The traditional diet of Greece and cancer.

[R.B.]

Number of views 44,444

I just visited and saw this and it made me smile; I like patters in numbers, looking forward to 55,555

Thank you very much for your interest and support everybody

I have learned a lot in the process

[Andrea Barnett Budin]

Hi RB,

It's always good to feel appreciated for all your hard work and well-intentioned efforts! And that you are.

Plus, you're right, as we give we learn, and grow and that is the marvelous part of giving of yourself. It's a WIN WIN situation!!

Love,
Andi

[R.B.]

A bit complicated but yet more evidence of the involvement of Omega 6 in breast cancers.

D6D is one of the enzymes that convert plant based Omega 6 (LA) and plant based Omega 3 to the longer fats of the same respective families. The amount of Omega 3 or 6 stored in cell membranes ready for conversion by these enzymes is proportional to the dietary intake.

AA is a longer chain Omega 6.

PGE2 is an oxidized from of AA.

So it is possible to change the processes that take place in these pathways though the choice of dietary intakes of fats.

As often discussed in general on a population wide basis we eat far to much plant based Omega 6 (50% to 70% of many vegetable oils), and too little Omega 3 both plant based and long chain including EPA and DHA, which are not found in many food in quantity. etc etc.



Cancer Sci. 2013 Jun;104(6):760-4. doi: 10.1111/cas.12129. Epub 2013 Mar 19.
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, MA, USA.
Abstract

Omega-6 (n-6) arachidonic acid (AA) and its pro-inflammatory metabolites, including prostaglandin E2 (PGE(2)), 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 PGE(2) 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 PGE(2) 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, PGE(2) levels were increased in cancerous tissue, particularly in ER- patients. The results showed that the endogenous AA synthetic pathway, D6D activity, and PGE(2) 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.

OR eat much less Omega 6 and more Omega 3, a whole food diet that has not been de-mineralised and oxidised in storage and processing etc . . . but to give this advice would not be very helpful if your future career depended on securing future funding for drugs research. . . there has to be a better way of looking at health provision, a market that is more aware that we all share a very small precious planet, and will need to be at our best to have any hope of keeping it that way, that allows researchers to both secure research funding to expand important knowledge and give optimal health advice !

[R.B.]

Thing are rarely simple, and still much is unknown; the mysteries of estrogen !

N-3 Poly-Unsaturated Fatty Acids Shift Estrogen Signaling to Inhibit Human Breast Cancer Cell Growth

http://www.plosone.org/article/info%...l.pone.0052838

WenQing Cao, ZhiFan Ma, Mark M. Rasenick, ShuYan Yeh, JiangZhou Yu

"These findings may not only provide the evidence to link n-3 PUFAs biologic effects and the pro-apoptotic signaling of estrogen in breast cancer cells, but also shed new insight into the potential application of n-3 PUFAs in BCa treatment."


"Introduction

Fish oil dietary supplements have become increasingly popular. They are consumed for a variety of ailments as well as for promotion of general health. Population and preclinical studies have suggested that n-3 PUFAs inhibit BCa growth and improve treatment outcomes [1]. Accumulating evidence states that n-3 PUFAs may exert an antitumor action by altering lipid composition of the plasma membrane, which may affect the physical and chemical properties of lipid rafts, consequently, affecting localization of and interactions among signaling components in the microdomains of cell membrane [2]–[4]. Recent studies in breast cancer cells also found that, n-3 PUFA could incorporate different components of the cell membrane to remodel membrane architecture [5], [6]. These suggested a potential mechanism underlying n-3 PUFA anti-cancer effect. N-3 PUFA treatment decreases EGFR signaling [7], and down-regulates CXCR4 signaling in MDA-MB-231 cells [8], which might play the important roles in the anti-BCa effect of n-3 PUFAs. While E2 signaling is crucial for BCa tumorigenesis and progression, fewer studies have addressed how n-3 PUFAs affect E2 signaling and biologic function in BCa cells. It is noteworthy that in the animal studies on chemo-preventive properties of n-3 PUFAs, estrogen does not override the inhibitory effect of high n-3 PUFA diet on BCa growth [9], implying that n-3 PUFAs might abrogate/reduce/reverse the pro-proliferative effect of estrogen.

Estrogen, a mitogen, stimulates cell proliferation and prevents cell death in many different cell types, and is an important risk factor for BCa development [10]. Anti-estrogen therapies have been widely employed to treat hormone dependent BCa. However, laboratory studies have suggested that estrogen stimulates the apoptosis in long-term estrogen deprivation of MCF-7 BCa cells, and switches from being a mitogenic agent to inhibiting growth and inducing apoptosis [11]–[13]. Two potential mechanisms underlying this paradoxical effect of estrogen have been suggested in the studies that can be triggered either through the extrinsic death receptor pathway [12] or via the intrinsic pathway of mitochondrial disruption and release of cytochrome C [11]. Nevertheless, it is not clear how estrogen might promote BCa cell apoptosis.

Based on the above scientific findings, we propose that n-3 PUFAs alter estrogen signaling cascades in BCa cells, and initiate/augment the inhibitory effect of E2 (or compounds binding to membrane E2 receptors) on breast cancer. In this study, we first found that n-3 PUFA treatment initiated the inhibitory effect of E2 on MCF-7 and T47D BCa cell growth, and increased cell apoptosis. While these effects of estrogen were independent of the classical estrogen receptors, ERα or ERβ, they required the presence of the estrogen-sensitive G protein coupled receptor (GPCR), GPER1. Data from this study could lead to novel insights into the usefulness of n-3 PUFAs in the treatment of BCa."