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Re: PTSD and adaptogens

Posted by Larry Hoover on November 8, 2002, at 8:55:29

In reply to Re: PTSD/Social Anxiety-Herbals » Larry Hoover, posted by pelorojo on November 7, 2002, at 18:39:17

> I'm happy to meet someone so knowledgeable!

I'm not so sure about that, but I have been spending a lot of time trying to make sense of the situation.

Thanks for your reply. Some comments/questions below:
> > There is some evidence that adaptogens may have much lesser effect the longer the chronic stress has continued. The HPA can become 'locked in' to a vicious cycle caused by what some call burn-out.
>
> Interesting, I had never read that. I thought the adaptogens were especially useful for chronic stress - it didn't occur to me that long-term stress would reduce their effectiveness.

You've probably come across the three-stage model proposed by Hans Selye, called the GAS model. It's useful, but I find it does not account for some of the characteristics of chronic PTSD.

Theories and models are simplifications, abstractions which connect observations together. It's kind of like a connect-the-dots picture, except the theory forces you to fit the dots to the abstraction. Consider the constellations. For the life of me, I don't see a bear when I look at the Big Dipper.

The theoretical underpinnings of the GAS model, and the effect of adaptogens, presume that it is possible to normalize glandular communications (endocrine and exocrine). However, studies on lab animals clearly show that stressors can permanently change the pattern and extent of hormonal responses to subsequent stressors. Such, I believe, is the case with PTSD.

That's what I was trying to suggest in my mention of Olympic athletes. There's a window of opportunity for optimizing how the body functions, which once passed, cannot be re-obtained. Call it aging. Call it a disease syndrome. Call it what you want. You can't go back.

> >
> > That said, gingko or Siberian ginseng have quite different modes of action when compared to e.g. rhodiola or witheria or licorice root. For example, licorice root blocks liver enzymes affecting interconversion of some of the steroids. I don't like the 'lumping together' of herbs like this.
> >
>
> Oh yeah - 'adaptogen' encompasses a large number of herbs with different modes of action and presumed benefits. I listed some of those I had identified as potentially useful. It's a tremendous amount of information to swallow at once so I'm hoping to gain some insight about the options on this board.

Options I understand. The issue is also one of interpretation. It is my belief (and I encourage you to come clearly to your own) that adaptogens ought not to be considered to be maintenance therapy. They can be helpful in short-term use, but should not be used beyond 3-4 weeks at a time.

If a particular adaptogen is chosen, and it seems to help, it then provides a guide for understanding just what it is in our body which is functioning at a non-optimal level. Then a strategy to augment the bodily function through dietary/supplemental nutrition manipulations should be sought out. I believe that goes to causation, rather than symptom-management. But you see, that is *my* model.

I mentioned licorice root. It has powerful impacts on some core liver enzyme functions, and both increases circulating cortisol while decreasing conversion to testosterone. Clearly, you don't want those changes to be permanent. But, they may serve to inform, if one listens to the language of the body.

If licorice root makes you feel better, you may want to consider adrenal fatigue. Temporarily increasing cortisol (which flies in the face of the GAS model) will inhibit ACTH secretion via the feedback modulation of the hypothalamus on the pituitary. Which then implies other interventions.

It's all exceedingly complex, but that's just how it is. I inform the mind, then let my intuition have a go at it. That's just what works for me.

Here's a little bit of science on licorice root:

Life Sci 1998;62(6):571-82

Effect of licorice and glycyrrhizin on murine liver CYP-dependent monooxygenases.

Paolini M, Pozzetti L, Sapone A, Cantelli-Forti G.

Department of Pharmacology, University of Bologna, Italy. paolini@biocfarm.unibo.it

This study is aimed to investigate the effect of the prolonged intake of conspicuous amounts of licorice (LE), or its natural constituent glycyrrhizin (G) on murine liver CYP-catalyzed drug metabolism. For this purpose the modulation of the regio- and stereo-selective hydroxylation of testosterone, together with the use of highly specific substrates as probes for different CYP isoforms such as ethoxyresorufin (CYP1A1), methoxyresorufin (1A2), pentoxyresorufin (2B1), p-nitrophenol (2E1) and aminopyrine (3A), were investigated. Daily doses of licorice root extract (3,138 or 6,276 mg/kg b.w. per os), or G (240 or 480 mg/kg b.w. per os), were administered to different groups of Swiss Albino CD1 mice of both sexes for 1, 4 or 10 consecutive days. While a single LE or G dose was unable to affect the multienzymatic CYP-system, using both schedules of repeated treatment, either LE or G were able to significantly induce hepatic CYP3A- and, to a lesser extent, 2B1- and 1A2-dependent microsomal monooxygenase activities, as well as 6beta- (mainly associated to CYP3A), 2alpha-, 6alpha- (CYP2A1, 2B1), 7alpha-, 16alpha- (CYP2B9) and 16beta-testosterone hydroxylase (TH) activities in male and female mice. Data on CYP3A modulation, the major isoform present in human liver, was confirmed by using Western immunoblotting with anti-CYP3A1/2 rabbit polyclonal antibodies raised against purified rat CYP3A. Northern blotting analysis using CYP3A cDNA biotinylated probe showed that the expression of such isozyme is regulated at the mRNA level. These results suggest that the induction of cytochrome P450-dependent activities by the prolonged intake of high LE or G doses, may result in accelerated metabolism of coadministered drugs with important implications for their disposition. The adverse effects associated with CYP changes such as toxicity/cotoxicity and comutagenicity may also have clinical consequences.

Exp Clin Endocrinol Diabetes 2002 Sep;110(6):257-61

History of the endocrine effects of licorice.

Armanini D, Fiore C, Mattarello MJ, Bielenberg J, Palermo M.

Department of Medical and Surgical Sciences -Endocrinology University of Padua.

Summary. The history of licorice as an officinal plant dates back thousands of years, and licorice is still appreciated as a medicinal root. Many of its endocrine properties can be derived from observations of Authors of the ancient world, when hormones were not known. Inappropriate use of licorice can produce pseudoaldosteronism, by inactivating 11beta-hydroxysteroiod-dehydrogenase and by binding to mineralocorticoid receptors. Licorice possesses many other therapeutic properties as to potentiate the action of cortisol, to reduce testosterone synthesis, especially in women, to exert an estrogen-like activity and to reduce body fat mass. The chronological development of research on these effects is described.


Yakugaku Zasshi 2000 Oct;120(10):849-62

A drug over the millennia: pharmacognosy, chemistry, and pharmacology of licorice.

Shibata S.

Shibata Laboratory of Natural Medicinal Materials, C/o Minophagen Pharmaceutical Co., Ltd., Tokyo, Japan.

Licorice, the root of Glycyrrhiza spp. (Fabaceae), has been used since ancient Egyptian, Greek, and Roman times in the West and since the Former Han era (the 2nd-3rd century B.C.) in ancient China in the East. In traditional Chinese medicine, licorice is one of the most frequently used drugs. In Japan, the oldest specimen of licorice introduced from China in the middle of the 8th century still exists in Shosoin, the Imperial Storehouse, in Nara. Extracts of licorice were recommended as a remedy for gastric ulcer by Revers of the Netherlands in 1946, which was soon withdrawn owing to its side effects. Carbenoxolon sodium, glycyrrhetinic acid (GA) hemisuccinate Na, was prepared from licorice to treat peptic ulcer in the UK. In Japan for the past 60 years, a glycyrrhizin (GL) preparation under the name of Stronger Neo-Minophagen C (SNMC) has been used clinically as an antiallergic and antihepatitis agent. GL and GA sometimes induce edema, hypertension, and hypokalemia in patients treated with higher doses and long-term administration. The mechanism of this side effect, pseudoaldosteronism, has been explained as due to the 11-hydroxy-steroid dehydrogenase inhibitory activity of GL and GA. The excess of endogenous cortisol produced combines with the renal mineral corticoid receptor, which promotes an aldosterone-like action. GL and GA reduce alanine transaminase (ALT) and aspartate transaminase (AST) values in the serum. This hepatoprotective effect has recently been explained as the inhibitory effects of GL and GA on immune-mediated cytotoxicity against hepatocytes and on nuclear factor (NF)-kappa B, which activates genes encoding inflammatory cytokines in the liver. To exclude the side effects and enhance the therapeutic activities, chemical modification of GL and GA has been performed. Deoxoglycyrrhetol (DG), homo- and heteroannular diene homologs of dihemiphthalates, showed a remarkable improvement in antiinflammatory, antiallergic, and antiulcer activities in animal experiments. Immunomodulating effects of GL, GA, and DG derivatives, which induce interferon-gamma and some other cytokines, have been demonstrated in relation with their antiviral activities. Antiinflammatory, antitumorigenic, and antimalarial effects of licorice flavonoids have also been investigated.


 

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poster:Larry Hoover thread:126446
URL: http://www.dr-bob.org/babble/20021108/msgs/126943.html