About our association with WAPF, if it helps some of yor enormous work
of running this site that would be a good thing. I whole heartily
agree with WAPF goals of less refined foods/more nutrient dense foods.
For years, however, I've had a big problem with one thing in their position
and that is their ferocious stand > against canola oil, flaunting ALL
available science and trial data. For most people, avoiding canola
type [cheap, high omega-3] oil is harmful and that stance, if widely
disseminated, would no doubt kill thousands [life without alpha-linolenic
acid, quite possibly THE most antiarrhythmic of the fatty acids]. I
happily live without statins but without canola or similar sources of n-3 I
would not dream of.
In objectable category: "These new-fangled fats can cause cancer, heart
disease, immune system dysfunction, sterility, learning disabilities, growth
problems and osteoporosis" Included is canola. http://www.westonaprice.org/know_your_fats/know_your_fats.html
general] and about canola specifically http://www.westonaprice.org/know_your_fats/conola.html
This stuff is so out-dated and dangerous, it makes my > skin crawl -and
even 44% erucic 22:1 -presumably factory generated-rapeseed in the Indo/meditarranean
trial turned out to be beneficial in CHD. This is the year 2003 and
properly processed canola is a vital food. Mary Enig, for whom I have
enormous like and respect, would not disagree with the Lyon trial data for
example but Sally Fallon dismisses canola out of hand as "highly
processed". The posted canola position is wrong, dead wrong, and
based on philosophy, not science. This frightens me as it violates
scientific and trial data, and the "first do no harm principle".
Food processing is part of life, like gravity, but it should of course be
done properly. This includes supplementation in many nutrients,
including the fatty acids, if this is shown beneficial. I personally
like thincs the way you created it -putting science before philosophy.
[do I sound upset? I am -and p.s. not rapeseed's erucic but low
selenium is causally linked to Keshan's disease -cardiomyopathy-, just check
I am not as sanguine about canola as you, Eddie. I understand that the
component is actually removed in the processing as it causes problems when
cooking with the stuff. I, too, wouldn't (couldn't?) want to live without
n-3 fatty acids, but there are far better sources, at least in this country.
Hello Barry. The funny thing is that it would be illegal to
process away a substantial amount of n-3 in any oil by careless processing
or by hydrogenation [without mention] and the actual Canadian labels
indicate that there must be very low trans --and the two store-shelf U.S.
samples analyzed for USDA show below 0.2% trans in canola oil, most n-6
based. I could not find a differential analysis by O'Keefe S mentioned in http://www.westonaprice.org/know_your_fats/conola.html
but if anyone has access to its reference 24, that would be appreciated: S
O'Keefe and others. Levels of Trans Geometrical Isomers of Essential Fatty
Acids in Some Unhydrogenated US Vegetable Oils. Journal of Food Lipids
1994;1:165-176. Eddie [I cc one of the top guys on ALA,
Serge Renaud, who would be a worthy addition to our http://www.thincs.org
Just a note regarding n-3 in canola. According to the Swedish National
Administration data base, Swedish canola contains:
10.7 % 18:3
P.S An upcoming thesis from Uppsala
University that might be of interest http://publications.uu.se/theses/abstract.xsql?lang=en&dbid=3424
Hello Ulf, that Swedish canola with 10.7% omega-3 seems good stuff, and
I understand all Finnish margarines and most salad oils now are
unhydrogenated canola based. One needs a username/password to access
that fisharticle in nature. To end, I add a gif to the bottom of this
e-mail illustrating the lack of CoQ10 warning in the U.S. statin ads -also
in my website http://www.health-heart.org/comments.htm
[in point 21.]
Regarding the issue of whether canola oil is needed to provide the world's
population with omega-3's or whether wild fish populations are sustainable,
what is your opinion (and that of everyone else as well) of the potential
for pasture-raised beef and other livestock to meet this need? I ask
this because in a recent order of grassfed beef that I receieved,
Grassland Beef (http://www.grasslandbeef.com/index.html )
claims that its beef has an omega-6/omega-3 ratio of 0.16 to 1 as opposed
to the statistics they give of 20 to 1 for grain-fed beef and 3 to 1 for
wild fish (not sure what type they are referring to).
These numbers seem much
higher than I expected, with a 125-fold increase over grainfed beef and an
almost 19-fold increase over "wild fish". But if
these numbers are true or at least in the right ballpark, doesn't
grass-fed beef at least give your beloved canola oil some stiff
This information was in
some literature that I can't email, but I was able to find it on the
website as well. Go to http://www.grasslandbeef.com/health.html and
click on the "Loin Analysis" in the upper right corner.
Hi Cory, That grass-beef analysis shows
2g/100g fat = 900 kcal gives about 1% of energy as ALA, that's about
ISSFAL's recommendation but that's a lot of fat! flax and canola
do it more calorie wise but it's known that meats do supply small but useful
amounts of the ALA. With low n-6 intake, that will get converted to
longer chain but as I've said before, fish oil is recommended separately.
There evidently ain't enough fish in the ocean but if one stops wasting fish,
the oil could be used directly rather than be fed to farmed salmon etc.
There's not enough "pasture" to go around either" so canola
Hi Eddie and Cory
The stupidity of us in the West is that, influenced by the cholesterolphobes,
we are taught to cut off the little fat there is on beef. We should keep the
animals out to pasture longer and eat the fat. Omega-3 at 1% of calories is
all that is needed for health, but as our healthiest energy source is fat,
not carbs, having more fat on the meat would not only increase n-3 intake,
it would obviously bring bigger health benefits, particularly as there is
also CLA included in beef fat.
Our article on conola which seems to have stirred so much controversy is
I think it is important to remember that we only need about 1.5 percent of
our total calories as omega-3 fatty acids. That's about 4 grams per
day, less than a teaspoon. One teaspoon of flax oil per day (flax oil
is about 50% omega-3's) will do it, less if you are eating whole foods such
as beef, cheese, butter, eggs, green vegetables, fish, nuts, grains and
legumes, all of which provide small amounts of omega-3 fatty acids.
Dear Sally, re your note at the end. Your stance on canola is
doing harm to people and isolates you from the balance of fatty acid
science -and, as Mary Enig knows, properly [or even normally] processed
canola is a unique and marvelous and available and cheap source of ALA and
of which ISSFAL suggests you consume 1% of your energy [mean U.S. and other
intake about 1/2 of "adequate"]
Your stance on canola is wrong, unscientific and will kill people.
The world is bigger than the one limited to those who have access to flax
seed. Grass fed beef, for example, at 3% fat of which 2% is n-3 ALA:
100 grams of make "GRASSLAND" beef has 0.06g ALA -of the ~2 grams
you need-, so you'd have to eat 7 pounds (3.3 kg/beef) of beef per day -not
very sustainable, for man, cattle and grassland alike.
Lyon and a similar trial showed about 70% less mortality and or MI on canola/rapeseed
and until you have anything more than a rat study to even suggest the
contrary [even ignoring other supportive animal, theoretical and cell
culture data], as I told you before, your stance first does harm. Your
"CONOLA" story is false and misleading and needs to be brought up
to current science and it does a disservice to the other 14 articles on your
WAPF fat page. Eddie [when science proves an idea wrong, corrections
And, P.S. nuts are a POOR source of ALA [only walnuts and butternuts are,
and there aren't enough of those trees around to supply mankind -with the
last butternut tree killed in my valley after the last flood of our mountain
Here's http://www.canolainfo.org [used
to be and probably still is a good site]
Dear all - Eddie mainly,
I find these conversations on what does, and does not contain Omega-3 fatty
acids baffling. I have never seen, so far, any evidence that I consider
robust, demonstrating the Omega-3 fatty acids have any major effect on the
rate of CHD. Where does this evidence come from? And whilst your at it, what
is the precise mechanism that links Omega-3 fatty acid consumption to
protection against CHD?
Malcolm, About alpha-linolenic acid. The evidence and links are to a
large degree in point 1. of my page http://www.health-heart.org/comments.htm*)
It's antiarrhythmic, stabilizes myocytes [heart muscle cells] and is the
balancing precussor of the series 3 prostaglandins [and provides fuel and,
in rats, makes cholesterol] and of the longer chain omega-3 DHA/EPA.
It hydrogenates [degrades/fries] away about 10x as fast as omega-6 linoleic
acid and ~100x as fast as mono. And while the WAPF conola [payola, canadian
oil con job] suggests mono is not that great, let's not forget that lard is
about 50% mono unsaturate also, with olive and canola, one of the main
sources available [but it's low in n-3].
*) the Feb. 1999 Circ. editorial by Alexander Leaf, probably THE most senior
of the fat scientists, pretty much states that it's the alpha-linolenic that
is the cardioprotective agent -and I've seen nothing much to disagree with
Eddie, Thanks for that, but I feel the need to be picky. Arrhythmia and
atherosclerosis are not, in any way, the same thing. Antiarrhtymic agents
may prevent sudden death, but they do not prevent atherosclerosis (the
underlying condition that we are all interested in?) Equally, monocytes have
no involvement in the development of atherosclerosis that I can see -
whatever role they may have in other CV disorders. Series 3 prostaglandins
are, no doubt, important. But I have seen no link between them and
The ability of a fatty acid to be hydrogenated, again, has no link with
atherosclerosis that I am remotely aware of.
The substrate for cholesterol, in man, is Acetyl Co A. You do not make
cholesterol from any fatty acid.
In short, I can still see no biologically plausible link between Omega-3
fatty acids and the prevention of the development of atherosclerosis. Fatty
acids, whatever their exact composition, are carried in the bloodstream in
lipoproteins. The great bulk of fatty acids are removed from the bloodstream
and taken straight into cells as part of a triglyceride, in which form they
are stored, primarily, to provide energy when needed. Fatty acids do not,
directly, interract with any other factor in the blood, or the artery walls.
In my understanding of atherosclerotic plaque formation you must either
damage an artery wall, or be pro-coagulant, or do both.
The cholesterol hypothesis is (I believe) completely wrong. But it did have
a reasonable, if facile, biological plausibility. I cannot, as yet, see any
coherant mechanism of action linking Omega-3 (or 6) to atherosclerosis. Am I
alone in this?
Malcolm. Picky is good and a great e-mail; that's what we're here for!
My take on heart disease is that [apart from deficiencies in magnesium and
potassium] it is at least in the nutrition department a higher than minimal
amount of homocysteine [or a lack of the nutrients that cause that] which is
causally related to athero or sclerosis. I have not seen an omega-3
link to sclerosis --except for the fact that eskimo / inuit on their Weston
A Price unprocessed high vitamin D and omega-3 diet don't die from heart
disease. It appears however that many populations have arterio/athero
sclerosis yet NOT to die from that situation. The difference to me
seems to be the alpha-linolenic n-3 as a superior anti-arrhythmic, which is
the phase that makes a heart attack fatal. Ergo, the surprising
results of the omega-3 trials, including GISSI that supplemented with fish
If it is as normal to sclerosis as it is to have wrinkles, the trick should
be to keep circulation going and to keep the myocyte gates happy so that the
heart keeps ticking despite a clot and vessel spasm/contraction.
Re cholesterol synthesis, Stephen Cunnane's experiments in young rats with
extremely fancy tagged alpha-linolenic suggest that it is especially this
omega-3 that gets rapidly used for energy [~90%] and that about 9% of it is
rapidly found in cholesterol [even in brain cholesterol -I just phoned him].
He confirmed that n-6 linoleic also winds up in cholesterol, of course also
via acetyl CoA [an acyl temporary stuck to a large vitamin built carrier
called CoA, the same stuff that carries the pre-mevalonate HMG before it's
turned into mevalonate unless you're on the Great Lipitor Experiment].
In other words, while canola may kill an aphid [as states the canola phobia
lobby], as will vitamin C, soap and lard, all four have useful functions [thus
I use all four] and then they move on after having done their good deeds.
Alpha linolenic leaves traces as the longer chain n-3 stuff, and it keeps
the muscle cell walls responsive to signals that make the heart cells
function happily. And, yes, their longer chain offspring is anti
coagulant which cannot be that bad [beats aspirin, heparin and warfarin].
**) P.S. 23 months ago I stopped my rental Renauld along a one lane windy
undulating paved French road to check out the field of canola or rapeseed
that had a funny blue color hue. Gazillions of aphids changing the
color of the entire field and that farmer, I'd guess, harvested little that
year. Our Canadian climate however is not aphid friendly and canola is
rarely sprayed against insects, yet they love the stuff.
***) P.S. #2: canola is a unique source especially for those few [I only met
one] individuals that react badly to the phyto-estrogens of flax.. and such
can be a substantial problem to those individuals
Conflict of interest: I'm a happy Canadian and have no financial interest in
canola or any other agricultural or industrial food product, unless it's om
my plate, and I've never seen payola in Canada either, but what's the link
to canola anyhow -except for the WAPF write up.
Hi Eddie and Malcolm
I worry about when we look at just one aspect of diet in disease patterns
without looking at the totality of it. This is frequently cited, as in
"The Mediterranean Diet" being high in olive oil. The truth here
is that the Mediterranean diet is high in all fats, but mostly from animal
It is true that Inuit/Eskimos have a diet that is high in fish and seal.
This may well be high in omega-3 fatty acids. But there are other peoples:
Maasai, Watusi, Sambura, Naga, Berber, et al, who also do not suffer from
heart diseases -- but don't eat any fish, canola oil or other foods that are
particularly high in omega-3 as far as I am aware. Wouldn't it be more
profitable to look at what they have in common?
In these cases, I would suggest that the reason they are disease free may be
a combination of several things ranging from lack of stress (lower levels of
fight or fright hormones circulating in their bloodstreams) to what they
DON'T eat -- the concentrated carbohydrates so common in the Western
High levels of blood glucose cause platelets to clump and make the blood
"sticky". MIs are caused by thromboses. But it isn't just sucrose
(the white granulated sugar we put in bowls on the table) that are the joker
in the pack, as far as our bodies are concerned all carbs are sugar. It
doesn't matter whether what we put in our mouths is sugar, jam, bread,
pasta, breakfast cereals or fruit. They all end up as the blood sugar,
glucose. And it is in people that eat lots of these foods that MIs are
prevalent, not is those who don't. Cause and effect?
Dear Malcolm, attached is a metaanalysis of
RCTs on the effect of n-3 on CHD and total
mortality.* It seems that this is indeed quite robust.
*Heiner C. Bucher, MD, MPH, Peter Hengstler,
MD, Christian Schindler, PhD, Gabriela Meier, MD. N-3 Polyunsaturated Fatty
Acids in Coronary Heart Disease: A Meta-analysis of Randomized Controlled
Trials Am J Med. 2002;112:298 –304.
Thanks for that paper, and I have read it.
What this paper clearly demonstrates is that omega-3 fatty acids have an
anti-arrhythmic effect. Which I have never disputed.
This effect reduces fatal MIs and sudden death (as reported). This is
exactly what you would expect, as sudden death and fatal MIs are almost
exclusively due to arrhythmias. As you will note from this paper, the rate
of non-fatal MI was increased in some of the Omega-3 arms.
In fact, if you add together the non-fatal and fatal MIs then you get a
pretty good match (I know that you can't really do this). This makes it
entirely clear that Omega-3 fatty acids have no impact on the rate of MIs,
what they do, however, is to make it less likely that you will die from an
MI. (I do not suggest that prevention of death from MI is anything
other than good, by the way.) Which means that they are not having any
effect on the underlying disease process - atherosclerotic plaque formation/atherothrombosis
- whatever you want to call it.
I never said that Omega-3 fatty acid wasn't anti-arrhythmic. I just said
there was no evidence that it had any impact on atherosclerotic plaque
formation. This paper confirms that.
Can anyone direct me toward a
"definitive" answer re dietary arachidonic acid? The literature
seems to be conflicted re whether or not dietary AA can enhance the
production of pro-inflammatory eicosanoids and cytokines or whether this is
counterbalanced by: a reduced endogenous production of AA and/or the
effects of other dietary factors such as increased
omega 3s, reduced omega 6s, and reduced dietary carbs and subsequent
controlled insulin and glucose levels. I would appreciate input.
Hello Barry, I'd generally agree with you
and let me add:
Many nutrients are essential and while there may be many pathways helping
redundancy [several ways to deal with homocysteine, get niacin or the
reverse paths between the omega-3 fatty acids] it seems smart to insure
optimal baselines of the essential nutrients [in my case I take a high
"potency" multi/mineral including Se; and extra Mg and a few grams
of C, niacin and betaine]. I would think that most successful cultures had
some source(s) of omega-3 fatty acids of which the need might have been
smaller before the onslaught of omega-6 linoleic and hydrogenation/processing.
50% of one eye component and ~7 % of brain fatty acids have to be omega-3,
and they have to be consumed somehow, even by the Berber.
What have these societies in common? Well, WA Price suggested
unprocessed foods and some source of fat with vitamin-hormone D [and some
other stuff]. 95% of us will have to deal from now on with large
amounts of industrially produced foods, and I'd agree with you that the
glucose/fructose category IS a problem [but I don't see much wrong with
fresh fruits that I see as happy primate food]. Things may well depend
on the glycemic index/-load and on the structural "intactness" of
the carbohydrate food.
The question that you pose can be rephrased as "can we have our
concentrated carbohydrates and still avoid/pospone our "modern"
degenerative diseases? Maybe with the addition of optimal amounts of
the known nutrients we can.
Be that as it may, 99% of our neighbors, if not ourselves, need substantial
omega-3, squeezed out of a mustard seed in a small mill, using nitrogen in a
fancier set up from flax, or in a large factory from canola/rapeseed using
vacuum in part of the process by Procter and Gamble.
P.S. What was originally "Mediterranean diet" was referred to as
one resembling that of Crete. That is of course misleading as Egyptian/French/Moroccan/Spanish
diets are equally "mediterranean". The M word should not be
used since all these countries and regions have proper names.
Hello Eric, I hope you're fine and enjoy the weather! I've
forwarded your question below re arachidonic acid (AA) to someone else and
will report further. What I understand about the truly fascinating COX
enzymes [and probably others that do similar things to the C20 highly
unsaturates] is that even linoleic acid competes to some degree and that EPA
is the most powerful regulator via that/those enzymes re the generation of
I've never paid much attention to AA, the most powerful of the C20 mothers,
since I figure that a healthy intake of n-3 and a limited intake of linoleic
n-6 would naturally balance the picture [and if not, there is aspirin and
Inuit/Eskimo and other animal diets are high in AA and that seems normally
not a problem. I'll keep all posted if I get more feed back.
P.S. The Ottoboni's book [figures 5-1 and 5-2] had something about insulin
influencing the fatty acids you're talking about.
I wanted to respond to Eddie's initial email
to Sally that started this chain. I apologize in advance for the fact
that this topic may be somewhat off track and maybe doesn't fit into the
mission of the THINCS group.
Eddie - Where does your figure of 3% fat content of grassfed beef come from? In
most cases, this seems to be MUCH too low. The grassfed chopmeat I buy
varies between 75% lean and 87% - never higher. So your estimate in
this scenario was off more than 4-fold at least and probably much more.
And what is the ALA content of whole milk and butter? Wouldn't these
products contribute significantly to omega-3 intake? Certainly meat is not
the only source of omega 3 in the diet, is it?
As for what is "sustainable" and what is not, that is very much
debateable. Do you have any studies showing that the raising of
livestock is, "calorie for calorie" or "nutrient for nutrient",
not "sustainable" or comparively less sustainable than the
cultivation of rapeseed?
As for canola oil being the the only way to get enough omega-3 to the
huddled masses of the world, lets say just for arguements sake that this is
true. But the fact is that omega-3 deficiency is NOT the most urgent
health issue for most of the 6 billion or so people in the
The most pressing concern, especially in the "third world" is
protein deficiency - a problem which canola oil does absolutely nothing for.
Did you ever see the sad photos of starving children with large, protuberant
bellies? That is a clear sign of protein deficiency, also
known as "Kwashiorkor". What is the short-term effect of an
omega-3 deficient diet? I doubt that it is as severe as the effects of
a protein deficient diet, which results in, growth failure, loss of muscle
<003193.htm> mass, generalized swelling (edema), decreased
immunity, all leading to Shock, coma and of course death.
Although protein deficiency is typically a disease of impoverished countries,
a US government report concluded that as many as 50% of elderly persons in
nursing homes in the U.S. suffer from protein-calorie malnutrition.
Also, not to belabor the point too much longer, but iron defiency is also a
much bigger issue in most of the world than omega-3 deficiency. I have
absolutely no idea of the iron content of canola oil, but I would assume
that it is very low, whereas most animal protein foods are
excellent sources of iron.
Lastly, many edible weeds which are commonly discarded in the idustrialized
world, such as purslane, are excellent sources of ALA. Purslane is the
richest source of ALA of any green leafy vegetable, but it intentionally
killed off by herbicides and even most organic farmers
I once called a local organic farmer and asked him if he had any purslane
for sale. He told me that he had none for sale, but plenty in his
fields, which we were free to pick and keep all we wanted at no cost.
Perhaps this is not the wisest use of the earth's natural omega-3 resources.
Eric - I can't answer the first part of your question -- I am unsure also
about the role of AA. However, as far as dietary AA is concerned I may be of
a little assistance. AA, which is omega-6, is listed as one of the three
essential fatty acids (EFA); the others being linoleic acid (LA), which is
also omega-6 and alpha-linolenic acid (ALA), which is omega-3. Although
included as an essential fatty acid, in fact AA can be synthesised in the
body from LA so
in this respect it is not an EFA.
Two of the three EFAs -- LA and ALA -- are found in plant oils; all three
are found in animal fats. If animal fats are not eaten, the body makes AA
from the LA in plant oil. If a very low-fat vegan type diet, or a diet of
only fatless meats such as turkey and skinned chicken is eaten, however,
with little or no LA, then the body will be deficient of both LA and AA.
When Stefansson and Andersen were experimenting in the Canadian north,
eating only the game they could catch, they only experienced illness when
they were forced to eat rabbits and caribou and their diet was deficient in
fats. As soon as they found seal, they were okay.
Cory, The 3% fat figure comes from the
chart the Grassland Beef company puts on the Web, i.e. the one that finds 3x
more omega-6 than omega-3 in a "wild fish" and about which I
raised doubt earlier [that's some strange fish that would not live long].
There are other sources of the 18:3n-3 ALA but meats are not a great source
[since you asked: whole milk and butter respectively 0.05% and 1.2% ALA, 50%
less than 18:2 LA and zero longer chain omega-3 according to http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl
. 700 kcal from butter would actually give you about 1.2 grams of ALA,
which is not a bad amount, but lots of tasty calories and not much room for
I've heard the purslane ALA story and I've yet to trip over this supposedly
common weed in N. America. It's not for sale in any stores I know.
0.1 or 0.2 g fat/100g plant, no breakdown in fatty acids http://www.nal.usda.gov/fnic/cgi-bin/measure.pl?11428xyz1100xyzPurslane%2c%20cooked%2c%20boiled%2c%20drained%2c%20without%20saltxyz
[picture at the very end of this e-mail] As you said, there are other health/deficiency
problems around the world but for any one who can afford a computer, the one
deficiency that is most related to MI and heart related death*) may well be
a lack of ALA [i.e. canola as the most common and cheapest source in the
Western world] and what started this subject was something you sent around
that contained the link to WAPF's Canadian canola/payola writeup.
*) and with homocysteine being one of the main underlying causes of
sclerosis, the most common precursor to MI.
POST SCRIPT: I just received a brief e-mail from Sally in which she suggests
that if you eat a lot of saturated fat, the body would tend to conserve more
omega-3. While this may or not be relevant [Americans carry around 1
or 2 kg of LA but very little ALA since it does not store well], that still
does not address WAPF's dangerous suggestion to avoid canola and making one
believe it was born as a result of Canadian payola. The fatty acid
composition is about perfect, according to ISSFAL [the International Society
for the Study of Fatty Acids and Lipids], and canola type oil addresses a
major problem at end stage heart disease, if not earlier -that's the
You may be interested in the following
response I received from an essential fatty acid researcher at a North
American university. Comments?
Dietary linoleic acid (LA, n-6) plus arachidonic acid (AA, n-6) are the two
sources of cellular AA in the human body. The typical N. Am. consumes about
15,000 mg/day of LA (and converts approx. 1-2 % or 150-300 mg/day into AA
via biosynthesis as a precursor). We eat only 100-200 mg of preformed AA/day.
One might expect that a vegan vegetarian (who never consumes any AA ) would
have about half the cellular level of AA. However, the AA levels in such
subjects are only moderately lower thereby supporting the rather more
efficient conversion of LA to AA when AA is not consumed. AA, when available,
can exhibit feedback control/inhibition of LA conversion to AA.
LA conversion to AA in also reduced somewhat by higher omega-3 intakes
although this is a relatively minor factor currently in N. Am. because of
our high omega-6: omeg a-3 (approx. 10:1) ratio. Lowering the intake of LA
and/or AA plus elevating the intake of omega-3 (LNA and particularly EPA/
DHA) can all be expected to reduce the formation of AA and AA-derived
eicosanoids (incl. pro-inflammatory leukotrienes/cytokines).
Amen. It never seems to be a lack of
arachidonic [maybe in some formula fed babies] but the problem is
controlling AA's pro-inflammatory / coagulant offspring [with aspirin being
the statin equivalent of the eicosanoid/prostaglandins].
I think too much stress has been laid on the Lyon trial.
First, from their papers it is very difficult to know what kind of diet
these people have eaten. Members of the treatment group evidently have
eaten more alfa-linolenic acid than those in the control group, but
exactly how great the difference was, or how much omega-6 or other
foodstuff they have eaten is impossible to know. Second, although there is
evidence that the omega-3 fatty acids have antiarrhytmic effects, the
optimal dose, which probably depends on the amount of omega-6 in the diet
also, is not known. If you eat much omega-6 you probably need more
omega-3 to get a good eicosanoid balance. Is it really wise to gorge in
omega-3 as long as our knowledge is so imperfect? It is not self-evident,
that just because omega-3 may prevent arrhytmia, we should eat as much of
it as possible. I have read, but don´t tell me where, that eskimoes whose
consumption of omega-3 is very high and that of omega-6 is very low have
little heart disease, but instead have bleeding disorders, some of which
may be fatal.
There is never a bleeding problem with ALA
and only with extreme amounts of fish oil. I believe there ARE upper
levels of ANY of the polyunsaturates; more is not always better [issfal:
3%en for LA upper level, 2% adequate and 1% for ALA adequate [no upper level
Uffe is right that an attempt was made in Lyon to change the basic diet,
however, while suggesting to eat more fish, by memory the part of the "canola
treatment" group analyzed consumed about 46 g/d and the non
intervention [non-canola] group 40 or 41g/d. Ditto for vegetable and
some other variables: all minor changes with by far the largest measured
change being, again by memory, a 160% increase in ALA [adipose if I recall
right]. Other dietary trials WITHOUT n-3 additions have not shown
It is probably wise to cut down on omega-6 linoleic and increase the ALA by
a factor 2, if ISSFAL and some trials are right, and if you're a typical
American or Brit [populations for which I've seen ALA consumption data]. E
[Lyon halted for mortality benefit reasons at half planned duration of study]