recreate ingredients question

[unitas27]

Recreate: herbal extract questions

Hi Usp,
I apologize if this has already been answered, but I had a couple questions regarding recreate's ingredients. I bought a bottle, and I see the 'engineered extract" being touted for most of it's ingredients.
Question 1: Thyrofast....it is basically olive leaf extract, which has been used in many fatburners. what makes "thyrofast" any better than regular olive leaf extract, is it standardized for oleuropein? If not, what is it standardized for?

Question 2: The cortisol modulator, which appears to be arabica coffee extract? What exactly is the chemical(s) in arabica coffee extract that mediates cortisol?

Thanks for you anticipated time regarding these questions. So far I really like the recreate formula, definately kicks thermogenesis into overdrive.

Thanks!
john

 

[Guest]

Hi Usp,
I apologize if this has already been answered, but I had a couple questions regarding recreate's ingredients. I bought a bottle, and I see the 'engineered extract" being touted for most of it's ingredients.
Question 1: Thyrofast....it is basically olive leaf extract, which has been used in many fatburners. what makes "thyrofast" any better than regular olive leaf extract, is it standardized for oleuropein? If not, what is it standardized for?

Question 2: The cortisol modulator, which appears to be arabica coffee extract? What exactly is the chemical(s) in arabica coffee extract that mediates cortisol?

Thanks for you anticipated time regarding these questions. So far I really like the recreate formula, definately kicks thermogenesis into overdrive.

Thanks!
john

Really who else uses Olive leaf and quotes the study in reference?

With both compounds, we follow a specific extraction procedures outlined in the respective studies so the end result is the same instead of purchasing a standardized herb. We begin with the whole and extract for the specifics outlined in the study.

 

[unitas27]

Really who else uses Olive leaf and quotes the study in reference?

With both compounds, we follow a specific extraction procedures outlined in the respective studies so the end result is the same instead of purchasing a standardized herb. We begin with the whole and extract for the specifics outlined in the study.

Ergopharms old Ergolean MC fat loss supp used olive leaf exract, ALRI''s T-X also uses olive leaf. I only found one article citing referencing Thyroid stimulation in regards to olive leaf extract.

Can you direct me to the abstract showing arabica coffee extract having cortisol regulating properties?

 

[Guest]

Ergopharms old Ergolean MC fat loss supp used olive leaf exract, ALRI''s T-X also uses olive leaf. I only found one article citing referencing Thyroid stimulation in regards to olive leaf extract.

Can you direct me to the abstract showing arabica coffee extract having cortisol regulating properties?

Reference is listed in the recreate writeup or just do a Pubmed search.

 

[Guest]

Ergopharms old Ergolean MC fat loss supp used olive leaf exract, ALRI''s T-X also uses olive leaf. I only found one article citing referencing Thyroid stimulation in regards to olive leaf extract.

Can you direct me to the abstract showing arabica coffee extract having cortisol regulating properties?

Atanasov AG, Dzyakanchuk AA, Schweizer RA, et al. Coffee inhibits the reactivation of glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1: a glucocorticoid connection in the anti-diabetic action of coffee? FEBS Lett. 2006 Jul 24;580(17):4081-5

 

[Bobaslaw]

Atanasov AG, Dzyakanchuk AA, Schweizer RA, et al. Coffee inhibits the reactivation of glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1: a glucocorticoid connection in the anti-diabetic action of coffee? FEBS Lett. 2006 Jul 24;580(17):4081-5

Have there been blood tests related to testosterone. My concern is that I am unsure whether the inhibition of 11B-HSD1 is primarily the reductase (cortisone into cortisol) and/or the dehydrogenase (cortisol into cortisone). This is a concern with respect to 11B-HSD1 dehydrogenase inhibition in the testes since the dehydrogenase is more abundant than reductase (ratio of 2:1 or more). Reduction of 11BHSD1 dehydrogenase in the testes causes "testicular cortisol" to be elevated (regardless of baseline cort levels), which blunts the Leydig Cells testosterone production and spermatogenesis. This is a known fact in multiple studies and it has been documented with the use of glycyrretic acid and transdermal 7-oxo.

 

[Mulletsoldier]

Have there been blood tests related to testosterone. My concern is that I am unsure whether the inhibition of 11B-HSD1 is primarily the reductase (cortisone into cortisol) and/or the dehydrogenase (cortisol into cortisone). This is a concern with respect to 11B-HSD1 dehydrogenase inhibition in the testes since the dehydrogenase is more abundant than reductase (ratio of 2:1 or more). Reduction of 11BHSD1 dehydrogenase in the testes causes "testicular cortisol" to be elevated (regardless of baseline cort levels), which blunts the Leydig Cells testosterone production and spermatogenesis. This is a known fact in multiple studies and it has been documented with the use of glycyrretic acid and transdermal 7-oxo.

Hi Boba,

I'd refer you back to your original thread, and the comments made by Matt Cahill in reference to the DHEA metabolites; however, I would further his comments in this respect, as C. Arabica is not involved as directly as DHEA in spermatogenesis. While I cannot say definitively, I highly, highly doubt it would have a negative effect on Test.

 

[Bobaslaw]

Hi Boba,

I'd refer you back to your original thread, and the comments made by Matt Cahill in reference to the DHEA metabolites; however, I would further his comments in this respect, as C. Arabica is not involved as directly as DHEA in spermatogenesis. While I cannot say definitively, I highly, highly doubt it would have a negative effect on Test.

So far oral 7oxo (per Matt and the studies) shows no issues with lowered test. Transdermal 7-oxo does, however, show lowered testosterone as it bypasses the liver and takes action in other tissues such as testes. Oral Glycyrrhizic Acid (licorice) does also show affinity for the testes, lowering testosterone.
I just want to find out more detailed info on the 11BetaHSD1method of action by Coffea Arabica.

My Questions to you:

1) Does Coffea Arabica target 11BetaHSD1 dehydrogenase as well as reductase.

2) Does Coffea Arabica exhibit any affinity for 11Beta HSD1 dehydrognase in the testes.

If you have any info regarding these questions that would be wonderful, since in my research I have not found any specific info with regard to these details as pertains to Coffea Arabica L.

Take Care

 

[Mulletsoldier]

So far oral 7oxo (per Matt and the studies) shows no issues with lowered test. Transdermal 7-oxo does, however, show lowered testosterone as it bypasses the liver and takes action in other tissues such as testes. Oral Glycyrrhizic Acid (licorice) does also show affinity for the testes, lowering testosterone.
I just want to find out more detailed info on the 11BetaHSD1method of action by Coffea Arabica.

My Questions to you:

1) Does Coffea Arabica target 11BetaHSD1 dehydrogenase as well as reductase.

2) Does Coffea Arabica exhibit any affinity for 11Beta HSD1 dehydrognase in the testes.

If you have any info regarding these questions that would be wonderful, since in my research I have not found any specific info with regard to these details as pertains to Coffea Arabica L.

Take Care

I will get ahold of the full-texts and get back to you!

 

[Guest]

So far oral 7oxo (per Matt and the studies) shows no issues with lowered test. Transdermal 7-oxo does, however, show lowered testosterone as it bypasses the liver and takes action in other tissues such as testes. Oral Glycyrrhizic Acid (licorice) does also show affinity for the testes, lowering testosterone.
I just want to find out more detailed info on the 11BetaHSD1method of action by Coffea Arabica.

My Questions to you:

1) Does Coffea Arabica target 11BetaHSD1 dehydrogenase as well as reductase.

2) Does Coffea Arabica exhibit any affinity for 11Beta HSD1 dehydrognase in the testes.

If you have any info regarding these questions that would be wonderful, since in my research I have not found any specific info with regard to these details as pertains to Coffea Arabica L.

Take Care

From our science team
"There are no studies evaluating such activity in testicular tissue. However, modulating 11B-HSD1 is not what causes the reduction in testosterone with plants like licorice, rather, licorice inhibits testosterone production by inhibiting 3B-HSD, 17B-HSD, 17-20 lyase and stimulating aromatase expression."

 

[Bobaslaw]

From our science team
"There are no studies evaluating such activity in testicular tissue. However, modulating 11B-HSD1 is not what causes the reduction in testosterone with plants like licorice, rather, licorice inhibits testosterone production by inhibiting 3B-HSD, 17B-HSD, 17-20 lyase and stimulating aromatase expression."

There is, in fact, a study on GA and 11B-HSD1 Cortisol mediated steroidogenesis suppression in the testes. Please see below:

Invalid Link Removed

Inhibition of 11β-Hydroxysteroid Dehydrogenase Enzymatic Activities by Glycyrrhetinic Acid In Vivo Supports Direct Glucocorticoid-Mediated Suppression of Steroidogenesis in Leydig Cells

Inhibition of 11β-Hydroxysteroid Dehydrogenase Enzymatic Activities by Glycyrrhetinic Acid In Vivo Supports Direct Glucocorticoid-Mediated Suppression of Steroidogenesis in Leydig Cells
GUO-XIN HU*, HAN LIN,, CHANTAL M. SOTTAS, DAVID J. MORRIS, MATTHEW P. HARDY|| AND REN-SHAN GE*,
From the * Institute of Molecular Toxicology and Pharmacology, School of Pharmacy, and the Institute of Neuroendocrinology and 2nd Affiliated Hospital, Wenzhou Medical College, Wenzhou, Zhejiang, People's Republic of China; the Population Council and The Rockefeller University, New York, New York; and the Department of Pathology and Laboratory Medicine, The Miriam Hospital, Brown University School of Medicine, Providence, Rhode Island.

Correspondence to: Dr Ren-Shan Ge, The Population Council, 1230 York Avenue, New York, NY 10021 (e-mail: [email protected]).


Previous studies have suggested that glucocorticoid (GC) can directly affect testicular testosterone (T) biosynthesis by Leydig cells through a receptor-mediated mechanism. Interconversion of corticosterone (CORT), the active form in rodents, and 11-dehydroCORT, the biologically inert 11-keto form, is catalyzed by 11βHSD1. This enzyme thus controls the intracellular concentration of active GC. We have postulated that elevated CORT levels resulting from stress exceed the Leydig cell's capacity for metabolic inactivation of CORT, resulting in suppressed T production. The present study tested whether inhibition of 11βHSD1 in vivo, by the administration of glycyrrhetinic acid (GA), increases intracellular active GC concentration and thereby affects serum T concentration and Leydig cell T production. Adult Sprague-Dawley rats were treated with vehicle (corn oil), CORT, GA, or GA + CORT. Serum luteinizing hormone (LH), CORT, and T levels were measured, as were the steroidogenic capacities of purified Leydig cells. Twofold elevations of CORT were achieved by the administration of either CORT or GA alone, but in both cases there was no effect on serum T levels. However, when CORT and GA were administered in combination, serum CORT levels increased 3.5-fold (to 420 ± 34 ng/mL) and serum T levels were reduced significantly (to 0.72 ± 0.07 ng/mL; control, 2.12 ± 0.23 ng/mL). Serum levels of LH were not affected by CORT, GA, or GA + CORT. Consistent with the reduced serum T levels following GA + CORT, steroidogenic enzyme expression and capacities were significantly reduced compared to control. These data support a role for 11βHSD1 in modulating intracellular CORT concentrations and, in turn, for a direct effect of GC on Leydig cells in response to stress.

 

[Guest]

There is, in fact, a study on GA and 11B-HSD1 Cortisol mediated steroidogenesis suppression in the testes. Please see below:

from USPLabscience department

"The conclusions that one can draw from this study would be that if you are a rodent, you should not take exogenous corticosterone and glycyrrhetinic acid concurrently if you wish to avoid a reduction in serum testosterone.

First, corticosterone is the major glucocorticoid in rodents, not humans. The principle glucocorticoid in humans is cortisol, which an 11B-HSD1 inhibitor would decrease. Secondly, the study design is rather poor with respect to drawing conclusions about the inhibition of 11B-HSD1, especially if applied to humans. One of the tenets in determining whether a given enzyme is responsible for a given effect is to use an inhibitor which is selective and at the very least, it shouldn't exhibit any outside enzymatic activity which would influence the end product that one is measuring. In this case, GA was a poor choice as it inhibits not simply 11B-HSD1, but also 17B-HSD and likely 3B-HSD as well as 17,20-lyase while also stimulating aromatase activity, all of which leads to a decrease in testosterone formation. This makes GA a very poor choice for determining whether inhibition of 11B-HSD1 influences testosterone production.

With respect to the rest of the study, as one will easily notice, there was no decrease in vivo when GA alone was administered. In fact, serum testosterone only decrease when both exogenous corticosterone and GA were administered. So, again, if you have the physiology of a rat where corticosterone is the principle glucocorticoid and you are taking exogenous corticosterone, then it would be a good idea to avoid taking GA. This study does not, however, support the notion that inhibition of 11B-HSD1, in humans, leads to a reduction in endogenous testosterone production."

 

[bpmartyr]

I have been accused of rodent like behavior at times by certain females of the "X" variety. Does that mean I am at greater risk of a lowered sperm count? If so, good. I have enough "mini me's" running around.

 

[Bobaslaw]

from USPLabscience department

"The conclusions that one can draw from this study would be that if you are a rodent, you should not take exogenous corticosterone and glycyrrhetinic acid concurrently if you wish to avoid a reduction in serum testosterone.

First, corticosterone is the major glucocorticoid in rodents, not humans. The principle glucocorticoid in humans is cortisol, which an 11B-HSD1 inhibitor would decrease. Secondly, the study design is rather poor with respect to drawing conclusions about the inhibition of 11B-HSD1, especially if applied to humans. One of the tenets in determining whether a given enzyme is responsible for a given effect is to use an inhibitor which is selective and at the very least, it shouldn't exhibit any outside enzymatic activity which would influence the end product that one is measuring. In this case, GA was a poor choice as it inhibits not simply 11B-HSD1, but also 17B-HSD and likely 3B-HSD as well as 17,20-lyase while also stimulating aromatase activity, all of which leads to a decrease in testosterone formation. This makes GA a very poor choice for determining whether inhibition of 11B-HSD1 influences testosterone production.

With respect to the rest of the study, as one will easily notice, there was no decrease in vivo when GA alone was administered. In fact, serum testosterone only decrease when both exogenous corticosterone and GA were administered. So, again, if you have the physiology of a rat where corticosterone is the principle glucocorticoid and you are taking exogenous corticosterone, then it would be a good idea to avoid taking GA. This study does not, however, support the notion that inhibition of 11B-HSD1, in humans, leads to a reduction in endogenous testosterone production."

Yes that study is pertinent and yes GA and Cort simulate the natural environment of the testes in this circumstance (in vivo).
Cortisol alone does not affect steroidogenesis because Leydig Cell 11B-HSD1 dehydrogenase is able to inactivete it. 11BHSD1 dehydrogenase is predominant in the testes over the reductase. Anyhow GA alone does not affect steroidogenesis either, as in this example there is no endogenous cort being accounted for since this is an in vivo experiment. Remember, in vitro we would have a level of cort in the testes that would affect steroidogenesis if 11B-HSD1 dehydrogenase is inhibited by GA.
Thus adding Cort and GA simulates fully the in vitro eqivelent action of GA on 11B-HSD1 while in the presence of native levels of cortisol in the testes
At least that is how I see it.

BTW, the rat model has always been used and applied to the human model with respect to many actions such as this.

The fact is that GA can inhibit 11Beta-OHSD1 in the testes if it makes it to that tissue, and multiple studies (I have links) show that inhibition if 11BHSD 1 in the testes will reduce steroidogenesis in the presence of elevated testicular cortisol.

 

[USPLabscience]

Yes that study is pertinent and yes GA and Cort simulate the natural environment of the testes in this circumstance (in vivo).
Cortisol alone does not affect steroidogenesis because Leydig Cell 11B-HSD1 dehydrogenase is able to inactivete it. 11BHSD1 dehydrogenase is predominant in the testes over the reductase. Anyhow GA alone does not affect steroidogenesis either, as in this example there is no endogenous cort being accounted for since this is an in vivo experiment. Remember, in vitro we would have a level of cort in the testes that would affect steroidogenesis if 11B-HSD1 dehydrogenase is inhibited by GA.
Thus adding Cort and GA simulates fully the in vitro eqivelent action of GA on 11B-HSD1 while in the presence of native levels of cortisol in the testes
At least that is how I see it.

BTW, the rat model has always been used and applied to the human model with respect to many actions such as this.

The fact is that GA can inhibit 11Beta-OHSD1 in the testes if it makes it to that tissue, and multiple studies (I have links) show that inhibition if 11BHSD 1 in the testes will reduce steroidogenesis in the presence of elevated testicular cortisol.

Dear Sir,

This study does not clearly show that GA's ability to inhibit 11B-HSD1 in the testicles is responsible for a decrease in testosterone production for the reasons I mentioned before, namely that it also inhibits enzymatic activity that is known to contribute to testosterone formation. I don't know how else I can explain this. Again, this is why GA makes a poor choice molecule as it is not a selective or pure 11B-HSD1 inhibitor, affecting 17B-HSD and likely 3B-HSD, aromatase and 17,20-lyase, all of which contribute to reduced serum testosterone. Because the author of a study makes a conclusion, does not make it a "fact", something which is not present in science to begin with. One of the main reasons studies are published is to allow those considered peers to critique, validate or point out errors in research. I think the choice of GA in this model is an obvious error. Again, I would reiterate that one of the tenets in determining whether a given enzyme is responsible for a given effect is to use an inhibitor which is selective and does not exhibit any outside enzymatic activity which would infuence the end product that one is measuring. This was not followed in this study.

This in vivo (in the living rat) experiment has exogenous corticosterone being added in addition to what is already present in the rat, along with GA, and only then was there a decrease in serum testosterone.

Unless one self-administers such glucocorticoids along with GA (not to be confused with a 11B-HSD1 inhibitor which does not affect 17B-HSD, 3B-HSD, etc.), there are no other conclusions that one could draw and certainly not what it seems you are implying, which would be that if a human being ingested an 11B-HSD1 inhibitor (not GA but one that does not affect 17B-HSD, 3B-HSD, etc.), their serum testosterone levels would decrease. That is quite a leap to take.

I am well aware of the use of rat and other rodents for study. However, they are simply "models" and are not used to draw direct conclusions for another species. Rodents and other animal models are used to confirm in vitro research and if promising enough, will warrant research in humans.

If you have any studies demonstrating a selective 11B-HSD1 inhibitor (i.e. a molecule which unlike GA doesn't affect 17B-HSD and other enzymes which catalyze the formation of testosterone), administered by itself (i.e., without concurrent administration of exogenous glucocorticoids) affecting serum testosterone, in vivo, I would be very interested in seeing them.