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GHenerate vs PowerFULL

Lets just summarize where we have got to:
1. Chinese plant unknown extract
2. A strong has been put forward involving siRNA. This work isn't easy and is expensive. It strongly suggests phyto-estrogen type properties.
3. This backs up the fairly crude publication done in mouse models.
4. This also backs up my idea that the plant appeared to promote yin (cool/female).

At a guess I would say that LG have extracted this from bark, otherwise it would say berries in the name
 
Lets just summarize where we have got to:
1. Chinese plant unknown extract
2. A strong has been put forward involving siRNA. This work isn't easy and is expensive. It strongly suggests phyto-estrogen type properties.
3. This backs up the fairly crude publication done in mouse models.
4. This also backs up my idea that the plant appeared to promote yin (cool/female).

At a guess I would say that LG have extracted this from bark, otherwise it would say berries in the name

As we discussed before this doesn't mean it is a bad thing. It could be a receptor antagonist and the other study you posted shows that elicits the PI3K as LG stated in their write up.

In addition, the fact hat they did an siRNA study doesn't mean anything. These types of experiments are done on a daily basis at most research universities and undergraduates at my university do them and I did when I was an undergraduate, too. I'm not saying the study is or isn't valid, I'm just saying that the fact they used RNA interference and silencing doesn't necessairly make it any better than the next.
 
Why is it that when a study is beneficial for a product and done on a mouse model it is acceptable, but if it has a negative connotation, then you get the old response of it was done on mice.

Cherry picking lines from studies is astounding to me. Yes they mentioned the PI3K in their write up, but failed to mention the phyto-estrogen as well. The first study I posted made me thing agonist not antagonist.
 
Well looking at Hwang YP, Jeong HG it basically says its a potent antioxidant.

The English is very poor - okay my typo rate is zillions but this ain't a peer reviewed journal. It could easily be misread.

It starts by making the assumption that Pueraria lobata is a phytoestrogen. Thats a slight problem here.

I presume the cell lines used are from ovary tissue, possibly hamster ovary - they could have used HeLa cells (human ovary). They simply say that free radical cell destruction (this isn't apoptosis) is mediated via Pueraria lobata increasing the gene expression of HO-1, which is the real antioxidant. They confirmed it via a few (presumably highly specific) metabolic inhibitors (toxcins).

Dunno what to think. However I ain't sure if this pathway is specific for estrogens or generic to any cell. They assume its estrogen specific - I'd question that. If they are right ... it will protect against ovary cancer.

LG Science thats a great marketing point!
 
I'm not saying the study is or isn't valid, I'm just saying that the fact they used RNA interference and silencing doesn't necessairly make it any better than the next.

The English is poor as I've said. It depends what system you are using but you try getting iRNA working from scratch then come back and give the rest of us a presentation. I know a guy that have dedicated years to getting iRNA up and running - well actually thats only half the story.

You are right though if the system is up and running the experiments are post-grad. You probably need some protein blots.
 
Why is it that when a study is beneficial for a product and done on a mouse model it is acceptable, but if it has a negative connotation, then you get the old response of it was done on mice.

;) arrgghh thats 'cause raw mice ain't trendy ;) Thing is you throw something at mice and cut them up to see if anything has happened. Lots of confounding effects - a specific mechanism (iRNA) limits the possibly confounders.

It can be hard getting iRNA working but it can't be a strong journal because they'd never allow it to be published because the English isn't clear. You've got to guess a bit to work out what they've done.
 
As we discussed before this doesn't mean it is a bad thing. It could be a receptor antagonist and the other study you posted shows that elicits the PI3K as LG stated in their write up.
.

Yep it will sure boost the chance of getting gyno... Just the thing you want on cycle.

Bit worrying LG say talk about PI3K suggests its the same extract as used here.
 
Yep it will sure boost the chance of getting gyno... Just the thing you want on cycle.

Bit worrying LG say talk about PI3K suggests its the same extract as used here.

Well from a quick literature search, we find evidence saying otherwise..

"The ERE-reporter activity induced by daidzein, genistein, and kaempferol was blocked by both ICI 182780 and 4-hydroxytamoxifen and partly blocked by puerarin."

Tang X, Zhu X, Liu S, Nicholson RC, Ni X. Phytoestrogens induce differential estrogen receptor beta-mediated responses in transfected MG-63 cells. Endocrine. 2008 Aug-Dec;34(1-3):29-35. Epub 2008 Oct 21.

and...

"Accordingly, the suppression of P450(arom) expression and activity by puerarin treatment may associate with the downregulation of transcription factor AP-1 or c-jun."


Li Y, Chen H, Yang S, Xie G. Decreased expression of aromatase in the Ishikawa and RL95-2 cells by the isoflavone, puerarin, is associated with inhibition of c-jun expression and AP-1 activity. Food Chem Toxicol. 2008 Dec;46(12):3671-6. Epub 2008 Sep 23.
 
The English is poor as I've said. It depends what system you are using but you try getting iRNA working from scratch then come back and give the rest of us a presentation. I know a guy that have dedicated years to getting iRNA up and running - well actually thats only half the story.

You are right though if the system is up and running the experiments are post-grad. You probably need some protein blots.

the experiments are done frequently by undergraduates researchers in our labs but I assume the difference here is we are comparing to a prominent US research oriented university where access to this technology is not uncommon.

Regardless, the point I was making was that their utilization of siRNA does not alone make the study more valid. You can't say that we threw the most money and high tech experiments at something and therefore we are right.
 
Just a few more interesting points on how it acts and its effects:


"Puerarin can inhibit the adhesion, invasion and migration of HO-8910 cells, plays an antagonist effect against the stimulation of estrogen on the malignant behavior of tumor cells."

Han J, Yu CQ, Shen W. Inhibitory effects of puerarin on invasion and metastasis of oophoroma cells HO-8910. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2009 Jul;29(7):632-5.


And, to further clear up that whole estrogen level increasing concern, I believe this was the study in question and if you look at their conclusion it doesn't give me, at least, much reason to worry about that and furthers the AI/SERM comparisons that LG was giving for the compound.


"The gonadotropin-releasing hormone level was increased (P < 0.05). CONCLUSION: Purariae-isoflavone can increase estrogen level to normal in ovariectomized rats by way of increasing the level of gonadotropin-releasing hormone. In normal rats, it has anti-estrogen effect."

NOTE: As my side note for those unfamiliar, godadotropin-releasing hormone is in fact the same as LH releasing hormone, its just a different name.

Qi BL, Qi BM. Effect of the purariae-isofiavones on estrogen level in normal and ovariectomized rats. Zhongguo Zhong Yao Za Zhi. 2002 Nov;27(11):850-2.
 
Some really good info in here.
 
^^^ just trying to figure what a supplement is doing - whats wrong with that? Kinda get jumpy when "phytoestrogen" is mentioned. Gingko blocks prolactin - could this stuff?

It (quote below) is saying something else not contrary. Its makes the point that puerarin is strongly believed to be a phytoestrogen. The question is what genes are the transcription factors regulating? What is ERE gene? E.g. suppressing prolactin? Whats the final outcome and how come we are trying to second guess a product when LG Science could simply tell us whats in the product.

Chinese medicine recognises the roots (e.g. ginseng), bark (this stuff), leaves (e.g. tea) and berries (this stuff). We are not really sure of the exact extract used.

I'll call it a day on this thread. Domestic hassle with New Year.

Well from a quick literature search, we find evidence saying otherwise..

"The ERE-reporter activity induced by daidzein, genistein, and kaempferol was blocked by both ICI 182780 and 4-hydroxytamoxifen and partly blocked by puerarin."

Tang X, Zhu X, Liu S, Nicholson RC, Ni X. Phytoestrogens induce differential estrogen receptor beta-mediated responses in transfected MG-63 cells. Endocrine. 2008 Aug-Dec;34(1-3):29-35. Epub 2008 Oct 21.

and...

"Accordingly, the suppression of P450(arom) expression and activity by puerarin treatment may associate with the downregulation of transcription factor AP-1 or c-jun."


Li Y, Chen H, Yang S, Xie G. Decreased expression of aromatase in the Ishikawa and RL95-2 cells by the isoflavone, puerarin, is associated with inhibition of c-jun expression and AP-1 activity. Food Chem Toxicol. 2008 Dec;46(12):3671-6. Epub 2008 Sep 23.
 
I am coming to this thread late.

It's a partial agonist of estrogen, which means it should block estrogen unless you are completely devoid of it (not really possibe for normal males)

Also it inhibits aromatase so it should lessen estrogen via that route too.

Also found a paper showing it reduces prolactin.


It's a pretty cool substance, don't read into the phytoestrogen since the partial agonist is a good thing (see how they compare it to tamoxifen)
 
...don't read into the phytoestrogen since the partial agonist is a good thing (see how they compare it to tamoxifen)

word. that is what I was trying to say with the antagonist vs agonist comments and the paper that explains in normal males (as you stated) it acts as an anti estrogen.

Some pretty sweet stuff you found, and I think we have covered many more studies on it in this thread than many other compounds have, haha

:D
 
It's a cool compound, plus the under the tongue delivery means it escapes the gut and doesn't get metabolized (which isn't really a concern anyway).

GHenerate is a truly amazing product. I just wish there was a way to make it as effective without being a liquid but it's not going to be the same any other way.
 
I applaud the sublingual delivary. Also bringing a Chinese herb under international quality control is very good news.

I'm gonna remain wary on this one. Clearly there is a lot of research in progress and alot to be discovered about it. It unquestionable strongly metabolically active.
Mice it supports ovary tissue
Antioxidant properties - cell lines only
Appears to have resveratrol type behaviour - what you are describing appears similar to what I understand about resveratrol
Metabolically active in the estrogen pathway

The label "phytoestrogen" is never a good label to wear: its why soya (soy) protein is no longer a force in sports supplements. I don't know of any study that undermines soy as a major protein source but I don't use it.

LG appear to be selling this as a Mucana puriens/1-carbody type replacement by increasing hGH by 500%+.

Ghenerate: I'm going look into the reviews and the logs rather than buy the product at the moment
 
word. that is what I was trying to say with the antagonist vs agonist comments and the paper that explains in normal males (as you stated) it acts as an anti estrogen.
No question you could be right: "partial agonist" is moving outside the classic definition of agonist/antagonist which was just turn on/turn off respectively. Admittedly this is an old definition.

"antagonist effect against the stimulation of estrogen"
Right there is no question in that study (which journal??) estrogen production was blocked. This was for tumour (tumor) cells. It appears to have switched behaviour from agonist to antagonist. That could be meant by "partial agonist", although literally it means "not switched fully on".

1HP mentioned that resveratrol is a aromatase inhibitor but will boost estrogens if the level is too low - I suspect this could be the "new" definition of "partial [receptor] agonist". I'm going to check this out later this year agonist/antagonist behaviour in resveratrol and log it (will be the "E2 log").

Some pretty sweet stuff you found, and I think we have covered many more studies on it in this thread than many other compounds have, haha

:D
Not really - we're a scrutiny committee.
 
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