[Lotus]

Thanks.
DGL Licorice Root 750-mg as strong as,equal= Licorice Root 450-mg/    (without side effects)right?
                                                 

Id like to know as well lotus I heard dgl licorice doesn't help as much non dgl. I heard after using non dgl licorice testosterone can drop 35 percent. I have had great results but I don't know how because I'm hard and horny all the time.

In large amounts, licorice containing glycyrrhizin can cause high blood pressure, salt and water retention, and low potassium levels, which could lead to heart problems. DGL products are thought to cause fewer side effects. Licorice can be found with glycyrrhizin removed; the product is called DGL (for “deglycyrrhizinated licorice”).
http://nccam.nih.gov/health/licoriceroot

Well the debate still goes on, you will find two opposing side's. My opinion is if you remove the glycyrrhizin you should still have the same constituents:

Constituents
• Triterpene saponins (3-15%): chief components glycyrrhetic acid, 18-
alpha-glycrrhetic acid, glycyrrhetic acid methyl ester, glabric acid, glabrolide,
uralenic acid
• Flavonoids: aglycones including liquiritigenin, isoliquiritigenin (its chalcone),
isolicoflavonol, isoliquiritin, licoricidin
• Isoflavonoids: aglycones formononetin, glabren, glabridin, glabrol, 3-
hydroxygIabrol, glycyrrhisoflavone
• Cumestan derivatives: glycyrol, isoglycyrol, liquocoumarin
• Hydroxycoumarins: including herniarin, umbelliferone, glycycoumarin, licopyranocoumarin
• Steroids: sterols, including beta-sitosterol, stigmasterol
• Volatile oil (very little): with anethole, estragole, eugenol, hexanoic acid


I'd rather have fewer side effects myself, so imo I'd choose DGL. I've done the homework on LR. Though someone can knock themselves out and do there own research if they prefer. (Good Luck cause it will leave you aggravated).

Just curious as this an old comment (3+ years ago) if DGL works. I've taken it off and on for acid reflux, but I'll consider taking it more often. Licorice is also in my Lyme protocol, but I need to find out which constituent are the active ones (whether it's glycyrrhizin or something else).
I also noticed beta-sitosterol is listed. It seems like so many foods and herbs have some amount of phytoestrogens, but it's often unclear if it's enough to block the more powerful estrogens. Cat's Claw is another herb in my Lyme protocol and it has beta-sitosterol, but I have no clue if it's enough to do any harm. I'm kind of just doing a little bit of everything because I don't know what's good or bad.

LR and dgl LR has its purposes, just not in use with estradiol, thanks for the question. Tbh, i was actually thinking of closing this thread out since I haven't posted anything for a bit....not for a lack of ideas lol, just heading in a different direction.
  

Btw, i did mention the science of LR will piss you off right? Nightshade, read the attached two studies below, you'll find the active constituents, my pick are aglycones and glycyrrhetic acid.

LR oxidizes NAPDH and inhibits P450 enzymes,  what's more interesting (imo) is the latter part. Meaning I see LR inhibiting aromatase, not potentiating it. Oh sure LR binds to estrogen receptors, but that's where I think it ends. My reasoning is what it isn't doing to the P450 enzyme, (i.e. not synthesizing it).

Agonistic and antagonistic estrogens in licorice root (Glycyrrhiza glabra)


Several fractions displayed higher responses than the maximum response obtained with the reference compound, the natural hormone 17β-estradiol (E2).


The roots of licorice are a rich source of flavonoids, in particular, prenylated flavonoids, such as the isoflavan glabridin and the isoflavene glabrene. Fractionation of an ethyl acetate extract from licorice root by centrifugal partitioning chromatography yielded 51 fractions.
One third of the fractions displayed estrogenic activity towards either one or both estrogen receptors (ERs; ERα and ERβ). Glabrene-rich fractions displayed an estrogenic response, predominantly to the ERα. Surprisingly, glabridin did not exert agonistic activity to both ER subtypes. Several fractions displayed higher responses than the maximum response obtained with the reference compound, the natural hormone 17β-estradiol (E2). The estrogenic activities of all fractions, including this so-called superinduction, were clearly ER-mediated, as the estrogenic response was inhibited by 20–60% by known ER antagonists. Most fractions displaying superinduction were rich in flavonoids with single prenylation. Glabridin displayed ERα-selective antagonism, similar to the ERα-selective antagonist RU 58668. Whereas glabridin was able to reduce the estrogenic response of E2 by approximately 80% at 6 × 10−6 M, glabrene-rich fractions only exhibited agonistic responses, preferentially on ERα.
http://www.ncbi.nlm.nih.gov/pmc/articles...po=7.50000

Two further LR studies to look at:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3889530/

https://www.google.com/url?q=http://www.irjponline.com/admin/php/uploads/1284_pdf.pdf&sa=U&ved=0ahUKEwiek4-xkcfXAhVW2GMKHbOyAxEQFggeMAU&usg=AOvVaw3ampJC5pP_pJjoTPbhbjLg