AP & decreased protein syntesis via COX2 suppression?

[Bobaslaw]

AP & decreased protein synthesis via COX2 suppression?

One thing I have not been able to find in my searches.

AP contains Phellodendron extract which is used also by companies such as Nexrutine. Nexrutine is a natural anti inflammitory and definitely works to suppress inflammation (1gram/day and up of Phellodendron Extract for this purpose) Phellodendron decreases COX2 production by suppressing the gene expression responsible for its production. Studies show this to be true of phellodendron, mainly from the alkaloid Berberine. Phellodendron contains mainly Berberine, Phellodendrine, Palmitine. This being said, my assumption would be that this would be similar to NSAIDs effect on protein synthesis. Less COX2 creates less PGE2 and PGFa from Arachidonic Acid. It is shown that these prostaglandins are responsible for protein synthesis.
So, does the level of COX2 suppression NOT outweigh the other factors that make up AP and its effect?

Please comment.

Thanks a bunch.

 

[bioman]

Perhaps..and I'm just shooting from the hip here..the increase in nutrient loading to the muscles may overcome this. AP/YG definitely lower inflammation levels, but I doubt they do it as extensively as something like Ibuprofen.

Even then, I hear of BBer's who had unknowingly taken NSAIDS for years while they trained and bulked and they still managed to put on muscle..so I have to wonder how important this relationship really is.

 

[xjsynx]

Perhaps..and I'm just shooting from the hip here..the increase in nutrient loading to the muscles may overcome this. AP/YG definitely lower inflammation levels, but I doubt they do it as extensively as something like Ibuprofen.

Even then, I hear of BBer's who had unknowingly taken NSAIDS for years while they trained and bulked and they still managed to put on muscle..so I have to wonder how important this relationship really is.

You have a valid point; however, how much muscle could they have put on if they did not take NSAIDS for years?

 

[AnonyMoose]

it would be nice if a usp labs rep chimed in. . .

 

[Guest]

it would be nice if a usp labs rep chimed in. . .

Hope a response from the owner will suffice.

_J Herb Pharmacother._ (javascript:AL_get(this, 'jour', 'J Herb
Pharmacother.') 2004;4(2):11-8. _Links_ (javascriptopUpMenu2_Set(Menu15364641)
Inhibition of COX isoforms by nutraceuticals.
_Seaver B_ (PubMed Home
entrez?Db=pubmed&Cmd=Search&Term="Seaver%20B"[Author]&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.
Pubmed_RVAbstractPlus) , _Smith JR_
(http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Search&Term="Smith%20JR"[Author]&itool=EntrezSystem2.PEntrez.Pu
bmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus) .
University of Montana, 441 S. 6th E., Missoula, MT 59812, USA.
Humans have two isoforms of Prostaglandin H Synthase or cyclooxygenase:
COX-1 and COX-2. COX-1 is cytoprotective. COX-2 inhibitors reduce inflammation
without the risk of ulceration and kidney damage. The ideal nutraceutical would
inhibit COX-2 synthesis while preserving COX-1 synthesis. The hypothesis for
this research was that COX inhibitors would fall primarily into three
categories: COX-2 specific inhibition, non-specific inhibition (COX-1 and COX-2),
and minimal inhibition. The human Cayman COX inhibitor screening assay was
used to determine the inhibitory concentration 50 (IC50) of COX-1/ COX-2
activity of each nutraceutical. The assay was run, in duplicate, with three
concentrations of a suspected inhibitor, a standard curve of eight concentrations, a
non-specific binding sample, and a maximum binding sample. The inhibition and
concentration of each sample was then put on a multiple regression best-fit
line and the IC50 determined. For comparison, ibuprofen, rofecoxib, naproxen,
and indomethacin were used. Positive results were seen for ipriflavone,
resveratrol, MSV-60, amentoflavone, ruscus extract and notoginseng. Glucosamine,
nexrutine, and berberine did not inhibit either isoform.
First, not all evidence suggests that there is significant COX-inhibitory
activity. See above. Second, one must consider the potency of COX-2 inhibition
and if the concentration seen in vitro will be able to be reached with the
dose in the product. Last, but not least, is the question of whether enough of
the compound(s) is distributed to skeletal muscle and if it is an effective
inhibitor in that tissue type. Considering all of that, it is highly unlikely
that AP would have any negative impact on protein synthesis. It is also
important to take into account that AP has a wide variety of biological effects
and thus a comparison with a compound or compounds which only have an effect
upon COX activity is difficult.

 

[prld2gr8ns]

Even then, I hear of BBer's who had unknowingly taken NSAIDS for years while they trained and bulked and they still managed to put on muscle..so I have to wonder how important this relationship really is.

ECA anyone.

 

[xjsynx]

Hope a response from the owner will suffice

....Considering all of that, it is highly unlikely
that AP would have any negative impact on protein synthesis. It is also
important to take into account that AP has a wide variety of biological effects
and thus a comparison with a compound or compounds which only have an effect
upon COX activity is difficult.

Well if that is the best you can do :yawn:

j/k

Glad you cleared that up, because I am running AP as we speak :woohoo:

 

[Aeternitatis]

Doubtful. Most herbal COX inhibitors do not have the same drawbacks as synthetic COX inhibitors. The one I'm still unsure about in this regard though is white willow bark. Other than that, herbal anti-inflammatories like ginger, turmeric, cat's claw, etc, are unlikely to have any significant negative effect. Many things are anti-inflammatory, but that does not mean they inhibit protein synthesis like aspirin or ibuprofen can. Creatine, for example, is anti-inflammatory.

 

[ahs4n]

What exactly is the point of Asprin in the ECA stack since Asprin is lowering protein synthesis? Does the asprin help the metabolism or something?

 

[Jayhawkk]

COX-2 inhibitors reduce inflammation
without the risk of ulceration and kidney damage.

I'm on a cox2 inhibitor and it clearly states there's a risk of kiney, liver and stomach damage but it's just less than that of regualar NSAIDS like naproxen. Just the working seems a bit misleading to me

**Nothing really to the claims of AP or USPL's statement but I thought I would chime in on that particular part.

 

[Aeternitatis]

What exactly is the point of Asprin in the ECA stack since Asprin is lowering protein synthesis? Does the asprin help the metabolism or something?

It's supposed to potentiate the caffeine and ephedrine. But in my experience, it makes no difference.

 

[ahs4n]

Thanks,man...if you can't tell yet...trying to research the E/C stack before I cut in August. Been hijacking these threads too much :/

 

[Guest]

In the case of the study cited before, demonstrating COX-2 inhibitor effects was in
"human colon cancer cell line" which is important because one A) those are not
normal cells and B) it is a different tissue type (i.e. not skeletal muscle).
In other words, cancerous cells are not "normal" and cells from the colon
are not from skeletal muscle. These are all very important things to consider
when looking at such studies.
As for what might be causing the benefits that some claim in terms of
anti-inflammatory effects perhaps it's through modulation of NF-kappaBeta or
perhaps it might be a selective effect only targeting leukotriene. Impossible to
say for certain but you certainly can have anti-inflammatory benefit without
targeting the COX enzymes.

 

[Jayhawkk]

Riiight...what?


lol

 

[strategicmove]

I'm on a cox2 inhibitor and it clearly states there's a risk of kiney, liver and stomach damage but it's just less than that of regualar NSAIDS like naproxen. Just the working seems a bit misleading to me

**Nothing really to the claims of AP or USPL's statement but I thought I would chime in on that particular part.

This excerpt from the article "Eating Your Way to Prostate Cancer" by William Faloon in the February 2007 edition of Life Extension Magazine might also help. (see attachment).

"To better understand the pathways by which arachidonic acid can cause arthritic, carcinogenic, and cardiovascular conditions, the flow chart below shows how arachidonic acid cascades down into damaging compounds in the body."

 

[Outside Backer]

whats funny is i know guys for years that took a advil before they go to the gym

big guys strong guys

im not real versed on COX2 but that is what is responsible for Pain and inflammation right

so let me see if Im on the right track

inflamation after a workout leads to growth and repair

an anti inflam would hinder growth and repair

so if u hinder cox-2 = hindering growth and repair

but ive read hindering cox-2 helps eleviate pain and in teh joints and what not. am I missing something


and I on the right track

 

[heebs10]

What exactly is the point of Asprin in the ECA stack since Asprin is lowering protein synthesis? Does the asprin help the metabolism or something?

asprin is also a weak thermo and so could increase the EC's effectiveness. not many people vouch for its effectiveness though

 

[strategicmove]

...Considering all of that, it is highly unlikely
that AP would have any negative impact on protein synthesis. It is also
important to take into account that AP has a wide variety of biological effects
and thus a comparison with a compound or compounds which only have an effect
upon COX activity is difficult.

Agree!

 

[jjohn]

Agree!

What a bump!!