*** Post your 11b-OH-Etiocholanolone & 5a/5b urine metabolite ratio results ***

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#21

And again, a low ratio this appears to be the culprit… no more debating over androgen insensitivity, neurosteroids or cortisol management…

All the thyroid and cortisol issues must stem from this because it is the main action of finasteride to disrupt 5-alpha reductase type 2, and what do we all have in common? we all used some form of a 5-AR-2 inhibitor.

I’ve thought it was this for sometime now, based on the combination of side effects I experienced and the role of 5-AR-2 in the body.

Now why did our bodies down regulate 5-AR-2 after coming off finasteride? Could it be some immune reaction with the CNS? Perhaps that is why drugs like morphine, and GHB and heroine have been shown to have some effect. They act directly on the CNS.

#22

Argument for 5aR being downregulated:

1.Low 3aDiolG

2.THF/5a-THF ratio shows low 5alpha activity (or high 5beta activity!)

Arguments against:

1.Normal DHT

2.All other 5alpha metabolites and ratios normal

(Of course these results against are less important when deciding 5aR activity, but the hormone tests would be very apparant in someone who is using Propecia for example.)

3.Symptoms unconnected to 5aR - muscle loss, bone problems, low body temperature, (anhedonia?) - do occur.

4.Why do people, like you and me, get worse after stopping? As you point out, thats a problem, because you have to invent some new other reason for 5aR to become downregulated, not connected to the damage finasteride should have caused. This surely points away from 5aR downregulation.

5.Our symptoms arent found in people who are currently using finasteride (or even dutasteride) to inhibit 5aR.

So the theory for Propecia destroying 5aR is compelling, but there are clear unavoidable problems with it. (ps Im not a cellular biologist).

(Personally I dont agree with it at the moment, Im a bit stuck on my current idea that the liver is deactivating our sex hormones, 3aDiolG is just a marker for DHT activity and high THF could be a marker for a liver problem, or something.)

#23

All of my primary sex hormones are in good ranges test is over 800 for example.

My 3adiolg is below range low.

My cortisol is well above range.

I’m getting my thyroid hormones run and should have the results maybe by early next week.

My DHT is in normal range but flucuates constantly. whereas my testosterone is consistantly over 800.

If its not 5AR2 than it must be an another enzyme, perhaps something we have yet to identify.

Personally I think it is 5ar2, and we didn’t recover after coming off because our bodies had a autoimmune response to the flush of 5ar2 activity and thus downregulated it in the CNS.

#24

What about people who developed sides on the drug, never had a brief recovery and have yet to experiance any sort of improvement? Do your theories incorperate this type of victim, if so please explain.

#25

… So maybe low 3aDiolG isnt necessarily due to low 5aR activity? The fact that DHT is normal (or in Mew’s case and a few others out of range high) it simply must still be working. Ill just take a moment to explore this idea.

The steps in the production of of 3alpha Androstanediol Glucurinide (3adiolG) goes something like this - Testosterone > 5aR > DHT > 3aHSD > 3aDiol > Glucuronyltransferase > 3aDiolG


3aHSD is the next step after 5aR that turns DHT into 3aDiol. It occurs before the androgen receptor, and is thought to control the access of DHT to the androgen receptor. 3aDiol is in fact the deactivated form of DHT.

Reasons I can imagine for low 3aDiolG:

(1) If there is less 5aR then there will be less 3aDiolG, since there is less intracellular DHT to deactivate.

(2) If there is less 3aHSD there will be less 3aDiolG.

However in that scenario less DHT will be deactivated and so surely more DHT will be available to activate the androgen receptor. I suppose only if there is less androgen receptors and less 3aHSD will we have the symptoms and the blood test results (something along the lines of Awor’s theory).

(3) Other enzymes are preventing the binding of DHT to the androgen receptor and the conversion of DHT to 3adiolG.

I have discovered that if the normal metabolism of sex hormones is increased then DHT will often fail to bind to the androgen receptor. This is due to increased conjugation by Sulfotransferase. There will also be less 3aDiolG due to a bias towards 3alpha Androstanediol Sulfate, or due to less DHT being deactivated by 3aHSD due to less DHT activating the androgen receptor.

#26

Oscar, you need to separate out 5 alpha reductase types 1, 2 and 3. Adiol-G is a marker for 5AR2 activity only (as well as peripheral androgen action, but that is a receptor effect and not something that produces DHT). The attraction of urinary metabolite ratios is that the three being discussed are markers for 5AR2 and nothing else.

In some 5AR1 is suppressed as well, leading to low DHT levels. In some others I suspect 5AR2 is highly depressed, so the 5AR1 pathway goes into hyperdrive making lots of DHT to try to compensate, but that still odes not provide 5AR2 for the prostate, brain, liver etc.

Perhaps we should split this thread into a technical discussion, and a separate place to collate the metabolite ratios and serum 11b-oH Etiocholanolone levels. In the meantime lets move technical discussions elsewhere.

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#27

I believe a correct reading of this thread viewtopic.php?t=761 shows that 3aDiolG is produced by 5aR types 1 & 2 but is mostly from type 2. Both types of 5aR also produce DHT, at a ration of 30%/70%.

The urinary markers show the activity of both 5aR types 1 & 2. (Otherwise the type 2 deficient people would have no 5alpha reduced metabolites in their urine!)

Thats the obvious conclusion. But, both 5aR types 1 & 2 are present in the brain and liver. If 5aR1 was ‘compensating’ this would be revealed in the urinary metabolites too. It doesnt show this. Also, levels of DHT do not correlate to severity of symptoms. Also, this doesnt match why people get worse after stopping, or the non-5aR related symptoms.

Or keep it all in one place, since this is an important set of results but not many people seem interested or realise the relevance of this thread.

#28

Is anyone able to determine how cortisol can have two sets of 5a/5b reduced metabolites? These are also the metabolites that come back showing an unusual pattern.

#29

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#30

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#31

Pls keep this thread on topic for posting results from bloodwork if possible. There are other sections for alternative theories etc.

#32

I believe that it is a metabolite of DHEA. Yes/No???

My results …

2 years post crash - no meds
THF - 956 (842-2800)
5a-TFH - 1399 (796-2456)
Ratio = 1.46 (.35-.95) (high 5AR activity)

THB - 80 (32-238)
5a-THB - 400 (132-588)

Testosterone - 13 (60-103)
DHT - 3.6 (0-13)

Androsterone - 4121 (478-4705)
Etiocholanolone - 2818 (689-3263)
Ratio = 1.46 (1.1-1.16) (medium-high or high 5AR activity)

11b-OHET - 415 (134-1186)

5 years post crash - 20mg hydrocortisone
THF - 3435 (842-2800)
5a-TFH - 2491 (796-2456)
Ratio = .725 (.36-.95) (medium 5AR activity)

THB - 185 (32-238)
5a-THB - 589 (132-588)

Testosterone - 63 (45-85)
DHT - 12 (0-13)
Ratio = 5.25 (7.9-15.2) pretty sure this is high 5AR activity

Androsterone - 3654 (478-4705)
Etiocholanolone - 1991 (689-3263)
Ratio = 1.8 (1.1-1.16) (high 5AR activity)

(at the same time I have low DHEA)

11b-OHET - 267 (134-1186) (low-side)

image7yt.jpg861×5123 872 KB

#33

more ranges

sdfvsd.jpg917×6974 1.03 MB

#34

As seen in the lab report above…they have a slightly different range.

a-TFH / TFH = (.35-.95)

A / E = (1.01-1.16)