natural cox2 inhibitor

[R.B.]

As well as taking fish oil the key for me is to balance the omega threes and sixes.

I am still trying to understand it all, but here is my current take on what may be a key bit of it it based on trials etc, I am strictly an amateur, but would not be posting if I had not read sufficient to be convinced balancing the omega threes and sixes is a key factor with many potential benifits and limited downsides.

Please see posts on omega three six, side effects n3s see Linus Pauling site, and do talk to your advisors. The influence of fats in the body is much more powerful than is commonly understood by us the wider population.

Trials have shown

PGE 2 (prostaglandin 2) is a percussor of CPY 19 (aromatase gene), which is a percussor of P450 (called aromatase) which is a percusor of edstradoil (a member of the oestrogen family).

Aromatase is present in breast tissue and a source of local oestrogen production in breast tissue.

PGE 2 is a cox 2 derivative.

There is a straight line realtionship between Cox2 and CPY 19 expression. Cox 2 up CPY 19 up.

More omega six means more omega six in the cell membranes more fuel for the cox 2 pathways etc. NO omega six = no Cox 2. The body cannot make it any other way. (when in balance with n3 OK -BUTexcess n6 appears to be the issue)

Cox 2 can only be produced from the omega sixes.

Omega threes moderation production of cox 2s.

RB

[al from Canada]

Just to further along this train of thought, here is an excellent link to the cytochrome P450 (CPY19) activation and specifically the interaction with breast cancer.
http://www.cancerindex.org/geneweb/CYP19.htm

Also, looking at your list of natural COX2 inhibitors... scullcap can be toxic and IS toxic to anyone with liver disease, inc. mets. Here is a phase 1 trial using this herb: http://www.abstracts2view.com/sabcs0...u=SABCS05L_136

There are also clinical trials going on testing very potent COX2 inhibitors and analogues of celebrex.

Al

[R.B.]

re LIST.

I make no comment on the list - they are simply the ingredients listed for that product copied form their site.

I have not looked at these to form a view.

There are other natural products some of which have been discussed on this site.

For me the starting point has to be dietary considerations to maintain effective digestion and adequate nutrition which includes a fundamental balancing the omega threes and sixes. (Me to - I'm working on it)

If your using the wrong engine oil, fuel additives might help but changing to the right oil should come before the accessories to maintain your engine.

Heres is another COX 2 linked post.

http://www.her2support.org/vbulletin...ad.php?t=24328



RB

[R.B.]

For those following my wanders through the world of omega three and six.

More evidence that there is strong link between Omega six derivative and PGE 2. (see post above on production on of aromatase etc)

RB



ABSTRACT

http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_DocSum


1: Endocrinology. 1989 Sep;125(3):1650-9. Related Articles, Links

Essential fatty acid deficiency delays the onset of puberty in the female rat.

Smith SS, Neuringer M, Ojeda SR.

Department of Anatomy, Hahnemann University, Philadelphia, Pennsylvania 19102-1192.

This study assessed the effect of a dietary deficiency in the essential fatty acids (EFA) linoleic and linolenic acids on the onset of female puberty. EFA deficiency was produced in female rats by means of a semipurified diet and was biochemically documented by analyzing serum and erythrocyte fatty acid levels of more than 30 fatty acids, including all members of the n-6 and n-3 series. Levels of linoleic acid (18:2 n-6) and all n-6 derivatives, particularly arachidonic acid, were strikingly reduced. A less pronounced but clear-cut decrease in n-3 fatty acids, including docosahexaenoic acid (22:6 n-3) was also found. The times of puberty and first ovulation, as assessed by the ages at vaginal opening and first diestrus, were significantly delayed in EFA-deficient rats. The mechanisms underlying this delay appear to reside at both hypothalamic and ovarian sites. Simulation of preovulatory plasma estradiol (E2) levels via implantation of E2-containing Silastic capsules evoked a LH surge 30 h later in control juvenile rats, but not in EFA-deficient animals, indicating a delay in the development of the hypothalamic component of E2-positive feedback in the latter group. This delay appears to be due at least in part to reduced prostaglandin E2 (PGE2) synthesis, as the ability of the neurotransmitter norepinephrine to induce PGE2 release from median eminence nerve terminals was markedly reduced in EFA-deficient rats compared with that in controls. The decrease in hypothalamic PGE2 release was related to the EFA deficiency and not to reduced PG synthase activity, as determined by HPLC analysis of PG synthase products derived from exogenous [14C]arachidonic acid. Basal and hCG-stimulated PGE2 synthesis was also compromised in ovaries from EFA-deficient rats. Depressed gonadal function resulting from the EFA deficiency was further evidenced by a reduced gonadotropin receptor content, a blunted E2 response to hCG in vitro, and an increase in mean serum FSH levels. These results suggest that the delay in puberty resulting from EFA deficiency is due to a reduced availability of arachidonic acid for synthesis of bioactive metabolites. This results in delayed development of both the hypothalamic and ovarian components of the reproductive axis.

PMID: 2759037 [PubMed - indexed for MEDLINE]