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The Science behind Syntherol

Big A

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This is an AWESOME article written by DatBTrue. It fully explains scientifically why and how Syntherol works and creates permanent muscle growth, not just from fascial stretching but also from increasing androgen receptor regulation.

http://www.synthetek.com/the-science-behind-syntherol/
 

Michael

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Big A, just clicked on link & at the bottom Dats article didn't show, it was blank. Please fix if you can!
 

Big A

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Big A, just clicked on link & at the bottom Dats article didn't show, it was blank. Please fix if you can!
It works fine for me.

You can also find it by going to the Synthetek site, look up Syntherol and at the bottom of the page you will find the link to it.
 

weight

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if sesmae oil last longer why couldny we used a synthol version of that to make gains last longer? has anyone experimented with sesame oil before, i once heard of someone who used oilve oil, i dont know what for thoe,
 

chemicalwarrior

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Weight, that's what I was left wondering as well. Also, if a person was the type who made their own brew, would it benefit them to use MCT oil or syntherol as the oil base for their mix and do site injections throughout a cycle?
 

VTliftVT

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Weight, that's what I was left wondering as well. Also, if a person was the type who made their own brew, would it benefit them to use MCT oil or syntherol as the oil base for their mix and do site injections throughout a cycle?
Did neither of you read the article? It clearly states MCT's benefits in the article....
 

chemicalwarrior

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Oh no, I got the benefits of MCT oil, that's clear. What's not clear is are there similar benefits + the longer clearing time of using sesame oil? I'm guessing no. But, it is a valid question.

Also, my other question was about adding say test prop powder to mct oil instead of typical safflower oil for injections. I've heard that since mct is a longer chained substance that it won't allow the aas to be as readily used from an injection. But, does it make it unable to be metabolized? Or does it just take longer?

I'm asking for anyone with experience of putting aas powder in your mct oil for site injects.
 

Conciliator

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There were a few comments I had.

First, Big A said in his PM that Syntherol works "from increasing androgen receptor regulation," however it doesn't appear that this is the case. Research on the effect of polysaturated fatty acids on androgenic action has found that the effects are not due to receptor up-regulation. For example, this paper, which was referenced in the one DatBTrue discussed, found that the increased AR transactivation "is not due to changes in cellular AR content or affinity of the receptor for the cognate DNA element; rather, this phenomenon seems to result from altered interaction of ligand-activated AR with other proteins in the transcription machinery."

Second, DatBTrue is confused about what the difference is between short-chain lipids (like caprylic acid) and triterpenoids. He states that caprylic acid "exerts its phytoandrogenic activity through triterpenoids." This is incorrect. Caprylic acid is caprylic acid and triterpenoids are something else. As the paper explained, "A series of bioassay-guided fractionation showed that the phytoandrogenic and hormone potentiating effects of E. ulmoides were mediated by distinct groups of phytocompounds; triterpenoids and short-chain lipids respectively." They're two different constituents of E. ulmoides with their own respective effects.

DatBTrue stated that "What they discovered is that the bark or caprylic acid by itself demonstrated androgenic activities by weakly activating Androgen Receptors (AR) in a dose-dependent manner... Caprylic acid at 50ng/ml produced a 6.4 fold LUC activity." However, this is not the case. The study used 50ng/ml of E. ulmoides extract, not caprylic acid. They specifically addressed what it was that was activating the androgen receptor: "Subsequent bioassay-guided purification of the androgenic extract using chromatographic and ESI-MS techniques revealed that this phytoandrogenic activity was being mediated by triterpenoids." They even stated this in the results section of the abstract, finding that "phytoandrogenic activity of E. ulmoides was mediated by plant triterpenoids binding cognately to the androgen receptor (AR) ligand binding domain." This is in contrast the the effects of the polysaturated fatty acids. It was incorrect for DatBTrue to ascribe the activation of the androgen receptor to caprylic acid when they specifically ascribed it in the paper to the triterpenoids.

Third, DatBTrue was correct in explaining that E. ulmoides potentiated the effect of androgens, "increasing activity to 240%." However, he left out that it also potentiated the effect of estrogens to the same extent. It seems disingenuous to me for that information to not be included. As the paper stated, "A similar synergistic effect was observed when E. ulmoides extract was tested in combination with estradiol in the presence of the estrogen receptor (ER) α (figure 9)." Caprylic acid would be expected to make not just the effect of androgens more potent, but estrogens as well.
 
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weight

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There were a few comments I had.

First, Big A said in his PM that Syntherol works "from increasing androgen receptor regulation," however it doesn't appear that this is the case. Research on the effect of polysaturated fatty acids on androgenic action has found that the effects are not due to receptor up-regulation. For example, this paper, which was referenced in the one DatBTrue discussed, found that the increased AR transactivation "is not due to changes in cellular AR content or affinity of the receptor for the cognate DNA element; rather, this phenomenon seems to result from altered interaction of ligand-activated AR with other proteins in the transcription machinery."

Second, DatBTrue is confused about what the difference is between short-chain lipids (like caprylic acid) and triterpenoids. He states that caprylic acid "exerts its phytoandrogenic activity through triterpenoids." This is incorrect. Caprylic acid is caprylic acid and triterpenoids are something else. As the paper explained, "A series of bioassay-guided fractionation showed that the phytoandrogenic and hormone potentiating effects of E. ulmoides were mediated by distinct groups of phytocompounds; triterpenoids and short-chain lipids respectively." They're two different constituents of E. ulmoides with their own respective effects.

DatBTrue stated that "What they discovered is that the bark or caprylic acid by itself demonstrated androgenic activities by weakly activating Androgen Receptors (AR) in a dose-dependent manner... Caprylic acid at 50ng/ml produced a 6.4 fold LUC activity." However, this is not the case. The study used 50ng/ml of E. ulmoides extract, not caprylic acid. They specifically addressed what it was that was activating the androgen receptor: "Subsequent bioassay-guided purification of the androgenic extract using chromatographic and ESI-MS techniques revealed that this phytoandrogenic activity was being mediated by triterpenoids." They even stated this in the results section of the abstract, finding that "phytoandrogenic activity of E. ulmoides was mediated by plant triterpenoids binding cognately to the androgen receptor (AR) ligand binding domain." This is in contrast the the effects of the polysaturated fatty acids. It was incorrect for DatBTrue to ascribe the activation of the androgen receptor to caprylic acid when they specifically ascribed it in the paper to the triterpenoids.

Third, DatBTrue was correct in explaining that E. ulmoides potentiated the effect of androgens, "increasing activity to 240%." However, he left out that it also potentiated the effect of estrogens to the same extent. It seems disingenuous to me for that information to not be included. As the paper stated, "A similar synergistic effect was observed when E. ulmoides extract was tested in combination with estradiol in the presence of the estrogen receptor (ER) α (figure 9)." Caprylic acid would be expected to make not just the effect of androgens more potent, but estrogens as well.
dam u must b a scientist
 

DatBtrue

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This statement goes right at me doesn't it?

"It was incorrect for DatBTrue to ascribe the activation of the androgen receptor to caprylic acid when they specifically ascribed it in the paper to the triterpenoids."​

From page 6 of the published portion of the study:

a.jpg

Equally effective were:

Ethanolic extract of coconut
Pure caprylic acid
E. ulmoides

The major constituent in all three is caprylic acid which as the authors show had the strongest augmenting effect.

So a blend of PFAs in Ethanolic extract of coconut the vast majority of which is caprylic acid replicated the hormone potentiating effect of E. ulmoides extract whose primary constituent is caprylic acid which all by itself in pure caprylic acid form replicated the hormone potentiating effect of E. ulmoides extract.

You don't need to rely on my statement which was based on my communication with Victor where he shared with me their unpublished data.

There is enough information in that study for you to understand if you really wanted to.

b.jpg
 

Conciliator

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This statement goes right at me doesn't it?

"It was incorrect for DatBTrue to ascribe the activation of the androgen receptor to caprylic acid when they specifically ascribed it in the paper to the triterpenoids."​

From page 6 of the published portion of the study:


Equally effective were:

Ethanolic extract of coconut
Pure caprylic acid
E. ulmoides

The major constituent in all three is caprylic acid which as the authors show had the strongest augmenting effect.
You're committing a red herring by changing the topic. The paper found that E. ulmoides had two effects. They were stated explicitly in the results section of the abstract. Those two effects were 1) a magnification of the transactivational response to androgens and 2) actual binding to the androgen receptor (AR agonism).

You incorrectly stated in your paper that caprylic acid is responsible for effect #2. It is NOT. They clearly found and stated that effect #2 was caused by phytoandrogenic triterpenoids. Caprylic acid and the phytoandrogenic triterpenoids are two different things. Caprylic acid does not exert a phytoandrogenic effect through triterpenoids, as you incorrectly asserted. The triterpenoids do that themselves.

What the paper did find was that effect #1 is due to the polysaturated fatty acids, and in particular, caprylic acid. In the quote above, you posted a part of the study talking about that. Yet it is not in dispute that caprylic acid causes effect #1. We both acknowledge it. Changing the topic doesn't change the fact that you were incorrect about effect #2. In your write up, your entire discussion surrounding this figure is flawed. You ascribed the effects of the phytoandrogenic triterpenoids to the "lipidic augmenter" caprylic acid.

Can you not just admit you made a mistake?
 

DatBtrue

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Conciliator; said:
...What the paper did find was that effect #1 is due to the polysaturated fatty acids, and in particular, caprylic acid. In the quote above, you posted a part of the study talking about that. Yet it is not in dispute that caprylic acid causes effect #1. We both acknowledge it.
Okay.

This was my intended focus though in demonstrating synergism:

"It is possible that AR and ER augmentation by both E. ulmoides extract and caprylic acid arise from a common tripartite synergism between the steroid receptors, sex steroids and fats, based on a phosphorylation mechanism."​

Phosphorylation rather then binding should have sufficed as the explanatory mechanism in regard to caprylic acid.

Conciliator; said:
Changing the topic doesn't change the fact that you were incorrect about effect #2. ...Can you not just admit you made a mistake?
Now Conciliator you used some harsh language with me such as red herring so by way of explanation...

The following phrase "were mediated by distinct groups of phytocompounds; triterpenoids and short-chain lipids respectively" defined phytocompounds to include short-chain lipids...

This led to this "phytocompounds in the E. ulmoides extract were able to compete with and displace bound 3H-labelled testosterone from the AR ligand binding domain"

Which then led to the following narrowing of terminology "subsequent bioassay-guided purification of the androgenic extract... revealed that this phytoandrogenic activity was being mediated by triterpenoids" ... which demonstrates your point concerning binding.

Obviously at that point (the third quoted line) but not before "short-chain lipids" are excluded, which I obviously missed.

Now there was no bad intent on my part.

The explanatory mechanism of lipid augmentation lies in a synergy that does not involve binding. Yes the distinction is important for accuracy and it would have been better if the authors would had included their notes on pure caprylic acid within the work rather then conveying them in an email which reconfirmed with little elaboration on the synergism because I believe the distinction would have been clear, especially if they segregated the topics instead of interweaving them.

A "magnification of the transactivational response to androgens" by caprylic acid is all that I was concerned about and did not need nor desire to even discuss triterpenoids.

By-the-way Mr. Ong was very excited about the possibility of lipidic augmenters as therapeutic tools.

Thank you Concilator I appreciate you and I always like to interact with bright people who read, read, read until their eyes bleed. :)
 

Conciliator

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The following phrase "were mediated by distinct groups of phytocompounds; triterpenoids and short-chain lipids respectively" defined phytocompounds to include short-chain lipids...

This led to this "phytocompounds in the E. ulmoides extract were able to compete with and displace bound 3H-labelled testosterone from the AR ligand binding domain"

Which then led to the following narrowing of terminology "subsequent bioassay-guided purification of the androgenic extract... revealed that this phytoandrogenic activity was being mediated by triterpenoids" ... which demonstrates your point concerning binding.

Obviously at that point (the third quoted line) but not before "short-chain lipids" are excluded, which I obviously missed.

Now there was no bad intent on my part.
I can see how that could be confusing. They call short-chain lipids "phytocompounds" and then later talk about "phytoandrogens," which could mistaken for the same thing. I don't think you were trying to mislead anyone. It appears to be an honest mistake. Now you just need to update the paper :)
Now Conciliator you used some harsh language with me such as red herring so by way of explanation...
I tend to come on strong, so don't take it as anything personal. While I voiced a few criticisms of the article, don't think that overall I didn't enjoy it. I thought it was very good. I admire your research on other topics like GH. And likewise, I appreciate people with whom I can discuss the nitty-gritty details. Keep up the good work.
 

malcom young

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damn, I'm just here for the easy reading stuff, and I've actually got some graduate classes under my belt
 

iprimate

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Not really, the error is still there and its an egregious error.

It seems you failed to grasp the basic structure of Ong and Tan's results. Consider how many times the two distinct mechanisms of AR activation by Eucommia are mentioned:

(i) Title of paper: "Novel phytoandrogens and lipidic augmenters from Eucommia ulmoides"

(ii) "Here, we report that the tree bark (cortex) of the Gutta-Percha tree Eucommia ulmoides possesses bimodal phytoandrogenic and hormone potentiating effects by lipidic components". (p.1, emphasis mine)

(iii) "(1) a phenomenal tripartite synergism exists between the sex steroid receptors (androgen and estrogen receptors), their cognate steroidal ligands and lipidic augmenters isolated from E. ulmoides, (2) phytoandrogenic activity of E. ulmoides was mediated by plant triterpenoids binding cognately to the androgen receptor (AR) ligand binding domain." (p.1, emphasis mine)

(iv) "the existence of phytoandrogens is reported in this study. Furthermore, a form of tripartite synergism between sex steroid receptors, sex hormones and plant-derived lipids is described for the first time." (p.1, emphasis mine)

(v) "A series of bioassay-guided fractionation showed that the phytoandrogenic and hormone potentiating effects of E. ulmoides were mediated by distinct groups of phytocompounds; triterpenoids and short-chain lipids respectively". (p.2, emphasis mine)

(vi) "Fraction AB with dominant phytoandrogenic activity was subsequently re-chromatographed in C-18 matrix using high performance liquid chromatography (HPLC) to obtain a phytoandrogenic fraction (AB-P1) of even greater purity. AB-P1 fraction was subjected to thin layer chromatography (TLC) and a phytoandrogenic triterpenoid fraction TLC4-5 was recovered for molecular mass measurement using electron spray ionization-mass spectroscopy (ESI-MS)." (p.3) [This concerns triterpenoids as an AR agonist]

(vii) "Subsequent 1H NMR and GC analyses of active fraction CB showed the major presence of the 8-carbon polysaturated fatty acid, caprylic acid, along with other lipids (figure 13 and table 1). Bioassays using pure caprylic acid and other polysaturated fatty acids (PFAs) correlated with the augmenting effect of E. ulmoides on the AR (figure 14) in varying degrees" (p.6) [This concerns the synergising effect of PFA and natural ligand on AR activation.]

(viii) "The novel discoveries reported in this study add phytoandrogens and lipidic augmenters to the emerging list of hormomimetics (such as phytoestrogens) known to exist in plants." (p.7, emphasis mine)

Obviously at that point (the third quoted line) but not before "short-chain lipids" are excluded, which I obviously missed.
Sorry but you missed at least seven slabs of text that either explain or reference the distinction between PFA/ligand synergy and phytoandrogenicity.

In any event, caprylic acid is not a triterpenoid. Triterpenoids have a C30 structure and caprylic acid has a C8 structure. That you could miscategorise caprylic acid as a triterpenoid suggests that you actually don't understand caprylic acid nor any of the triterpenoids.

Further, it is unclear that Eucommia even contains caprylic acid. Takeshi et al (2001) conclude "the main components of the bark are iridoids and lignans" (p. 1058). Don't get excited, caprylic acid is neither an iridoid nor a lignan. Lignans are phytoestrogens. What did Takeshi et al find in Eucommia ?



No Caprylic acid in sight.

Sellers of bulk Eucommia don't sell it as a source of caprylic acid. It either has no caprylic acid (and Ong and Tan botched up and that is a distinct possibility since no-one has replicated their results (Google Scholar turns up 1 article and 2 books, so its a paper of little significance) or the quantities of caprylic acid are negligibly small.

Finally, the article doesn't actually answer whether fascia stretching is the mechanism by which SEOs primarily work.

I'd mark your article a solid E (on the scale A=Excellent, F=Fail). Conflating triterpenoids and PFA is a grave error and the paper doesn't tell me anything about the supposed mechanical mechanism of SEO on fascia besides retelling the anecdotes about Platz and Parrillo.
 
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ironman5151

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Between DatBTrue and Concillator....I feel dumb :food-;mil

Nice read though
 

Big A

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The Science behind Syntherol article has been updated according to the discussion in this thread.
 

Big Danny

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I finally got around to reading this yesterday. BRILLIANT!
 

J4CKT

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Great read, very interesting.
 

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