Evolutionary Muse Presents: BMP

And, of course, why the selectivity of BMP activation (and downstream SMAD activation) is critical....

Invalid Link Removed 2009 Jun;296(6):C1248-57. doi: 10.1152/ajpcell.00104.2009. Epub 2009 Apr 8.
[h=1]Smad2 and 3 transcription factors control muscle mass in adulthood.[/h]Invalid Link Removed[SUP]1[/SUP], Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
[h=3]Invalid Link Removed[/h]
[h=3]Abstract[/h]Loss of muscle mass occurs in a variety of diseases, including cancer, chronic heart failure, aquired immunodeficiency syndrome, diabetes, and renal failure, often aggravating pathological progression. Preventing muscle wasting by promoting muscle growth has been proposed as a possible therapeutic approach. Myostatin is an important negative modulator of muscle growth during myogenesis, and myostatin inhibitors are attractive drug targets. However, the role of the myostatin pathway in adulthood and the transcription factors involved in the signaling are unclear. Moreover, recent results confirm that other transforming growth factor-beta (TGF-beta) members control muscle mass. Using genetic tools, we perturbed this pathway in adult myofibers, in vivo, to characterize the downstream targets and their ability to control muscle mass. Smad2 and Smad3 are the transcription factors downstream of myostatin/TGF-beta and induce an atrophy program that is muscle RING-finger protein 1 (MuRF1) independent. Furthermore, Smad2/3 inhibition promotes muscle hypertrophy independent of satellite cells but partially dependent of mammalian target of rapamycin (mTOR) signaling. Thus myostatin and Akt pathways cross-talk at different levels. These findings point to myostatin inhibitors as good drugs to promote muscle growth during rehabilitation, especially when they are combined with IGF-1-Akt activators.
 
dsade said:
And, of course, why the selectivity of BMP activation (and downstream SMAD activation) is critical.... Invalid Link Removed 2009 Jun;296(6):C1248-57. doi: 10.1152/ajpcell.00104.2009. Epub 2009 Apr 8. [h=1]Smad2 and 3 transcription factors control muscle mass in adulthood.[/h]Invalid Link Removed[SUP]1[/SUP], Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed. [h=3]Invalid Link Removed[/h] [h=3]Abstract[/h]Loss of muscle mass occurs in a variety of diseases, including cancer, chronic heart failure, aquired immunodeficiency syndrome, diabetes, and renal failure, often aggravating pathological progression. Preventing muscle wasting by promoting muscle growth has been proposed as a possible therapeutic approach. Myostatin is an important negative modulator of muscle growth during myogenesis, and myostatin inhibitors are attractive drug targets. However, the role of the myostatin pathway in adulthood and the transcription factors involved in the signaling are unclear. Moreover, recent results confirm that other transforming growth factor-beta (TGF-beta) members control muscle mass. Using genetic tools, we perturbed this pathway in adult myofibers, in vivo, to characterize the downstream targets and their ability to control muscle mass. Smad2 and Smad3 are the transcription factors downstream of myostatin/TGF-beta and induce an atrophy program that is muscle RING-finger protein 1 (MuRF1) independent. Furthermore, Smad2/3 inhibition promotes muscle hypertrophy independent of satellite cells but partially dependent of mammalian target of rapamycin (mTOR) signaling. Thus myostatin and Akt pathways cross-talk at different levels. These findings point to myostatin inhibitors as good drugs to promote muscle growth during rehabilitation, especially when they are combined with IGF-1-Akt activators.
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this resembles a post you made about HUNG... Is hung BMP?
 
dsade said:
Not at this time....there are still very valid concerns of mine with oversuppression of MyoStatin and blowback. The body has developed all pathways because they serve a function, and throwing it out of whack too dramatically tends to lead to unforseen problems.

I'm still of the opinion that a shifting of the balance towards protein synthesis is the way to go.
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Interesting, so do you think going over 200mg of Epi-(-) will have over supperssion of it? which may lead to diminishing returns? I felt the double dose of myo worked well, but once i tried 3 serves for a week with not much difference at all


also exited to read about bmp
 
Jackedjack said:
this resembles a post you made about HUNG... Is hung BMP?
Click to expand...

Hey....this is about BMP...but if you think they might be related I would have to say you are on the right track. Very observant.
 
dsade said:
Hey....this is about BMP...but if you think they might be related I would have to say you are on the right track. Very observant.
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Evomuse is probably the most innovative company I can think of. I cannot wait until all of these upcoming products are released. But for the myostatin issue, there are humans with a deficiency and they seem relatively fine, so what is the main concern with too much prolonged down-regulation of myostatin? Does it have effect with muscle growth on organs i.e the heart?
 
Jackedjack said:
Evomuse is probably the most innovative company I can think of. I cannot wait until all of these upcoming products are released. But for the myostatin issue, there are humans with a deficiency and they seem relatively fine, so what is the main concern with too much prolonged down-regulation of myostatin?
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For one:

Invalid Link Removed 2009 Aug;27(4):247-54. doi: 10.1080/08977190903052539.
[h=1]Myostatin in tendon maintenance and repair.[/h]Invalid Link Removed[SUP]1[/SUP], Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
[h=3]Invalid Link Removed[/h]
[h=3]Abstract[/h]Myostatin, a negative regulator of muscle growth, has recently been found to be expressed in tendons. Myostatin-deficient mice have weak and brittle tendons, which suggest that myostatin could be important for tendon maintenance. Follistatin expression in the callus tissue after tendon transection is influenced by loading. We found that follistatin antagonises myostatin, but not GDF-5 or OP-1 in vitro. To study if myostatin might play a physiological role in soft tissue, we transected 64 rat Achilles tendons and studied the gene expression for myostatin and its receptors at four different time-points during healing. Intact tendons were also studied. All samples were studied with or without mechanical loading. Unloading was achieved with botulinum toxin injections in the calf muscles. The expression of the myostatin gene was more than 40 times higher in intact tendons than in the callus tissue during tendon healing. The expression of myostatin was also influenced by loading status in both intact and healing tendons. Thereafter, we measured the mechanical properties of healing tendons after local myostatin administration. This treatment increased the volume and the contraction of the callus after 8 days, but did not improve its strength. Our results indicate that myostatin plays a positive role in tendon maintenance and that exogenous protein administration stimulates proliferation and growth of early repair tissue. However, no effect on further development towards connective tissue formation was found.


PMID:19591015 [PubMed - indexed for MEDLINE]
 
I did know about the tendon issue, but never saw it as a concern in humans as human tendons are stronger than mice in Vito. Does epi compare to legit follistatin when it comes to myostatin suppression? I doubt it does, but how close does it come to follistatin. Also do you have any medical articles on clinical experiments of myostatin suppression in humans?
 
Jackedjack said:
I did know about the tendon issue, but never saw it as a concern in humans as human tendons are stronger than mice in Vito. Does epi compare to legit follistatin when it comes to myostatin suppression? I doubt it does, but how close does it come to follistatin. Also do you have any medical articles on clinical experiments of myostatin suppression in humans?
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I'm not sure that anyone has gotten that deep into the research, but I am definitely keeping my ears open. Let me know if you run across anything.
 
Invalid Link Removed
This is not a study on myostatin reduction in humans, but a study done to see if lowered myostatin, does induce muscle hypertrophy. It seems there results are not what we would expect, I will read and find out the reason.
 
Jackedjack said:
Invalid Link Removed
This is not a study on myostatin reduction in humans, but a study done to see if lowered myostatin, does induce muscle hypertrophy. It seems there results are not what we would expect, I will read and find out the reason.
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My god, the formatting!

Damn, my head hurts already.
 
Jackedjack said:
So far, what I have taken from little research and this thread, this product intends to use the many protein factors such as BMP 2/7 to manipulate the rate of protein synthesis along with much more. This is all based around the idea that the bones in our body are the ultimate endocrine organ. This is only one part of it, if you can manipulate these BMP's you can now manipulate many more BMP's for whatever you need to use them for I.e changing fat cells into brown adipose cells to fight obesity. This is only one part of the product though, there seem to be many more parts In motion making research important if you want to understand this.
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Oh wow ok that seems really cool. I'll have to do some of my own research on this. Thank you for the explanation
 
dsade said:
I'll be finalizing Seethe this week, but I'm going to release the full retail of Virile Mane, with the new ingredients, first to generate revenue.

So, to let you guys into the schedule, we're looking at:

Another run of BRITE
Retail Virile Mane
Slintensity
BMP
Demolish
SEETHE
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nice to see the schedule, i'm guessing hung is still a long way off if it didn't make it in.
Have you thought about possibly doing a sticked thread of the schedule where you can edit the first post to update as it progresses? With so many things in the works it sure would make it easier for us to keep up to date with how far away all the cool new stuff is
Also, are you still thinking of doing another run of glycomyx?
 
dsade said:
I'll be finalizing Seethe this week, but I'm going to release the full retail of Virile Mane, with the new ingredients, first to generate revenue.

So, to let you guys into the schedule, we're looking at:

Another run of BRITE
Retail Virile Mane
Slintensity
BMP
Demolish
SEETHE
Click to expand...


This is going to put me in the poor house. But at least i'll be happy!
 
jmr79x said:
This is going to put me in the poor house. But at least i'll be happy!
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lol this, EvoMuse is ruining my resolution of spending less on supplements!!
 
BMPs are really a fascinating area of study, including interactions with IGF-1, mTOR, PI3K, etc. All of these signalling cascades affect protein turnover, or establish a balance between MPS and protein degradation.
 
dsade said:
I'll be finalizing Seethe this week, but I'm going to release the full retail of Virile Mane, with the new ingredients, first to generate revenue.

So, to let you guys into the schedule, we're looking at:

Another run of BRITE
Retail Virile Mane
Slintensity
BMP
Demolish
SEETHE
Click to expand...


No mention of HEAT or Leptigen Rebirth. I take it these are much further out than the others above?
 
How in the world have I missed this thread? Very interesting stuff here Matt!! You never cease to amaze me with your innovation. Seriously, hat's off to you dude.
 
enhanced said:
How in the world have I missed this thread? Very interesting stuff here Matt!! You never cease to amaze me with your innovation. Seriously, hat's off to you dude.
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He cranks out the latest and greatest at a pace that is head spinning!
 
This I know. I've been a follower of his for a number of years now. Definitely a pioneer.
 
Does anyone else just get really sexually aroused when reading all of the science for stuff like this? lol

Seriously, this is better than like all the Harry Potter books (if that's your sorta thing...lol).

Cannot wait to try this one out (with MyoSynergy and X-Factor).
 
MidwestBeast said:
Does anyone else just get really sexually aroused when reading all of the science for stuff like this? lol

Seriously, this is better than like all the Harry Potter books (if that's your sorta thing...lol).

Cannot wait to try this one out (with MyoSynergy and X-Factor).
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Reading (well written and informative) product descriptions is definitely an enjoyable thing for me personally... I also do tend to touch myself inadvertently... Or perhaps I really do mean to?
 
chedapalooza said:
Reading (well written and informative) product descriptions is definitely an enjoyable thing for me personally... I also do tend to touch myself inadvertently... Or perhaps I really do mean to?
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This just made me chuckle because I thought of a Jim Gaffigan bit where he talks about bologna and how it's apparently implied that balogna makes you lie because of the "you're full of it" phrase. He then comments on never lying and says "...or maybe that's just the bologna talking..." lol
 
MidwestBeast said:
This just made me chuckle because I thought of a Jim Gaffigan bit where he talks about bologna and how it's apparently implied that balogna makes you lie because of the "you're full of it" phrase. He then comments on never lying and says "...or maybe that's just the bologna talking..." lol
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Haha yea
 
Studies are dribbling in on the Facebook page
 
Invalid Link Removed
 
sprintsss said:
When will this be in stock for purchase?
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I have a finance meeting this afternoon. We might be able to get this out in 2-3 weeks, if it goes well.
 
And this:

Proc Natl Acad Sci U S A. 2013 Feb 26;110(9):E798-807. doi: 10.1073/pnas.1215236110. Epub 2013 Feb 6.
BMP4-mediated brown fat-like changes in white adipose tissue alter glucose and energy homeostasis.
Qian SW1, Tang Y, Li X, Liu Y, Zhang YY, Huang HY, Xue RD, Yu HY, Guo L, Gao HD, Liu Y, Sun X, Li YM, Jia WP, Tang QQ.
Author information
Abstract

Expression of bone morphogenetic protein 4 (BMP4) in adipocytes of white adipose tissue (WAT) produces "white adipocytes" with characteristics of brown fat and leads to a reduction of adiposity and its metabolic complications. Although BMP4 is known to induce commitment of pluripotent stem cells to the adipocyte lineage by producing cells that possess the characteristics of preadipocytes, its effects on the mature white adipocyte phenotype and function were unknown. Forced expression of a BMP4 transgene in white adipocytes of mice gives rise to reduced WAT mass and white adipocyte size along with an increased number of a white adipocyte cell types with brown adipocyte characteristics comparable to those of beige or brite adipocytes. These changes correlate closely with increased energy expenditure, improved insulin sensitivity, and protection against diet-induced obesity and diabetes. Conversely, BMP4-deficient mice exhibit enlarged white adipocyte morphology and impaired insulin sensitivity. We identify peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC1α) as the target of BMP signaling required for these brown fat-like changes in WAT. This effect of BMP4 on WAT appears to extend to human adipose tissue, because the level of expression of BMP4 in WAT correlates inversely with body mass index. These findings provide a genetic and metabolic basis for BMP4's role in altering insulin sensitivity by affecting WAT development.

PMID:
23388637
[PubMed - indexed for MEDLINE]
PMCID:
PMC3587258
 
dsade said:
And this: Proc Natl Acad Sci U S A. 2013 Feb 26;110(9):E798-807. doi: 10.1073/pnas.1215236110. Epub 2013 Feb 6. BMP4-mediated brown fat-like changes in white adipose tissue alter glucose and energy homeostasis. Qian SW1, Tang Y, Li X, Liu Y, Zhang YY, Huang HY, Xue RD, Yu HY, Guo L, Gao HD, Liu Y, Sun X, Li YM, Jia WP, Tang QQ. Author information Abstract Expression of bone morphogenetic protein 4 (BMP4) in adipocytes of white adipose tissue (WAT) produces "white adipocytes" with characteristics of brown fat and leads to a reduction of adiposity and its metabolic complications. Although BMP4 is known to induce commitment of pluripotent stem cells to the adipocyte lineage by producing cells that possess the characteristics of preadipocytes, its effects on the mature white adipocyte phenotype and function were unknown. Forced expression of a BMP4 transgene in white adipocytes of mice gives rise to reduced WAT mass and white adipocyte size along with an increased number of a white adipocyte cell types with brown adipocyte characteristics comparable to those of beige or brite adipocytes. These changes correlate closely with increased energy expenditure, improved insulin sensitivity, and protection against diet-induced obesity and diabetes. Conversely, BMP4-deficient mice exhibit enlarged white adipocyte morphology and impaired insulin sensitivity. We identify peroxisome proliferator-activated receptor gamma coactivator 1-? (PGC1?) as the target of BMP signaling required for these brown fat-like changes in WAT. This effect of BMP4 on WAT appears to extend to human adipose tissue, because the level of expression of BMP4 in WAT correlates inversely with body mass index. These findings provide a genetic and metabolic basis for BMP4's role in altering insulin sensitivity by affecting WAT development. PMID: 23388637 [PubMed - indexed for MEDLINE] PMCID: PMC3587258
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Very cool
 
blurryimage said:
I think this was ment for the BRITE thread
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Nope...this is BMP related. BMP and Brite will work synergistically to hasten the Brite cell formation.
 
blurryimage said:
I think this was ment for the BRITE thread
Click to expand...

Nope...this is BMP related. BMP and Brite will work synergistically to hasten the Brite cell formation.
 
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