The traditional diet of Greece and cancer.

i live in greece. unfortunately the hospitals here in greece are full of cancer patients, especially in crete.
my mother has metastatic breast cancer, since she was a child she followed a very healthy nutrition but unfortunately this did'nt helped to prevent the disease.
The truth is that -at the moment- she never had symptoms of the disease. she feels very good, full of energy, she does a lot of things every day.
from this point of view, maybe this could be a sign that greek diet helps cancer patients to have a good qol and live with dignity.
take care
lorenzo

[R.B.]

Thank you for your post.

I am glad your mother has a good qol.

I was sorry to hear of the suggestion of high numbers of cases in Crete. I would be positive to know of corners that had managed to avoid the increase that are being seen in numbers.

The articles do refer to the pre 1960 diet, and I guess was based on then (1960) statistics.

The introduction in dietary changes, vegetable oils, vegetable oils in processed foods etc may have changed the comparative cancer ratio bringin them more in line with other western countries since then.

It is not something I have specifically looked at.

Also sadly there are always going to be those for whom diet may offer better qol but have some sort of predisposition, exposure to other environmental factors etc.

Thank you agin for your post.

I hope your mother continues to enjoy a good qol. grape vines, Tavernas feta, juicy fresh peaches, local honey, feta basil and tomatoes come to mind but that was some years ago.

RB

[RobinP]

RB thanks so much for the omega three balancing dietary posts which are prudent for overall healthy living and to help prevent many disease conditions. I think it has made me more conscious of what I, my kids and husband eats which is a good thing. Afterall, we are what we eat to a certain degree, and also as the above abstracts suggests we are what mother ate while we were in utero as well. Of course, I agree that genetics and environment also plays into the equation and defines our weakness, strengths and our suspectibility to disease.

[R.B.]

I have see trial that suggest negative impacts for trans fats including blocking the pathways to make long chain fats which could compromise immune function, exacerbate related conditions, and as previously posted potentially impact on risks of cancer etc.

Margerines come in different "shapes" and sizes with different levels of polyunsaturates contents and thrans fats etc.

But you may like to try this with your brand, and some butter as a contol.

The author has a way with words.

RB





http://www.healthy-communications.co...margerine.html

Subject Butter or Parkay?
Date Sat, 18 Mar 2006

Margarine was originally manufactured to fatten turkeys. When it killed the
turkeys, the people who had put all the money into the research wanted a
payback so they put their heads together to figure out what to do with this
product to get their money back. It was a white substance with no food
appeal so they added the yellow coloring and sold it to people to use in
place of butter. How do you like it? They have come out with some clever
new flavorings.

DO YOU KNOW... the difference between margarine and butter?

Read on to the end...gets very interesting!

Both have the same amount of calories.

Butter is slightly higher in saturated fats at 8 grams compared to 5 grams.

Eating margarine can increase heart disease in women by 53% over eating
the same amount of butter, according to a recent Harvard Medical Study.

Eating butter increases the absorption of many other nutrients in other
foods.

Butter has many nutritional benefits where margarine has a few only because
they are added!

Butter tastes much better than margarine and it can enhance the flavors of
other foods.

Butter has been around for centuries where margarine has been around for
less than 100 years.

And now, for Margarine. Very high in trans fatty acids.

Triple risk of coronary heart disease.

Increases total cholesterol and LDL (this is the bad cholesterol) and
lowers HDL cholesterol, (the good cholesterol)

Increases the risk of cancers up to five fold.

Lowers quality of breast milk.

Decreases immune response.

Decreases insulin response.

And here's the most disturbing fact.... HERE IS THE PART THAT IS VERY
INTERESTING!

Margarine is but ONE MOLECULE away from being PLASTIC..

This fact alone was enough to have me avoiding margarine for life and
anything else that is hydrogenated (this means hydrogen is added, changing
the molecular structure of the substance).

You can try this yourself

Purchase a tub of margarine and leave it in your garage or shaded area.
Within a couple of days you will note a couple of things

* no flies, not even those pesky fruit flies will go near it (that should
tell you something)

* it does not rot or smell differently because it has no nutritional value
nothing will grow on it. Even those teeny weeny microorganisms will not a
find a home to grow.

Why? Because it is nearly plastic. Would you melt your Tupperware and
spread that on your toast?


Share This With Your Friends.....(If you want to "butter them up")

[RhondaH]

IF I "splurge" on my diet, I would rather use the REAL thing (i.e. butter, sugar) instead of the margarine, splenda, etc. as it seems that all the "stuff" they put in the food to lower the calories and/or fat, we have YET to know what it will do to our bodies and while YES, it may be helping us lose weight, do we REALLY know what it is doing to our bodies that's why everything is "real". It just seems like all the low fat, artificially sweetened food (with fewer) calories MAY be doing us more harm than good. Well, I have to go now as I'm off to the market to pick up my 40lbs of organic blueberries (sounds like a lot, BUT I use them as well as other berries...already froze 25lbs of strawberries...in Diana Dyers phytochemical shake that I have every day) AND I'm splurging and making a blueberry cobbler...mmm. Take care and God bless.

Rhonda

[R.B.]

See also previous post re DHA reducing bone loss and here a 2006 trial as well



"Bone marrow from LF-CO animals appeared to be more resistant to araC treatment than either MF group. Thus, DHA, fed as DHASCO, has advantages over low or moderate n-6 diets and chow as it is has both hypolipidemic- and bone marrow-enhancing properties in weanling Fischer 344 rats. This suggests that DHA supplementation may be useful in adjuvant chemotherapy."




http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9076666

1: Lipids. 1997 Mar;32(3):293-302. Links
Incorporation of long-chain n-3 fatty acids in tissues and enhanced bone marrow cellularity with docosahexaenoic acid feeding in post-weanling Fischer 344 rats.

* Atkinson TG,
* Barker HJ,
* Meckling-Gill KA.

Department of Human Biology and Nutritional Sciences, University of Guelph, Ontario, Canada.

We wanted to examine the effects of an oil rich in docosahexaenoic acid (DHA), without eicosapentaenoic acid, on the composition of membrane phospholipid in a variety of tissues. Our in vitro studies had previously shown that DHA could modify glucose and nucleoside transport in cells in culture and also increase selectivity of the nucleoside drug, arabinosylcytosine (araC) toward tumor cells. Here we wanted to examine what effect DHA supplementation would have in the whole animal in terms of the chemosensitivity of normal bone marrow, the dose-limiting tissue during chemotherapy, to araC. The purpose was to determine whether fatty acid supplementation might be useful as an adjuvant to chemotherapy. We fed diets containing 5% (w/w) low fat-corn oil (LF-CO group), 10% moderate fat-safflower oil (MF-SO group), or 10% DHASCO (MF-DHA group) to weanling Fischer 344 rats for 8-9 wk. Feed intake and growth were not different between the different diets. Similarly, treatment of animals with the chemotherapeutic drug araC did not differentially affect growth, feed intake, or tissue fatty acid composition for the different diet groups. Fatty acid compositions of bone marrow, liver, red blood cells, plasma phospholipid and triglyceride, as well as skeletal and cardiac muscle, were substantially different between the dietary groups. The DHASCO oil contained 46% DHA (22:6n-3) and resulted in profound incorporation of DHA in all tissues examined. The most dramatic response was seen in skeletal muscle of MF-DHA fed animals where DHA represented 46% of membrane phospholipid fatty acids. This is likely to have consequences to muscle function. Although DHASCO contains a similar level of saturated fatty acids (42%), few differences in saturates were noted between the various dietary groups for most of the tissues examined. Both LF-CO and MF-SO diets were hypercholesterolemic, and the LF-CO was also hypertriglyceridemic compared to the chow-fed animals. Animals fed the MF-DHA diet had the lowest triglyceride levels of any of the treatment groups and cholesterol levels comparable to chow-fed animals. MF-DHA had substantially higher numbers of colony-forming units-granulocyte macrophage (CFU-GM) as reflected in a twofold higher bone marrow cellularity than either chow or LF-CO animals, suggesting expansion of the bone marrow compartment with DHA feeding. Although higher than LF-SO, the number of CFU-GM in MF-SO animals was not significantly higher than animals fed chow. Bone marrow from LF-CO animals appeared to be more resistant to araC treatment than either MF group. Thus, DHA, fed as DHASCO, has advantages over low or moderate n-6 diets and chow as it is has both hypolipidemic- and bone marrow-enhancing properties in weanling Fischer 344 rats. This suggests that DHA supplementation may be useful in adjuvant chemotherapy.

PMID: 9076666 [PubMed - indexed for MEDLINE]



http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16102959


1: J Nutr Biochem. 2006 Apr;17(4):282-9. Epub 2005 Jun 21.Click here to read Links
Dietary ratio of n-6/n-3 PUFAs and docosahexaenoic acid: actions on bone mineral and serum biomarkers in ovariectomized rats.

* Watkins BA,
* Li Y,
* Seifert MF.

Center for Enhancing Foods to Protect Health, Lipid Chemistry and Molecular Biology Laboratory, Purdue University, West Lafayette, IN 47907-2009, USA. baw@purdue.edu

Hypoestrogenic states escalate bone loss in animals and humans. This study evaluated the effects of the amount and ratio of dietary n-6 and n-3 polyunsaturated fatty acids (PUFAs) on bone mineral in 3-month-old sexually mature ovariectomized (OVX) Sprague-Dawley rats. For 12 weeks, the rats were fed either a high-PUFA (HP) or a low-PUFA (LP) diet with a ratio of n-6/n-3 PUFAs of 5:1 (HP5 and LP5) or 10:1 (HP10 and LP10). All diets (modified AIN-93G) provided 110.4 g/kg of fat from safflower oil and/or high-oleate safflower oil blended with n-3 PUFAs (DHASCO oil) as a source of docosahexaenoic acid (DHA). Fatty acid analyses confirmed that the dietary ratio of 5:1 significantly elevated the amount of DHA in the periosteum, marrow and cortical and trabecular bones of the femur. Dual-energy X-ray absorptiometry measurements for femur and tibia bone mineral content (BMC) and bone mineral density showed that the DHA-rich diets (HP5 and LP5) resulted in a significantly lower bone loss among the OVX rats at 12 weeks. Rats fed the LP diets displayed the lowest overall serum concentrations of the bone resorption biomarkers pyridinoline (Pyd) and deoxypyridinoline, whereas the bone formation marker osteocalcin was lowest in the HP groups. Regardless of the dietary PUFA content, DHA in the 5:1 diets (HP5 and LP5) preserved rat femur BMC in the absence of estrogen. This study indicates that the dietary ratio of n-6/n-3 PUFAs (LP5 and HP5) and bone tissue concentration of total long-chain n-3 PUFAs (DHA) minimize femur bone loss as evidenced by a higher BMC in OVX rats. These findings show that dietary DHA lowers the ratio of 18:2n-6 (linoleic acid)/n-3 in bone compartments and that this ratio in tissue correlates with reduced Pyd but higher bone alkaline phosphatase activity and BMC values that favor bone conservation in OVX rats.

PMID: 16102959 [PubMed - indexed for MEDLINE]

[R.B.]

For those of you who may have read the "very thought provoking" http://www.her2support.org/vbulletin...ight=provoking post on the man who claimed to have significantly impacted on lung cancer by balancing the omega threes and sixes here is some more evidence that would support such a possibility.

RB

http://carcin.oxfordjournals.org/cgi...tract/26/4/779

Decreased n-6/n-3 fatty acid ratio reduces the invasive potential of human lung cancer cells by downregulation of cell adhesion/invasion-related genes
Shu-Hua Xia, Jingdong Wang and Jing X. Kang*

Departments of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA

* To whom correspondence should be addressed. Tel: +1 617 726 8509; Fax: +1 617 726 6144; Email: kang.jing@mgh.harvard.edu

Recent studies have shown opposing effects of n-6 and n-3 fatty acids on the development of cancer and suggest a role for the ratio of n-6 to n-3 fatty acids in the control of cancer. However, whether an alteration in the n-6/n-3 fatty acid ratio of cancer cells affects their invasive potential has not been well investigated. We recently developed a genetic approach to modify the n-6/n-3 ratio by expression of the Caenorhabditis elegans fat-1 gene encoding an n-3 desaturase that converts n-6 to n-3 fatty acids in mammalian cells. The objective of this study was to examine the effect of alteration in the n-6/n-3 fatty acid ratio on the invasive potential of human lung cancer A549 cells. Adenovirus-mediated gene transfer of the n-3 desaturase resulted in a marked reduction of the n-6/n-3 fatty acid ratio, particularly the ratio of arachidonic acid to eicosapentaenic acid. Cell adhesion assay showed that the cells expressing fat-1 gene had a delayed adhesion and retarded colonization. Matrigel assay for invasion potential indicated a 2-fold reduction of cell migration in the fat-1 transgenic cells when compared with the control cells. An increased apoptosis was also observed in the fat-1 transgenic cells. Microarray and quantitative polymerase chain reaction revealed a downregulation of several adhesion/invasion-related genes (MMP-1, integrin-{alpha}2 and nm23-H4) in the fat-1 transgenic cells. These results demonstrate that a decreased n-6/n-3 fatty acid ratio reduces the invasion potential of human lung cancer cells by probably downregulating the cell adhesion/invasion-related molecules, suggesting a role for the ratio of n-6 to n-3 fatty acids in the prevention and treatment of cancer.

[R.B.]

Fats in milk will obviously depend on feed as cows like us are what they eat.

So I suppose you need to know what your organics cows ate but a Uk trial suggests organic milk has a better fat profile.

High levels of vegetable seed in feed are likely to produce high six contents.

Interestingly swiss cows from alpine pastures seem to have high omega three content.

RB


http://www.dairy-science.org/cgi/con...ract/89/6/1938

Comparing the Fatty Acid Composition of Organic and Conventional Milk
K. A. Ellis*,1, G. Innocent*, D. Grove-White{dagger}, P. Cripps{dagger}, W. G. McLean{ddagger}, C. V. Howard§ and M. Mihm#

* Division of Animal Production and Public Health, University of Glasgow Veterinary School, Bearsden Road, Bearsden, Glasgow, G61 1QH, UK
{dagger} Division of Livestock Health and Welfare, University of Liverpool, Faculty of Veterinary Medicine, Leahurst, Neston, CH64 7TE, UK
{ddagger} Department of Pharmacology & Therapeutics School of Biomedical Sciences, Sherrington Buildings, Ashton Street, Liverpool, Merseyside, L69 3GE, UK
§ Centre for Molecular Biosciences, University of Ulster, Cromore Road, Coleraine, Co. Londonderry, BT52 1SA, UK
# Division of Cell Sciences, Institute of Comparative Medicine, University of Glasgow Veterinary School, Bearsden Road, Bearsden, Glasgow, G61 1QH, UK

1 Corresponding author: k.ellis@vet.gla.ac.uk

During a 12-mo longitudinal study, bulk-tank milk was collected each month from organic (n = 17) and conventional (n = 19) dairy farms in the United Kingdom. All milk samples were analyzed for fatty acid (FA) content, with the farming system type, herd production level, and nutritional factors affecting the FA composition investigated by use of mixed model analyses. Models were constructed for saturated fatty acids, the ratio of polyunsaturated fatty acids (PUFA) to monounsaturated fatty acids, total n-3 FA, total n-6 FA, conjugated linoleic acid, and vaccenic acid. The ratio of n-6:n-3 FA in both organic and conventional milk was also compared. Organic milk had a higher proportion of PUFA to monounsaturated fatty acids and of n-3 FA than conventional milk, and contained a consistently lower n-6:n-3 FA ratio (which is considered beneficial) compared with conventional milk. There was no difference between organic and conventional milk with respect to the proportion of conjugated linoleic acid or vaccenic acid. A number of factors other than farming system were identified which affected milk FA content including month of year, herd average milk yield, breed type, use of a total mixed ration, and access to fresh grazing. Thus, organic dairy farms in the United Kingdom produce milk with a higher PUFA content, particularly n-3 FA, throughout the year. However, knowledge of the effects of season, access to fresh grazing, or use of specific silage types could be used by producers to enhance the content of beneficial FA in milk.

Key Words: organic farming • fatty acid • n-3 fatty acid • conjugated linoleic acid



http://circ.ahajournals.org/cgi/cont...ract/109/1/103

Basic Science Reports
High {omega}-3 Fatty Acid Content in Alpine Cheese
The Basis for an Alpine Paradox
Christa B. Hauswirth, MD; Martin R.L. Scheeder, Dr sg agr; Jürg H. Beer, MD

From the Department of Medicine, Kantonsspital Baden, and the Federal Institute of Technology, Zürich, Switzerland.

Correspondence to J.H. Beer, MD, Department of Medicine, Kantonsspital Baden, 5404 Baden, Switzerland. E-mail hansjuerg.beer@ksb.ch

Received June 17, 2003; revision received August 21, 2003; accepted August 22, 2003.

Background— {alpha}-Linolenic acid (ALA) may protect from cardiovascular disease. Because fresh alpine grass contains high amounts of ALA, we hypothesized that the levels of {omega}-3 fatty acids would concentrate to nutritional relevance in the cheese of milk from cows with alpine grass feeding compared with cheese from silage and concentrate feeding; the newly available cheese produced from cows fed with linseed supplementation should contain even higher ALA concentrations.

Methods and Results— Forty different cheeses were analyzed by gas chromatography for their fatty acid profile: (1) 12 from well-defined alpine regions around Gstaad, Switzerland; (2) 7 commercially available English cheddar cheeses; (3) 6 cheeses from cows fed with linseed supplementation; (4) 7 industrial-type Emmentals; and (5) 8 alpine cheeses with partial silage feeding. The alpine cheese contained 4 times more linolenic acid (C18:3{omega}-3) compared with cheddar, more total {omega}-3 fatty acids, and showed a significantly lower n-6:{omega}-3 ratio. Conjugated linoleic acid (C18:2 c9/t11) was 3-fold higher, whereas the amount of palmitic acid was 20% lower. The Emmental reached 40% of the ALA content compared with alpine cheese, and surprisingly, cheese from linseed-supplemented cows contained only 49% of that of the alpine cheese (P<0.001 for each trait in the 5 cheese groups).

Conclusions— Cheese made of milk from cows grazed on alpine pastures had a more favorable fatty acid profile than all other cheese types. Alpine cheese may be a relevant source of ALA and other cardioprotective fatty acids.


Key Words: nutrition • fatty acids • coronary disease • diet • death, sudden

[R.B.]

ABSTRACT

"The omega-3 fatty acids continue to accumulate research that suggests that they may prevent a variety of diverse chronic diseases and potentially some acute clinical scenarios. In the first part of this article, the potential for these compounds to prevent certain cardiovascular conditions are discussed. In the second part, the potential for an impact in arthritis, numerous areas of cancer research, depression, maternal and child health, neurologic diseases, osteoporosis, and other medical disciplines are also briefly covered. "








http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: Urol Oncol. 2005 Jan-Feb;23(1):36-48.Click here to read Links
An introduction to dietary/supplemental omega-3 fatty acids for general health and prevention: part II.

* Moyad MA.

Phil F. Jenkins Director of Complementary & Alternative Medicine, Department of Urology, University of Michigan Medical Center, Ann Arbor, 48109-0330, USA. moyad@umich.edu

The correction of a subtle nutritional deficiency that may reduce the risk of a future chronic disease is indeed a challenge. However, some specific examples in the past, such as the addition of folic acid to prevent neural tube defects and calcium and vitamin D to prevent osteoporosis, should provide some encouragement that some conditions can be prevented with the appropriate addition of a deficient compound. One of the most intriguing current and future impacts on public health may come from a higher intake of omega-3 fatty acids, such as alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). The omega-3 fatty acids continue to accumulate research that suggests that they may prevent a variety of diverse chronic diseases and potentially some acute clinical scenarios. In the first part of this article, the potential for these compounds to prevent certain cardiovascular conditions are discussed. In the second part, the potential for an impact in arthritis, numerous areas of cancer research, depression, maternal and child health, neurologic diseases, osteoporosis, and other medical disciplines are also briefly covered. The future appears bright for these agents, but specifically which conditions, who qualifies, testing, frequency, adequate sources, future trials, and numerous other questions need to be addressed and answered before the potential impact can catch up to the recent hype.

PMID: 15885582 [PubMed - indexed for MEDLINE]

[R.B.]

Blocking delta destaurase 5 will inhibit the formation of Archnidonic acid the omega six raw material for the eisosanoid pathways.

It may aslo push the omega six to DGLA conversion via the series one pathway which is reported as producing less inflamatory agents that the series two pathways.

This presumably acounts for its reported anti inflamatory properties.

But does it also block the 5 pathway for omegas threes long chain fabrication in the body (DHA and EPA)? (AMENDMENT I have just found a trial which suggests it does not which makes it a really interesting dietary adjunct) [Trial see below)

Also if excess omega six souces is a factor in inflamtion in a persons body the consequences in blocking the elongation pathways. The body has been supplied with the omega six and has to do something with it - burn it in exercise or for energy - store it in fat - and if there is too much of it in the circulation trials suggest things start going wrong with inapproriate oxidation leading heart conditions.

All of which might lead on to the conclusion that the easiest long term option is not getting to much in the first place.

RB




http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=1291640

1: J Nutr Sci Vitaminol (Tokyo). 1992 Aug;38(4):353-63. Links
Effects of sesamin and curcumin on delta 5-desaturation and chain elongation of polyunsaturated fatty acid metabolism in primary cultured rat hepatocytes.

* Fujiyama-Fujiwara Y,
* Umeda R,
* Igarashi O.

Institute of Environmental Science for Human Life, Ochanomizu University, Tokyo, Japan.

Effects of sesamin and curcumin on delta 5-desaturation and chain elongation of polyunsaturated fatty acid (PUFA) were studied in rat primary cultured hepatocytes. When sesamin was added to culture medium containing 20:4 (n-3), rat hepatocytes after 24 h of incubation produced 20:5 (n-3) from 20:4 (n-3), whereas when incubated with 20:3 (n-6), the metabolite by delta 5-desaturation did not accumulate, and consequently, the ratio of 20:3 (n-6)/20:4 (n-6) increased with the amount of sesamin added. Curcumin was more effective than sesamin in this respect. Both sesamin and curcumin interfered with chain elongation of PUFAs. An addition of 18:3 (n-6) or 18:4 (n-3) increased the cellular concentrations of 20:3 (n-6) or 20:4 (n-3), respectively, but the simultaneous addition of sesamin or curcumin inhibited the chain elongation of C18 acids (the fatty acids with 18 carbons) into corresponding C20 and C18 acids. Similarly, the elongation from C20 of n-3 and n-6 families to C22 was also inhibited with sesamin and curcumin. These results suggested that: 1) sesamin and curcumin inhibited delta 5-desaturation of n-6 fatty acid, but not n-3 fatty acid in rat hepatocytes; 2) curcumin was more effective than sesamin; 3) chain elongation was also inhibited by sesamin and curcumin.

PMID: 1291640 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9610840

1: Prostaglandins Leukot Essent Fatty Acids. 1998 Mar;58(3):185-91. Links
Dietary alpha-linolenic acid increases TNF-alpha, and decreases IL-6, IL-10 in response to LPS: effects of sesamin on the delta-5 desaturation of omega6 and omega3 fatty acids in mice.

* Chavali SR,
* Zhong WW,
* Forse RA.

Department of Surgery, Harvard Institute of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.

Sesamin (a non-fat portion of sesame seed oil) inhibits delta-5 desaturase activity resulting in an accumulation of dihomo-gamma-linolenic acid (DGLA) which can displace arachidonic acid (AA) and decrease the formation of pro-inflammatory mediators. We investigated the effects of consumption of diets containing 0.25wt% sesamin and 15 wt% safflower oil (SO) (providing 12% of the added fat as linoleic acid) or a 15 wt% 2:1 mixture of linseed oil and SO (LOSO) (providing 6% alpha-linolenic acid and 6% linoleic acid) for 3 weeks on the liver membrane fatty acid composition and on the production of prostaglandin (PG) E2, TNF-alpha, IL-6 and IL10 in mice. Consumption of sesamin-supplemented SO and LOSO diets resulted in a significant increase in the levels of 20:3omega6 (DGLA), suggesting that sesamin inhibited delta-5 desaturation of omega6 fatty acids. In animals fed LOSO diets, the levels of alpha-linolenic acid, eicosapentaenoic acid (EPA) and of docosahexaenoic acid (DHA) were elevated with a concomitant decrease of arachidonic acid (AA) in the liver membrane phospholipids. Further, in animals fed LOSO diets with or without sesamin, an increase in the circulating levels of TNF-alpha was associated with a concomitant decrease in PGE2. Despite a lack of differences in the levels of AA, the PGE2 levels were significantly lower in mice fed sesamin-supplemented SO compared to those fed SO alone. Thus, these data suggest that irrespective of the availability of a specific fatty acid as a substrate, through regulating the PGE2 synthesis, the production of TNF-alpha could be modulated.

PMID: 9610840 [PubMed - indexed for MEDLINE]

[R.B.]

1: Neuro Endocrinol Lett. 2005 Dec;26(6):745-51. Links
In chronic fatigue syndrome, the decreased levels of omega-3 poly-unsaturated fatty acids are related to lowered serum zinc and defects in T cell activation.

* Maes M,
* Mihaylova I,
* Leunis JC.

M-Care4U Outpatient Clinics, and the Clinical Research Center for Mental Health, Antwerp, Belgium.

There is now evidence that major depression is accompanied by decreased levels of omega3 poly-unsaturated fatty acids (PUFA), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). There is a strong comorbidity between major depression and chronic fatigue syndrome (CFS). The present study has been carried out in order to examine PUFA levels in CFS. In twenty-two CFS patients and 12 normal controls we measured serum PUFA levels using gas chromatography and mass spectrometry. We found that CFS was accompanied by increased levels of omega6 PUFAs, i.e. linoleic acid and arachidonic acid (AA), and mono-unsaturated fatty acids (MUFAs), i.e. oleic acid. The EPA/AA and total omega3/omega6 ratios were significantly lower in CFS patients than in normal controls. The omega3/omega6 ratio was significantly and negatively correlated to the severity of illness and some items of the FibroFatigue scale, i.e. aches and pain, fatigue and failing memory. The severity of illness was significantly and positively correlated to linoleic and arachidonic acid, oleic acid, omega9 fatty acids and one of the saturated fatty acids, i.e. palmitic acid. In CFS subjects, we found significant positive correlations between the omega3/omega6 ratio and lowered serum zinc levels and the lowered mitogen-stimulated CD69 expression on CD3+, CD3+ CD4+, and CD3+ CD8+ T cells, which indicate defects in early T cell activation. The results of this study show that a decreased availability of omega3 PUFAs plays a role in the pathophysiology of CFS and is related to the immune pathophysiology of CFS. The results suggest that patients with CFS should respond favourably to treatment with--amongst other things--omega3 PUFAs, such as EPA and DHA.

PMID: 16380690 [PubMed - indexed for MEDLINE]

[R.B.]

If you are debating the best way to get your fish omega threes and sixes the articles below would provide arguments for fish oil or wild fish however humble, and thats without looking at other issues.

I must admit the figures made my draw drop.

The conversion rate from wild fish as food to farmed fish is apparently about 4 or 5 to 1.

A high price to fill our shelves with particular fish types?

I am not against farming fish to preserve wild stocks but where is the environmental "value" balance.

RB


Antarctic Krill: a case study on the ecosystem implications of fishing
http://72.14.221.104/search?q=cache:...ient=firefox-a


ABSTRACT

The fish farming industry already uses up
around 75% of the world’s fish oil and
around 40% of the world’s fish meal. By
2010, these figures might go up to 90% and
56% respectively, according to predictions
by the International Fish Meal and Fish Oil
Manufacturers Association (IFOMA). FAO
has indicated that by 2010, farmed salmon and trout alone could consume 620,000 tonnes
of fish oil (Staniford 2002). With demand exceeding supply and rising prices, fish oil has
been labelled “the new blue gold” (Staniford 2001).

http://72.14.221.104/search?q=cache:...ient=firefox-a


ABSTRACT

"Number 8
Winter 2001
Effects of Aquaculture on World Fish Supplies
SUMMARY
Global production of farmed fish, shrimp, clams, and oysters more than doubled in weight and value during the
1990s while landings of wild-caught fish remained level. Many people look to this growth in aquaculture to relieve
pressure on ocean fish stocks, most of which are now fished at or beyond capacity, and to allow wild populations to
recover. Production of farmed fish and shellfish does increase world fish supplies. Yet by using increasing amounts of wild-
caught fish to feed farmed shrimp and salmon, and even to fortify the feed of herbivorous fish such as carp, some sectors
of the aquaculture industry are actually increasing the pressure on ocean fish populations.
The available scientific evidence indicates that some types of aquaculture are on a destructive path that poses a
threat not only to wild fish stocks but also to the industry’s own long-term potential. One of the most disturbing trends is
the rapid expansion and intensification of shrimp and salmon farming and culture of other high-value carnivorous marine
fish such as cod, seabass, and tuna. Production of a single kilogram of these species typically uses two to five kilograms
of wild-caught fish processed into fish meal and fish oil for feed.
Besides this direct impact on wild fish stocks, some aquaculture as currently practiced degrades the marine
environment and diminishes the ecological life support services it provides to fish, marine mammals, and seabirds, as well
as humans. These impacts include
• Destruction of hundreds of thousands of hectares of mangrove forests and coastal wetlands for construction
of aquaculture facilities
• Use of wild-caught rather than hatchery-reared finfish or shellfish fry to stock captive operations, a practice
that often leads to a high rate of discarded bycatch of other species
• Heavy fishing pressure on small ocean fish such as anchovies for use as fish meal, which can deplete food for
wild fish such as cod, as well as seals and seabirds
• Transport of fish diseases into new waters and escapes of non-native fish that may hybridize or compete with
native wild fish
As aquaculture production continues to expand and intensify, both its reliance and its impact on ocean fisheries are
likely to increase. The balance between farmed and wild-caught fish, as well as the total supply of fish available for human
consumption, will depend on future trends in aquaculture practices. If the goal of aquaculture is to produce more fish for
consumers than can be produced naturally, then it will become increasingly counterproductive to farm carnivores that must
be fed large amounts of wild-caught fish that form the foundation of the ocean food chain. Indeed, non-carnivorous
species such as marine mollusks and carps account for most of the current net gain in world fish supplies from aquaculture.
Without clear recognition of its dependence on natural ecosystems, the aquaculture industry is unlikely to develop
to its full potential or continue to supplement ocean fisheries. We recommend the adoption of four priority goals for
aquaculture:
• Encourage farming of species lower on the food web – that is, fish with herbivorous or omnivorous diets or
filter feeders such as oysters
• Improve feed management and efficiency in industrial aquaculture systems and develop substitutes for fish-
derived feed ingredients
• Develop integrated fish farming systems that use multiple species to reduce costs and wastes while increasing
productivity
• Promote environmentally sound aquaculture practices and resource management
Governments have a key role to play in developing regulations to protect coastal ecosystems and in reexamining
subsidies to unsustainable marine fisheries. Development agencies are strategically placed to help in developing and
implementing sustainable production practices and in financing otherwise economically and socially unattainable reforms in
developing countries. If public and private interests act jointly to reduce the environmental costs generated by fish farm-
ing, present unsustainable trends can be reversed and aquaculture can make an increasingly positive contribution to global
fish supplies..............."
Cover (clockwise from top): shrimp ponds in Honduras (courtesy CODDEFFAGOLF); basket of milkfish (J. Primavera); harvesting catfish in
Mississippi (K. Hammond, courtesy USDA).

[R.B.]

Having done some more searches on the subject of fish farming there is contoversy about the "conversion" rate.

Here is another link to an article on conversion which contains three figues and one from the industry to balance things.



RB


http://www.davidsuzuki.org/Oceans/Fi...n/Net_Loss.asp

Net loss of wild fish to produce farmed salmon

A total of 2.7 to 3.5 tonnes of wild fish are used to make 1 tonne of farmed salmon

ABSTRACT



"Since a salmon farm in BC currently uses between 1.3 and 1.7 tonnes of dry feed (ie: FCR of 1.3 to 1.7) to make one tonne of farmed salmon, then the total amount of wild fish used to make one tonne salmon is between 2.7 and 3.5 tonnes (ie: the FCR multiplied by 2.08). It should be noted that in practice, BC salmon farms do not often reach the lower FCR of 1.3 which is achievable only when feed is used very efficiently on the farm. Rather than taking pressure off ocean resources then, salmon farming is currently adding greatly to that pressure..........................Much more research needs to be done and it is unclear when, or if the day will come when farmed salmon will be vegetarian. In the meantime, the stress on the ocean ecosystem will increase as salmon aquaculture expands globally. The consumption of 6.2 tonnes of wild fish for each tonne of salmon produced not only means less food for humans, but also for the many ocean species that rely on these fish as part of their food chain. Currently, the continued expansion of salmon farming is not sustainable.."



http://www.wfga.net/issues.asp?id=37

The Environmental Impact Of Salmon Farms

[R.B.]

Please also see prior posts on COX inhibitors and DHA.

This is prostate but there seems to be some communality of mechanisms in many cancers.

RB



1: Int J Cancer. 2006 Apr 27; [Epub ahead of print]Click here to read Links
Docosahexaenoic acid in combination with celecoxib modulates HSP70 and p53 proteins in prostate cancer cells.

* Narayanan NK,
* Narayanan BA,
* Bosland M,
* Condon MS,
* Nargi D.

Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY.

The role of cyclooxygenase-2 (COX-2) and the mechanism by which it influences the development and behavior of prostate cancer is unclear. Selective COX-2 inhibitors may be effective against prostate cancer via COX-2-independent mechanisms. But administration of high doses of COX-2 inhibitors over longer period of time may not be devoid of side effects. There is increasing interest in using COX-2 inhibitors in combination with other chemopreventive agents to overcome the issue of toxicity. However, the molecular mechanisms underlying their combined actions are not well understood. Therefore, the present study was designed to determine the effects of low doses of docosahexaenoic acid (DHA) in combination with celecoxib on the molecular targets at the proteins level in rat prostate cancer cells. Two-dimensional gel electrophoresis, in combination with mass spectrometry analysis, was used for protein identification. Western blot analysis confirmed the proteins identified. Paraffin-embedded tissue sections from the rat prostate tumor were used to detect base level expression of heat shock protein 70 (HSP70) and p53. The rate of cancer cell growth was inhibited more effectively (p < 0.01) by DHA in combination with celecoxib at lower doses (2.5 muM each). A total number of twelve proteins were differentially expressed by the combined action of DHA and celecoxib at low doses. It was interesting to note that these agents activated both HSP70 and p53 proteins. Activation of HSP70 by the combined actions of DHA and celecoxib in the presence of wild-type p53 reveals a unique COX-2 independent mode of action against prostate cancer. (c) 2006 Wiley-Liss, Inc.

PMID: 16646082 [PubMed - as supplied by publisher]

[R.B.]

More links between repoduction and prostaglandins. " Although the mechanism by which prostaglandins modulate these changes remains unclear, much evidence suggests that prostaglandins and their receptors and downstream signalling pathways are involved in angiogenesis and in alterations in cell adhesion, morphology, motility, invasion and metastases. "

Whilst omega threes and GLA both produce separte series of prosaglandins series 1 and series 3 the limited materila I have read links 1 and 3 to moderating roles in cell maturation etc, and series 2 which are derived from omega six and AA are the drivers.

More questions

RB



http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15380812

1: Trends Endocrinol Metab. 2004 Oct;15(8):398-404.Click here to read Links
Prostaglandin receptor signalling and function in human endometrial pathology.

* Jabbour HN,
* Sales KJ.

MRC Human Reproductive Sciences Unit, Centre for Reproductive Biology, The University of Edinburgh Academic Centre, 49 Little France Crescent, Edinburgh EH16 4SB, Scotland, UK. h.jabbour@hrsu.mrc.ac.uk

Prostaglandins are bioactive lipids that exert an autocrine or paracrine function by binding to specific G-protein-coupled receptors (GPCRs) to activate intracellular signalling and gene transcription. Prostaglandins are key regulators of reproductive processes, including ovulation, implantation and menstruation. Prostaglandins have been ascertained to have a role in various pathological changes of the reproductive tract including menorrhagia, dysmenorrhea, endometriosis and cancer. Although the mechanism by which prostaglandins modulate these changes remains unclear, much evidence suggests that prostaglandins and their receptors and downstream signalling pathways are involved in angiogenesis and in alterations in cell adhesion, morphology, motility, invasion and metastases. The potential role of prostaglandin receptors in pathological changes of the endometrium has significance for the future development of therapeutic interventions.

PMID: 15380812 [PubMed - indexed for MEDLINE]

[R.B.]

http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16310177

Fishing for prostanoids: deciphering the developmental functions of cyclooxygenase-derived prostaglandins.

* Cha YI,
* Solnica-Krezel L,
* DuBois RN.

Department of Medicine and Cancer Biology, Cell and Developmental Biology, Vanderbilt University Medical Center and Vanderbilt Ingram-Cancer Center, Nashville, TN 37232-2279, USA.

Prostaglandin G/H synthases (PGHS), commonly referred to as cyclooxygenases (COX-1 and COX-2), catalyze a key step in the synthesis of biologically active prostaglandins (PGs), the conversion of arachidonic acid (AA) into prostaglandin H(2) (PGH(2)). PGs have important functions in a variety of physiologic and pathologic settings, including inflammation, cardiovascular homeostasis, reproduction, and carcinogenesis. However, an evaluation of prostaglandin function in early development has been difficult due to the maternal contribution of prostaglandins from the uterus. The emergence of zebrafish as a model system has begun to provide some insights into the roles of this signaling cascade during vertebrate development. In zebrafish, COX-1 derived prostaglandins are required for two distinct stages of development, namely during gastrulation and segmentation. During gastrulation, PGE(2) signaling promotes cell motility, without altering the cell shape or directional migration of gastrulating cells. During segmentation, COX-1 signaling is also required for posterior mesoderm development, including the formation of vascular tube structures, angiogenesis of intersomitic vessels, and pronephros morphogenesis. We propose that deciphering the role for prostaglandin signaling in zebrafish development could yield insight and ultimately address the mechanistic details underlying various disease processes that result from perturbation of this pathway.

PMID: 16310177 [PubMed - indexed for MEDLINE]

[R.B.]

A different cancer but same general direction of importance of omega three six balance.

I am scratching my head over aspects of the diagram but will work on it.


RB



http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: J Carcinog. 2006 Mar 27;5:9.Click here to read Click here to read Links
The yin and yang of 15-lipoxygenase-1 and delta-desaturases: Dietary omega-6 linoleic acid metabolic pathway in prostate.

* Kelavkar U,
* Lin Y,
* Landsittel D,
* Chandran U,
* Dhir R.

Department of Urology and University of Pittsburgh Cancer Institute, 5200 Center Ave,, SHMC-Suite G-37, Pittsburgh, PA, 15232, USA. kelavkarup@upmc.edu.

ABSTRACT : One of the major components in high-fat diets (Western diet) is the omega (omega, n)-6 polyunsaturated fatty acid (PUFA) called linoleic acid (LA). Linoleic acid is the precursor for arachidonic acid (AA). These fatty acids are metabolized to an array of eicosanoids and prostaglandins depending upon the enzymes in the pathway. Aberrant expression of the catabolic enzymes such as cyclooxygenases (COX-1 and/or -2) or lipoxygenases (5-LO, 12-LO, 15-LO-1, and 15-LO-2) that convert PUFA either AA and/or LA to bioactive lipid metabolites appear to significantly contribute to the development of PCa. However, PUFA and its cellular interactions in PCa are poorly understood. We therefore examined the mRNA levels of key enzymes involved in the LA and AA pathways in 18 human donor (normal) prostates compared to 60 prostate tumors using the Affymetrix U95Av2 chips. This comparative (normal donor versus prostate cancer) study showed that: 1) the level of 15-LO-1 expression (the key enzyme in the LA pathway) is low (P < 0.001), whereas the levels of delta-5 desaturase (P < 0.001, the key enzyme in the AA pathway), delta-6 desaturase (P = 0.001), elongase (P = 0.16) and 15-lipoxygenase-2 (15-LO-2, P = 0.74) are higher in donor (normal) prostates, and 2) Contrary to the observation in the normal tissues, significantly high levels of only 15-LO-1; whereas low levels of delta-6 desaturase, elongase, delta-5 desaturase and 15-LO-2 respectively, were observed in PCa tissues. Although the cyclooxygenase (COX)-1 and COX-2 mRNA levels were high in PCa, no significant differences were observed when compared in donor tissues. Our study underscores the importance of promising dietary intervention agents such as the omega-3 fatty acids as substrate competitors of LA/AA, aimed primarily at high 15-LO-1 and COX-2 as the molecular targets in PCa initiation and/or progression.

PMID: 16566819 [PubMed - in process]

[R.B.]

More of the same.

RB



http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16611404

1: Neoplasia. 2006 Feb;8(2):112-24.Click here to read Links
Prostate Tumor Growth and Recurrence Can Be Modulated by the omega-6mega-3 Ratio in Diet: Athymic Mouse Xenograft Model Simulating Radical Prostatectomy.

* Kelavkar UP,
* Hutzley J,
* Dhir R,
* Kim P,
* Allen KG,
* McHugh K.

Department of Urology and Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA, Email: kelavkarup@upmc.edu.

Evidence indicates that a diet rich in omega (omega)-6 polyunsaturated fatty acids (PUFAs) [e.g., linoleic acid (LA)] increases prostate cancer (PCa) risk, whereas a diet rich in omega-3 decreases risk. Precisely how these PUFAs affect disease development remains unclear. So we examined the roles that PUFAs play in PCa, and we determined if increased omega-3 consumption can impede tumor growth. We previously demonstrated an increased expression of an omega-6 LA-metabolizing enzyme, 15-lipoxygenase-1 (15-LO-1, ALOX15), in prostate tumor tissue compared with normal adjacent prostate tissue, and that elevated 15-LO-1 activity in PCa cells has a protumorigenic effect. A PCa cell line, Los Angeles Prostate Cancer-4 (LAPC-4), expresses prostate-specific antigen (PSA) as well an active 15-LO-1 enzyme. Therefore, to study whether or not the protumorigenic role of 15-LO-1 and dietary omega-6 LA can be modulated by altering omega-3 levels through diet, we surgically removed tumors caused by LAPC-4 cells (mouse model to simulate radical prostatectomy). Mice were then randomly divided into three different diet groups-namely, high omega-6 LA, high omega-3 stearidonic acid (SDA), and no fat-and examined the effects of omega-6 and omega-3 fatty acids in diet on LAPC-4 tumor recurrence by monitoring for PSA. Mice in these diet groups were monitored for food consumption, body weight, and serum PSA indicative of the presence of LAPC-4 cells. Fatty acid methyl esters from erythrocyte membranes were examined for omega-6 and omega-3 levels to reflect long-term dietary intake. Our results provide evidence that prostate tumors can be modulated by the manipulation of omega-6mega-3 ratios through diet and that the omega-3 fatty acid SDA [precursor of eicosapentaenoic acid (EPA)] promotes apoptosis and decreases proliferation in cancer cells, causing decreased PSA doubling time, compared to omega-6 LA fatty acid, likely by competing with the enzymes of LA and AA pathways, namely, 15-LO-1 and cyclooxygenases (COXs). Thus, EPA and DHA (major components of fish oil) could potentially be promising dietary intervention agents in PCa prevention aimed at 15-LO-1 and COX-2 as molecular targets. These observations also provide clues as to its mechanisms of action.

PMID: 16611404 [PubMed - in process]

[R.B.]

"Modulation of cancer development with low n-6/n-3 ratio diets containing specific dietary FA could be a promising tool in cancer intervention in the liver."


http://www.ncbi.nlm.nih.gov/entrez/q...ubmed_DocSum1: Lipids. 2004 Oct;39(10):963-76. Links
Dietary modulation of fatty acid profiles and oxidative status of rat hepatocyte nodules: effect of different n-6/n-3 fatty acid ratios.

* Abel S,
* De Kock M,
* Smuts CM,
* de Villiers C,
* Swanevelder S,
* Gelderblom WC.

Medical Research Council, Tygerberg, South Africa. stefan.abel@mrc.ac.za

Male Fischer rats were fed the AIN 76A diet containing varying n-6/n-3 FA ratios using sunflower oil (SFO), soybean oil (SOY), and SFO supplemented with EPA-50 and GLA-80 (GLA) as fat sources. Hepatocyte nodules, induced using diethylnitrosamine followed by 2-acetylaminofluorene/partial hepatectomy promotion, were harvested, with surrounding and respective dietary control tissues, 3 mon after partial hepatectomy. The altered growth pattern of hepatocyte nodules in rats fed SFO is associated with a distinct lipid pattern entailing an increased concentration of PE, resulting in increased levels of 20:4n-6. In addition, there is an accumulation of 18:1 n-9 and 18:2n-6 and a decrease in the end products of the n-3 metabolic pathway in PC, suggesting a dysfunctional delta-6-desaturase enzyme. The hepatocyte nodules of the SFO-fed rats exhibited a significantly reduced lipid peroxidation level that was associated with an increase in the glutathione (GSH) concentration. The low n-6/n-3 FA ratio diets significantly decreased 20:4n-6 in PC and PE phospholipid fractions with a concomitant increase in 20:5n-3, 22:5n-3, and 22:6n-3. The resultant changes in the 20:4/20:5 FA ratio and the 20:3n-6 FA level in the case of the GLA diet suggest a reduction of prostaglandin synthesis of the 2-series. The GLA diet also counteracted the increased level of 20:4n-6 in PE by equalizing the nodule/surrounding ratio. The low n-6/n-3 ratio diets significantly increased lipid peroxidation levels in hepatocyte nodules, mimicking the level in the surrounding and control tissue while GSH was decreased. An increase in n-3 FA levels and oxidative status resulted in a reduction in the number of glutathione-S-transferase positive foci in the liver of the GLA-fed rats. Modulation of cancer development with low n-6/n-3 ratio diets containing specific dietary FA could be a promising tool in cancer intervention in the liver.

PMID: 15691018 [PubMed - indexed for MEDLINE]

[R.B.]

Interesting RB



http://grande.nal.usda.gov/ibids/index.php


Impact of fish oil and melatonin on cachexia in patients with advanced gastrointestinal cancer: a randomized pilot study.
Author: Persson,-C; Glimelius,-B; Ronnelid,-J; Nygren,-P
Citation: Nutrition. 2005 Feb; 21(2): 170-8
Abstract: OBJECTIVE: The effect of fish oil (FO), melatonin (MLT), or their combination and dietary advice on cachexia and biochemistry variables reflecting cachexia were investigated in patients with advanced gastrointestinal cancer. METHODS: Twenty-four patients not amenable to standard anticancer treatment and with documented weight loss and/or decreased serum albumin were included. They were randomized to 30 mL/d of FO, which provided 4.9 g of eicosapentaenoic acid and 3.2 g of docosahexanoic acid, or 18 mg/d of MLT for 4 wk. During the next 4 wk, all patients had FO and MLT. Serum or plasma was analyzed for tumor necrosis factor-alpha, interleukin-1beta, soluble interleukin-2 receptor, interleukin-6, and interleukin-8 and the fatty acids eicosapentaenoic acid, docosahexanoic acid, arachidonic acid, and linoleic acid. RESULTS: Serum levels of eicosapentaenoic acid and docosahexanoic acid increased as expected with FO. No major changes in biochemical variables and cytokines were observed with any intervention. In the FO group, 5 of 13 patients (38%) showed weight stabilization or gain compared with 3 of 11 patients (27%) in the MLT group. After combining interventions, approximately 63% of patients showed such responses. CONCLUSIONS: FO, MLT, or their combination did not induce major biochemical changes indicative of a strong anticachectic effect. Nonetheless, the interventions used may have produced a weight-stabilizing effect.