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Re: Urine Test to Measure Neurotransmitter Levels? Larry Hoover

Posted by Elroy on May 16, 2005, at 12:49:50

In reply to Re: Urine Test to Measure Neurotransmitter Levels? Elroy, posted by Larry Hoover on May 16, 2005, at 10:42:36

Yes, as part of ongoing testing have had a few dexamethasone suppression tests. Have always suppressed. Anywhere from moderately to significantly. Last dex suppression test was a result of a 1.2 ug/DL.


> I've re-organized your post a bit.
>
> > Anyway, I recall some info about licorice. As I recall, there's two types. Actually only one type but processed differently?? One type boosts the adrenal glands and could actually increase production of cortisol while other type is an effective "anti-cortisol" product. Can't remember offhand which is which. Let's see, something like non-deglycyrrhinized licorice and deglycyrrhinized licorice, but can't recall which does which (darn brain fog!).
>
> > Do you have any links to further information on that process?
>
> DGL is the one that does not affect cortisol. Regular (unprocessed) licorice root affects cortisol. But, rather than increasing cortisol production, literally, it inhibits the conversion of cortisol to cortisone, via the enzyme 11beta-hydroxysteroid dehydrogenase type 2. This actually enhances the systemic cortisol signal, and shuts down the adrenal gland production, via cortisol receptors in the hypothalamus. This sounds contrary to what you seek, but:
>
> Food Chem Toxicol. 2002 Oct;40(10):1525-7.
>
> Liquorice (Glycyrrhiza glabra) and the adrenal-kidney-pituitary axis in rats.
>
> Al-Qarawi AA, Abdel-Rahman HA, Ali BH, El Mougy SA.
>
> The effect of oral administration of a water freeze-dried extract of Glycyrrhiza glabra (liquorice) has been studied at doses of 100, 250 and 500 mg/kg in rats on the plasma concentration of cortisol, adrenocorticotrophic hormone (ACTH), aldosterone, renin, sodium (Na) and potassium (K). The results indicated that treatment induced dose-dependent and mostly significant decreases in the concentration of cortisol, ACTH, aldosterone and K. There were concomitant dose-dependent increases in the concentrations of renin and Na. The results suggest a strong and dose-dependent suppression of the adrenal-pituitary axis, accompanied by stimulation of renin production from the kidney.
>
> When I was looking at this more closely, in response to your questions, I began to see an apparent contradiction between human and animal studies. It seems my suggestion was informed by study of rats. They are different than us.
>
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8733012
>
> They have different receptors than we do, and thus their response to cortisolic regulators is different than ours. *OR*, the time-dependency of the measures accounts for the differences.
>
> I've been "thinking this through" as I wrote this post. Despite the apparent contradictions, it seems that mifepristone and licorice have a similar mechanism.
>
> > I found your comment (as follows) very interesting:
> >
> > QUOTE: Licorice tricks your hypothalamus and pituitary into thinking the adrenals are pumping out excess cortisol, and they shut down their adrenal stimulatory activity. The whole system should go into a temporary rest phase. END QUOTE
>
> That would be mediated by hypothalamic response to cortisolic receptor binding (GR and MR).....but it depends on your initial ACTH (and CRH, but they are usually very closely linked). And....
>
> > Let's see. CRH levels, I am not sure about. ACTH levels have always been pretty much mid range, occasional upper normal range. My lab's reference range is 5 - 50 and I've run the range from a 16 to a 36. Mostly in the 16-25 range.
>
> Your ACTH is in the normal range despite excessive cortisol. You seem like you're not responding to excess cortisol already (i.e. I presume normal CRH).
>
> And that leads directly to the following:
>
> > I have been so convinced of this that I have spoke very strongly with my endo about looking into an attempt at RU486 therapy to "re-set" the HPA Axis.
>
> That sounds like an excellent option. I was unaware of the selective GR antagonism of this drug. On its face, it sound like it has a very similar mechanism of action as does licorice, except I don't know if licorice antagonizes the GR receptor. You'll note in your last reference that mifepristone has the short term effect of increasing cortisol. So would licorice. The idea, I suppose, is to shock the sytem back into a more normal "rhythm", like shocking a heart that is beating too fast. I suspect the short-term increase in cortisol ought to be seen as a side-effect of the therapy. The true intent is to get the hypothalamus back into balance.
>
> The advantages of mifepristone would be direct medical supervision and very controlled dosage. Also, you know it has GR antagonism.
>
> For both licorice and mifepristone, the treatment period should be no more than 3-4 weeks.
>
> No matter what course you take (if you do), you're pretty much in uncharted territory. Have you ever done a dexamethasone suppression test? It would confirm the GR non-responsivity issue.
>
> > Also, your info about samE maybe being too "stimulating" appears to be right on the mark. Am even still trying to take 1/4 tablet of Tyrosine without too much stimulation (especially in the result of having the prostatitis type pain - burning urethra - flare up and the anxiety feelings enhance somewhat). 1/4 tablet is 125 mgs in my case (maybe I need to find 100 mg tablets and cut them down??? or maybe just let go that angle for right now and assume that I've actually got more than sufficient dopamine / adrenaline levels???).
>
> I would stay away from something that seems to clearly aggravate some of your symptoms.
>
> I am really wondering if anything I talk about is of any use to you at all.
>
> Regards,
> Lar


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poster:Elroy thread:493827
URL: http://www.dr-bob.org/babble/20050516/msgs/498500.html