The traditional diet of Greece and cancer.

[R.B.]

More about the importance of lipid rafts ^ (see previous post) and the possibility they have a very special role in HER2

This explains the active HER2 receptors (Docking stations built into the cells outer wall (membrane) into which the HER2 protein fits like a key) are only found in a particular areas of the double skin fat/protein/cholesterol bubbles that form the outer layer of cells (think bubble). The particular areas in which active HER2 receptors are apparently exclusively found are called lipid rafts (Special functional areas within the surface of the bubble that contain greater amounts of close packed fats)

It also explains that the docking locks come in three types, on activated by one HER2 protein (monomer), another type by a pair of HER2s (homodimer) and a third by an HER2 combined with another, probably specific, substance (heterodimer).

The results also suggest that there may be a connection between an increased number of HER2 docking locks and more numerous areas of lipid rafts in the cell membrane.

The HER2 protein may look something like this
http://en.wikipedia.org/wiki/File:Tr...mplex_1N8Z.png see Wikipedia http://en.wikipedia.org/wiki/HER2/neu

The paper explains DHA may alter the structure of the rafts so possibly disrupting the docking locks which ultimately may lead to higher cell death rates in cells expressing more HER2 receptors.

ABSTRACT

http://www.ncbi.nlm.nih.gov/pubmed/22749134

J Nutr Biochem. 2012 Jun 27. [Epub ahead of print]
Lipid raft disruption by docosahexaenoic acid induces apoptosis in transformed human mammary luminal epithelial cells harboring HER-2 overexpression.
Ravacci GR, Brentani MM, Tortelli T Jr, Torrinhas RS, Saldanha T, Torres EA, Waitzberg DL.
Source

Department of Oncology Medical School, University of São Paulo, 01246-903 São Paulo, Brazil; Department of Gastroenterology Medical School, University of São Paulo-LIM 35, 01246-903 São Paulo, Brazil.
Abstract

In HER-2-overexpressing breast cells, HER-2 receptors exist on the cell surface as monomers, homodimers and heterodimers. For signal activation and transduction to occur, HER-2 must be localized to lipid rafts. Therefore, we hypothesized that the amount of lipid rafts on the cell membrane would be a factor in HER-2 signaling. To test this, we used HB4a (an untransformed human mammary epithelial cell line) and HB4aC5.2 cells. HB4aC5.2 cells are HB4a derivatives that have been transfected with five copies of pJ5E.c-ErbB-2 and express approximately 900 times more HER-2 than HB4a cells. In these cells, HER-2 overexpression was accompanied by increased lipid rafts in cell membranes, a hyperactivation of downstream Akt and ERK1/2 proteins, and an increased rate of cell growth compared to HB4a. In addition, HER-2 overexpression was associated with an increased activation of FASN, a key enzyme involved in cellular lipogenesis. Its final product, palmitate, is frequently used to synthesize lipid rafts. We further hypothesized that treatment with docosahexaenoic acid (DHA), an omega-3 fatty acid, would disrupt the lipid rafts and lead to a growth arrest. In HB4aC5.2 cells, but not HB4a cells, we found that DHA treatment disrupted lipid raft; inhibited HER-2 signaling by decreasing activation of Akt, ERK1/2 and FASN proteins; and induced apoptosis.Although little is known about lipid rafts, our data support the idea that disturbances in these microdomains induced by DHA may represent a useful tool for controlling the signaling initiated by HER-2 receptors and its therapeutic potential in the treatment of HER-2 positive breast cancer.

[R.B.]

BMC Cancer. 2012 Aug 15;12(1):355. [Epub ahead of print]
Omega-3 fatty acids are protective against paclitaxel-induced peripheral neuropathy: A randomized double-blind placebo controlled trial.
Ghoreishi Z, Esfahani A, Djazayeri A, Djalali M, Golestan B, Ayromlou H, Hashemzade S, Asghari Jafarabadi M, Montazeri V, Keshavarz SA.
Abstract

ABSTRACT:
BACKGROUND:

Axonal sensory peripheral neuropathy is the major dose-limiting side effect of paclitaxel.Omega-3 fatty acids have beneficial effects on neurological disorders from their effects on neurons cells and inhibition of the formation of proinflammatory cytokines involved in peripheral neuropathy.
METHODS:

This study was a randomized double blind placebo controlled trial to investigate the efficacy of omega-3 fatty acids in reducing incidence and severity of paclitaxel-induced peripheral neuropathy (PIPN). Eligible patients with breast cancer randomly assigned to take omega-3 fatty acid pearls, 640 mg t.i.d during chemotherapy with paclitaxel and one month after the end of the treatment or placebo. Clinical and electrophysiological studies were performed before the onset of chemotherapy and one month after cessation of therapy to evaluate PIPN based on "reduced Total Neuropathy Score".
RESULTS:

Twenty one patients (70 %) of the group taking omega-3 fatty acid supplement (n = 30) did not develop PN while it was 40.7 %( 11 patients) in the placebo group(n = 27). A significant difference was seen in PN incidence (OR = 0.3, .95 % CI = (0.10-0.88), p = 0.029). There was a non-significant trend for differences of PIPN severity between the two study groups but the frequencies of PN in all scoring categories were higher in the placebo group (0.95 % CI = ([MINUS SIGN]2.06 -0.02), p = 0.054).
CONCLUSIONS:

Omega-3 fatty acids may be an efficient neuroprotective agent for prophylaxis against PIPN. Patients with breast cancer have a longer disease free survival rate with the aid of therapeutical agents. Finding a way to solve the disabling effects of PIPN would significantly improve the patients' quality of life.Trial registrationThis trial was registered at ClinicalTrials.gov (NCT01049295).

[rhondalea]

Thanks for that study.

During chemo, I took 4.252 grams of fish oil daily, for a total of 800mg DHA and 1600mg EPA. I thought it was ALCAR that prevented me from experiencing any neuropathy, but it now appears that the high dose fish oil may have played a role.

[R.B.]

BMC Med. 2012 May 21;10:50.
New insights into the health effects of dietary saturated and omega-6 and omega-3 polyunsaturated fatty acids.
de Lorgeril M, Salen P.
Source

Laboratoire Cœur & Nutrition, TIMC-IMAG, Université Joseph Fourier-CNRS, Faculté de Médecine, Grenoble, France. michel.delorgeril@ujf-grenoble.fr
Abstract

Cardiovascular diseases and cancers are leading causes of morbidity and mortality. Reducing dietary saturated fat and replacing it with polyunsaturated fat is still the main dietary strategy to prevent cardiovascular diseases, although major flaws have been reported in the analyses supporting this approach. Recent studies introducing the concept of myocardial preconditioning have opened new avenues to understand the complex interplay between the various lipids and the risk of cardiovascular diseases. The optimal dietary fat profile includes a low intake of both saturated and omega-6 fatty acids and a moderate intake of omega-3 fatty acids. This profile is quite similar to the Mediterranean diet. On the other hand, recent studies have found a positive association between omega-6 and breast cancer risk. In contrast, omega-3 fatty acids do have anticancer properties. It has been shown that certain (Mediterranean) polyphenols significantly increase the endogenous synthesis of omega-3 whereas high intake of omega-6 decreases it. Finally, epidemiological studies suggest that a high omega-3 to omega-6 ratio may be the optimal strategy to decrease breast cancer risk. Thus, the present high intake of omega-6 in many countries is definitely not the optimal strategy to prevent cardiovascular disease and cancers. A moderate intake of plant and marine omega-3 in the context of the traditional Mediterranean diet (low in saturated and omega-6 fatty acids but high in plant monounsaturated fat) appears to be the best approach to reduce the risk of both cardiovascular diseases and cancers, in particular breast cancer.

PMID:
22613931
[PubMed - in process]
PMCID:
PMC3394202

Free PMC Article here http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3394202/

[R.B.]

Lani kindly posted this comment / paper summary which identifies COX1 and COX2 related genes as possible targets in HER2 related cancer. Interestingly COX 1 and COX 2 are key enzymes in the Omega 6 pathways in that they convert Omega 6 fats to active derivatives. NSAIDS intervene in these pathways in different ways and prevent formation of these products. . . In very simplistic terms reducing the amount of plant based Omega 6 in the diet to under 4% of calories and increasing Omega 3 which competes for space in the cell membrane will also reduce the amount of Omega 6 COX products made by the body.

The full free version of the paper referred to in the above post includes the following comment. "In animal studies, omega-6 PUFAs have a strong mammary tumor-enhancing effect [21,22]. In order to exert their carcinogenic effects, they must first undergo an oxidative metabolization, mainly through the lipoxygenase and cyclooxygenase pathways [23,24]. " COX is the short form for cyclooxygenase, the same COX 1 and COX 2 family as Lani is talking about above. COX enzymes prefer Omega 6s. So give COX enzymes a ready supply of Omega 6 and the right conditions and they will get busy. Incidentally LOX enzymes prefer Omega 3s, but will also use Omega 6s particularly when Omega 3s are in short supply . . .



http://her2support.org/vbulletin/showthread.php?t=56001


"I have railed for years on the need to divide her2+ bc into subtypes in order to discover the best targets/ combination treatment for each subtype

I have also railed for years to encourage bone marrow sampling to discover if the disseminated tumor cells there could tell which patients needed systemic therapy as well as local treatment (surgery and/or radiation therapy) and to discover whether the initial therapy was successful or whether additional therapy against other targets is needed

I have not hidden that I believe in the cancer stem cell "theory" of breast cancer

Here scientists have found (in mice, but results corroborated when evaluating a cohort of human breast cancer patients accumulated by vantViver) that an 8 gene signature derived from cancer stem cells of her2+ breast cancer (in mice)
can stratify her2+ breast cancer patients prognoses and serve as targets for therapy.

Two of the genes can be affected by over the counter NSAIDs (cox1 and cox2) and an already FDA approved drug in use for many years -an iron chelator used for iron poisoning and inherited iron deposition diseases is available as well.

I am hopeful studies in this direction will help stratify her2+ breast cancer into groups (even though every patients tumor is unique) which can be treated similarly ie similar targets, turning her2+ breast cancer into an annoying chronic disease or even curing it.

I hope this approach can be used against other forms of cancer as well

Proteomics. 2012 Sep 19. doi: 10.1002/pmic.201200103. [Epub ahead of print]
Proteomic profiling of cancer stem cells derived from primary tumors of HER2/Neu transgenic mice.
Kanojia D, Zhou W, Zhang J, Jie C, Lo PK, Wang Q, Chen H.
Source
Department of Biological Science, Centre for colon cancer, University of South Carolina, Columbia, SC 29208, USA.
Abstract
HER2 overexpression leads to mammary tumorigenesis and its elevated levels leads to increase in cancer stem cells (CSCs), invasion and metastasis. CSCs are resistant to radiation/chemotherapeutic drugs and are believed to be responsible for recurrence/relapse of cancer. CSCs are isolated using flow cytometry based sorting, although reliable, this technology hinders the convenient identification of molecular targets of CSCs. Therefore to understand the molecular players of increased CSC through HER2 overexpression and to develop meaningful targets for combination therapy, we isolated and characterized breast CSCs through convenient tumorsphere culture. We identified the altered protein expression in CSC as compared to non-CSC using LC-MS/MS and confirmed those results using qRT-PCR and western blotting. Ferittin Heavy Chain 1 was identified as a candidate gene which is involved in iron metabolism and iron depletion significantly decreased the self-renewal of CSCs. We further performed in silico analysis of altered genes in tumorsphere and identified a set of genes (PTMA, S100A4, S100A6, TNXRD1, COX-1, COX-2, KRT14 and FTH1), representing possible molecular targets, which in combination showed a promise to be used as prognostic markers for breast cancer.
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
PMID: 22997041"

[KDR]

Could this be summarized, i.e., what is a good ratio of O3 to O6 by example. Thank you.
Karen

[R.B.]

(In Progress - I will revisit this over the next few days and amend it - if I put it in a word folder I will be less motivated to get it finished (-



Hi KDR

I simply cannot believe it is over a year that I have been meaning to respond to your question !!!

The reason I did not respond straight away is that the answer is not simple, biology it seems rarely is.

I will try and summarize a few thoughts that may help identify key issues.

1. Omega 3 and 6 fats are families made from a basic Omega 3 and a basic Omega 6 building block, which cannot be made by mammals but which can be made by plants. The fact that these fat must be got in the diet, and are hugely influential in body function is of immeasurable functional significance. Each member of each family has different functions. In general terms Omega 6 products promote inflammation, blood vessel formation, cell migrations and related activities. Omega 3s tend to be counter inflammatory, reduce blood vessel formation etc. It is complex, and these are generalizations.

2. With the help of our cells, and or the bacteria in our guts, we can make almost all other fats. Bacteria make short fats. We can make a 16 carbon saturated fat palmitic acid, which can be elongated and double bonds added to make other fats including oleic acid; the fat found in olive oil. We also have mechanisms to break fats down to shorter units

3. The plant based Omega 6 is an 18 carbon chain, with 2 double bonds.

4. The plant based Omega 3 is an 18 carbon chain with 3 double bonds.

5 The plant based Omega 3 and 6 can be elongated and double bonds added to make longer fats. DHA and EPA are longer fats of the Omega 3 family. GLA has one more double bond, and arachidonic acid is a longer fat and has more double bonds; both are from the Omega 6 family.

6. Plant based Omega 3 and 6 is very common because it is found in all 'green' plant based material, but in relatively small amounts; parts per thousand. Plant based Omega 6 is only found in quantity in plant reproductive material, seeds nuts and grains. Plant based Omega 3 is occasionally found in quantity in seeds, nuts and grains but not very often.

7. So in a wild diet we would have got slightly more plant based Omega 3 than 6 for most of the year with a boost of mainly Omega 6 in the fruiting and seeding seasons. In the wild seeds and nuts were not that plentiful, and very much weather dependent. On a year round basis we are maybe looking at an average intake of about 2% of calories, maybe a bit more or less depending on the particular diet. Modern intake of the Omega 6 plant based fat is maybe 10% and up to 25%, so a vast increase over our pre agricultural ancestors. The main source by far is vegetable oils.

8 Our cells can convert the plant based fats using two enzymes to the longer fats in the family. Conversion becomes increasingly difficult as the fats get longer. Conversion is much more efficient at lower intake levels. Imbalances heavily disrupt conversion. Some people are genetically less efficient converters, maybe up to 40% less efficient, and more often include celtic types/ maybe descendents of people who dwelled near the oceans ( the ocean dweller bit is postulation).

9. Importantly and probably because of estrogen ( and progesterone?) women convert plant based fats to long chain fats eg plant based Omega 3 to DHA about 10 times more efficiently than men do. This is arguably of huge importance and helps define some of the gender differences. It also magnifies the effect of Omega 3 and 6 dietary imbalances and deficiencies. These fats are fundamental to the reproductive processes and pathways including the hormonal pathways. Breast tissue concentrates these fats in breast milk to supply them to the infant, so they have a particularly important role in the breast in general terms.

10. A small amount of long chain fat Omega 3 and 6 can be got through the diet taking advantage of conversion by other animals. Long chain Omega 3s are primarily found in marine animals. Wild animals (pastured herbivores, fowl, etc) have higher Omega 3 levels than grain fed animals.

11. Omega 3 and 6 are rival siblings. The amount of each in the cell membranes reflects the amount in the diet. Both compete for the elongation conversion enzymes. An excess of either will create imbalances. Too much Omega 6 will magnify the effects of Omega 6, and too much Omega 3 will magnify the Omega 3 pathways at the expense of Omega 6 activity, which is why a balance is so important. It is not just the amount of Omega 3 and 6 that go out of balance but all their downstream products and effects. including inflammation, blood vessel formation, cell migration, cell structure, cell function at a host of levels etc etc.

In summary

You are aiming to balance plant based Omega 3 and 6, and get adequate long chain Omega 3s. Long chain Omega 6s are more readily available than 3s due to our modern food chain and higher plant based Omega 6 intake / body fat stores. Most but by no means not all will have adequate long chain Omega 6; for example breast feeding women are often lowish in long chain Omega 6.

As a vast generalization most vegetable oils are best avoided partially because they contain lots of Omega 6 and partly because of what processing does to them. Some have other useful properties - eg cold pressed olive is rich in antioxidants, so it is best to look them up, http://nutritiondata.self.com/ but the majority are high or very high in Omega 6, and often contain almost no Omega 3. They are starting to try and breed plants which are higher in Omega 9 or have a better 3:6 balance, but there is still the issue of processing and onward treatment in food preparation.

Most of us are short of Omega 3s so adding an Omega 3 rich source eg a little flax seed or oil - there are others - is logically a good idea.

Avoid industrial chicken which is very high in Omega 6, because they are fed almost exclusively on grains.

Many processed foods products will contain vegetable oils so are best avoided, and particularly so crisps cooked in vegetable oils; it is not just the vegetable oils per se but what treatment temperature cooking etc does to them which is arguably such an issue.

Try and get some oily marine foods / marine foods generally, and or supplement with fish oil in modest amounts. Omega 3 in fish muscle are in a different form to those in fish fats, and are metabolized differently, so marine foods provide a wider range of Omega 3 related products than fish oil, and marine foods contain lots of other useful nutrients.

Nuts are rich in minerals and other nutrients, and so I am ambivalent about them in larger quantities, and for them in smaller quantities.

Most have a historic excess of Omega 6, which the body likes to store in the body fats. Our omega 6 in body fat has increased from maybe 4% in the 1950s to up to 25% today. It can take a significant amount to time to re-balance the body fat content - years - but interestingly breast tissue changes much faster. So it is going to take a while to re-balance the body tissues.

There is some evidence that the benefits of fish oil e.g. EPA and DHA tail off around 2.5 to 3 grams (EPA plus DHA combined total) a day.

The optimal amount of plant based Omega 3 e.g. flax oil is less clear - the issues are very complex. Johana Budwig interestingly reported good results with flax oil and cottage cheese in the diet, and was robustly supported by her patients. The explanations were based in the knowledge of the day and lack clarity, but make some sense in a very fuzzy intuitive way - these fats are central to plant function; and plants derive their energy from light; Omega 3 it is suggested may have an important role in photosynthesis; Omega 6 is central to plant reproduction - so they may also have important roles in humans and have proved to do so. We do not really know as much about the metabolism of plant based Omega 3 as we should. Interestingly her suggestions also include sun (vitamin D), 'fermented foods' good for gut function / source of short chain fats, no refined foods etc - so lots that is familiar. Unfortunately there does not appear to be any references to her clinical notes etc, which information would provide a much clearer view of what her protocol was and how effective it was, so I post information about her with a cautionary caveat, and particularly as to some of the claims that are made by sites promoting 'her' protocol, which sites also often promote some pretty quirky treatments which good or bad should not be confused with my simple premis that Omega 3s and in this case plant based Omega 3 has highly influential roles in cellular metabolism.

I do think and the trial based evidence on this site supports a general premis that excess Omega 6 and lack of Omega 3 may increase the risk of cancer, and that the Omega 3 and 6 families and their downstream products have their own individual roles, some of which have received more research attention than others.

Getting adequate plant based and long chain Omega 3s and reducing excessive intake of plant based Omega 6s, as part of a healthy diet may well reduce the risk of cancer. Work by Budwig, anecdotal evidence etc raises the question if taking larger amounts of plant based Omega 3 and longer chain Omega 3s than would be found in the natural diet as a initial strategy to try and rebalance body fats, and cellular function at many levels, is a useful strategy in the prevention / slowing / reduction of recurrence etc.

The importance of wider diet, adequate vitamin D and related fat soluble vitamins, iodine, and a host of other nutrients, cannot be stressed enough. The Omega 3;6 balance may prove to be a highly significant factor in the risk of cancer, but it is only one of many.

[R.B.]

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


LA is the plant based Omega 6 linoleic acid

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

PGE2 is a downstream product of Omega 6

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


Also see following post



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

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

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

© 2013 Japanese Cancer Association.

[R.B.]

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

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

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


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

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

The whole article is available on the link above

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

[Andrea Barnett Budin]

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

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

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

Andi

[R.B.]

Hi Andi

I love your positive outlook and smiley posts.

Both fish oils and krill oils are high in Omega 3. The amount of long chain Omega 3 also called EPA and DHA per 1gram (1000mg) of oil depends on the marine source of the oil, as well as the extraction and refining process used in the particular oil product, and varies hugely; so check the label when considering which brand to purchase.

The primary difference between fish and krill oil are the structures to which Omega 3 is attached, which affects the way and location in which it is mainly used in the body. To understand this you need to know a little about how fats are organised in different tissues.

Fat is most commonly attached to another substance most commonly in either pairs or sets of three; image toast in toast racks, the toast is the fat and the rack the binding substance. In cell membranes fats are generally found in pairs, two slices of 'toast' to a 'rack' (phospholipids). Fat in fat cells is always found in threes, three slices of toast to a rack (triglycerides).

The toast racks used in cell membranes and fat storage are different designs; and to make things more complicated whilst there is only one design of rack for fat storage there are several models used in cell membranes.

Fish oil are extracted from fish, and crustaceans like Krill, by a combination of pressure and solvents. The ratio of storage fat to membrane fat in the krill or fish body will determine the ratio of phospholipids to triglycerides.

Krill do not contain much body storage fat compared to oily fish, and so krill oil contains mainly membrane fats (phospholipids). Oily fish contain lots of storage fat so fish oil contains mainly triglycerides.

Cell membrane fat is less resistant to oxidation than storage fat, so when they process oily fish they generally remove the cell membrane fat from fish oil products because it is easier to produce a stable product with a good shelf life; so even though membranes fats were present in the fish they do not make it into fish oil.

Krill are processed into other food products, such as protein etc, which involves removing the oil, so they started at looking at ways to process and conserve the oil rich in cell membrane fats as an Omega 3 rich product, and found ways to do so. They were helped because the krill contained a powerful antioxidant that helped protect these membrane fats from oxidation. The result is Krill oil, which contains omega 3 and other fats, and is mainly in the form of fats found in the cell membrane rather than storage fats.

Once they are in the body, the fats in cell membrane form can be directly used in the structure of cell membranes. In contrast storage fats would first have to be broken down and remade into cell membrane fats. Omega 3 rich membrane based fats are important to the function of many tissues, (and particularly the brain) which is why Krill oil may have some advantages over fish oil in so far as cell membrane function goes.

Omega 3 rich storage fats have important roles in the body too. The body will also use the Omega 3 fish oil storage based fats, but in different ways, and some of the storage fats will be converted to membrane fats for use in the cell membranes.

There are still more layers to this; not all the oil you eat ends up in the same form once it has been digested. When storage fats and cell membrane fats are digested, they are stripped down to the toast rack structure with just one fat attached, and either one or two free fats. A proportion of what is digested then gets put back together again in the original structure, but a proportion is also used as building blocks for other products including storage fats. So after digestion only a proportion of the Omega 3 rich cell membrane fats from the Krill oil eaten will be available directly for use in cell membranes in the body, while in comparison storage fats that remain in the same form after digestion would need to be reprocessed and adapted before they could be used in the cell membranes.

So krill oil is a very useful supplement along with fish oil; both provide much needed Omega 3s albeit in different forms. But they are generally both ‘solvent’ extracted so may not contain the full spectrum of fats and structures that would be found in whole food. It is also important to be cautious about miracle claims for one or other, and the advantages for krill over fish oil; they are going to do slightly different things, benefits of one over the other are not as clear cut as reports would suggest, as results depend on tissues examined, dosages, form of Omega 3s, exactly what you are looking at etc. Krill oil tends to be more expensive too, but does usefully provide the fats largely in Omega 3 rich membrane form, which you will not get in fish oil (because of the way it is processed) but will get to varying extents in fish and other marine products.

So if you are going to supplement some of both would seem a reasonable strategy, and as previously identified do not loose sight of the importance of the humble plant based Omega 3 rich foods such as flax.

Natural foods have to be the best source. Some oily fish and interestingly offal etc are good sources of membranes fats; but because we feed our livestock on grain they do not have the Omega 3 levels they should, as well as potentially containing too much Omega 6; and in reality we do not tend to eat offal any more. Brain was a traditional source of membrane Omega 3s but that is off the menu on a precautionary basis due to potential uncertainties as to the origin of neurological conditions in cattle that occurred some while ago (certainly in the UK).

The best options are the marine foods themselves, which raises the issue of the sustainability of supply. . .

I hope that helps. Thank you for your kind words they are appreciated.

P.S. Look for the phospholipid and Omega 3 content on Krill oil labels because it varies a lot between products - hopefully with both a decent phospholipid and Omega 3 content a good proportion of the phospholipids will be high in Omega 3.

P.P.S. For those unable to afford Krill a good quality fish oil is still an excellent way to get Omega 3s - but as ever fish and marine products contain a much wider range of important nutrients; but not everybody has access to or can afford fish and fish oil is a much better option than a significant Omega 3 / 6 imbalance.

P.P.P.S The amount of Omega 3 that people may want to take at the outset of a dietary change to rebalance these fats in the body might sensibly be higher, but taking large quantities for years is probably not a good idea for a wide range of reasons.

P.P.P.P.S Very very very importantly it is in significant part ultimately about balance between Omega 3 and 6. It is equally important to reduce the Omega 6 intake; the amount of omega 3 needed rises with rising Omega 6. Ultimately it is simply not possible to compensate for an excess of Omega 6 even by taking excessive amounts of Omega 3.

[Andrea Barnett Budin]

Thanks RB. So thorough and complex. Will process. Appreciate you sharing. A little Omega 3 and a little Krill is what I think I'm seeing. So interesting. So essential to everyone's life!!!! My nephew takes this and he's healthy and in his 40s. My husband has consented to take it. I am working on my dghtrs.

Plus co-enzyme Q10, plus Carnitine, plus Alpha Lipoic Acid, plus D, plus B's (especially 12 for energy!!!!!), calcium, C. Basic to wellness...

So kind of you to take the time to respond, RB...

[AlaskaAngel]

RB, thank you for taking the time to give us a better description and mental picture of how it all works. I understand it a bit better for that.

A.A.

[Becky]

Never told you guys this but I think I have told you I am a sales rep. However, in more detail, I am a sales rep for a major chemical company. I sell for many divisions of the company but only to our distributors who then sell to small and medium sized end users who can't meet our minimum orders (hence they buy from our distributors). Last year our Human Nutrition group decided to put their products into distribution and I have the one National distributor that does this. Hence - training. I just got back from a big training seminar (2 days) on Omega 3 (we are a huge producer). So, I asked the question on how to sell our products more effectively over Krill. The big answer is don't. They are different products and you do need to take both. As RB stated, there is virtually no way to get the phospholipids that Krill provides. Phospholipids are also important. Also, if you are not sure of the Fish Oil source you are buying from, buy the higher strength softgels (usually named "Triple Strength" etc). These softgels use the highest purity fish oil. They are highly refined (with membrane separation not chemical separation) and are heavy metal free. Do not buy salmon fish oil as they use salmon (duh) which is a large fatty fish and could have heavy metal contaminates. Most fish oil (if not all) use anchovy or sardines fished off the Peruvian coast. These are small fish hence far, far less natural heavy metal contamination.

On the flip side, I also sell sodium nitrate for hot dogs

[karen z]

RB
Can you recommend name brands/dosages for those folks who want to get seriously started on taking both Krill and Omega 3?

[NEDenise]

Becky,
I've found that if I spread the fish oil on the hotdogs...I get a nice anti-oxidant buzz going!
Denise
PS - India relish is also good!

[Andrea Barnett Budin]

Denise -- you spread the Fish Oil on hot dogs??? Huh?

Sounds weird but if you say so, I'm thinking...

How about on the zucchini pancakes I have for dinner?

You actually cut open the capsule? I am lost here. Please explain ...

[NEDenise]

Joking! Hello! Remember who you're talking to my friend!

Wouldn't crack open that capsule on a bet!
Denise

[Andrea Barnett Budin]

I think you had me with THE ANTI-OXIDANT BUZZ GOING...

Thanks for clearing that up. (I'm sooo literal... Silly...)

Andi

[NEDenise]

You crack me up!

How about dishin' up the recipe for those zucchini pancakes though. I LOVE zucchini anything!
Denise
I'm not planning to put fish oil on them!