal with normal levels of DHT & T, and still have enough free AR available, to not downregulate 5-AR enzyme in the brain.

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What about our sexual symptoms? 5AR2?

Yes, I think so, most of my sexual issues were fixed while being on creatine, but since 5AR2 and 5AR1 are on opposite sides of the same coin, it caused increased brain fog. This isnā€™t a problem in a normal body with adequate amounts of androgen receptors in the brain, but with our low AR density any increase of 5AR2 (more accurately, T/DHT) to normal will suppress 5AR1 in the brain even further.

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The MediHerb tribulus has shot up to an astonishing 100 USD per bottle on Amazon rendering this a very expensive experiment for anyone who wants to try it.

VemoHerb seems to be rated weaker by the few members here who have compared both.

I was looking for other tribulus supplements which could be of comparable strength, and I found this, it seems to be a recently released product:

According to the specifications it should be about as strong as the MediHerb one (if we are to believe the protodioscin standardization rating), if anyone is willing to try ā€¦ Iā€™m about to run out of VemoHerb so might do that next.

fvckthepfs

My sleep is fucked since creatine crash, soon after my creatine crash my sleep seem to not be affected and while after it get really bad, I was sleeping 6 hour some time even more no problem with the sleep, now I am sleeping 3 hours and unable to go back to sleep again.
who is your sleep with creatine ?

Last time I messed with it was in November or so, but during the time I was mainly having issues with brain fog, sleep was fine (no worse than usual).

But ever since PFS I can barely sleep through the night, have to wake up to go to bathroom and then have trouble falling back asleep, always wake up around 3-4 AMā€¦

When I am on Trib or increase T/DHT I sleep better.

This is getting fucking ridiculous, my testicles are bigger and solid than ever, my nigh sleep is shorter I sleeping now 3 hours, my libido dropped after my second crash of creatine, my orgasm are very intense and my skin is more oiled.
Seem that creatine crash me, but tribulus is giving me positive result, maybe my libido is fuck because the lack of sleep.

I will make a very long fasting and only taking Tribulus and Water. I started today.
I will create a protocol taking note and if work it will be posted here in this discussion.

Also I want to make an appointment to this place.

https://www.utsouthwestern.edu/education/medical-school/departments/neurology/programs/rare-brain-disorders/clinic.html

I believe that this is the right place to go, please leave me opinions.

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I would go if I were you, also tell them about the rest of us on the forum they might find interest in our case.

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That is the idea, It going to be in the name of all us.
I truly believe that the center have the potential to find an answer, it is one of the a few center of this kind on the whole nation and probably in the world, I think this place had should been the main center of investigation of our condition since the beginning.

Baylor is taking to long and to be honest I do not have any hope on Baylor study.

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You da man! Hope you can bring back some positive info for us!

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I have to make an appointment first, I hope that they will accept me, I will call then on 05/28/19, I keep you posted.

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I canā€™t believe mediherb tribulus shot up in price. I literally got it before it went up on eBay for $57 after shipping I checked the seller and he no longer is selling it, heā€™s probably going to also make the price higher now, the standard process website doesnā€™t sell it either anymore when they had it a few days ago wtf?

Totally impotent again, big crash, not sleeping at all.

This give me an complete idea of what PFS is.

1- 5Ī±-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 5Ī±R 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-1Ī² in late pregnant rats.

4- Patients with AD show an increased glucocorticoid production compared to healthy elderly control subjects. In addition, an increased 5Ī±-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 5Ī±-reduced metabolites of cortisol was established (Rasmuson et al., 2001). 3Ī±-OH-5Ī±-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 ā€œburn-out syndrome.ā€ ā€œBurn-out syndromeā€ 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 Alzheimerā€™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, ā€œburn-outā€ 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**ā€œburn-outā€ syndrome**= PSF

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