The traditional diet of Greece and cancer.

[R.B.]

Another paper adding support to the general contention that in the context of a western diet Omega 6s increase and Omega 3s decrease risk of breast cancer.

Positive tumors were found to have an association with a saturated fat, I have not seen the full paper but it occurs to given palmitic acid is also made in the body a plasma phospholipid content increase could in part or whole reflect wider dysbiosis in other lipid metabolic pathways.


http://www.foodconsumer.org/newsite/...808160946.html

http://www.ncbi.nlm.nih.gov/pubmed/27146840
ABSTRACT

Cancer Causes Control. 2016 Jun;27(6):759-73. doi: 10.1007/s10552-016-0753-2. Epub 2016 May 4.
Plasma phospholipids fatty acids, dietary fatty acids, and breast cancer risk.
Bassett JK1, Hodge AM2, English DR2,3, MacInnis RJ2,3, Giles GG2,3,4.
Author information
Abstract
PURPOSE:

This study prospectively investigates associations between fatty acids assessed in plasma phospholipids (PPL) and diet, and breast cancer risk, including subgroups defined by hormone receptor status.
METHODS:

We performed a case-cohort analysis within the Melbourne Collaborative Cohort Study using a random sample of 2,021 women and 470 breast cancer cases. At baseline, fatty acids were assessed in PPL and estimated from diet using a 121-item food frequency questionnaire. Hazard ratios (HR) and 95 % confidence intervals (CI) were estimated using Cox regression.
RESULTS:

Breast cancer risk was positively associated with %PPL saturated fatty acids (SFA); HRQ5vsQ1 = 1.64 (95 % CI 1.17-2.30); p trend = 0.004. Positive associations were found for ER+ or PR+ tumors for %PPL SFA and palmitic acid and for ER-/PR- tumors for %PPL n-6 polyunsaturated fatty acid (PUFA), TFA, TFA 16:1, and TFA 18:1n-7 (all p homogeneity <0.05). Breast cancer risk was inversely associated with dietary docosapentaenoic acid (DPA); HRQ5vsQ1 = 0.57 (95 % CI 0.40-0.82); p trend = 0.001 [with similar inverse associations observed for dietary docosahexaenoic (DHA) and eicosapentaenoic acid (EPA)] and positively associated with dietary n-6:n-3 PUFA. Inverse associations for ER-/PR- tumors were found for dietary dihomo-γ-linolenic acid (DGLA) for older women (p homogeneity = 0.04).
CONCLUSIONS:

Breast cancer risk was positively associated with %PPL SFA and the ratio of dietary n-6 to n-3 PUFA and inversely associated with dietary long-chain n-3 PUFA intake. Some associations between fatty acids and breast cancer varied by age and tumor phenotype defined by hormone receptor status. Increased intake of fish and other foods rich in long-chain n-3 PUFAs and reduced n-6 PUFA intake might reduce breast cancer risk.

[R.B.]

The Role of n-3 Polyunsaturated Fatty Acids in the Prevention and Treatment of Breast Cancer

Full PDF available for free

Complex as ever but the general direction of travel seems clear

www.mdpi.com/2072-6643/6/11/5184/pdf

[R.B.]

Just a quick post for the moment; this is what I have been up too for a while; having the honor of being asked to write some 6 chapters in a edited Springer Publication. (A university type reference book)

The chapters argue the physiological importance of plant based Omega 3 linolenic acid ALA and Omega 6 linoleic acid LA in evolutionary terms as well as on physiology and energetics.

There is a limited amount of material on cancer; the chapters look more widely at the impact of and implications of imbalances, and oxidation of LA and ALA, in the context of a western nutrient depleted diet, on the occurrence of western non-communicable diseases including cardiovascular, obesity dementia's, and more widely behavioral change, trends to aggression etc, set within an evolutionary framework.

Some of the ideas are new and arguably potentially of significant importance. As above the University Books are expensive, but may be found in some libraries. (just to be clear I and other contributors received no payment or reward beyond a free copy and the honor of contributing).

This thread that has been running since 2005 was in part the start of the journey that lead to these chapters being written. so thank you all very much for your interest and support over the years.



http://www.springer.com/gp/book/9783...53.About_eBook

http://link.springer.com/chapter/10....319-40458-5_27
http://link.springer.com/chapter/10....319-40458-5_28
http://link.springer.com/chapter/10....319-40458-5_29
http://link.springer.com/chapter/10....319-40458-5_30
http://link.springer.com/chapter/10....319-40458-5_31
http://link.springer.com/chapter/10....319-40458-5_32

[R.B.]

As ever complicated stuff, but very simplistically 13HODE is an oxidised product of Omega 6 linoleic acid, (AKA 'FA oxygenases') and one of the most common oxidised lipids in plasma by a long way (exactly which is the most common differs between groups but they are all oxidized derivatives of linoleic acid - more research required as to why)

The preferred substrates of the 'LO' lipoxygenase enzymes are linolenic and linoleic (probably in that order - arguably an evolutionary consequence of their centrality in plant function), so simplistically if there is lots of linoleic acid (plant derived Omega 6) in the circulation, and not much linolenic acid (plant derived Omega 3) the the LO enzyme is going to work on oxidizing the linoleic acid including to 13HODE.

13HODE is found in oxidised vegetable oils along with other oxidised products, as well as being created by the activity of oxidizing enzyme activity, including that of LO, on ingested linoleic acid in the body (remember linoleic acid cannot be got from the diet and must be made in the body; it is an essential nutrient we must have enough to be healthy but arguably excess and more so where the Omega 3 linolenic acid is low, in the context of an overly processed, antioxidant depleted, western diet, is a significant factor in western diseases.)

The conclusion below needs to be mulled in the wider context of papers referred to in this thread, but adds more weight to the contention that excess Omega 6 in vegetable oils and other sources in the context of a nutrient depleted and nutrient damaged western diet is a factor in risk of cancer occurrence and progression.

The full free paper is accessible through the link below, and below is a abstract of the concluding paragraph at the end of the paper.

Fatty Acid Metabolites in Rapidly Proliferating Breast Cancer
Joseph T. O’Flaherty,1 Rhonda E. Wooten,2 Michael P. Samuel,2 Michael J. Thomas,2 Edward A. Levine,3 L. Douglas Case,4 Steven A. Akman,5 and Iris J. Edwards6,*
Anthony Peter Sampson, Editor

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3642080/

"In conclusion, the metabolites and pathophysiology behind the contributions of FA oxygenases to poor survival in breast cancer has been ill-defined. We find that among the metabolites of the oxygenases known or found here to stimulate breast cancer cell proliferation, 13-HODE stands alone in associating with rapidly proliferating, rapidly dividing, aggressive grade, and perhaps metastasizing breast cancer. Three oxygenases make 13-HODE but correlation studies suggest that its major producer in rapidly proliferating breast cancer is 15-LO-1. Since 15-LO-1 makes other metabolites that are not characterized for proliferative activity in breast cancer cells or measured here, 13-HODE’s contribution to proliferation, division, and metastasis may be complemented or even superseded by other products of 15-LO-1. This caveat also applies to the trends of PGE2 and D2 to be negatively associated with these parameters of aggressive disease. Nonetheless, our results indicate that 13-HODE is a marker for breast cancer severity and the 15-LO-1/13-HODE pathway is associated with a rapidly proliferating, dividing, and possibly metastasizing phenotype. We propose that the over expression of this pathway speeds breast cancer’s growth and spread. Over expression of the other oxygenase-metabolite pathways, including the CO/PGE2/D2 pathways, do not use this specific mechanism to worsen the disease."

[R.B.]

Bump - Hi all I will update this in the next few days.