Re: licorice dosing

[Guest guest]

on <jamesinspace@y...> wrote:

> Essentially, is it possible to maximise the thrombin

> inhibition whilst minimising inhibition of 18 beta

> HSD? What dose and frequency would you suggest, how

> about 100mg GA (eg, 1g Baschetti extract) per day with

> breakfast, or well before breakfast if you intend to

> boost cortisol as well?

I went off for six months because I was doing so great. I started

getting worse after a month off baschetti and then started

investigating my allergies by going on a serious rotational diet. I

discovered sufite sensitivity and a host of allergies to all sorts of

fillers. The allergies to supplement fillers (magnesium sterate,

silca, etc) stimulated my kidneys and caused my to become dehydrated

within 12 hours. I can't believe how sensitive I have become to so

many things. I especially can't believe how difficult it was to

uncover these allergies. What the heck, I've only been working on

this for 20 years.

Anyway, I was very excited about finding these allergies and was

almost convinced that I didn't have CFS...I just had allergies. But

now I am seeing a different picture. It seems that the " Complement

System " is the culprit in food and chemical allergies and is also

very active in the kidneys. Licorice inhibits complement so the

baschetti I was taking was, in a way, was masking the allergies.

When I went off for a long period, the allergies became more dramatic

and easier to detect.

Now I discover that 18 beta GA from licorice extract also

desensitizes the immune response and prevents the proliferation of

mast/immune cells, thus playing a role in toning down the incipient

stage of inflammation. (see 1st abstract below)

18 beta GA also markedly inhibited the release of histamine from

antigen-stimulated mast cells so it looks like I might have

overlooked an important way in which licorice extract can help a PWC.

(see 2nd abstract below)

18 beta GA in licorice extract acts as a thrombin inhibitor...it also

inhibits the complement system...acts to desensitize antigen

repsonse....and also acts to inhibit histamine. Besides this it

boost cortisol bioactivity. But licorice extract does have its

negatives...the herb increase estrogen levels, which can be a problem

in CFS since estrogen stimulates nitric oxide and lowers blood

pressure. Low doses of an estrogen blocker like tomoxifen might be

necessary to gain full benefit.

As far as dosing, I'm started my new regiment at 3 grams day and will

quickly ramp up to 5 grams based on response. I'm also going to

devide the dose up over the day. Dosing of licorice extract is an

individual thing because the actual dose of 18 beta GA getting into

the blood is dependant on gut flora that favors a none nutrient

environement. The differences in individual gut flora is great so is

the difference in gut flora based on time of day, etc. No two people

will repond the same. If anyone recommends a set dose of licorice

extract for everyone they don't know the workings of the herb. We

will respond based on what lives in our intestine so we need to

experiment and find what works best for ourselves at different times

of the day and after different foods. Of course, licorice extract

will alter the gut flora after a few weeks so we need to be prepared

to change dose as our intestinal flora changes. Sound confusing yet?

Before starting licorice extract, I would recommend everyone go off

everything they can and get on a rotation diet to identify food and

chemical allergies first since the herb looks like it might tend to

mask allergies and make them difficult to indentify.

This brings up another point. It takes about 3 hours before 18 beta

GA reaches maximum in the blood stream and another 3 hours until it

is mostly gone. This was ideal when taking licorice to boost cortisol

since it tended to lower feedback by not working all day long. But

when taking licorice for the above effects, it might be better to

devide your daily allotment in two doses or even three.

If 18 beta GA is masking allergies and you took it once a day in the

morning as has been the practice, I can see how it might be possible

to digest an allergen in the morning and not be affected, whereas you

ingest the same allergen late in the day when GA is gone from the

blood and you really feel like crap because the protection from

licorice had worn off.

Anyway, there is a lot I don't know about dosing so I can't really

answer your question properly. Best to experiment a little.

Dave

********************************************************************

Biochem Pharmacol 1991 Jun 1;41(11):1725-30

Desensitization by glycyrrhetinic acid of other stimulatory substance-

induced increases in intracellular calcium in a variety of cell types.

Hayashi Y, Hirai S, Negishi M, Okumura T, Ichikawa A

Department of Physiological Chemistry, Faculty of Pharmaceutical

Sciences, Kyoto University, Japan.

The effects of glycyrrhizin and its aglycone, glycyrrhetinic acid, on

the cytoplasmic free calcium concentration ([Ca2+]i) in mastocytoma P-

815 cells, DNP-Ascaris (antigen) sensitized mast cells, hepatocytes,

fibroblasts and endothelial cells were investigated. In these cell

types, glycyrrhetinic acid in the concentration range of 20 to 100

microM caused an increase in [Ca2+]i and inhibited calcium increases

induced by an antigen (mast cells), ATP, phenylephrine (hepatocytes)

and thrombin (fibroblasts and endothelial cells). Stimulation with

phenylephrine, in place of glycyrrhetinic acid, did not inhibit

subsequent calcium increases induced by phenylephrine or ATP. On the

other hand, glycyrrhizin at concentrations up to 100 microM neither

caused an increase in [Ca2+]i nor inhibited calcium increases induced

by other stimulatory substances. These results suggest that the

inhibition of the calcium-mediated signal pathway may participate in

the cytostatic actions of glycyrrhetinic acid.

**********************************************************************

Biochem Pharmacol 1989 Aug 1;38(15):2521-6

Effects of glycyrrhizin and glycyrrhetinic acid on dexamethasone-

induced changes in histamine synthesis of mouse mastocytoma P-815

cells and in histamine release from rat peritoneal mast cells.

Imanishi N, Kawai H, Hayashi Y, Yatsunami K, Ichikawa A

Department of Health Chemistry, Faculty of Pharmaceutical Sciences,

Kyoto University, Japan.

The effects of glycyrrhizin and its aglycone, glycyrrhetinic acid, on

dexamethasone-induced changes in the histamine synthesis of

mastocytoma P-815 cells and in the histamine release from antigen-

stimulated rat peritoneal mast cells were investigated.

Glycyrrhetinic acid but not glycyrrhizin, at concentrations from 20

to 35 microM, almost completely inhibited the dexamethasone-induced

increases in both the histamine content and histidine decarboxylase

activity of cultured mastocytoma P-815 cells. Glycyrrhetinic acid,

however, showed practically no inhibition of [3H]dexamethasone

binding to the cytoplasmic receptor. On the other hand,

glycyrrhetinic acid but not glycyrrhizin markedly inhibited the

release of histamine from antigen-stimulated rat mast cells, and

intensified the inhibitory activity induced by dexamethasone.

Glycyrrhetinic acid inhibited the antigen-induced release and

incorporation of [3H]arachidonic acid in immunized rat mast cells.

The administration of glycyrrhizin into rats, in contrast to the in

vitro treatment of the cells with glycyrrhizin, markedly inhibited

histamine release from antigen-stimulated rat mast cells. These

results suggest that glycyrrhetinic acid inhibited dexamethasone-

induced changes in the histamine synthesis of mastocytoma P-815

cells, and in the histamine release from rat mast cells. On the other

hand, glycyrrhizin may exert its effect after conversion to

glycyrrhetinic acid in vivo.