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Speaking of supplements that won't die....

 

 

Ecdysteroids: A novel class of anabolic agents?
M K Parr 1, F Botrè 2, A Naß 1, J Hengevoss 3, P Diel 3, G Wolber 1
Affiliations expand
PMID: 26060342 PMCID: PMC4447764 DOI: 10.5604/20831862.1144420

Abstract
Increasing numbers of dietary supplements with ecdysteroids are marketed as "natural anabolic agents". Results of recent studies suggested that their anabolic effect is mediated by estrogen receptor (ER) binding. Within this study the anabolic potency of ecdysterone was compared to well characterized anabolic substances. Effects on the fiber sizes of the soleus muscle in rats as well the diameter of C2C12 derived myotubes were used as biological readouts. Ecdysterone exhibited a strong hypertrophic effect on the fiber size of rat soleus muscle that was found even stronger compared to the test compounds metandienone (dianabol), estradienedione (trenbolox), and SARM S 1, all administered in the same dose (5 mg/kg body weight, for 21 days). In C2C12 myotubes ecdysterone (1 µM) induced a significant increase of the diameter comparable to dihydrotestosterone (1 µM) and IGF 1 (1.3 nM). Molecular docking experiments supported the ERβ mediated action of ecdysterone. To clarify its status in sports, ecdysterone should be considered to be included in the class "S1.2 Other Anabolic Agents" of the list of prohibited substances of the World Anti-Doping Agency.

 

Keywords: anabolic effect; beta-ecdysone; doping in sport; ecdysteroids; estrogen receptor beta; muscle hypertrophy.

 

 

FFT

 

 

 

 

Regulatory Toxicology
Published: 23 May 2019
Ecdysteroids as non-conventional anabolic agent: performance enhancement by ecdysterone supplementation in humans
Eduard Isenmann, Gabriella Ambrosio, Jan Felix Joseph, Monica Mazzarino, Xavier de la Torre, Philipp Zimmer, Rymantas Kazlauskas, Catrin Goebel, Francesco Botrè, Patrick Diel & Maria Kristina Parr 
Archives of Toxicology volume 93, pages1807–1816(2019)Cite this article


Recent studies suggest that the anabolic effect of ecdysterone, a naturally occurring steroid hormone claimed to enhance physical performance, is mediated by estrogen receptor (ER) binding. In comparison with the prohibited anabolic agents (e.g., metandienone and others), ecdysterone revealed to be even more effective in a recent study performed in rats. However, scientific studies in humans are very rarely accessible. Thus, our project aimed at investigating the effects of ecdysterone-containing products on human sport exercise. A 10-week intervention study of strength training of young men (n = 46) was carried out. Different doses of ecdysterone-containing supplements have been administered during the study to evaluate the performance-enhancing effect. Analysis of blood and urine samples for ecdysterone and potential biomarkers of performance enhancement has been conducted. To ensure the specificity of the effects measured, a comprehensive screening for prohibited performance-enhancing substances was also carried out. Furthermore, the administered supplement has been tested for the absence of anabolic steroid contaminations prior to administration. Significantly higher increases in muscle mass were observed in those participants that were dosed with ecdysterone. The same hypertrophic effects were also detected in vitro in C2C12 myotubes. Even more relevant with respect to sports performance, significantly more pronounced increases in one-repetition bench press performance were observed. No increase in biomarkers for liver or kidney toxicity was noticed. These data underline the effectivity of an ecdysterone supplementation with respect to sports performance. Our results strongly suggest the inclusion of ecdysterone in the list of prohibited substances and methods in sports in class S1.2 “other anabolic agents”.

 

 

Sam, can you get the FT of this one?

 

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So the experimental group that got  200mg gained 1.5kg  and the group that got 800mg of ecdy/day gained 2kg of lean mass over 10 weeks while placebo group lost 1/2kg.

 

Also saw better increase in squat and bench but difference was not significant.

 

Not too shabby.

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  • 1 month later...
20 hours ago, STENDEC said:

Yes.

 

My sense is that HMB is effective when you are getting insufficient leucine.

 

Which is why I think it seems to work in the lab but not so well in the real world where most users are getting tons of leucine. 

Got it, looking for a decent source of Ecdysterone now.  There are only a few on Amazon.  

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  • 7 months later...

Mol Nutr Food Res. 2014 Sep;58(9):1861-72. doi: 10.1002/mnfr.201300806. Epub 2014 Jun 27.
Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone
Maria Kristina Parr 1, Piwen Zhao, Oliver Haupt, Sandrine Tchoukouegno Ngueu, Jonas Hengevoss, Karl Heinrich Fritzemeier, Marion Piechotta, Nils Schlörer, Peter Muhn, Wen-Ya Zheng, Ming-Yong Xie, Patrick Diel
PMID: 24974955 DOI: 10.1002/mnfr.201300806

 

Abstract
Scope: The phytoectysteroid ecdysterone (Ecdy) was reported to stimulate protein synthesis and enhance physical performance. The aim of this study was to investigate underlying molecular mechanisms particularly the role of ER beta (ERβ).

 

Results: In male rats, Ecdy treatment increased muscle fiber size, serum IGF-1 increased, and corticosteron and 17β-estradiol (E2) decreased. In differentiated C2C12 myoblastoma cells, treatment with Ecdy, dihydrotestosterone, IGF-1 but also E2 results in hypertrophy. Hypertrophy induced by E2 and Ecdy could be antagonized with an antiestrogen but not by an antiandrogen. In HEK293 cells transfected with ER alpha (ERα) or ERβ, Ecdy treatment transactivated a reporter gene. To elucidate the role of ERβ in Ecdy-mediated muscle hypertrophy, C2C12 myotubes were treated with ERα (ALPHA) and ERβ (BETA) selective ligands. Ecdy and BETA treatment but not ALPHA induced hypertrophy. The effect of Ecdy, E2, and BETA could be antagonized by an ERβ-selective antagonist (ANTIBETA). In summary, our results indicate that ERβ is involved in the mediation of the anabolic activity of the Ecdy.

 

Conclusion: These findings provide new therapeutic perspectives for the treatment of muscle injuries, sarcopenia, and cachectic disease, but also imply that such a substance could be abused for doping purposes.

 

Keywords: Dietary supplement; Ecdysterone; Estrogen receptor beta; Skeletal muscle; Traditional Chinese medicine.

 

 

 

Related study, not on ecdy specifically

 

 

FASEB J. 2012 May;26(5):1909-20. doi: 10.1096/fj.11-194779. Epub 2012 Jan 25.
Selective estrogen receptor-β activation stimulates skeletal muscle growth and regeneration
Martina Velders 1, Burkhardt Schleipen, Karl H Fritzemeier, Oliver Zierau, Patrick Diel
Affiliations expand
PMID: 22278942 DOI: 10.1096/fj.11-194779

There is increasing evidence suggesting that estrogens augment skeletal muscle regeneration processes after injury. To study the contribution of estrogen receptors α and β (ERα and ERβ) during muscle regeneration, skeletal muscles of ovariectomized (OVX) rats, as well as ERα- and ERβ-knockout (αErko and βErko) mice, were injured with a myotoxin (notexin). OVX rats were simultaneously treated with the ER-selective ligands genistein, ERα agonist 16α-LE2 (alpha), ERβ agonist 8β-VE2 (beta), or 17β-estradiol (E(2)). OVX rats showed significantly elevated serum creatine kinase (CK) activity after muscle injury compared to intact sham-treated animals. Treatment with ER ligands significantly reduced CK activity. TNF-α, IL-10, and MCP-1 expression served to characterize immune responses. Treatment with all ER ligands, but particularly E(2) and beta, reduced TNF-α, but elevated MCP-1 and IL-10 expression. PCNA and MyoD expression served to define satellite cell activation and proliferation and were found to be up-regulated by beta and E(2). To further study muscle regeneration responses, expression of the embryonic myosin heavy chain (MHC) was analyzed. Beta and E(2) but not alpha increased embryonic MHC expression compared to OVX. The absence of ERβ in βErko mice negatively affected CK activity levels and expression of satellite cell and muscle regeneration markers (MHC embryonic, MyoD, Pax7) compared with αErko and wild-type mice. In a classic Hershberger assay using male rats, beta stimulated muscle growth, accompanied by a strong induction of IGF-1 expression. Our data provide evidence that ERβ signaling is involved in the regulation of skeletal muscle growth and regeneration by stimulating anabolic pathways, activating satellite cells and modulating immune responses.

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There's also a 2006 study that showed no effect in humans and a couple from the late 1980s that I can't find but which were described this way in the 2006 study that contradicted the results.

 

The most often cited scientific study on ecdysterone was published in Scientific Sports Bulletin by Simakin. This study sought to determine the effect of ecdysterone on muscle tissue mass and fat mass, while testing for hormonal changes in the subjects. Seventy-eight highly trained male and female athletes served as subjects in one of three experimental groups: protein, protein and ecdysterone, and placebo. Those consuming just protein, showed only a slight increase in muscle mass for the 10 day period of time, while the placebo group experienced a slight reduction in lean muscle. The addition of ecdysterone in conjunction with protein intake resulted in a 6–7% increase in lean muscle tissue with nearly a 10% reduction in fat. Finally, Gadzhieva and colleagues reported that 3-weeks of Ekdisten, leveton, and Prime Plus (combination of Ekdisten and pure protein) supplementation during training increased skinfold determined muscle mass, decreased fat mass, and increased total work during training. Additionally, Ekdisten and Prime Plus supplementation appeared to promote the greatest gains during training. These studies found that ecdysterone might increase work capacity, decrease fat mass, and increase lean muscle mass.

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