Saw this posted on another forum. There are some sulfurophane supps out there but according to my research they are innefective see heregenetics. 2012 Dec 1;7(12):1379-90. doi: 10.4161/epi.22609. Epub 2012 Oct 23.Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells.
Fan H, Zhang R, Tesfaye D, Tholen E, Looft C, Hölker M, Schellander K, Cinar MU.
Institute of Animal Science; Animal Breeding and Husbandry Group; University of Bonn; Bonn, Germany.
Satellite cells function as skeletal muscle stem cells to support postnatal muscle growth and regeneration following injury or disease. There is great promise for the improvement of muscle performance in livestock and for the therapy of muscle pathologies in humans by the targeting of myostatin (MSTN) in this cell population. Human diet contains many histone deacetylase (HDAC) inhibitors, such as the bioactive component sulforaphane (SFN), whose epigenetic effects on MSTN gene in satellite cells are unknown. Therefore, we aimed to investigate the epigenetic influences of SFN on the MSTN gene in satellite cells. The present work provides the first evidence, which is distinct from the effects of trichostatin A (TSA), that SFN supplementation in vitro not only acts as a HDAC inhibitor but also as a DNA methyltransferase (DNMT) inhibitor in porcine satellite cells. Compared with TSA and 5-aza-2'-deoxycytidine (5-aza-dC), SFN treatment significantly represses MSTN expression, accompanied by strongly attenuated expression of negative feedback inhibitors of the MSTN signaling pathway. miRNAs targeting MSTN are not implicated in posttranscriptional regulation of MSTN. Nevertheless, a weakly enriched myoblast determination (MyoD) protein associated with diminished histone acetylation in the MyoD binding site located in the MSTN promoter region may contribute to the transcriptional repression of MSTN by SFN. These findings reveal a new mode of epigenetic repression of MSTN by the bioactive compound SFN. This novel pharmacological, biological activity of SFN in satellite cells may thus allow for the development of novel approaches to weaken the MSTN signaling pathway, both for therapies of human skeletal muscle disorders and for livestock production improvement.
PMID: 23092945 [PubMed - in process] PMCID: PMC3528693 [Available on 2013/12/1]
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LinkOut - more resourcesSo cannot use supplemental forms because they won't work.Sulforaphane works as a potent catalyst to boost Phase 2 enzymes in the body. These detoxification enzymes trigger ongoing antioxidant action for at least 72 hours. As a result, the indirect antioxidant activity of sulforaphane lasts significantly longer than that of direct antioxidants, such as vitamins C, E and beta carotene, although it also boosts the regeneration of the active forms of these vitamins. Furthermore, three-day-old sprouts have a much higher concentration of glucoraphanin than the average mature broccoli (73 mg v. 11 mg per serving, respectively), which means one ounce of broccoli sprouts contains as much glucoraphanin as over 1.25 pounds (20 ounces) of average market-stage broccoli. However, the range of glucoraphanin varies considerably with the variety of broccoli grown, so that in market broccoli, there is at least a 15-fold range of glucoraphanin (Brown et al., J.Am. Hort. Soc. 2002). The highest concentration of glucoraphanin is found in the seed. Eating the raw, unsprouted seed could provide high amounts of sulforaphane, but seeds also contain the antimetabolite erucic acid, which is metabolized during sprouting, so eating seeds is not recommended.
Prepared extracts of either broccoli seeds or broccoli sprouts typically lose their myrosinase activity. As a result, the content of glucoraphanin may remain, but without the presence of the myrosinase, the ability to convert the bioactive sulforaphane has been lost. Based on some limited evidence from animal studies, the colonic microflora may have some myrosinase-like activity. One study suggests this may provide no more than 8% conversion. A human study showed there is such large interindividual variability in the population of colonic microflora in humans, such that any conversion to sulforaphane is not only limited, but also unpredictable. Other researchers have similarly found there is limited sulforaphane bioavailability in broccoli sprouts preparations in which the myrosinase has been destroyed.
My research revealed that sulfurophane which is found in broccoli and broccoli sprouts has a host of health
benefits outside the myostatin inhibition. It is found in Broccoli sprouts at up to 50x the amount in the same weight of broccoli. Broccoli Sprouts cost 4 bucks for 4 ounces at the local heath food store so... screw that... I've started growing my own to get it in its effective form. There is approximately 2 mg of Sulurophane in a pound of broccoli, (once its constituents are activated by chewing) which means there would be 40-100 mg's in a pound of sprouts.
My question is, how many pounds of sprouts would I need to eat to consume enough sulfurophane to test the theory of Myostatin inhibition? i.e. more muscle growth