New (-)epicatechin research

[brundel]

Anything to increase absorption? I thought I had seen EGCG potentially increased absorption.

EGCG didnt do much in testing.
I do know something that does though .
Youll see it soon enough. Kasaj and Half are both taking it already.

Really though you dont NEED absorption enhancement. 200mg gave a 250% increase in follistatin. This is much higher than I had thought. Like more than 3x higher than I expected it to be. This study ran extensive bloodwork. It also showed that even long term use is completely safe.

 

[kisaj]

You guys are going to be so happy to try to current product we are testing out. I keep trying to guess what is in it because there are some profound effects and I haven't got it right yet.

 

[Auslifter]

People be saying epi-(-) is bunk all the time, even now with me been off it since i ran 4 bottles i can notice the difference in endurance, that's for sure. the volume of my workouts on it was nuts compared to now have had to cut back my sets quite allot. strength is still the same, accept reps have decreased with the same weight on a fair few of my regular exercises.

 

[brundel]

People be saying epi-(-) is bunk all the time, even now with me been off it since i ran 4 bottles i can notice the difference in endurance, that's for sure. the volume of my workouts on it was nuts compared to now have had to cut back my sets quite allot. strength is still the same, accept reps have decreased with the same weight on a fair few of my regular exercises.

At this point anyone who knows the research knows that (-)-epicatechin elevates follistatin. This is a fact not my opinion.
So people who say it doesnt work are also saying that they believe that follistatin does not work then right?

Fact:
Follistatin significantly lowers myostatin.
Fact:
Reduced myostatin increases anabolic potential.


Fact:
Follidrone/(-)-epicatechin increases follistatin (on average to 250% above normal after 5 days) which in turn reduces myostatin and therefore increases anabolic potential.

"expressing follistatin-288aa (rAAV6:Fst-288) markedly increased muscle mass and force-producing capacity concomitant with increased protein synthesis and mammalian target of rapamycin (mTOR) activation."


another Myostatin inhibitor....the point being reduced myostatin = muscle growth.
"We therefore sought to test the hypothesis that in vivo inhibition of myostatin using an injectable myostatin propeptide (GDF8 propeptide-Fc) would increase both muscle mass and bone density in aged (24 mo) mice. Male mice were injected weekly (20 mg/kg body weight) with recombinant myostatin propeptide-Fc (PRO) or vehicle (VEH; saline) for four weeks. There was no difference in body weight between the two groups at the end of the treatment period, but PRO treatment significantly increased mass of the tibialis anterior muscle (+ 7%) and increased muscle fiber diameter of the extensor digitorum longus (+ 16%) and soleus (+ 6%) muscles compared to VEH treatment

Youll notice that muscle size increased while weight stayed stagnant. This is why weight is not a solid indicator if Follidrone is working or not.
As I have stated multiple times....it appears that there is a concurrent increase in metabolism which tends to decrease bodyfat levels. THere are studies showing a significant increase in fat burning with epicatechin. So, you MUST eat alot during Follidrone cycles if you want to increase weight and really get everything you can out of it.


REF:
http://jcb.rupress.org/content/197/7/997.full
http://www.ncbi.nlm.nih.gov/pubmed/23832079

 

[GreenMachineX]

Awesome stuff.

 

[NoAddedHmones]

One of the new anabolics, a mixed product that includes (-)-epicatechin and 2 other anabolic ingredients will be ready I think in about a month.

Do you have access to the full text of the abstract i posted?

 

[GreenMachineX]

One of the new anabolics, a mixed product that includes (-)-epicatechin and 2 other anabolic ingredients will be ready I think in about a month.

Are both the other ingredients novel?

 

[brundel]

Do you have access to the full text of the abstract i posted?

Maybe, let me look when I get to my work or home comp.

 

[brundel]

Are both the other ingredients novel?

Yes sir.
Very interesting stuff.

 

[NoAddedHmones]

Maybe, let me look when I get to my work or home comp.

 

[kissdadookie]

This new study is very promising. The only possible concern is with half-life as going by the new human in vivo data, it's best to keep the (-)epi circulating in ones system. Perhaps more frequent dosing for best results?

The endurance benefits could possibly be due to increase in nitric oxide.

mod edit: read the rules. last warning.

 

[TeamTGB]

Lets use a scenario of someone going to run a cycle and many claim there is a rise in myostatin around the 8 week mark, would utilizing follidrone give a good benefit to your cycle?

 

[brundel]

Lets use a scenario of someone going to run a cycle and many claim there is a rise in myostatin around the 8 week mark, would utilizing follidrone give a good benefit to your cycle?

Absolutely! This is one of the best times for a non natty user to take Follidrone. In fact i have several friends, including an ifbb pro that uses Follidrone as a tool toward the end of their cycles specifically because it makes a huge difference.

 

[Afi140]

If this study helped sway any skeptics we have 10% off right now! Link is itt with discount code.

http://anabolicminds.com/forum/supplement-deals/264619-blr-supplement-sale.html

 

[kissdadookie]

Have 4 bottles of a (-)epi product arriving today. Going to see how it goes. Going to do split dosing, 100/100.

Btw, for folks that haven't looked at the study carefully enough or was kind of confused as to what dosing caused the results at the end of the 5 days, that was 50 mg of (-)epi 2 x's per day for 5 days. Someone had to clarify that for me as I wasn't sure either at first.

 

[NoAddedHmones]

Have 4 bottles of a (-)epi product arriving today. Going to see how it goes. Going to do split dosing, 100/100. Btw, for folks that haven't looked at the study carefully enough or was kind of confused as to what dosing caused the results at the end of the 5 days, that was 50 mg of (-)epi 2 x's per day for 5 days. Someone had to clarify that for me as I wasn't sure either at first.

What dose you going with ED?

 

[kissdadookie]

What dose you going with ED?

100 mg twice a day. So basically like in the study except each dose is double the studied BID dose. I'm thinking 6 hours apart. First dose first thing in the morning preworkout.

6 hours apart because it supposedly peaks at around 1.5-2 hours then drops off. So in 6 hours, I would think that it would be a good time to dose again to get another spike going whilst your follistatin is still elevated but the compound has mostly left your body from the first dose.

 

[NoAddedHmones]

100 mg twice a day. So basically like in the study except each dose is double the studied BID dose. I'm thinking 6 hours apart. First dose first thing in the morning preworkout. 6 hours apart because it supposedly peaks at around 1.5-2 hours then drops off. So in 6 hours, I would think that it would be a good time to dose again to get another spike going whilst your follistatin is still elevated but the compound has mostly left your body from the first dose.

Okay. Will be interesting to see the effects it has on you at that dose.

 

[kissdadookie]

Okay. Will be interesting to see the effects it has on you at that dose.

I still don't exactly have all that high hopes for it ATM, but hey, I'm willing to give most things a try. LoL. I'm already 4 bottles deep out of pocket on this experiment.

 

[Auslifter]

I still don't exactly have all that high hopes for it ATM, but hey, I'm willing to give most things a try. LoL. I'm already 4 bottles deep out of pocket on this experiment.

i experimented with 4 bottles of folli at a higher dose pwo did 3 caps ED 5x a week all pre workout had amazing results. I did 100mg epi-(-) from Myo solo and didn't get much at all. then also double dosed Myo, when it was first released since i got a good deal on it, 1 serve in the morning and pre and had very good resluts again with endurance and strength. I think it's simply dose related but interested to see how you go also

 

[kissdadookie]

i experimented with 4 bottles of folli at a higher dose pwo did 3 caps ED 5x a week all pre workout had amazing results. I did 100mg epi-(-) from Myo solo and didn't get much at all. then also double dosed Myo, when it was first released since i got a good deal on it, 1 serve in the morning and pre and had very good resluts again with endurance and strength. I think it's simply dose related but interested to see how you go also

From the abstract of the study (wish I had the full study to go through, but I'm not THAT deep into it that I want to buy access to it), if you're just going by effects of a single bolus dose, yes, the higher the dose the more acute the effect. If you looked at the trend from use over a period of time, there appears to be two things going on.

1) There is a "build up" effect over time even if it's 50 mg once a day (maybe the body becomes more sensitive to it? it's probably not some sort of saturation effect or else that wouldn't explain why several hours post last dose, follistatin levels drops back down dramatically, or maybe it is, I don't know)

and

2) There is also an effect correlating to how long you have the compound in your system for (thus a few hours after the last dose, follistatin levels drop dramatically and likely if you gave it ~12 hours or perhaps less post last dose, you're likely going to be back at baseline again) thus a multiple times a day dosing I would think would be ideal.

 

[Auslifter]

From the abstract of the study (wish I had the full study to go through, but I'm not THAT deep into it that I want to buy access to it), if you're just going by effects of a single bolus dose, yes, the higher the dose the more acute the effect. If you looked at the trend from use over a period of time, there appears to be two things going on.

1) There is a "build up" effect over time even if it's 50 mg once a day (maybe the body becomes more sensitive to it? it's probably not some sort of saturation effect or else that wouldn't explain why several hours post last dose, follistatin levels drops back down dramatically, or maybe it is, I don't know)

and

2) There is also an effect correlating to how long you have the compound in your system for (thus a few hours after the last dose, follistatin levels drop dramatically and likely if you gave it ~12 hours or perhaps less post last dose, you're likely going to be back at baseline again) thus a multiple times a day dosing I would think would be ideal.

another thing to note, dosing to close to food i found it messed with absorption, on days i didn't leave at least 2-2.5 hours after eating my pwo meal if i took it 1 hour after effects were nothing close to what they were when i dosed on an empty stomach. and as for the build up effect, i can see what you mean since there were weeks i didn't have that insane endurance and ability to perform huge amounts of volume compared to previous weeks then a week later it comes back again and your able to go nuts again

 

[kisaj]

//http://anabolicminds.com/forum/supplement-science/264728-ever-wonder-whats.html#post4839469

A new member decided to test out the purity of Follidrone and found what has always been said about the quality being put out.

 

[kissdadookie]

//http://anabolicminds.com/forum/supplement-science/264728-ever-wonder-whats.html#post4839469

A new member decided to test out the purity of Follidrone and found what has always been said about the quality being put out.

Who the heck ever really questioned the purity of the (-)epi. We just want to know how much actual (-)epi is in a full serving of Follidrone. At this point I think you guys should disclose that information now. I don't see how that would signal other companies to copy your dosage, because we already have competing (-)epi products which we know the amount of (-)epi per full serving, with the newest one having been disclosed as being 100 mg per cap, 2 caps being the full serving size.

 

[kisaj]

I have no idea what you are so riled up about. Settle down. If Brundel wants to disclose, he can.

...but, since you are already pissy, this has always been a question surrounding (-)epi as people report some work better than others.

 

[kissdadookie]

I have no idea what you are so riled up about. Settle down. If Brundel wants to disclose, he can.

Not riled up. Just pointing out the obvious there. For as long as I can remember since Follidrone first came out, people more or less just wanted to know how much actual (-)epi was in each full serving. At first it was understandable that Brundel didn't want to disclose the information, as there were no competing (-)epi products on the market really at the time. Now we have plenty. We have Olympus Lab's claiming to have what appears to be 300 mg? Then we have the newest one that came out supposedly having 200 mg. So I don't see why anybody would try to "steal" your dosage because I would think that OL's claimed 300 mg is probably the highest we're going to get.

So not trying to "attack" you or anything like that or "attack" Brundel/BLR, I'm just being blunt here, there's not much he's protecting by withholding the amount per full serving because we already have products that have disclosed amounts per full serving that is very high dosed at this point.

While I have you here, new SERM-like product for BLR, according to Brundel, he's been testing it on people for ~2 years, any bloodwork for any of those people whom he had been testing it on? Not trying to poo poo the product, it's just something myself and likely many others are curious about because that is a big deal when deciding if we want to use an OTC PCT or stick with tried and true RC/pharma.

 

[kisaj]

If that is really your argument, then don't start it with comments dismissing purity as that is the topic almost every (-)epi discussion surrounded when it was released and still is brought up. Again, if Brundel decides to release any mg information, that is his choice- not mine.

 

[NoAddedHmones]

If that is really your argument, then don't start it with comments dismissing purity as that is the topic almost every (-)epi discussion surrounded when it was released and still is brought up. Again, if Brundel decides to release any mg information, that is his choice- not mine.

Who was the main culprit who repeatedly raised it in a fear mongering market tactic?

 

[kissdadookie]

If that is really your argument, then don't start it with comments dismissing purity as that is the topic almost every (-)epi discussion surrounded when it was released and still is brought up. Again, if Brundel decides to release any mg information, that is his choice- not mine.

There's FAR more questions going WAY back which questioned the AMOUNT of (-)epi not the PURITY of the (-)epi. I started my post the way I started to point out what most people were REALLY wondering about, how much (-)epi was in the product. I think you may be confusing efficacy based on dose to actual quality/purity concerns. Remember, the whole online contention with the product using rice flour was based on people not know how much actual (-)epi was in there, not the purity of the (-)epi in the product. Two different things.

 

[digitalducki]

BSL? u mean BLR?

 

[kissdadookie]

BSL? u mean BLR?

Thanks. Fixed

 

[kissdadookie]

I did notice this morning whilst doing conditioning work, that I inflated a bit quicker than I usually do. Could be a total coincidence or it could be the (-)epi. Less gassed as well.

 

[kissdadookie]

Anybody notice BP changes from it? I felt there was something different with my BP yesterday and today, so I did some cuff readings. It's down a few points. Could be coincidence and not a huge change in readings but obvious changes. Will keep an eye on it.

 

[TheConMan]

There are many research and studies that link follistatin increase with cancer growth and metastasis.

Unfortunately I'm not allowed to post links to the research papers, but you can google "follistatin cancer" and
see for yourselves.

Most cancer victims don't realize they have the disease untill it has
progressed significantly in their body. Basically they are unaware of
the disease lingering in their system until it activates a few years
down the road.

Therefor supplementing with significant epicatechin doses, wich raise
follistatin concentration, is like playing russian roulette with your life.

-TheConMan

 

[wolfpack893]

Hmmm, this is interesting considering you just joined the forum yesterday and this is your first post...smh go to another forum to troll

 

[brundel]

Abstract

Follistatin is essential for skeletal muscle development and growth, but the intracellular signaling networks that regulate follistatin-mediated effects are not well defined. We show here that the administration of an adeno-associated viral vector expressing follistatin-288aa (rAAV6:Fst-288) markedly increased muscle mass and force-producing capacity concomitant with increased protein synthesis and mammalian target of rapamycin (mTOR) activation. These effects were attenuated by inhibition of mTOR or deletion of S6K1/2. Furthermore, we identify Smad3 as the critical intracellular link that mediates the effects of follistatin on mTOR signaling. Expression of constitutively active Smad3 not only markedly prevented skeletal muscle growth induced by follistatin but also potently suppressed follistatin-induced Akt/mTOR/S6K signaling. Importantly, the regulation of Smad3- and mTOR-dependent events by follistatin occurred independently of overexpression or knockout of myostatin, a key repressor of muscle development that can regulate Smad3 and mTOR signaling and that is itself inhibited by follistatin. These findings identify a critical role of Smad3/Akt/mTOR/S6K/S6RP signaling in follistatin-mediated muscle growth that operates independently of myostatin-driven mechanisms.


We know that reduced myostatin can lead to increased muscle growth potential but follistatin also increases muscle mass independently through different pathways.

 

[TheConMan]

Hmmm, this is interesting considering you just joined the forum yesterday and this is your first post...smh go to another forum to troll

mod edit: nope

 

[TheConMan]

Abstract

Follistatin is essential for skeletal muscle development and growth, but the intracellular signaling networks that regulate follistatin-mediated effects are not well defined. We show here that the administration of an adeno-associated viral vector expressing follistatin-288aa (rAAV6:Fst-288) markedly increased muscle mass and force-producing capacity concomitant with increased protein synthesis and mammalian target of rapamycin (mTOR) activation. These effects were attenuated by inhibition of mTOR or deletion of S6K1/2. Furthermore, we identify Smad3 as the critical intracellular link that mediates the effects of follistatin on mTOR signaling. Expression of constitutively active Smad3 not only markedly prevented skeletal muscle growth induced by follistatin but also potently suppressed follistatin-induced Akt/mTOR/S6K signaling. Importantly, the regulation of Smad3- and mTOR-dependent events by follistatin occurred independently of overexpression or knockout of myostatin, a key repressor of muscle development that can regulate Smad3 and mTOR signaling and that is itself inhibited by follistatin. These findings identify a critical role of Smad3/Akt/mTOR/S6K/S6RP signaling in follistatin-mediated muscle growth that operates independently of myostatin-driven mechanisms.


We know that reduced myostatin can lead to increased muscle growth potential but follistatin also increases muscle mass independently through different pathways.

No one doubts the effectiveness of follistatin increase. What concerns people is that it causes angiogenesis wich causes tumor progression and metastasis.

 

[Jiigzz]

No one doubts the effectiveness of follistatin increase. What concerns people is that it causes angiogenesis wich causes tumor progression and metastasis.

Actovation of mTOR (the anabolic protein) can accelerate tumour growth as well. Drinking a protein shake can activate mTOR.

At the end of the day, alot of things that promote growth in normal cells ABSOLUTELY has the potential to cause growth in cancerous cells but to avoid them is like not driving a car in the off chance you might crash.

 

[TheConMan]

Actovation of mTOR (the anabolic protein) can accelerate tumour growth as well. Drinking a protein shake can activate mTOR.

At the end of the day, alot of things that promote growth in normal cells ABSOLUTELY has the potential to cause growth in cancerous cells but to avoid them is like not driving a car in the off chance you might crash.

LOL apples vs oranges. The degree of impact on mTOR activation by a protein shake is not slightly comparable to the effects of plasma follistatin increase.

 

[Jiigzz]

LOL apples vs oranges. The degree of impact on mTOR activation by a protein shake is not slightly comparable to the effects of plasma follistatin increase.

Maybe you should research epi and cancer. Seems almost the opposite to what you are saying. Agreeably I havent looked at the research but you can search mtor and cancer and find equally alarming studies.

 

[kisaj]

You can find anything you want to support any argument. It's the beauty of the Internet.

 

[TheConMan]

You can find anything you want to support any argument. It's the beauty of the Internet.

Nice attempt to deflect my point... try harder. I wouldn't call unbiased medical research papers as "ANYTHING" (as you call it). Ultimately these are what make this industry to progress. I have nothing against the company you represent. Quite frankly I think epicatechin supplement (like Folli) is a breakthrough, BUT it comes with a big price (your health) and it's of people's best interest to be informed about it.

 

[Jiigzz]

You can find anything you want to support any argument. It's the beauty of the Internet.

The important thing is how appliciable what he is saying is to the studies he has found.

I see over expression of follistatin being repeatably mentioned, but over expression is different to supplemental use - I.e. faulty feedback mechanisms for a prolonged period perhaps (years? Months? Decades? Idk). But I doubt a 8-12 week run will cause what is being said.

A lot of important factors are being missed. We are talking supplemental cacethins lol

 

[TheConMan]

Maybe you should research epi and cancer. Seems almost the opposite to what you are saying. Agreeably I havent looked at the research but you can search mtor and cancer and find equally alarming studies.

It is dose dependent. Epicatechins have benefits, but at high doses as the ones contained in supplements of this kind have more cons than pros. Unless you don't care to possibly get cancer for just a couple of extra pounds of muscles.

 

[kisaj]

Nice attempt to deflect my point... try harder. I wouldn't call unbiased medical research papers as "ANYTHING" (as you call it). Ultimately these are what make this industry to progress. I have nothing against the company you represent. Quite frankly I think epicatechin supplement (like Folli) is a breakthrough, BUT it comes with a big price (your health) and it's of people's best interest to be informed about it.

Relax, it was a general comment towards any argument someone wants to have. Did you really join here to get defensive right off the bat?

 

[Volvo140G]

Big pimpin spendin cheeeeeez

 

[Jiigzz]

It is dose dependent. Epicatechins have benefits, but at high doses as the ones contained in supplements of this kind have more cons than pros. Unless you don't care to possibly get cancer for just a couple of extra pounds of muscles.

Can you provide the evidence that supplemental epicatethins can cause cancer? Or the dose response relationship between follistatin and cancer? The duration in which follistatin must be increased and the percentage in which it must be increased, whether there are faulty feedback mechanisms contributing to the effect, how the follistatin was induced (injection or was it just a measure of levels) and whether you can correlate epicatethin to cancer (a natural increased versus one by faulty machinery)

I'll liken this argument to another I repeatedly hear - We at SNS sell supplemental Arachidonic Acid which has evidence showing it can lead to systemic inflammation in the body - this evidence is a primary reason why people will not take it (who are informed on such matters), however what the argument fails to consider is the population in which Arachidonic Acid is more harmful than beneficial. Arachidonic acid supplementation is ONLY harmful when lipid perioxidsation products are also mixed - which are not included In supplemental capsules.

Studies done for up to 50 days (our recommended safety limit) show supplemental ARA at <2g HAS ZERO effect on pro-inflammatory markers and several showing reduction in IL-6 (which means a REDUCTION in pro inflammation).

And further A meta-analysis by Cambridge University looking for associations between heart disease risk and individual fatty acids reported a significantly reduced risk of heart disease with supplemental ARA and EPA DHA.

But yet we are repeatedly told to limit it. Why? Because the typical American diet is so pro-inflammatory that people correlate ARA (given its nature) to the effects rather than their diet as a whole. Limiting processed foods and other things can reduce perioxidation of lipids.

In short, finding a study that shows and effect MUST be related to the population we are a part of (using supplemental epi for example). In soft sciences, you can not just find an end product of something and then attribute it to EVERYTHING that raises that variable.

 

[TheConMan]

Can you provide the evidence that supplemental epicatethins can cause cancer? Or the dose response relationship between follistatin and cancer? The duration in which follistatin must be increased and the percentage in which it must be increased, whether there are faulty feedback mechanisms contributing to the effect, how the follistatin was induced (injection or was it just a measure of levels) and whether you can correlate epicatethin to cancer (a natural increased versus one by faulty machinery)

I'll liken this argument to another I repeatedly hear - We at SNS sell supplemental Arachidonic Acid which has evidence showing it can lead to systemic inflammation in the body - this evidence is a primary reason why people will not take it (who are informed on such matters), however what the argument fails to consider is the population in which Arachidonic Acid is more harmful than beneficial. Arachidonic acid supplementation is ONLY harmful when lipid perioxidsation products are also mixed - which are not included In supplemental capsules.

Studies done for up to 50 days (our recommended safety limit) show supplemental ARA at <2g HAS ZERO effect on pro-inflammatory markers and several showing reduction in IL-6 (which means a REDUCTION in pro inflammation).

And further A meta-analysis by Cambridge University looking for associations between heart disease risk and individual fatty acids reported a significantly reduced risk of heart disease with supplemental ARA and EPA DHA.

But yet we are repeatedly told to limit it. Why? Because the typical American diet is so pro-inflammatory that people correlate ARA (given its nature) to the effects rather than their diet as a whole. Limiting processed foods and other things can reduce perioxidation of lipids.

In short, finding a study that shows and effect MUST be related to the population we are a part of (using supplemental epi for example). In soft sciences, you can not just find an end product of something and then attribute it to EVERYTHING that raises that variable.

I'd provide you with some of the evidence you inquired, however I'm not allowed to post links on this forum as of yet. Thus you need to look it up on pubmed and google scholar documents. As you mentioned there are some faulty or unknown mechanism taking place because the reasearch on this subject is fairly new and elaborated. But there are quite a few studies showing the relation between (-)epi, follistatin increase, angiogenesis and tumor progression.

BTW I appreciate you clarifying the subject on aRa, wich in many cases has been linked to the production of the dangerous enzyme called 5-lipoxygenase and the stimulation of prostate cancer cells proliferation.

 

[Jiigzz]

I'd provide you with some of the evidence you inquired, however I'm not allowed to post links on this forum as of yet. Thus you need to look it up on pubmed and google scholar documents. As you mentioned there are some faulty or unknown mechanism taking place because the reasearch on this subject is fairly new and elaborated. But there are quite a few studies showing the relation between (-)epi, follistatin increase, angiogenesis and tumor progression.

BTW I appreciate you clarifying the subject on aRa, wich in many cases has been linked to the production of the dangerous enzyme called 5-lipoxygenase and the stimulation of prostate cancer cells proliferation.

Awesome man, you can provide the links and just leave a few spaces in the URL and i'll look for myself. FWIW I'm not saying there ISNT a link, I just try point out the dangers in seeing the end product (follistatin being increased) when the intervention (supplementation) may not have the same effect. There are usually confounders which must be considered.

As ARA is our own product, I have done plenty of research on it so it seemed like the most valid comparison.