[twinklepose]

Soooo, in layman's terms... what's it all mean?!

[spanky]

I think it means that "Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR)" neutralizes 5alpha-dihydrotestosterone (DHT). Where you can get "Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR)" is a mystery to me. It is also unclear to me what the total health effects would be.

http://www.ncbi.nlm.nih.gov/pubmed/12810547

file:///C:/Users/Bill/Downloads/30451.pdf

However, it may be that certain SSRIs might provide it. http://en.wikipedia.org/wiki/3-alpha-HSD

Unfortunately, the last thing I would recommend is taking SSRIs, unless your really, really need them.

[twinklepose]

I think it means that "Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR)" neutralizes 5alpha-dihydrotestosterone (DHT). Where you can get "Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR)" is a mystery to me. It is also unclear to me what the total health effects would be.

http://www.ncbi.nlm.nih.gov/pubmed/12810547

file:///C:/Users/Bill/Downloads/30451.pdf

However, it may be that certain SSRIs might provide it. http://en.wikipedia.org/wiki/3-alpha-HSD

Unfortunately, the last thing I would recommend is taking SSRIs, unless your really, really need them.

Had to Google that. As it happens, I do take Paroxetine anyway, for anxiety and depression. Been taking it for years and it's saved my life. The alternative was a living hell.

Sooooo, is that good for NBE then?

[spanky]

I think it means that "Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR)" neutralizes 5alpha-dihydrotestosterone (DHT). Where you can get "Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR)" is a mystery to me. It is also unclear to me what the total health effects would be.

http://www.ncbi.nlm.nih.gov/pubmed/12810547

file:///C:/Users/Bill/Downloads/30451.pdf

However, it may be that certain SSRIs might provide it. http://en.wikipedia.org/wiki/3-alpha-HSD

Unfortunately, the last thing I would recommend is taking SSRIs, unless your really, really need them.

Had to Google that. As it happens, I do take Paroxetine anyway, for anxiety and depression. Been taking it for years and it's saved my life. The alternative was a living hell.

Sooooo, is that good for NBE then?

It would take a lot more knowledge than I have to answer with any certainty.

[Lotus]

This is a bit over simplified but Hydroxysteroid Dehydrogenases (HSDs) act like a gate-keeper just before steroids (hormones) bind to receptors (synthesis). Furthermore, these "gate-keepers" can flip the switch (a light switch) on/off to allow passage to the cell receptors. So in essence, they can inhibit or promote hormone activity. Finding a new class of HSD's is the next step, Aldo-keto reductases (AKRs) can help us get there.

By acting as ketosteroid reductases or hydroxysteroid oxidases these AKRs can either convert potent sex hormones (androgens, estrogens and progestins) into their inactive metabolites or they can form potent hormones by catalyzing the reverse reaction[/b]. In this manner they may regulate occupancy and trans-activation of steroid hormone receptors.

[Lotus]

I think it means that "Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR)" neutralizes 5alpha-dihydrotestosterone (DHT). Where you can get "Type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2, aka-AKR)" is a mystery to me. It is also unclear to me what the total health effects would be.

http://www.ncbi.nlm.nih.gov/pubmed/12810547

file:///C:/Users/Bill/Downloads/30451.pdf

However, it may be that certain SSRIs might provide it. http://en.wikipedia.org/wiki/3-alpha-HSD

Unfortunately, the last thing I would recommend is taking SSRIs, unless your really, really need them.

Had to Google that. As it happens, I do take Paroxetine anyway, for anxiety and depression. Been taking it for years and it's saved my life. The alternative was a living hell.

Sooooo, is that good for NBE then?

I agree spanky, the side effects alone are risky. Antipsychotics up-regulate prolactin, some antidepressants downregulate estrogen. Certain foods up-regulate GABA and dopamine nuerotransmitters. Almonds and walnuts are 2 good examples, plus, many others food choices to choose from too.

Here's an example of how an androgen actually up-regulates GABA.

The testosterone-derived neurosteroid androstanediol is a positive allosteric modulator of GABA (A) receptors.

Abstract
Testosterone modulates seizure susceptibility, but the underlying mechanisms are obscure. Recently, we demonstrated that testosterone affects seizure activity via its conversion to neurosteroids in the brain. Androstanediol (5alpha-androstan-3alpha,17beta-diol) is an endogenous neurosteroid synthesized from testosterone. However, the molecular mechanism underlying the seizure protection activity of androstanediol remains unclear. Here, we show that androstanediol has positive allosteric activity as a GABA(A) receptor modulator. In whole-cell recordings from acutely dissociated hippocampus CA1 pyramidal cells, androstanediol (but not its 3beta-epimer) produced a concentration-dependent enhancement of GABA-activated currents (EC(50) of 5 microM). At 1 microM, androstanediol produced a 50% potentiation of GABA responses. In the absence of GABA, androstanediol has moderate direct effects on GABA(A) receptor-mediated currents at high concentrations. Systemic doses of androstanediol (5-100 mg/kg), but not its 3beta-epimer, caused dose-dependent suppression of behavioral and electrographic seizures in mouse hippocampus kindling, which is a model of temporal lobe epilepsy. The ED(50) value for antiseizure effects of androstanediol was 50 mg/kg, which did not produce sedation/motor toxicity. At high (2x ED(50)) doses, androstanediol produced complete seizure protection that lasted for up to 3 h after injection. The estimated plasma concentrations of androstanediol producing 50% seizure protection in the kindling model (10.6 microM) are within the range of concentrations that modulate GABA(A) receptors. These studies suggest that androstanediol could be a neurosteroid mediator of testosterone actions on neuronal excitability and seizure susceptibility via its activity as a GABA(A) receptor modulator and that androstanediol may play a key role in men with epilepsy, especially during the age-related decline in androgen levels.

[Lotus]

The illustration shows the positions of HSD's (Hydroxysteroid Dehydrogenases) see how it's involved between positions?, pretty significant huh?. The arrows mean up & down regulation between positions. (That includes the half arrows between the HSD's). Previously HSD's, we're thought to be anti-androgens, but they can be influenced as stated previously, cool, eh.

This is a bit over simplified but Hydroxysteroid Dehydrogenases (HSDs) act like a gate-keeper just before steroids (hormones) bind to receptors (synthesis). Furthermore, these "gate-keepers" can flip the switch (a light switch) on/off to allow passage to the cell receptors. So in essence, they can inhibit or promote hormone activity. Finding a new class of HSD's is the next step, Aldo-keto reductases (AKRs) can help us get there.

   

[Lotus]

Androgens from adrenal pathway (DHEA & DHEAS) go through a back doors of sorts to 4 Dione (androstenedione), which in turn can be synthesized by aromatase to E1.


Btw, did you know that the skin acts as one big hormone receptor!, that's right, beneath the layers of skin sits all the hormone molecules. Estrogens sit inside the fat tissues (aka adipose), the process of first pass metabolism is generally ignored, meaning the liver. And in this case offers one of the biggest opportunities to get at hormones that are in the "free" state (the active hormones).
This illustrates a transdermal application, but you get the idea.



   

[pom19]

My goodness Lotus, you are good at what you do. Thanks again, POM

[Lotus]

My goodness Lotus, you are good at what you do. Thanks again, POM

That's nice of you to say POM, thank you.