The traditional diet of Greece and cancer.

[pibikay]

Interesting. What does FADS stand for?

[Jackie07]

Am J Clin Nutr. 2010 May;91(5):1368-76. Epub 2010 Mar 24.
FADS1 FADS2 gene variants modify the association between fish intake and the docosahexaenoic acid proportions in human milk.

Moltó-PuigmartÃ* C, Plat J, Mensink RP, Müller A, Jansen E, Zeegers MP, Thijs C.
Department of Nutrition and Food Science, Faculty of Pharmacy, University of Barcelona, Barcelona, Spain.
Abstract

BACKGROUND: The genes encoding Delta(5)- and Delta(6)-desaturases (FADS1 FADS2 gene cluster) were reported to be associated with n-3 (omega-3) and n-6 (omega-6) fatty acid proportions in human plasma, tissues, and milk. Docosahexaenoic acid (DHA) can be supplied especially by dietary fish or fish oil and synthesized from alpha-linolenic acid through a pathway involving these desaturases.
OBJECTIVE: We evaluated whether FADS gene variants modify the effect of maternal fish and fish-oil intake on plasma and milk DHA proportions.
DESIGN: FADS1 rs174561, FADS2 rs174575, and intergenic rs3834458 single nucleotide polymorphisms were genotyped in 309 women from the KOALA Birth Cohort Study in The Netherlands. Plasma was collected at 36 wk of pregnancy, and milk was collected at 1 mo postpartum. Fish and fish-oil intake was assessed by using a food-frequency questionnaire at 34 wk of pregnancy and updated for the week of milk collection. Gene-diet interactions were tested by linear regression analysis.
RESULTS: DHA proportions were lower in women homozygous for the minor allele than in women who were homozygous for the major allele (DHA proportions in plasma phospholipids: P < 0.01; DHA proportions in milk: P < 0.05). Fish intake ranged from 0 to 2.5 portions of fatty fish/wk, and 12 women took fish-oil supplements during pregnancy. DHA proportions in plasma phospholipids increased with increasing fish and fish-oil intake, irrespective of the genotype. DHA proportions in milk increased only with fish and fish-oil intake in the major-allele carriers.
CONCLUSION: Lower proportions of DHA in milk from women who were homozygous for the minor allele could not be compensated for by increasing fish and fish-oil intake, possibly because of limited incorporation into milk.

[R.B.]

pibikay

^ This may help

FADS = Fatty acid desaturase

http://en.wikipedia.org/wiki/Fatty_acid_desaturase


Jackie 07

Could the failure of dietary DHA to raise DHA in breast milk be because even with additional intake the women were still not making enough to meet the needs of the foetus / their own needs and that higher intakes than used may have raised levels in breast milk. Other papers seem to suggest that in general supplementation raises DHA in breast milk

The effects of fish oil supplementation in pregnancy on breast milk fatty acid composition over the course of lactation: a randomized controlled trial.

Dunstan JA, Mitoulas LR, Dixon G, Doherty DA, Hartmann PE, Simmer K, Prescott SL.

School of Paediatrics and Child Health, The University of Western Australia, Crawley WA 6009.
Abstract

This study evaluated the longitudinal effect of fish oil in pregnancy on breast milk fatty acid composition and infant outcomes. In a randomized, controlled trial, 98 women received 2.2 g docosahexaenoic acid (DHA) and 1.1 g eicosapentaenoic acid (EPA) or olive oil from 20 wk of gestation until delivery. Fatty acid composition in breast milk (at 3 d, 6 wk, and 6 mo) and infant erythrocyte membranes (at 1 y) were determined by gas liquid chromatography. Breast milk fatty acids were examined in relationship to growth and development. Compared with control group, breast milk from women who received fish oil had proportionally higher DHA and EPA levels at 3 d and 6 wk after delivery, but this difference was no longer apparent by 6 mo. Infant DHA status at 1 y of age was directly related to DHA levels at 3 d, 6 wk, and 6 mo postpartum (but not to antenatal supplementation). Both EPA and DHA in breast milk were positively correlated with Griffith's developmental scores including hand and eye coordination. Thus, supplementation in pregnancy was associated with increased n-3 long-chain polyunsaturated fatty acids (LCPUFAs) in breast milk, particularly in early lactation, and this was positively associated with infant DHA status at 1 y.

Thanks for posting that link I will bear the contents in mind.

[R.B.]

More emphasis as to the importance of fats in cancer.


Cancer Biol Ther. 2011 Apr 15;11(8):724-31. Epub 2011 Apr 15.
Fatty acids as potential adjunctive colorectal chemotherapeutic agents.
Fauser JK, Prisciandaro LD, Cummins AG, Howarth GS.
Source

University of Adelaide, Adelaide, Australia; The Queen Elizabeth Hospital, Woodville, South Australia, Australia.
Abstract

Fatty acids (FA) are bioactive molecules which have potential as adjunctive chemotherapeutic agents. FA are classified as short-, medium; or long-chain on the basis of the number of carbon atoms in the aliphatic chain and have been reported to induce apoptosis in vitro in a range of cancer cell types, including breast, tongue, cervix and colorectal. However, to date the chain length exerting optimal anti-neoplastic properties remains undefined. Short chain fatty acids, such as butyrate (C4:0), have induced high rates of in vitro apoptosis, presumably related to epigenetic modification, cell cycle arrest and activation of pro-apoptotic genes. Medium chain fatty acids have demonstrated in vivo and in vitro cytotoxic and anti-microbial properties; however, scant evidence currently exists on their anti-neoplastic potential. Longer unsaturated fatty acids (C16-24: ω3-9), including conjugated linoleic acid and eicosapentaenoic acid, also exhibit in vitro anti-proliferative actions, including induction of oxidative stress and modification of intracellular signalling pathways. Although incorporation of FA into CRC chemotherapy regimens is in its infancy, evidence is accumulating to allow identification of the FA chain length capable of exerting the most effective anti-neoplastic activity.

PMID:
21430438
[PubMed - in process]

[R.B.]

In essence the fat composition of the breast tissue is diet sensitive.

A trial looking at the impact of dietary EPA + DHA suggests that in terms of tissue composition there was not any significant benefit in more that 2.52 grams a day.


Full Free Text



http://www.ncbi.nlm.nih.gov/pmc/arti...tool=pmcentrez

ω-3 Fatty acid supplements in women at high risk of breast cancer have dose-dependent effects on breast adipose tissue fatty acid composition1,2,3
Lisa D Yee,corresponding author Joanne L Lester, Rachel M Cole, Julia R Richardson, Jason C Hsu, Yan Li, Amy Lehman, Martha A Belury, and Steven K Clinton

Background: Preclinical evidence of the preventive benefits of ω-3 (n–3) polyunsaturated fatty acids (PUFAs) in breast cancer continues to fuel interest in the potential role of dietary fat content in reducing breast cancer risk. The dose of fish-oil/ω-3 PUFAs needed to achieve maximal target tissue effects for breast cancer prevention remains undefined.
Objective: To determine the dose effects of ω-3 fatty acids on breast adipose tissue fatty acid profiles, we conducted a study of 4 doses of ω-3 PUFAs in women at high risk of breast cancer.
Design: In this 6-mo randomized open-label study, 48 women with increased breast cancer risk received 1, 3, 6, or 9 capsules/d of an ω-3 PUFA supplement that provided 0.84, 2.52, 5.04, and 7.56 g docosahexaenoic acid (DHA) + eicosapentaenoic acid (EPA) daily, respectively. Subjects made monthly visits, at which time pill counts were made and fasting blood samples were collected to determine fatty acid profiles; anthropometric measurements were made, breast adipose tissue samples were collected, and laboratory tests of toxicity (alanine aminotransferase, LDL cholesterol, and platelet function) were made at baseline and at 3 and 6 mo.
Results: All doses led to increased serum and breast adipose tissue EPA and DHA concentrations, but the response to 0.84 g DHA+EPA/d was less than the maximum possible response with ≥2.52 g/d. Body mass index attenuated the dose response for serum tissue DHA and EPA (P = 0.015 and 0.027, respectively) and breast adipose tissue DHA (P = 0.0022) in all of the treatment groups. The incremental increase in DHA and EPA correlated inversely with baseline fat and serum values. Compliance over 6 mo was 92.9 ± 9.2% and was unaffected by treatment arm. No severe or serious toxicities were reported.

Conclusions: Daily doses up to 7.56 g DHA+EPA were well tolerated with excellent compliance in this cohort at high risk of breast cancer. Body mass index and baseline fatty acid concentrations modulated the dose-response effects of ω-3 PUFA supplements on serum EPA and DHA and breast adipose tissue DHA.

[pibikay]

Thanks All.We have been away for a week at Kangra Valley in Himachal.Hence my late reply

[R.B.]

http://www.ncbi.nlm.nih.gov/pubmed/21569413

Lipids Health Dis. 2011 May 12;10(1):73. [Epub ahead of print]
Effects of n-3 PUFAs on breast cancer cells through their incorporation in plasma membrane.
Corsetto PA, Montorfano G, Zava S, Jovenitti IE, Cremona A, Berra B, Rizzo AM.
Abstract

ABSTRACT:
BACKGROUND:

PUFAs are important molecules for membrane order and function; they can modify inflammation-inducible cytokines production, eicosanoid production, plasma triacylglycerol synthesis and gene expression. Recent studies suggest that n-3 PUFAs can be cancer chemopreventive, chemosuppressive and auxiliary agents for cancer therapy. PUFAs could alter cancer growth influencing cell replication, cell cycle, and cell death. The question that remains to be answered is how n-3 PUFAs can affect so many physiological processes. We hypothesize that n-3 PUFAs alter membrane stability, modifying cellular signalling in breast cancer cells.
METHODS:

Two lines of human breast cancer cells characterized by different expression of ER and EGFR receptors were treated with AA, EPA or DHA. We have used the MTT viability test and expression of apoptotic markers to evaluate the effect of PUFAs on cancer growth. Phospholipids were analysed by HPLC/GC, to assess n-3 incorporation into the cell membrane.
RESULTS:

We have observed that EPA and DHA induce cell apoptosis, a reduction of cell viability and a decrease of Bcl2 and procaspase-8 expression. Moreover, DHA slightly reduces the concentration of EGFR but EPA has no effect. Both EPA and DHA reduce the activation of EGFR. N-3 fatty acids are partially metabolized in both cell lines; AA is integrated without being further metabolized. We have analysed the fatty acid pattern in membrane phospholipids where they are incorporated with different degrees of specificity. N-3 PUFAs influence the n-6 content and vice versa.
CONCLUSIONS:

Our results indicate that n-3 PUFA feeding might induce modifications of breast cancer membrane structure that increases the degree of fatty acid unsaturation. This paper underlines the importance of nutritional factors on health maintenance and on disease prevention.

[R.B.]

Int J Cancer. 2011 Mar 15;128(6):1434-41. doi: 10.1002/ijc.25703. Epub 2010 Nov 23.
Dietary polyunsaturated fatty acids and breast cancer risk in Chinese women: a prospective cohort study.
Murff HJ, Shu XO, Li H, Yang G, Wu X, Cai H, Wen W, Gao YT, Zheng W.
Source

Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37203-1738, USA. harvey.j.murff@vanderbilt.edu
Abstract

Breast cancer is the most common cancer in women. Controversy exists regarding the role of dietary fat in breast cancer etiology. We investigated the association of dietary polyunsaturated fatty acids (PUFAs) and the ratio of n-6 PUFAs to marine-derived n-3 PUFAs with breast cancer risk in the Shanghai Women's Health Study, a prospective cohort study including 72,571 cancer-free participants at baseline. Dietary fatty acid intake was determined using food frequency questionnaires. We used Cox proportional hazards analysis to estimate the relative risks (RRs) and 95% confidence intervals (CIs) for the association of breast cancer risk with dietary fatty acids consumption. In 583,998 person-years of follow-up, we identified 712 breast cancer cases. We found no association of breast cancer risk to dietary intake of linoleic acid, arachidonic acid, α-linolenic acid or marine-derived n-3 PUFA. We found a statistically significant interaction between n-6 PUFA intake, marine-derived n-3 PUFA intake and breast cancer risk (p = 0.008). Women with lower intake (the lowest tertile) of marine-derived n-3 PUFA and higher intake (the highest tertile) of n-6 PUFA had an increase risk for breast cancer (RR = 2.06; 95% CI = 1.27-3.34) compared to women with higher intake (the highest tertile) of marine-derived n-3 PUFAs and lower intake (the lowest tertile) of n-6 PUFAs after adjusting for potential confounders. The relative amounts of n-6 PUFA to marine-derived n-3 PUFAs may be more important for breast cancer risk than individual dietary amounts of these fatty acids.

[R.B.]

Expert Review of Anticancer Therapy
August 2011, Vol. 11, No. 8, Pages 1151-1153 , DOI 10.1586/era.11.106
(doi:10.1586/era.11.106)


Omega-3 fatty acids: a potential booster for tamoxifen therapy?
Lucas Tadeu Bidinotto, Ricardo López de Cicco & Jose Russoâ€*

http://www.expert-reviews.com/doi/fu...586/era.11.106


Quote from paper


"In summary, there are several pathways by which omega-3 fatty acids can act in an anticancer response. The downregulation of the CDK1-cyclin B1 complex, resulting in prolongation of the G2-phase, and the downregulation of the MAPK pathway may be responsible for slowed breast cancer growth. Increased lipid peroxidation along with the accumulation of ROS and downregulation of Akt may be responsible for an increased apoptotic index. The improvement of the immune response against tumors and the lack of inflammatory cytokines in the tumors of animals fed omega-3-rich diets and treated with tamoxifen contribute to the impairment of tumor growth. The improvement of wasting syndrome in patients with advanced cancer may contribute to their overall health. Finally, the increased membrane fluidity may improve the internalization of chemotherapeutic drugs. Therefore, the combination of these mechanisms represents a potential boost to tamoxifen therapy."

[R.B.]

Effects of n-3 PUFAs on breast cancer cells through their incorporation in plasma membrane
Paola A Corsetto,1 Gigliola Montorfano,1 Stefania Zava,1 Ilaria E Jovenitti,1 Andrea Cremona,1 Bruno Berra,1 and Angela M Rizzocorresponding author1
1Dipartimento di Scienze Molecolari Applicate ai Biosistemi, UniversitÃ* degli Studi di Milano, Italy

(Full Free Text)

http://www.ncbi.nlm.nih.gov/pmc/arti...tool=pmcentrez

Background
PUFAs are important molecules for membrane order and function; they can modify inflammation-inducible cytokines production, eicosanoid production, plasma triacylglycerol synthesis and gene expression. Recent studies suggest that n-3 PUFAs can be cancer chemopreventive, chemosuppressive and auxiliary agents for cancer therapy. N-3 PUFAs could alter cancer growth influencing cell replication, cell cycle, and cell death. The question that remains to be answered is how n-3 PUFAs can affect so many physiological processes. We hypothesize that n-3 PUFAs alter membrane stability, modifying cellular signalling in breast cancer cells.

Methods
Two lines of human breast cancer cells characterized by different expression of ER and EGFR receptors were treated with AA, EPA or DHA. We have used the MTT viability test and expression of apoptotic markers to evaluate the effect of PUFAs on cancer growth. Phospholipids were analysed by HPLC/GC, to assess n-3 incorporation into the cell membrane.
Results
We have observed that EPA and DHA induce cell apoptosis, a reduction of cell viability and the expression of Bcl2 and procaspase-8. Moreover, DHA slightly reduces the concentration of EGFR but EPA has no effect. Both EPA and DHA reduce the activation of EGFR.
N-3 fatty acids are partially metabolized in both cell lines; AA is integrated without being further metabolized. We have analysed the fatty acid pattern in membrane phospholipids where they are incorporated with different degrees of specificity. N-3 PUFAs influence the n-6 content and vice versa.

Conclusions
Our results indicate that n-3 PUFA feeding might induce modifications of breast cancer membrane structure that increases the degree of fatty acid unsaturation. This paper underlines the importance of nutritional factors on health maintenance and on disease prevention.

[R.B.]

Hi All

Apologies I managed to duplicate a reference above.

The ongoing saga of dental infection continues, and my suspicion that dental infections can fog the brain remains. My childhood hockey accident broken root filled and refilled and apisectomied tooth [twice] appears to have been reinfecting the bone through escape of bacteria living in the space where the post sits - the tooth and a neighbouring tooth have now been removed - not a good look (-: - but hopefully the recurring infection in the bone in the area and likely higher in the face which has been going on to greater and lesser extent for several years, now may clear up.

This is a fascinating summary adding to the evidence excess linoleic acid (plant based 18 carbon Omega Six which makes up 50 - 70 % of the fat in many vegetable oils, and arguably which many of us get too much of) is a factor in BC.


Int J Biochem Cell Biol. 2011 Sep 16. [Epub ahead of print]
Linoleic acid induces an EMT-like process in mammary epithelial cells MCF10A.
Espinosa-Neira R, Mejia-Rangel J, Cortes-Reynosa P, Salazar EP.
Source

Departamento de Biologia Celular, Cinvestav-IPN, Av. IPN # 2508, San Pedro Zacatenco, Mexico, DF 07360, Mexico.
Abstract

Epidemiological studies and animal models suggest an association between high levels of dietary fat intake and an increased risk of developing breast cancer. Epithelial-mesenchymal-transition (EMT) is a process, by which epithelial cells are transdifferentiated to a mesenchymal state, and it has been implicated in cancer progression, including invasion and metastasis. Linoleic acid (LA) induces proliferation and invasion in breast cancer cells. However, the role of LA on the EMT process in human mammary epithelial cells remains to be studied. In the present study, we demonstrate that LA induces a transient down-regulation of E-cadherin expression, accompanied with an increase of Snail1, Snail2, Twist1, Twist2 and Sip1 expressions. Furthermore, LA induces FAK and NFκB activation, MMP-2 and -9 secretions, migration and invasion. In summary, our findings demonstrate, for the first time, that LA promotes an EMT-like process in MCF10A human mammary epithelial cells.

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID:
21945809
[PubMed - as supplied by publisher]

[R.B.]

More Omega 3 and 6 mechanisms which affect cancer cell function (-:

Omega 6 derivatives are the main natural activators of pathways in which cannabis derivatives are also active, which has a host of implications, including in controlling mood, food intake, weight gain etc. As well as influencing brain function these Omega 6 compounds are also active in many cells, including the reproductive system. This paper suggests they affect proliferation in cancer cells.

It looks as if Omega 3 derivatives have different roles in these pathways to Omega 6 derivatives and once again the balance between the two appears to affect cell function. ( FYI anandamide and 2-arachidonoylglycerol are omega 6 based products - see below)

The involvement of cannabis receptors begs the question does cannabis affect cancer (increase or decrease) by inhibiting the access of other compounds to these pathways - scientists are looking a the effects of cannabis derivatives on cancer - and that in turn would depend on the balance of natural activators produced in the body, including through the Omega 3 and 6 pathways but the wider implications ??? These receptors are found widely in the body including in the brain, and I value the function of mine.



Prostaglandins Leukot Essent Fatty Acids. 2011 Oct 11. [Epub ahead of print]
Omega-3 N-acylethanolamines are endogenously synthesised from omega-3 fatty acids in different human prostate and breast cancer cell lines.
Brown I, Wahle KW, Cascio MG, Smoum-Jaouni R, Mechoulam R, Pertwee RG, Heys SD.
Source

Translational Medical Sciences, Division of Applied Medicine, School of Medicine and Dentistry, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
Abstract

Omega-3 (n-3) fatty acids inhibit breast and prostate cancer cell growth. We previously showed that N-acylethanolamine derivatives of n-3 (n-3-NAE) are endocannabinoids, which regulate cancer cell proliferation. These n-3-NAE are synthesised in certain cells/tissues, after supplementing with fatty acids, however, no one has assessed whether and to what extent this occurs in cancer cells. We determined levels of endogenous n-3-NAEs in hormone sensitive and insensitive prostate and breast cancer cells and subsequent effects on other endocannabinoids (anandamide and 2-arachidonoylglycerol), before and after supplementing with DHA and EPA fatty acids, using HPLC tandem mass spectrometry. This is the first study reporting that n-3-NAEs are synthesised from their parent n-3 fatty acids in cancer cells, regardless of tumour type, hormone status or the presence of fatty acid amide hydrolase. This could have important implications for the use of n-3 fatty acids as therapeutic agents in breast and prostate cancers expressing cannabinoid receptors.

Copyright © 2011 Elsevier Ltd. All rights reserved.

PMID:
21995886
[PubMed - as supplied by publisher]

[R.B.]

This is neat because it relates the Omega 3:6 profile of strictly controlled diet to what is happening in prostate cancer cells in living humans. The diet was tested in the time frame whilst patients were awaiting surgical removal of cancerous tissue, which tissue was then available for examination as to the effect of the different diets on cancer cell fat composition, structure, cell division rate, etc. The trial is small but has prompted a bigger trial


http://www.newswise.com/articles/you...e-cancer-cells

You are What You Eat: Low-Fat Diet with Fish Oil Slowed Growth of Human Prostate Cancer Cells
Released: 10/25/2011 7:00 AM EDT
Source: University of California, Los Angeles (UCLA), Health Sciences

"Newswise — A low-fat diet with fish oil supplements eaten for four to six weeks prior to prostate removal slowed down the growth of prostate cancer cells – the number of rapidly dividing cells – in human prostate cancer tissue compared to a traditional, high-fat Western diet.

Done by researchers at UCLA’s Jonsson Comprehensive Cancer Center, the short-term study also found that the men on the low-fat, fish oil supplement diet were able to change the composition of their cell membranes in both the healthy cells and the cancer cells in the prostate. They had increased levels of omega-3 fatty acids from fish oil and decreased levels of omega-6 fatty acids from corn oil in the cell membranes, which may directly affect the biology of the cells, though further studies are needed, said Dr. William Aronson, the study’s first author and a researcher with UCLA’s Jonsson Comprehensive Cancer Center.

The study also found that blood obtained from patients after the low-fat, fish oil diet program slowed the growth of prostate cancer cells in a test tube as compared to blood from men on the Western diet, which did not slow cancer growth.

“The finding that the low-fat, fish oil diet reduced the number of rapidly dividing cells in the prostate cancer tissue is important because the rate at which the cells are dividing can be predictive of future cancer progression,” Aronson said. “The lower the rate of proliferation, the lesser the chances that the cancer will spread outside the prostate, where it is much harder to treat.” . . .

"- the “treatment” was indeed reaching the targeted organ because of the changes in the prostate cell membrane’s fatty acid composition." . . .

"Diet studies often are difficult to evaluate because getting patients to comply with dietary changes can be challenging. However, the food eaten by men in both arms of this study was precisely controlled, Aronson said. The meals were prepared by chefs in the UCLA Clinical Translational Research Center and delivered in bulk to study participants several times a week. Participants also met with a dietician, kept food diaries and were required to return uneaten food."


"
The study appeared Oct. 25, 2011 in Cancer Prevention Research, a peer-reviewed journal of the American Association for Cancer Research."

[Andrea Barnett Budin]

For goodness sakes -- IS THERE NO END TO THE MANY WAYS IN WHICH OMEGA 3 BENEFITS US ALL...???

Hi, RB! Can you list some of the diseases and ailments Omega 3 can alter our lives? Just in a neat little package. (I've read your book, and am ever impressed with it's messages.)

I know people in their 40s, 50s, 60s, 70s, and 80s who are on to this life-saver!

I take 2 a day. Every day...

[R.B.]

Hi Andrea

Great to your positive posts. Thanks for the kind words. The book is not very well written, but the science in it is generally fine, and I am well received at specialist conferences on lipids on the strength of it. It raises important issues, is thought provoking, but is a bit disjointed and best read in small sections - it leaves lots of questions and that is because this is a developing area of science and much is still simply not known - if the book gets you to realise that excess Omega 6 (and not enough Omega 3) in our diet is an important issue it is a positive step - I stand by some of the more sweeping claims - excess Omega 6 will be seen in the future to be a very serious health issue - I have largely rewritten an expanded book, which is much fuller and more confidently written, and ties in other areas, but I need to find some serious time to finish it - the researchers that are doing all the fine work that made the book and rewrite possible are way ahead of their time.

One of the pieces of good news is that the US military are beginning to take the subject seriously, and they really do have the power to influence food production and composition.

Excess Omega 6 is strongly connected with the ability to reproduce and all of the processes that entails. Excess omega 6 is a factor in many western conditions, and particularly those that are inflammation related. I will try and find time over the weekend to add a list.

(For anyone who has read the biography at the back the issue is still ongoing, and it was disclosed at a recent Freedom of Information Tribunal seeking disclosure of a secret practice direction dealing with the closure of Royal wills that the document related to a secret illegitimate royal child; so the claim may not be as batty as it sounds.)

[R.B.]

Some of you may also have seen the vitamin D threads in the nutrition section that suggest those with 'higher' levels of vitamin D on average have a lower risk of BC / recurrence.

The body is enormously complicated and interlinked as is evidenced by the paper below. The study suggests there may be links between the vitamin D pathways and Omega 6 pathways. PGE2 (a prostaglandin) is an oxidised downstream product of the 20 carbon fat called arachidonic acid (a member of the Omega 6 family, its name is explained by the fact it was first isolated from a spider). PGE2 features in lots of body functions, including inflammation, and hormone production.

The paper suggests links between a combination of increased Omega 6 PGE2 and lower Vitamin D (calcitriol) in breast cancer patients - double trouble.

Another paper on vitamin D and cancer below suggests a mechanism. Vitamin D is suggested to regulate enzymes that produce and dispose of prostaglandins including one called COX2, which is the enzyme that allows PGE2 to be made.

As a very broad generalisation Omega 3 competes for the same enzymes as Omega 6, and those with lower Omega 6 tend to have lower levels of Omega 6 products including PGE2 in their systems. In this way increased Omega 3 and lower Omega 6 may reduce the risk of a number of conditions including an array of cancers including BC and prostate cancer

A significant number of non-steroidal drugs commonly block the production or action of PGE2, which may explain why they and asprin may be associated with a reduction in the risk of cancer - but have other side effects



"Prostaglandin Metabolising Enzymes and PGE2 are Inversely Correlated with Vitamin D Receptor and 25(OH)2D3 in Breast Cancer

http://ar.iiarjournals.org/content/30/5/1673.abstract

Abstract

Background: Breast cancer is associated with inflammatory processes based on an up-regulation of cyclooxygenase-2 (COX-2) expression. The antiproliferative effects of calcitriol (1,25(OH)2D3) mediated via the vitamin D receptor (VDR) render vitamin D a promising target in breast cancer therapy. First data suggest a correlation between vitamin D and prostaglandin metabolism. Materials and Methods: We determined the expression of VDR, COX-2, 15-PGDH and the prostaglandin receptors EP2/EP4 in normal and malignant breast tissue by real-time PCR and Western blot analysis, as well as 25(OH)2D3 and PGE2 plasma levels from healthy and breast cancer patients. Results: Significantly higher COX-2, lower VDR and lower EP2 and EP4 receptor protein levels in the malignant tissue and a significantly lower 15-PGDH protein level in normal breast tissue were detected. Breast cancer patients older than 45 years, diagnosed and sampled in the wintertime had significantly lower 25(OH)2D3 and higher PGE2 serum levels. Conclusion: The inverse correlation between VDR and both COX-2 and 15-PGDH, as well as between PGE2 and 25(OH)2D3 levels, suggests a possible link between VDR-associated target genes and prostaglandin metabolism."

Vitamin D and cancer: current dilemmas and future research needs1,2,3
Cindy D Davis
1 From the Nutritional Sciences Research Group, National Cancer Institute, Rockville, MD

2 Presented at the National Institutes of Health conference "Vitamin D and Health in the 21st Century: an Update," held in Bethesda, MD, September 5–6, 2007.


(the paper includes the following quote)

"Vitamin D regulates many genes involved in prostaglandin metabolism. 1,25(OH)2D inhibits COX-2 expression and activity, inhibits expression of prostaglandin receptors, and increases prostaglandin catabolism by increasing expression of 15-prostaglandin dehydrogenase (25). In combination, these 3 mechanisms reduce prostaglandin levels and signaling, thereby attenuating the growth-stimulatory effects of prostaglandins in prostate cancer (25). Furthermore, 1,25(OH)2D and naproxen (a nonsteroidal antiinflammatory drug) act synergistically in vitro and inhibit prostate cancer cell growth more effectively than either alone in patients on the basis of a slowing of the prostate-specific antigen doubling time (25). Thus, by understanding the molecular targets for vitamin D, researchers can develop more effective strategies for cancer prevention and treatment. "

[R.B.]

A cautionary tale for those with troublesome root fillings.

For those of you who may have noted my observations starting in 2007 as to an ongoing infection in the jaw I finally went to see a top London Maxi-facial Consultant with the support of an excellent new dentist.

The Noted Consultant confirmed what I have always suspected that the bone at the corner of the nose was / had been infected. I have unsuccessfully spent 5 years and more, based on my analysis of the symptoms (sometime symptoms including pain, red eye lid, tender bones round eye, swollen gland at the back of the skull, skin reddening and flaking, swelling, acid night-time discharges, blocked lacrimal duct, bad tastes /breath from affected nostril, fluid discharge / sensitivity from the nose during exercise, abbesses in that segment of the jaw, eye glued shut etc) trying to convince a wider range of dentists, my doctor, the hospital et al that I had a wider jaw / skull infection, and had had an MRI, 2 CTs, OPGs etc etc etc.

It took the Noted Consultant about 10 seconds (almost instant with no hesitation) of looking at the copy of the disc of a year old CT scan before he pointed to the damaged bone, which he then showed me on a 3D image of the skull. You could not miss it - a black space surrounded by grey about the size of my thumbnail at the base of the entrance to the nose - exactly where all this time I have been pointing,with my finger half stuck up my nose, pleading plaintiffully "the problem is here". I have no idea if he had better software, or why it was so easy for him, using an existing CT to almost instantly come to that conclusion that there was damaged / infected bone, when after many x-rays etc the fact had eluded others for several years .

The upshot is that hopefully the infection should clear now the incisor, root filled as a child following a hockey accident, and subsequently apisectomied twice etc etc. the likely source of infection, had recently been removed, (when the tooth was extracted the putrid smell confirmed that area round the crown post was evidently a bacterial Hilton, and bacterial safehaven from antibiotics etc - 4 root filled teeth all in the same segment have now been the source of bone infection - including one more that died following an adjacent apisectomy, and including the offending incisor which resulted in infection to the bone around the entrance to the nose - I have not needed any other dental work for 15 years so this is not due to poor maintenance, and gums appeared healthy etc.) I now have to wait six months to find out if the bone has healed. It looks like the song "All I want for Christmas is my two front teeth" will resonate for a while yet. It is still an intermittent source of pain at a low level, and the occasional source of bad tastes / smells in the affected nostril but is much improving, as hopefully is my brain fuzz / anxiety.

On the positive side I suspect if my diet was not as good as it is (always room for improvement) that there is a chance it could have spread. Also I now know what it is, that my analysis was right, and I can no longer be treated with a certain amount of disdain by some medical / dental professionals who made it pretty clear that they viewed my symptoms as being in my imagination.

[Andrea Barnett Budin]

I always say, Listen to your Inner Voice. You may call it your gut. By any name, it is your Spirit talking to you. And it can be counted on for excellent guidance.

By the same token, if you are with a doc who is very nice but... Look elsewhere for answers. Don't waste time with those that think your pain is a manifestation of your imagination. Nor stay with a doc who responds to your questions as you try to get your brain around something -- You don't have to understand, let me do the worrying. WRONG.

If a doc shows disdain for your mention of 2nd opinions, know that any really good doc welcomes more input. Is that comfortable in his or her own skin.

If the problem persists, go bigger. It may be inconvenient, but you may have to travel to an expert who can tell in a heartbeat what's happening to you. These are pearls.

I had 4 oncs at one time. Each was brilliant, each had a slightly different take on my situation. One was a stem cell guy (1 of an additional 2 who specialized in this, as I was considering such a transplant and was gathering information) -- this one was an hour away from my then home in NY, and at first in a dark, dank basement office. Finally he moved to a grand institute. Either way, there were always longgggg lines waiting to get to him. Even if you had the first appointment.

I was mid chemo and feeling really rotten. But both my husband and I loved this genius and felt we'd make an exception for his inconvenient location(s) and the 2 hour waits. In general, we refuse to go to anyone who leaves you hanging for hrs. But this guy was worth the wait.

Hope you're feeling way better, RB!

That doc, BTW, was one of 2 oncs who said, next time bring me your CT scans so I can have "my" radiologist read them. And so we did. And both, independent and unaware of one another, disagreed w/my regular radiologist's report. It was those 2, back in '99, who each said, I don't believe what I am looking at are tumors (splattered throughout my liver). They appear to be the dead remains of tumors. Cyst-like. Filled w/fluid.

What does this mean, we asked my wonderful and inconvenient onc?! It means, he paused and beamed his familiar smile, and sang out -- You are... in... cautious... remission!

And so it was! And has remained so since '99.

Listen to your Inner Voice and follow wherever it guides you. Your Spirit loves you more than any human being on this earth.

Sending healing energy to you all,

Andi

[Jackie07]

Almost missed the very important messages posted by R.B. and Andrea. No, their conversation today was not about diet, but somehing that's cruicial to our survival.

Everyone, please read the previous two postings by these two ladies. They are both long-time survivors and full of wisdom.

[R.B.]

HI Jackie07,

Many thanks for your very kind words. I have been posting on this board for quite a few years now, and am honoured that you thought I was female, but am a man with a particular interest in this devastating cancer.

Hi Andrea,

I had no idea you had gone through a misdiagnosis, your thoughts are always inspirational.

Doctors do their very best but the body is very complex, and sometimes as you say, we just have to go with our gut analysis and try and answer our concerns