Re: Fish Oil and Oxidation Products

[Guest guest]

Hi Rodney,

Bill Lands has done a lot of the work and here is his page. Several years

ago he was quite good with his emails.

http://efaeducation.nih.gov/sig/eicosa1.html

What you need to understand is basically the eicosanoid balance controls how

the cell senses and reacts to external stress. Four types of fatty acids in

the cell membranes basically control the level of these short range

signalling eicosanoids which are:

Omega 3 EPA

Omega 3 DHA

Omega 6 DGLA

Omega 6 AA

Basically the first three fatty acids form the " Good " eicosanoids which

moderate stress reaction while the last is a responsible for the " Bad "

eicosanoids which elevate stress reactions. Food choices totally control the

amount and ratio in the cell membranes. While the conversion from the short

chain to the long chain forms and the relationship is somewhat complex due

to the same enzymes being responsible for elongation and double bonding, the

big problem is too much AA and too little EPA. Eating preformed EPA reduces

the conversion of the " good " Omega 6 DGLA to the " bad " Omega 6 AA and is

party why elevated levels of EPA reduce / restore proper cell stress

handling as the EPA both increases the good eicosanoids while reducing the

bad eicosanoids. Of course eating preformed AA can significantly reduce the

beneficial effects of the EPA.

The free KIM software was especially developed to allow individuals and

health professionals to run " What Ifs " and learn how various types of food

alter the tissue / cell ratios. As I said before, with eicosanoids you are

very literally what you eat.

Barry Sears diet was all about controlling the enzyme which does the DGLA to

AA conversion by controlling insulin to a tight range. I was never a fan of

his method and saw little research which supported that you could

significantly influence the DGLA to AA conversion just by controlling

insulin. Eating preformed EPA does the job of controlling excess DGLA to AA

conversion very well and is one reason I believe we are structured to eat

preformed EPA.

Anyway download KIM, watch the tutorials, input your diet and see what

tissue / membrane ratios you get. You just may learn something new about

eating for optimal health and nutrition.

Greg

[ ] Re: Fish Oil and Oxidation Products

> Hi Greg:

>

> Thank you for those links. Especially the first one which provides

> quite a few relevant references. However, from looking at the titles

> I do not see any that refer to *ratios* of w-6/w-3 fats. Nor do I

> see titles which suggest empirical benefit for any particular ratio.

> Although almost all of them do indicate either benefit from dietary

> intake of additional w-3, or potential for harm from excessive

> amounts of w-6. I will take a closer look at them on the weekend.

>

> Also, I see there is a 'Contact Us' link on one of those pages. So I

> will contact them and ask the same question.

>

> If I can persuade myself that there is a health-maximizing 'sort-of-

> magic' ratio of dietary fat intake I will pay much closer attention

> to the precise amounts of my intake of the various fats than I have

> been to date. All I have been doing up until now is reducing my

> overall fat intake as much as possible consistent with satisfying

> micronutrient RDAs, while eating perhaps 100 grams of fish daily -

> often high-fat fish, but not always - and a few nuts from time to

> time. I have also taken some trouble to avoid 14:0 which presumably

> is important. And based on the titles of the papers listed that does

> not seem to be addressed in this material either. This may be an

> issue since many sources of w-3s also contain 14:0.

>

> If I find anything of interest I will post it.

>

> Thanks again for raising this issue. I realize this may be an aspect

> of nutrition that up until now I have not paid enough attention to.

>

> Rodney.

>

>

>>

>> Hi Rodney,

>>

>>

>> I'm not an expert on eicosanoid signalling and how it is effected

> by the

>> balance in Omega 3 and 6 fatty acids in the cell membrane but those

> in the

>> NIH who created the web site are. I also suggest posting isolated

> papers can

>> be found to support almost any point of view and posting such

> papers do

>> little to support anything more than a personal point of view as,

> with

>> respect, we are not experts in the field.

>>

>> However the creators of the site are eicosanoid signalling experts,

>> have looked at all the papers, have created some of the papers

> themselves

>> and have attempted to put it all together in a such a way that

> intelligent

>> lay folks can understand what balancing eicosanoid production is

> all about

>> I suggest these to review:

>>

>> http://efaeducation.nih.gov/sig/annotated2.html

>> http://efaeducation.nih.gov/sig/relatedw.html

>> http://efaeducation.nih.gov/sig/video.html

>> http://efaeducation.nih.gov/sig/overview1.html

>> http://efaeducation.nih.gov/sig/workshop1.html

>>

>> Greg

>

>

>

>

>

>

[Guest guest]

Hi Greg:

I said that, over the weekend, I would look at the references you

provided regarding your view that it is important to maintain a

dietary intake ratio of 4:1 for omega-6 to omega-3 . Here is what I

have done:

I took a look for the abstracts of the first ten papers in the list

you referenced, provided by the source you appear to depend on for

your information, at:

http://efaeducation.nih.gov/sig/annotated2.html

I took only those papers for which authors' names are listed (so that

I could easily locate the papers at Pubmed).

This is what I found:

1. Ridker PM Manson JE Buring JE Goldhaber SZ Hennekens CH (Dated

1991): The abstract makes no mention of any kinds of fat. The study

appears to have examined just the effects of low dose aspirin on

CVD. So it apparently has no relevance to the issue under discussion.

2. delogeril M: Pubmed has no record of an author by this name.

3. Brown M: Pubmed has 319 PAGES of references under this name.

Perhaps you would like to find the reference for us? Assuming you

have reason to suppose it may be relevant.

4. Burr ML Fehily AM S Welsby E King S Sandham S (Dated 1989 -

seventeen years ago): The last part of the abstract of this paper

indicates that: " The differences between the diets of the groups

given and not given advice on fish and fibre were substantial; the

difference attributable to advice on fat has been somewhat less than

anticipated, partly because of failure to comply with advice and

partly because of spontaneous changes in the diets of control

subjects. " Note that this does not refer to differences in health.

Just differences in what the subjects consumed after being given

advice. There is no reference in the abstract to ratios of fats.

Indeed the terms " omega-6 " and " omega-3 " do not appear. Let alone

mentioning a 4:1 ratio. So this appears to have no relevance at all

to the present discussion.

5. de Deckere EA Korver O Verschuren PM Katan MB (Dated 1998): For

the purposes of the present discussion the following quote from the

abstract appears to be the most relevant: ...

" ......... The ratio of total n-3 over n-6 PUFA (linoleic acid) is

not useful for characterising foods or diets because plant and marine

n-3 PUFA show different effects, and because a decrease in n-6 PUFA

intake does not produce the same effects as an increase in n-3 PUFA

intake. "

Far from supposedly supporting what you are saying, this paper

appears to contradict it.

6. Simopoulos AP Leaf A Salem N Jr: (Dated 1999) This was not a

study, but a brief paper reporting what happened at a workshop, and

the recommendations of the participants. The suggestions for

adequate intakes (NOT for recommended optimal intakes), were 4.44g

for LA; 2.22g for ALA; and 0.65g for EPA+DHA. This represents a

ratio of omega-6 to omega-3 of 1·55:1 .............. NOT 4:1.

Furthermore, it isn't a study providing evidence of benefit - which

is what we need to see - it is, again, people expressing opinions,

without providing support.

7. The next two references: Both authored by Mohrhauer H and Holman

RT are dated 1963. I think we can safely ignore them.

8. Nair SS Leitch JW Falconer J Garg ML (Dated 1997): This paper

discusses the benefits of omega-3 fats for reducing the incidence of

dangerous cardiac arrhythmias, and speculates about possible

mechanisms by which the benefits occur. The abstract does not

mention the term " omega-6 " , let alone use the word " ratio " or the

numbers 4 or 1. And the benefit described has been quite often

discussed here over the years, so for most of us it is not news.

9. Hock CE Holahan MA Reibel DK: This paper (dated 1987 - nineteen

years ago) studied " The effect of dietary fish oil on myocardial

phospholipids and ischemic damage to the heart ........ in the

rat. " (by comparing the differences in the effects of menhaden oil

versus corn oil). In the abstract it notes: " ........ dietary

menhaden oil resulted in significant elevations in the percent of

fatty acids in the total phospholipids that were saturated, the n-3/n-

6 ratio and the double-bond index. The changes in total phospholipids

were not uniform for all phospholipid classes. Although the n-3/n-6

ratio was increased in each of the individual phospholipids

examined ..... " .

In other words, it observed that the ratios of the fats **in

myocardial phospholipids** were different when feeding menhaden oil

than when feeding corn oil. The abstract doesn't mention anything

about ratios of DIETARY fat INTAKE, which is what our discussion is

about. So, of course, it has no information about whether one ratio

of fat intake was better than another.

10. Kang JX Leaf A (Dated 1994): This study investigated

the " Effects of long-chain polyunsaturated fatty acids on the

contraction of neonatal rat cardiac myocytes. " It found that: " The

omega 3 PUFA from fish oils, EPA; C20:5 (n-3) and DHA; C22:6 (n-

3), ..... profoundly reduced the contraction rate of the cells

without a significant change in the amplitude of the contractions. "

Also found: " Two other PUFAs, linoleic acid C18:2 (n-6) and

linolenic acid C18:3 (n-3) also exhibited similar but less potent

effects compared with EPA or ETYA. In contrast, neither the

monounsaturated fatty acid oleic acid [C18:1 (n-9)] nor the saturated

fatty acids stearic acid (C18:0), myristic acid (C14:0), and lauric

acid (C12:0) affected the contraction rate. " So it suggests a

possible link in the chain of causation by which omega-3 helps

prevent arrhythmia. This is interesting, but does not appear to have

relevance to beneficial ratios of dietary intake of omega-6 to omega-

3.

----------------------------------

I suppose I could go through another ten of your references, or 20,

or 50. But I really do not feel inclined to do so. If you are

persuaded to express as much conviction as you do about the 4:1 ratio

based on information like that above - which, remember, are the

sources you suggested we look at - then good luck to you. But count

me out.

If you wish to provide justification for what you have been posting

here lately, namely that a 4:1 ratio of omega-6 to omega-3 is vitally

important for cardiovascular health, I invite you to do the

following: Find three or four studies where the ratio of omega-6 to

omega-3 **intake** was varied (in humans, monkeys or other mammals

with a disease suceptibility similar to that of humans) and in which

a statistically significant U-curve relationship was found where the

low point (maximum health benefit) in the curve was somewhere between

a 3:1 and 5:1 ratio. Then post accessible references (preferably

Pubmed) for the papers.

But if you cannot find studies like those described in the above

paragraph then you might as well give up trying to convince me.

Because, imo, that is the kind of information you would need to be in

possession of, not only to convince me, but also **yourself**, about

what you are saying.

Rodney.

--- In , " Rodney " <perspect1111@...>

wrote:

>

> Hi Greg:

>

> Thank you for those links. Especially the first one which provides

> quite a few relevant references. However, from looking at the

titles

> I do not see any that refer to *ratios* of w-6/w-3 fats. Nor do I

> see titles which suggest empirical benefit for any particular

ratio.

> Although almost all of them do indicate either benefit from dietary

> intake of additional w-3, or potential for harm from excessive

> amounts of w-6. I will take a closer look at them on the weekend.

[Guest guest]

> Find three or four studies where the

> ratio of omega-6 to

> omega-3 **intake** was varied (in humans, monkeys or

> other mammals

> with a disease suceptibility similar to that of

> humans) and in which

> a statistically significant U-curve relationship was

> found where the

> low point (maximum health benefit) in the curve was

> somewhere between

> a 3:1 and 5:1 ratio. Then post accessible

> references (preferably

> Pubmed) for the papers.

As several of the 2005, and 2006 papers I posted on

this topic stated, while this is an interesting topic

with some support, these isnt any clinical evidence to

support any specific ratio right now.

There is evidence against consuming too much Omega 6,

and for lowering total fat intake (especially specific

types of fat), and for adequate intake of Omega 3, and

" some " for preformed EPA/DHA.

Also, it is immportant to understand what an AI is as

many of the numbers posted here by Greg and the NIH

wesbite on EFAs are " suggested " ALs. These are

averages for groups based on obesrvations and not

specific individual daily needs.

Adequate Intake (AI): When sufficient scientific

evidence is not available to estimate an average

requirement (EAR) , Adequate Intakes (AIs) will be

set. These are derived though experimental or

observational data that show a mean intake which

appears to sustain a desired indicator of health, such

as calcium retention in bone. The AIs should be used

as a goal for individual intake where no RDAs exist.

Estimated Average Requirement (EAR): The intake that

meets the estimated nutrient need of 50% the

individuals in a specific group. This figure will be

used as the basis for developing the RDA and can be

used by nutrition policy-makers to evaluate the

adequacy of nutrient intakes for population groups.

Anyone of us is welcome to take this information and

turn it into the " gospel " but for now, these are all

" suggestions " based on " obeservations " of " averages "

in " groups " .

Like CR-ON, it is hardly an exact science, and we all

get to apply it how we think best from our

interpretation of the date.

Regards

Jeff