Amazing article on omega3 and BC prevention...

seafood.ucdavis.edu/consumer/HardmanOmega3.pp

After reading this article, I couldn't believe that omega 3 has been found to decrease RAS, the downstreaming pathway of Her2. Also, omega 3 increase BCL2, a cancer suppressor gene. RB I know your going to like this article.

seafood.ucdavis.edu/consumer/HardmanOmega3.ppt

Still didn't work just google seafood.ucdavis.edu/consumer/HardmanOmega3.ppt

http://www.seafoodandhealth.org/docu...ardman_000.pdf

http://www.pubmedcentral.nih.gov/art...?artid=1097743

http://www.healthcentral.com/newsdetail/408/525189.html

[R.B.]

Thank you for the posts. The trial is intrigueing. I have seen it or similar before, but not the others. There are a very large number of trials emphasising the importance of maternal nutrition for a host of reasons. Why they have not received wider recognition is a true puzzle.

I am delighted to see the subject getting a wider airing.

My amateur wanderings which may or not make sense-

I am convinced at a personal level that the omega threes and sixes and the ratios of ingestion are intimately bound in the process for a host of reasons for a segement of cancers.

This is very amateurish stuff as I have only the vaguest of understanding of fragements of the parts but the overall might make some sense as a part of the whole?

It would make sense at a wider level in terms of providing a link to the status of the environment and its fecundity.

DHA and eostrogen have a cylical relationship of interdependence. The body uses oestrogen as the DHA demand lever, and when levels are sufficient oestrogen will in turn dampen down demand through the production of DHA which moderates the AA eicosanoid pathway so PGE2, aromatase etc.

A cyclical balance between DHA and AA could conceivably control to some extent the fertility cycle. AA upgrades testosterone and progesterone series one and two eicosanoids. DHA upgrades oestrogen and series three.

As AA rises aromatse rises - more oestrogen - more DHA which damps down AA series one and two through EPA series three derivatives and diversion of desaturase to an omega three preference. (Does oestrogen control the desaturase omega three six balance when supply paramaters etc are in bal)

Lower oestrogen in men would logically link to lower DHA higher AA levels and AA promotes tostesterone.

Higher oestrogen in women to higher DHA required for foetal development and allowing the fertility cycle in part.

The differnece in women and men being ovarian / testes signalling?

Pregnancy would trigger DHA eostrogen production etc to remain high by release of signals at implantation, rather than the cycle continuing.

Personally at a simplistic level I think as previously partially posted the body is trying to make DHA and failing - no raw materials - blocked pathways - trans fats, excess omega six, and other blocking factors.


Part of that aromatase cycle is excess PGE derivatives, more aromatase more oestrogen, very high inflamatory factor production but no targets and no cyclical shut down leading to autoimmune type degreadation of the genes - combined with excess archnidonic acid which triggers testoserone and progesterone - and derivates series 1 as well as 2 which somehow together trigger reproductive pathways used in maturation and implantation in response to ovarian triggers.

RB

[heblaj01]

Wanda Elaine Hardman has done a lot of research on fatty acids (in vitro & in animals but not on humans) over the years & published several papers including a 4 page review of the scientific data in the december 2004 issue of the Journal of Nutrition:

International Research Conference on Food,Nutrition, and Cancer

(n-3) Fatty Acids and Cancer Therapy1
W. Elaine Hardman2
Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808

http://jn.nutrition.org/cgi/reprint/...urcetype=HWCIT

[R.B.]

Thank you very much for that. It looks like a very useful summary. I will spend some time reading it.

I think I may have seen it before, but I skim an awful lot, and had not "registered" it. I saw the P450 mechanism in "aromatse inhibitors in the treatment of breast cancer" but who knows how we work at more subliminal levels.

Whilst the above post thoughts are wanderings all the elements above are based on reading a large number of trials.

I just do not have the knowledge to "understand" a lot of what I am reading, or be at all certain I am putting it together right.

Increasing eostrogen does increase DHA production - reported in several trials from different hormone perspectives.

The very generally unconsidered area is the influenence of threes AND sixes - for me its a bit like a traditional dual pan scales, and once it is significantly out of balance you have a problem. I do not understand why more trials do not look at the influence of both in conjunction.

Thanks again

RB