Suppressed 3a-hydroxysteroid may be the cause?

#83

My body odor did go away for over a year after developing this condition, but oddly enough returned sometime during 2018. I can’t pinpoint exactly when it came back or what brought it back, but I once again noticed that I needed to use deodorant and wear a different shirt every day again. It was a nice return to semi-normalcy, but it didn’t really come with any resolution in other symptoms.

On a related note, my BO has actually decreased a little bit since starting broccoli sprouts. I suppose that’s good evidence of it suppressing DHT.

#84

Did you start eating Broccoli sprouts on purpose? and will you stop ?

#85

What’s BO ?

I’m seeing changes with Sulforaphane but not what I expected. Sleep is not better.

However, I have more motivation, I’m more focused and brain fog is gone. I’m also in a better mood, having more emotions.

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#86

Body Odor

#87

i think GABA is more responsible for sleep isnt it?

i know allo should help with that as well but maybe you need direct allo to correct levels like what sage is doing

#88
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#89

Keep us posted about sulforaphane!

#90

Ok. So body odors do have something to do with pfs symptoms. My body odors are gone again. So yes, it may have to do with taking both Pine Pollen and Horny Goat Weed at the same time. That’s a finding by itself (for those interested in having to put deodorant. Lol)

I think Sulforaphane is not going to give spontaneous response like taking 5-HTP or L-Dopa. (or a testocaps, they always gave me a rush). I’m at 200 mg a day now. If after sometime I still don’t see effects, I’ll try with DMSO. Truth is, I do have some feelings that seem to come from the past. But it’s not obvious at this point.

I’ll keep you posted.

#91

Confirmed for body odors. If I take both Pine Pollen and Horny Goat Weed things return to normal.

About Sulforaphane:

I had a bad night of sleep last night. 4/10 . The weird thing is I was tired at bed time and went to sleep fast but I just kept waking up and falling in a light sleep, dreaming all the time. The dreaming zombie state as I call it. I usually feel not rested after a night like that.

I made five changes in my regimen:

I’m taking Creatine. It could be it but it’s said to be to be non-stimulant and can be taken even before sleep. (for non-pfs people anyway). It boosts testosterone and androgen, but only if you exercise which I haven’t done that much. I’m in the load up period and still suppose to load up for 3 days but I’ll just take the maintenance dose for now until I can fix my sleep.

I’m taking 4.5 mcg of Boron if adding my multivitamin. I doubt this makes a difference. The upper limit is 20 mcg. 10 mcg is used to boost testosterone.

I’m taking Horny Goat Weed once in the morning. Could be that, but it’s supposed to affect testosterone and sex drive, not sleep. Plus I stopped One day and sleep was bad anyway.

Sulforaphane. Yesterday I took around 300 mg. It did make me feel calm yet confident and motivated during the day, and I was sleepy before bed. But I slept bad while just a week ago, before any changes in my regimen, I was saying sleep was getting better. ( 8.5 or 9/10) Today I will reduce to less than 100mg and see what happens.

Sleep patterns: The 2 months school vacation just started in Thailand last week. My sleep patterns are all messed up. I go to sleep at the same time but wake up at 8 instead of 6:30. So instead of 8 hours, I get 9 and half and that, by itself, has always caused bad nights on the next night.

So I’ll fix my night pattern, that’s the best educated guess I can take as oversleeping has always resulted in bad sleep the next night. I’ll cut down Sulforaphane to less than 100mg until I get better sleep. If after fixing my sleep patterns I still can’t sleep good, I’ll have to cut Sulforaphane.

Following my regular rules,Sulforaphane didn’t significantly make me feel better while I did have bad side effects. I still cannot attribute those to Sulforaphane but after fixing my sleep pattern, I’ll know what’s the cause of this bad sleep.

#92

Hi. Do you have any study regarding this fact? Thank you

#93

I looked again and I have been wrong. My sources were from a hair loss forum and it was incomplete.

5-ar produces DHT and 3a-HSD eliminates DHT in the muscles. Both are working together and are essential to produce ALLO and other important neurosteroids.

However, as far as I’m concerned in raising 3a-HSD levels (with Sulforaphane), I will also want to raise 5-ar levels to make sure I have normal DHT.

#94

And to answer to myself on this post, I did fix the sleep patterns and slept better. Sleep is no longer an issue as long as I don’t sleep more than 8 hours.
I decreased Sulforaphane to 50 mg a day which seems to be adequate and I found that it was either improving the effect of Tyrosine, or using it at a much faster pace. As a result, after taking Sulforaphane I stopped having brain fog and became more focused. I also have an inner calm I haven’t felt for a very long time (years) but I ended up depleting my Dopamine and Serotonin. (felt demotivated, unhappy, depressed, and unsure of myself)
So I continued to take 5-HTP 100 mg, L-Dopa 350 mg, L-Tyrosine 375 mg, all three two times a day and I also take half a dose of St-John’s worth (300 mg, it’s a plant extract) which is a unique non selective, all neurotransmitter re-uptake inhibitor to prevent my Tyrosine, Serotonin and Dopamine from being depleted.
5-HTP and St-John’s Worth are dangerous together so I monitoring how I feel carefully, taking only small doses of that herb and I’m ready to stop it the moment I feel a dopamine or a serotonin rush (after months of testing those, I know how too little or too much of those feels like). Stopping St-John’s Worth would let my body flush the extra neurotransmitters. At the same time, to make sure, I would also stop the intake of the neurotransmitter that seems over-abundant.
And considering Tyrosine seems to have a greater effect, I’m taking a small dose of Phenylalanine (350mg per day) to prevent depleting that one as well. Tyrosine and Phenylalanine are the precursors of the neurosteroids responsible for regulating the nucleus acumbens, where all the Dopamine receptors are located. (I could name those neurosteroids, they have long, funny chemical names that look like they come from a Star Trek episode)

For a second day in a row, I felt more normal than I did in years. Even more normal than when I was taking fin (in the end, it was making me very irritable).
I’m not suggesting any of you try what I’m doing. As a matter of fact, it can be dangerous. I’m just documenting what I’m doing and the effects it has on me.

I’m looking forward to a good night of sleep and a fully motivated, productive day tomorrow.

I’ll keep you posted (more on Amino Acid For neurological symptoms)

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#95

where are you guys reading that pfs has low 3a-HSD activity?? data we have points to the other direction


https://sci-hub.tw/https://doi.org/10.1016/j.jsbmb.2017.04.003

also like @Ozeph said 5ar and 3a-HSD are antagonists why would you want to increase the latter?? makes zero sense to me

#96

My statement that 5ar and 3a-HSD are antagonist is incorrect. I got it from a dubious source and could not verify it from trustworthy study.

Here’s where it says Allopregnanolone is particularly affected by pfs: Couldn’t find it online so here’s a copy:
The metabolism path is incomplete, it’s both 5ar and 3a-HSD that transforms progesterone and Deoxycorticosterone into it metabolites. Considering many of us shows GABA abnormalities but still have 5a-DHT I theorized that 3a-HSD was the one missing.

Allopregnanolone – How to Increase the 5-Alpha-Reduced Allopreg
In Neurosteroids by Tyler SJanuary 30, 20174 Comments

Allopregnanolone (allopreg for short) is a powerful neurosteroid that has been in the headlines recently ever since the deadly “post finasteride syndrome”. Allopreg is considered a neurosteroid that has numerous neuroprotective properties that range anywhere from the importance of the regulation of emotion and its therapeutical use in depression and anxiety may not only involve GABAergic mechanisms, but also includes enhancement of neurogenesis, myelination, neuroprotection, and regulatory effects on HPA axis function. When your body is under stress, allopregnanolone acts as the body’s natural tranquilizer or anti stress mechanism to help dampen the response [here]. It is highly involved in many mental disorders including mood disorders, depression, anxiety, sleep disorders and seizures. One of allopreg’s main role in the central nervous system is activating the GABA (A) receptor (taurine also does this) which provides many of those anti stress properties [here].

image

Now if you take a look at the chart above, you can see how finasteride (or any 5 alpha reductase inhibitor) can negatively impact the proper synthesis of not only allopregnanolone but also another important neurosteroid, tetrahydrodeoxycorticosterone (another anti stress mechanism). Allopreg is synthesized from progesterone which then gets converted into the direct precursor, 5a-DHP (5a-dihydroprogesterone).

Through the series of coenzymes (NAD/NADH) allopreg is now established in the brain.
Now to put into perspective how powerful allopreg really is- it’s actually under development under the name “Ganaxolone” for the treatment of seizures, anxiety, epilepsy, Alzheimer’s, Parkinson’s etc. The difference is that Ganaxolone is allopreg’s synthetic brother [here].

Why are the mental effects (anxiety, memory loss, poor stress tolerance) of finasteride or any 5 alpha reductase inhibitor so severe? Well, there is a significant amount of 5AR expression in the brain and it fits in line with anything that disrupts that function like finasteride which absolutely destroys allopreg in the brain along with MANY other neurosteroid/steroids in the body besides just shutting down the conversion of DHT only. It was hard to find this study especially on male humans, but the results are pretty astounding [here].

This is only after 5 months, also keep in mind that the study notes 5mg of finasteride, but 1mg vs 5mg are pretty much the same in terms of 5AR inhibition in the body and brain [here].

image

As you can see, anything with a negative (-) number is taking a hit- allopreg being the absolute worse. So much for just being DHT only.

Alright, enough bashing 5ARi’s now it’s time to take a look at how to optimize allopregnanolone both for optimizing mental properties long term and also for anyone recovering from 5 alpha reductase inhibitors.

So as noted from the first master chart above that displays the entire hormone cascade, there a few different ways to increase neurosteroids in general but mainly allopreg:

• Oral pregnenolone at higher doses was shown to increase allopregnanolone significantly.

• Caffeine was shown to increase pregnenolone, progesterone and allopreg in the brain [here]. The trick with caffeine is to take it after eating food and enough sugar to avoid the stress (cortisol) response when lack of glucose is available.
• Progesterone, which is one of allopreg’s precursors can raise allopreg levels [here]. If you are a male, probably wouldn’t go to high on the dose to avoid any potential anti androgenic effects or just simply supplement with oral pregnenolone instead to let your body regulate the conversion of progesterone synthesis.
• Supplementing with the direct precursor to allopreg, 5a-DHP works pretty damn well too. It’s hard to find, but one legit vendor does offer it [here]. I have experimented with 5a-DHP on my pet rat and the effects seem almost identical to a benzodiazepine- without the foggy memory issues which means that it is getting directly converted into allopreg.
• Glycine is another amino acid that can increase allopreg [here]. I found doses 6+ grams was best used before bed.
Another quick tip is whichever method you decide to take, supplementing with a small amount of niacinamide concurrently with any method will help enhance the conversion of neurosteroid activity by increasing the coenzyme (NAD/NADH) [here].

Allopreg in the bio-identical form is not available from any legit vendors after doing some quick searching around- mostly vendors looking to sell to a business (commercial use). Leveraging the precursors would actually be safer in optimizing serum allopreg levels since your body can regulate it better.

Ozeph’s Note: I tried Pregnenolone at high dose. I became hyper and unbalanced and it addictive. It has to be tapper down slowly. I also tried (and still using) Sulforaphane as for me it’s very efficient at clearing brain fog and keeping me motivated. I’m also singing songs in my head while taking it, which I don’t do when not on it. I can say my ability to feel happy is greater with Sulforaphane. Studies shows increased 3a-HSD when taking Sulforaphane.

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#97

please post the link to this study so people can understand the methodology and interpret it themselves

the one i posted measured specifically cerebrospinal fluid e.g brain levels and we have evidence of excess allopreg/gaba-agonism in PSSD too

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#98

Got positive changes with glycine, but these improvements diminish very quickly. I got noticeable Increase in ‘‘visual’’ libido and stronger boner. And 6G of glycine making my body feel tense.

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#99

The thing is, the study you posted would reflect what happens while taking an SSRI.

Is there any evidence that this is the same as PSSD?

Many PFS patients have normal serum DHT levels, for instance. This was also the case found in Melcagni’s study.

I don’t the the typical effect of a medication during use can be translated to apply to these post-drug conditions.

#100

I don’t have the link to the study. Maybe it can be found by google searching the first paragraph.

The study is about pfs, with normal DHT levels. It points out at a lack of 5ar as the reason for not having Allo, I just wanted to add that it’s both 5ar and 3a-HSD that creates Allopregnanolone and 5a-THDOC.

I agree with Dubya_B that the suggested treatment for increasing Allo is for normal people (or non-pfs pet rats) and may not work for pfs patients. It didn’t for me.

#101

which study?

i feel its important to note patterns like high dhea / low androstenedione in PFS, its the exact opposite in hyperandrogenism

why are we even talking about serum levels?

of course not, we are the perfect example