[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.