CEE: All HYPE?

NO HYPE said:
(1) As opposed to last time when I didn't? :blink: .... Not once, did I alter the meaning of your words.

(2) Hey, I've got an idea.... let's not.... :wave:.... :dance: .... :wave:

1) Whether you realized it or not, you did everytime. You just became more and more bold with it.

2) Wise choice. :gore:
 
If we put the OP's post aside, I'd like to see a poll of people who feel CEE worked better for them than old micronized creatine. And if it worked better than dicreatine malate (which I like). I'm not sure CEE is more effective for me personally. I'd don't really care about the price, although the CEE taste puts me off.
 
dagecko said:
So I was reading a post on another forum I visit and saw this:

"Here's a mail I recently received from some friends (PhDs) in the Ex Sci/Nut Biochem community. It discusses the potential dangers and (flawed marketing picture) associated with the use of Creatine Ethly Ester:


1) CEE is a true covalently bonded ester and is absorbed into blood and
tissues as the intact molecule. This is the picture that the
manufacturers would have us believe and is the basis for why they claim
CEE is superior to creatine monohydrate. However, inside cells CEE
will be unreactive with creatine kinase and may be a potential
competitive or non-competitive inhibitor to the enzyme. This would
make it toxic to brain, heart, testes, muscle and all other CK
containing tissues. People by now should be dying, but clearly are not
and this means 2) and 3) are the more likely. Nonethess, CEE should be
treated as a potentially toxic phrarmaceutical and in the US should be
treated as a drug, which requires multi species studies
to estimate LD50's and potential sites of tissue damage etc. However, recently I have been told that CEE did get new dietary ingredient status (scary).

2) CEE is hydrolysed to creatine on absorption from the gut. In this
case CEE offers no advantage over creatine monohydrate which has a
bioavilability of 100%. Indeed if hydrolysis of CEE is less than 100%
then it will be inferior to the monohydate. But in the case of
hydrolysis there are no circumstances in which it could be better than
the monohydrate in increasing tissue creatine levels. Obviously CEE
manufacturers would prefer 1) except that they then shoot themselves in
the foot over the issue of potential toxicity.

3) CEE is not a true covalently bonded ester. The whole of this is a scam
with the compound ionising in solution to free creatine, as does the
monohydrate and all salts of creatine. In this case CEE would again
represent no advantage over creatine monohydrate, except to the seller
who can double the price.

The failure of the US sports nutrition community (industry and the
universities) to call for closer examination of CEE seriously questions its
credibility in the eyes of many scientist in this country and the world. A simple water solvation test would answer 3), i.e. whether or not it was a covalent or ionisable derivative of creatine. The work time would be about one hour. Investigation of whether CEE is a competitive or non-competitive inhibitor of creatine kinase would take 2-3 hours. If either of these occured then clearly CEE must be investigated in at least two species to investigate lethality and potential organ damage. If on the other hand CEE is ionisable then I see no reason why a bioavailability study should not be undertaken comparing this, on a molar/molar basis, with
creatine monohydrate. My guess is that plasma AUC would be identical.
Again a very simple study.

None of this is rocket science but could spare a few lives, if the
manufacturers claims on the absorption of CEE are to believed."

After reading this it made me wonder on the true value of CEE and why it's so highly regarded as being superior. Is it all hype? :think:


My "problem" with the understanding behind CEE has nothing to do with all this so much. It has to do with the fact there are no studies on Pubmed about CEE!

Regular monohydrate is well studied.

Other forms like Magnesium creatine chelate I can buy into easier than CEE simply because bonding MG++ to Creatine seems pretty predictable.
 
Phosphate bond said:
My "problem" with the understanding behind CEE has nothing to do with all this so much. It has to do with the fact there are no studies on Pubmed about CEE!

Regular monohydrate is well studied.

Other forms like Magnesium creatine chelate I can buy into easier than CEE simply because bonding MG++ to Creatine seems pretty predictable.


The fact that there are no studies doesn't say much.

Try to find reputable studies of any creatine aside from monohydrate, and you will come up empty handed.

Monohydrate has been around a long time. The facts of mono are pretty much set in stone. For studies to be conducted on any of the newer forms of creatine, there would most likely need to be more significant factors other than increased absorbtion rates and reduction of water retention.

CEE is monohydrate with an ester attached, and esterification is a proven method of enhancing efficiency. I'm not sure I understand why the other forms seem so much more believable.
 
NO HYPE said:
The fact that there are no studies doesn't say much.

Try to find reputable studies of any creatine aside from monohydrate, and you will come up empty handed.

Monohydrate has been around a long time. The facts of mono are pretty much set in stone. For studies to be conducted on any of the newer forms of creatine, there would most likely need to be more significant factors other than increased absorbtion rates and reduction of water retention.

CEE is monohydrate with an ester attached, and esterification is a proven method of enhancing efficiency. I'm not sure I understand why the other forms seem so much more believable.


Well with CEE the idea is that passive diffudion helps absorption right? That would only happen in the gut because:

1. The ester hasn't had time to be removed

2. The intestine to bloodstream is not going against a concentration gradient (since the bloodstream conc of creatine is lower than the gut there is no active pumping of creatine needed to cause it to move from one place to another)

3. The stuff I am mentioning is #2 wouldn't happen in muscle because there is a uphill conc gradient from bloodstream to muscle --therefore passive diffsuion wouldn't work here (opposite to that happening in gut to bloodstream) . Plus the Ethyl ester likely gets cleaved off in the liver. Because of this I doubt CEE really increases muscle creatine levels. To me CEE just seems like something that may increase gut absorption of creatine. But I question whether gut absorption of creatine is really even a problem? Is absorption of creatine monohydrate in the intestine a problem in all those creatine monohydrate studies that have been done? Obviously not considering even 3 grams of Monohydrate have been shown to saturate muscle levels.

4. Some of the water retention stuff surrounding CM may have to do with too high of doses (that's just my guess) I haven't heard of anyone taking 20 grams of CEE like I have with Monohydrate.

That's why I am doubting CEE's effectivesness. The other forms like Magnesium creatine chelate are no big deal. Its just Mg++ and creatine. But both of those things have merit separately.
 
I have been using various forms of CEE for the past year and just recently decided to go back to regular creatine mono which I had used off and on since the mid 90's. After one month on it, I have decided to stay on it....aside from it being cheaper, I actually find that I respond better to it. I have been busting through plateaus on all core exercises.

Gumbo
 
Phosphate bond said:
Well with CEE the idea is that passive diffudion helps absorption right?


Pardon the delayed response.

As for you're statement about passive diffusion or passive transport.... in my opinion, that's not the premise behind CEE's increased absorbtion rates.

Wether it is active or passive transport, diffusion or facilitated diffusion, after the ester is cleaved off (wich I believe occurs prior to reaching the liver) CEE.... or should I say, the remaining substance, creatine, will take the same path to the cells as monohydrate. It's just that once it arrives, seeing how it is minus the sodium molocule, it will permeate the cell membrane quicker and more efficiently than monohydrate.
 
NO HYPE said:
Pardon the delayed response.

As for you're statement about passive diffusion or passive transport.... in my opinion, that's not the premise behind CEE's increased absorbtion rates.

Wether it is active or passive transport, diffusion or facilitated diffusion, after the ester is cleaved off (wich I believe occurs prior to reaching the liver) CEE.... or should I say, the remaining substance, creatine, will take the same path to the cells as monohydrate. It's just that once it arrives, seeing how it is minus the sodium molocule, it will permeate the cell membrane quicker and more efficiently than monohydrate.

How will CEE (minus the ethyl ester that got cleaved off before it reached the blood stream) penetrate the cell better?

Isn't CEE minus ethyl ester just creatine monohydrate?
 
Phosphate bond said:
How will CEE (minus the ethyl ester that got cleaved off before it reached the blood stream) penetrate the cell better?

Isn't CEE minus methyl ester just creatine monohydrate?


Alright, this is how I understand it.

Esterification is the process of joining two molecules together to eliminate an extra molecule. The attachment of an ester to creatine monohydrate eliminates the sodium molecule thereby rendering it identical to creatine already present in the body.

The seperation of the ester (ethanol) occurs rapidly after ingestion. This means that the remaining creatine molecule is smaller than that of creatine monohydrate, thereby enabling it to permeate the cell wall quicker and more efficiently.

This process also eliminates bloating by eliminating the extra molecule that sits outside the cell, once it is saturated.
 
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