The traditional diet of Greece and cancer.

[R.B.]

D6D is short hand for one of the two enzymes that convert the plant based Omega 3 and 6 to the long fats.


LA is the plant based Omega 6 linoleic acid

AA arachidonic acid is an important elongated fat made form the plant based Omega 6.

PGE2 is a downstream product of Omega 6

Excessive Omega 6 tends to overwhelm the D6D enzyme creating an excess of downstream product. Omega 3 if present would help counterbalance that effect.


Also see following post



Cancer Sci. 2013 Feb 18. doi: 10.1111/cas.12129. [Epub ahead of print]
Delta-6-desaturase activity and arachidonic acid synthesis are increased in human breast cancer tissue.
Pender-Cudlip MC, Krag KJ, Martini D, Yu J, Guidi A, Skinner SS, Zhang Y, Qu X, He C, Xu Y, Qian SY, Kang JX.
Source

Laboratory for Lipid Medicine and Technology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Abstract

Omega-6 (n-6) arachidonic acid (AA) and its pro-inflammatory metabolites, including prostaglandin E2 (PGE2 ), are known to promote tumorigenesis. Delta-6 desaturase (D6D) is the rate-limiting enzyme for converting n-6 linoleic acid (LA) to AA. Our objective was to determine if AA synthesis, specifically D6D activity, and PGE2 levels are increased in cancerous breast tissue, and whether these variables differ between estrogen receptor positive (ER+) and negative (ER-) breast cancers. Gas chromatography was performed on surgical breast tissue samples collected from 69 women with breast cancer. Fifty-four had ER+ breast cancer, and 15 had ER- breast cancer. Liquid chromatography-mass spectrometry was used to determine PGE2 levels. Lipid analysis revealed higher levels of LA metabolites (C18:3 n-6, C20:3 n-6, and AA) in cancerous tissue than in adjacent noncancerous tissue (P < 0.01). The ratio of LA metabolites to LA, a measure of D6D activity, was increased in cancerous tissue, suggesting greater conversion of LA to AA (P < 0.001), and was higher in ER- than in ER+ patients, indicating genotype-related trends. Similarly, PGE2 levels were increased in cancerous tissue, particularly in ER- patients. The results showed that the endogenous AA synthetic pathway, D6D activity, and PGE2 levels are increased in breast tumors, particularly those of the ER- genotype. These findings suggest that the AA synthetic pathway and the D6D enzyme in particular may be involved in the pathogenesis of breast cancer. The development of drugs and nutritional interventions to alter this pathway may provide new strategies for breast cancer prevention and treatment.

© 2013 Japanese Cancer Association.

[R.B.]

As a follow on from the above the D6D conversion enzyme activity has been shown to have an important role in cancer promotion and blocking it has been shown to significantly reduce tumor growth.

They suggest blocking this pathway and increasing Omega 3 intake of both plant and long chain fats may be an interesting potential treatment strategy.

Increasing Omega 3 intake and reducing Omega 6 intake will help rebalance these pathways.


Inhibiting Delta-6 Desaturase Activity Suppresses Tumor Growth in Mice
Chengwei He,1,4 Xiying Qu,1 Jianbo Wan,1 Rong Rong,1 Lili Huang,1 Chun Cai,2 Keyuan Zhou,2 Yan Gu,3 Steven Y. Qian,3 and Jing X. Kang1,2,*
Wolf-Hagen Schunck, Editor

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3480421/

The whole article is available on the link above

"Arachidonic acid (AA), an omega-6 (n−6) polyunsaturated fatty acid, is converted through three major pathways– the cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 epoxygenase pathways–into bioactive lipid mediator eicosanoids, including prostaglandins (PGs), leukotrienes (LTs), and epoxyeicosatrienoids (EETs), respectively [5], [6] (Figure S1). These metabolites have crucial roles in chronic inflammation and cancer [5]–[7]. Increased AA metabolism and eicosanoid formation is a common feature of various types of cancer cells [8], [9]. AA-derived pro-inflammatory eicosanoids, particularly PGE2 and LTB4 which are produced by tumor cells and their surrounding stromal cells, are key mediators in their crosstalk and can accelerate tumor growth and metastasis through several mechanisms [5], including: 1) directly activating their receptors on tumor cells to induce cell proliferation, survival, migration, and invasion through multiple signaling pathways in both autocrine and paracrine manners, 2) directly inducing cancer cells to secrete growth factors, pro-inflammatory mediators and angiogenic factors that turn a normal microenvironment into one that supports tumor growth and spread, and 3) directly binding receptors on stromal cells to promote a tumor-supportive microenvironment by inducing angiogenesis and evading attack by the immune system"

[Andrea Barnett Budin]

Should I be taking Krill Oil vs my Omega 3's?

I don't need a symposium answer, just a simple explanation for a simple girl, please.

RB, you are the go-to guy on this topic and you've always been sooo great to all of us, your Sisters. Thanks for remembering us.

Andi