thorus2000

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Maybe I missed it. What about the shelf life of the product and the temperature stability?

My rat unfortunately suffers from PFS. It uses Zopiclone , Gabapentin and sometimes Trazodone to Sleep, Tianeptine against anxiety.
The idea is to use 5a-DHP to gradually reduce this cocktail. Good idea?
 
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haidut

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I have been having severe brain fog lately, likely a finasteride complication. I noticed that every time I drink a glass of wine the fog clears. Alcohol is a GABA-A agonist, and so is 5a-DHP, so I tried 1mg of 5a-DHP on the tongue and within 10 minutes I could feel the fog clearing. Now it's like 50% gone, and I feel as if my eyesight is a little sharper.

@haidut what do you think the reason for this is? Could this give us some clue into post-finasteride syndrome's neurological effects?

Well, finasteride is known to suppress allopregnanolone synthesis and this is one of the main proposed explanations of its negative effects on brain function. Aside from GABA agonism, allopregnanolone also has antidepressant, anti-estrogenic and anti-inflammatory effects so just taking a pure GABA agonist like a benzo will probably not be enough to replicate the effects fully. Alcohol is a short term antidepressant due to its NMDA antagonism properties and n the short run also raises allopregnanolone levels. So, alcohol and 5a-DHP likely have similar effects in the short term and long term alcohol consumption quickly becomes predominantly serotonergic and endotoxin-inducing.
 

haidut

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thorus2000

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That is correct and one of the reasons I went with 5a-DHP. It does not sit on the pathway to estrogen like regular progesterone does. I still doubt that progesterone itself would raise estrogen that much to cause spider veins, but some people complained about that so I did not want to exclude it as possibility. 5a-DHP can only be converted to allopregnanolone and other steroids but not estrogen.

I know a man who was treated with progesterone (100 mg capsules) for several months due to sleep problems. During this time, prominent veins developed on the shins and forearms. It is no 100 % clear that Prog is the reason but possible. Is this reversible?
 

MCurtone

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I know a man who was treated with progesterone (100 mg capsules) for several months due to sleep problems. During this time, prominent veins developed on the shins and forearms. It is no 100 % clear that Prog is the reason but possible. Is this reversible?
Are we talking about skinny red veins, commonly seen in "spiderveins" or are we talking big green veins, which actually look very androgenic?

For example:

http://millervein.wpengine.com/wp-content/uploads/2018/02/iStock-671005188-1280x806.jpg



OR

 

haidut

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I know a man who was treated with progesterone (100 mg capsules) for several months due to sleep problems. During this time, prominent veins developed on the shins and forearms. It is no 100 % clear that Prog is the reason but possible. Is this reversible?

As the user above me responded already, prominent veins is not the same as spider or varicose veins.
 

haidut

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I don't think it is even related to prominent veins. Prominent veins implies bulging out, while these are more like crevices or at least concave. Looks like some kind of change in muscle and/or subcutaneous fat. I would ask a doctor, but I don't think progesterone is the reason.
 

thorus2000

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I don't think it is even related to prominent veins. Prominent veins implies bulging out, while these are more like crevices or at least concave. Looks like some kind of change in muscle and/or subcutaneous fat. I would ask a doctor, but I don't think progesterone is the reason.
Thanks Haidut
 
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As many of you know by now, I have acquired an interest lately to research the connection between the process of saturation of various nutrients and steroids and the effects of this saturation on the properties of these substances. After doing some work on androgens such as androsterone and 11-keto DHT, I started researching the effects of various progestins / progestogens, especially metabolites of progesterone. As most people familiar with this forum know, progesterone occupies a rather prominent role in metabolic therapy due to its multitude of systemic beneficial effects such as opposition to estrogen, PUFA, aging, degeneration, infections, serotonin, prolactin, NO, etc. After reviewing the metabolic pathways of progesterone, especially in the brain, one metabolite immediately caught my eye. That metabolite was 5α-Dihydroprogesterone (5α-DHP).
5α-Dihydroprogesterone - Wikipedia

5α-DHP is formed from progesterone by the activity of the enzyme 5α-reductase (5-AR) - the same enzyme that converts T into DHT. I noticed that 5α-DHP levels rise sharply during pregnancy in most mammals (including humans) and in some species are the only progestogen as that species (horses) produces almost no regular progesterone. 5α-DHP is also the direct precursor to the neurosteroid allopregnanolone.
Allopregnanolone - Wikipedia

Allopregnanolone is the current darling of the pharma industry (since everything else failed) and is in clinical trials for almost every conceivable brain or mood condition including epilepsy, Alzheimer, Parkinson, TBI, MS, ALS, depression, schizophrenia, bipolar disorder, PTSD, suicidal tendencies, etc. Those trials are being conducted with both bioidentical allopregnanolone and its bastardized synthetic cousin Ganaxolone.
Ganaxolone - Wikipedia

Early animal studies and subsequent human ones showed that it is progesterone metabolites formed by the activity of the enzyme 5-AR that are primarily responsible for the beneficial effects of progesterone in the brain and in so many conditions. Administration of a 5-AR inhibitor like finasteride reliably lowers levels of not only DHT but also of 5α-DHP and allopregnanolone. The administratios of a 5-AR inhibitor abolished almost all positive effects of progesterone in the brain. This suggests that it is the 5-AR metabolites of progesterone such as 5α-DHP and allopregnanolone that are primarily responsible for the benefits of progesterone in all these conditions. Reductions in brain allopregnanolone are widely recognized as the single most important factor in mental health (especially depression, suicide, and the infamous "brain fog"). Virtually all SSRI drugs that have shown some effectiveness raise levels of allopregannolone in the brain. However, in people who are under stress, have neurological damage, have endured treatment with finsateride, or are simply loaded with PUFA the enzyme 5-AR is downregulated both in levels and in activity. As such, simply supplementing with progesterone may not have the desired effects of raising allopregnanolone. This may be one of the reasons why progesterone seems to lose effectiveness as an anti-depressant in older people - i.e. they have much lower expression and activity of 5-AR compared to younger people. However, with the widespread PUFA assault even young people are showing signs of diminished neurological responsiveness to progesterone when administered as a supplement. One option would be to supplement allopregnanolone. However, allopregnanolone is not available OTC or by prescription in any country. In addition, due to the recent successful trials with both bioidentical and synthetic allopregnanolone derivatives, the future of allopregnanolone as a freely available chemical looks rather bleak. In all likelihood, one the FDA approved allopregnanolone or Ganaxolone for any condition, the company behind the trial will petition FDA to start regulating allopregnanolone as a drug. In addition, while allopregnanolone has a great track record as neurosteroid, it has no progesterone effect - i.e. it is not an agonist of the progesterone receptor. Agonism of the progesterone receptor has a multitude of other benefits including opposition to estrogen, prolactin, serotonin, NO and variety of other mediators tat serve to inhibit metabolism. Thus, ideally the substance to be supplemented with should have the properties of allopregnanolone (or easily convert into it) while also having the properties of progesterone through the progesterone receptor. The steroid 5α-DHP is exactly such substance, and for now it seems to not be subject to any clinical trials or legal threats. It is a direct precursor of allopregnanolone and as such should elevate allopregnanolone levels even in people with strongly downregulated 5-AR - i.e. sufferers of the so-called post-finasteride syndrome (PFS), older people or people under severe stress or PUFA loads. Just like progesterone 5α-DHP is capable of reducing estrogen receptor levels inside the cells and knock the estrogen out of the cells. It also inhibits prolactin release, just like progesterone. More importantly, it achieve these benefits in doses 2-3 times lower than progesterone. And last but not least, 5α-DHP is not a metabolic precursor to estrogen, cortisol, and aldosterone like regular progesterone is.
Furthermore, 5α-DHP (like other 5-AR derived steroids) can serve as raw material for synthesis of potent androgens such DHT, androstanedione, and androsterone. And unlilke other precursors such as DHEA, 5α-DHP does not seem to activate the same negative feedback mechanisms upon its conversion to DHT or other androgens.
Finally, to top it all off, 5α-DHP does not seem to possess anti-androgenic effects like regular progesterone. This should make it a bit more convenient for supplementation in males who are wary of using progesterone supplements. I think the saturation of the steroid is what removes some if its anti-androgenic effects while preserving the activation of the progesterone receptor.

Disclaimer: The fact that this post and product description contain quotes from Ray Peat does not mean he endorses/approves of this product. His opinions on a chemical may change when new evidence becomes available in the future, so future inquiries about a chemical, solvent, ingredients, etc contained in this product may elicit a different response than his quotes included in this post. Please seek his opinion independently on any chemical, solvent, ingredient, etc that you may have concerns/questions about.

The units listed on the label are just for measurement purposes. They do not indicate or suggest optimal dose. Please note that similar to the products sold by companies like BlueSky, this product if for lab/research use only. The product can be ordered from the link below:
http://www.idealabsdc.com/lab

*******************************************************************************
5α-Dihydroprogesterone (5α-DHP) is a metabolite of progesterone through the action of the enzyme 5α-reductase (5-AR). It is an agonist of the progesterone receptor with similar potency to progesterone, and just like progesterone it is an agonist of the GABA receptor. As a result, 5α-DHP has been shown to possess a number of properties ascribed to progesterone, including anti-estrogenic, anti-prolactin, sedative, anxyolitic, anti-depressant, neuprotective, anti-aging, pro-metabolic, pro-thyroid, and anti-proliferative. Unlike progesterone, 5α-DHP is not a metabolic precursor to cortisol, estrogen and androsterone. However, due to its 5-AR derived nature 5α-Dihydroprogesterone (5α-DHP) can serve as a pro-hormone to potent androgens such as DHT, androstanedione, and androsterone through a recently discovered alternative pathway. 5α-DHP is also a direct precursor to allopregnanolone and can elevate its levels even in cases of severely downregulated 5-AR activity due to stress, PUFA overload, or administration of 5-AR like finasteride or dutasteride. Finally, unlike progesterone, 5α-DHP seems to have little or no anti-androgenic effects.

Drops per container: about 240
Each drop contains the following ingredients:

5α-Dihydroprogesterone (5α-DHP): 1 mg

Other ingredients: add product to shopping cart to see info
*******************************************************************************

References:

1. Po-hormone for DHT / androgen agonist / progesterone agonist
5α-Dihydroprogesterone (5α-DHP) Is Androgen/Progesterone Agonist And Pro-hormone For DHT

2. Anti-estrogen effects
5α-Dihydroprogesterone (5α-DHP) Is More Effective Than Progesterone As Estrogen Antagonist

3. Anti-prolactin effects
5α-Dihydroprogesterone (5α-DHP) Is More Effective Than Progesterone In Lowering Prolactin

4. GABA agonist and neurosteroid
5α-Dihydroprogesterone (5α-DHP) - The Primary Progestogen Neurosteroid

5. Effects on neurodegenerative conditions
5α-Dihydroprogesterone (5α-DHP) - Potent Role In Neurodegenerative Conditions
Hey Georgi, I read on allthingsmale.com a few months ago that Accutane works through lowering RoDH and it’s already known that it inhibits 5 AR type 1. It’s no wonder it causes so many issues if you look at the classic vs backdoor pathway. My question is will increasing retinol intake increase RoDH?
 

haidut

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Hey Georgi, I read on allthingsmale.com a few months ago that Accutane works through lowering RoDH and it’s already known that it inhibits 5 AR type 1. It’s no wonder it causes so many issues if you look at the classic vs backdoor pathway. My question is will increasing retinol intake increase RoDH?

I think retinol has a U-curve effect - i.e. increasing RoDH in lower doses and inhibiting it in high. By high doses, I mean 200,000+ IU daily or a retinyl ester of some sort.
 

TiltMaster

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I'm pretty new to all of this so excuse me for asking stupid questions. When taking dutasteride for hair loss, some negative mental/neurological side effects can occur. In theory, would taking 5a-DHP while also taking dutasteride help one to keep ones hair and maintain a decent level of neurosteroids as well? Or are there, in this case (if one wants to keep taking dutasteride), better ways through other pathways to boost the level of neurosteroids?

A few more questions:

1) What would the dosage be in mg/kg? I think I've read that 5mg/day is a decent doasage? And if one would take it once a day, does the timing matter?

2) What about the shelf life? Haven't been able to find that in the shop. For how long will the mixture be stable and at what temp should it be stored?

3) Are there any good articles about tolerance developping when administering 5a-DHP? I couldn't find any while googling. Or maybe somebody has anecdotal evidence?

Thanks in advance for any help!
 
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Kray

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That is correct and one of the reasons I went with 5a-DHP. It does not sit on the pathway to estrogen like regular progesterone does. I still doubt that progesterone itself would raise estrogen that much to cause spider veins, but some people complained about that so I did not want to exclude it as possibility. 5a-DHP can only be converted to allopregnanolone and other steroids but not estrogen.
Haidut, could women try 5a-DHP in lieu of progesterone or pregnenolone, and take that with a small dose of DHEA ?
 
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I'm pretty new to all of this so excuse me for asking stupid questions. When taking dutasteride for hair loss, some negative mental/neurological side effects can occur. In theory, would taking 5a-DHP while also taking dutasteride help one to keep ones hair and maintain a decent level of neurosteroids as well? Or are there, in this case (if one wants to keep taking dutasteride), better ways through other pathways to boost the level of neurosteroids?

A few more questions:

1) What would the dosage be in mg/kg? I think I've read that 5mg/day is a decent doasage? And if one would take it once a day, does the timing matter?

2) What about the shelf life? Haven't been able to find that in the shop. For how long will the mixture be stable and at what temp should it be stored?

3) Are there any good articles about tolerance developping when administering 5a-DHP? I couldn't find any while googling. Or maybe somebody has anecdotal evidence?

Thanks in advance for any help!

I cannot answer your questions. Just a note: If you're playing with 5-Alpha-Reductase-Inhibitors, pls beware that 5AR is involved in more steroidal pathways than just the ones of DHT & DHP! If you want to know which pathways are affected, you can check the following steroidal pathway map for the number 1.3.1.22 (which is their code for 5AR; you could also type 5alpha into the search function, then all affected steroids should get marked red; strangely that doesn't work for DHT...).

KEGG PATHWAY: Steroid hormone biosynthesis - Homo sapiens (human)
 
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I think retinol has a U-curve effect - i.e. increasing RoDH in lower doses and inhibiting it in high. By high doses, I mean 200,000+ IU daily or a retinyl ester of some sort.
Thanks for the reply Georgi! 5a-DHP seems like a great product that really covers all the bases.
 
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