This document "Dr. Duke’s Phytochemical and Ethnobotanical Databases List of Plants for 5-Alpha-Reductase-Inhibitor" is the phytochemical and ethnobotanical database of the list of 5-Alpha Reductase inhibitory plants of the American botanist James A. Duke (1929 -2017). Author of numerous scientific publications on botanical medicine. These plants are to be avoided like the plague!
Dr. Duke's Phytochemical and Ethnobotanical Databases List of Plants for 5-Alpha-Reductase-Inhibitor
Nice find. Worth flagging that Echinacea is on there which you’ll see in lots of health food stores.
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Si, It is comparable to that of Serenoa repens (Chemical Coun 3)
However it’s very strange.
I ate a lot of this plant’s product and I never experienced any symptoms or crash.
There is also Theobroma cacao in the same Chemical Count of Serenoa Repens, Silybum marianum, Rosa canina and Tribulus terrestris.
I ate a lot of cacao (especially in young age), milk thistle, yogurt at Rosa canina and supplement of Tribulus terrestris and many others in that list. No side effects except for Serenoa Repens.
Maybe concentration (total ppm) is more relevant and for sure the metabolic pathway to reduce 5ar.
There is no other explanations.
I’m speaking now with my dad (he is a doc) and he tells me that also testosterone and glucocorticoids inhibit 5ar but none of us developed pfs from them.
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Yes, it can be, in the last place there is Glycine Max and that is Soy! Soy isoflavones are known to inhibit 5-alpha reductase type II. All true! Let me know what your father says 
While healthy people are unlikely to develop pfs from exposure to what are (I assume) low strength 5ar inhibitors, those with PFS who have an impaired system are likely more sensitive to inhibition.
Some people here have suffered worsened conditions as a result of exposure to milk thistle and I recommend caution when it comes to considering what effect these things may or may not have on your condition.
@Andrea, as your father is a doctor, would he be willing to talk to other PFS patients? Has he read the papers from the studies?
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Yeah.
Soy in China is very popular. However there are no people claimed pfs or similar problem.
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Yeah my dad has read several papers from previous studies included Traish’s last paper about epigenetics.
He said me that substantially these papers tell nothing.
Traish and many other speak about neurosteroids impairments that induce PFS and AR issues. Well, a simple SSRI like paroxetine should fix all the problems. In real life this not happened.
The opinion of my dad and also the endocrinologists based also on the informations provided by Goodman and Gilman’s The Pharmacological Basis of Therapeutics (it’s like holy bible for doctors) and many other manuals, is about a metabolic impairment due to an endocrine disruptor (5ari, pathogens…) that shutdown hpa axis gives an imbalance between sympathetic and parasympathetic nervous system (maybe between also enteric nervous system).
This create a communication problem between central nervous system and peripheral nervous system.
In fact, a simple dose of pseudoephedrine fix all the mental sides (I’m in GOD MODE).
For the possibility to talk to other PFS patient, my dad is very busy with work (he’s a medical director) and furthermore he can’t give you online diagnosis (he should do a medical examination).
Fortunately I speak frequently with my dad and others physicians so I can inform you about therapies that can work.
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Thanks Andrea, I wasn’t really looking for help for me, I was thinking that it would be helpful to make a network of doctors who could help compare notes and breakthroughs and inform skeptical doctors.
That your Dad has cured some of your symptoms is incredible, it would be the kind of information that other doctors could benefit from. It would be easier to convince a doctor to treat a patient using a doctor’s testimony than with a forum post, even if the information is the same.
I’m really pleased to hear that you’re doing better though. 
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Your dad think the cause of PFS is HPA axis problem?
not epigentics changes, ARoverexpression?
I want to know more about it!
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Surely there is an imbalance in HPA axis because it responded quickly to hypoglycemia and hypoglycemia is a marker to reset HPA axis.
About epigenetic changes at the moment we have no data.
AR overexpression is possibile but a simple down regulator of the androgen receptor like milk thistle should fix the problem. In real practice it doesn’t work.
There are too many strange things (like Netflix series 
).
I hope the studies will find the root cause.
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Milk thistle doesnt down regulate the AR, it blocks DHT from binding to the AR. Big difference. Its poison and crashed many guys.
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Milk Thistle (silymarin) reduces nuclear androgen receptor levels and down-regulates several androgen-regulated genes primarily by inhibiting the transactivation activity of the AR.
I took this stuff and I hadn’t any issues, however everyone can respond differently.
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As Invictus says, it is my understanding that some people have massively worsened their condition with milk thistle. Be careful if you’re thinking of rolling the dice.
I took milk thistle after discontinuing proviron (never took Finesteride). Now I am thinking the reason why I am suffering from PFS (even despite never taking Finesteride) is because of this.
I have a feeling either only T or E are binding to my Receptors instead of DHT. I’m wondering how I am going to get my receptors to receive DHT again…
Do we know how to make our receptors more receptive to DHT again? Maybe I need to stop Estrogen for a prolonged period, so the receptors only receive T and DHT. This assumption comes from the following;
When testosterone enters a target cell, three things can happen
#1. Testosterone attaches to an androgen receptor and causes a moderate androgenic effect on the cell.
#2. An enzyme called 5-a-reductase converts testosterone into DHT, an androgen hormone that is 10x more powerful than testosterone. DHT then attaches to the androgen receptor and causes a huge androgenic effect on the cell.
#3. An enzyme called aromatase converts testosterone into oestrogen, which then attaches to a different receptor and exerts oestrogen effects on the cell – kind of the opposite of androgen effects.
No matter how high the circulating testosterone levels are, if the body’s androgen receptors are sleeping on the job, then #3 will always happen! This results in a relative androgen insufficiency – a much higher level of oestrogenic activity than androgenic activity in the body.
These are my bloods;
S Testosterone 21.2 nmol/L (9.9 - 27.8 )
SHBG 23 nmol/L (17 - 56 )
S Albumin 43 g/L (36 - 47)
Free Test 555 pmol/L (170 - 670)
S Cort 483 nmol/L (133 - 537)
Prolactin 463 mIU/L (90 - 400)
S Oestradiol 130 pmol/L (< 160)
S DHEAS 7.5 umol/L (2.4 - 11.6)
S FSH 5.5 IU/L (1.5 - 9.7)
S LH 4.4 IU/L (1.8 - 9.2)
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Well, that theory has been voiced a number of times. The problem is that people who have attempted to manipulate their body’s response have often caused worsening. I urge you to go carefully if you are considering this course of action.
Yes. very delicate. Thanks